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KRIPPS HEALTHY LIFESTYLES

Volume 1, Number 1, Spring 2007

Introduction: Our Purposes


Welcome to the first edition of the Kripps Pharmacys Kripps HEALTHY LIFESTYLES
newsletter. We are pleased to offer you our view of the exciting world of nutritional supplements,
products created to help prevent, mitigate, or assist reversal of human diseases, and to provide
contributions to the foundations of optimal health throughout ones life. Our intended viewpoint is to
be as scientifically objective as we can; we rely on our own experience and experiments,
observational feedback from our many helpful and dedicated customers, and upon an enormous
library of historical and current research from genetics, biochemistry, biology, nutrition-dietetics and
related sciences.
Those familiar with the supplements industry will have noted through the years the conflicting
reports from different areas of research about product efficacy, safety, and ingredient quality control.
In our view, the discrepancies and debates are to be expected. We believe the basic sciences
applied to human heath still remain in their early stages of development. Consider, for example, the
amazing advances in chemistry and biology in the last 200 years (1), or the advances in
investigative and diagnostic imaging techniques (1) that have occurred during the last 100 years,
both of which have contributed to definitive discoveries in modern genetics and molecular biology.
Humans have a long history of medicine-making, from our earliest herbal formulations to
contemporary pharmacogenomics, yet this history is understandably replete with misunderstanding
based on partial understanding of the basic science of the formulations used. By trial and error
these early applications were cautiously or incautiously developed in attempts to avoid toxic sideeffects for the users. Today we appreciate the immense complexity of human health and illness.
Our buoyant health remains of primary importance to us so much so we are liable to willingly
believe in the usefulness of ancient or contemporary formulations, even when they have been
fraudulently designed to take advantage of us when we are most vulnerable, during illness, or if we
are ignorant of scientific developments. And prescriptions and supplements, even when offered to
us with well-meaning honesty, still can be useless or worse, notwithstanding the self-induced
placebo effect we may unconsciously encourage in their use.
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May 2007

These predicaments have persisted throughout recorded history. Deception, mistakes and
misunderstandings occur at all levels of medical treatment, and in our opinion will continue to occur
indefinitely. Lasting, fundamental knowledge is hard won, and it is in the nature of humans and their
societies that individuals will continue to take advantage of others relative ignorance.
Epidemiologically, statistics indicate morbidity and mortality from allopathic medications remain too
high; whereas, to date, the reported side effects from nutritional supplements remain minimal. The
question of the reporting-comprehensiveness about adverse effects from both conventional and
complementary biochemical interventions remains controversial. Kripps believes a combination of
conventional pharmacology plus orthomolecular nutrigenomic pharmacology will lead to the future
of medical biochemistry and will profoundly affect our choices for healthy lifestyles.
Science has been characterized as a long history of learning how to not fool ourselvesthe first
principle is that you must not fool yourself, and you are the easiest person to fool. So, you have to
be very careful about that. After youve not fooled yourself, its easy not to fool other scientists. You
just have to be honest in a conventional way after that. (2) To prevent premature conclusions, the
most rigorous protocol for a biomedical experiment design with human subjects is the prospective,
large, randomized, double-blind, placebo-controlled clinical trial (randomized controlled trial (RCT)
(3- 6). Most of the reports we will be referring to in the newsletter do not meet this standard, for a
variety of reasons. The RCT experiments are statistically intricate to design, time-consuming to
implement, costly to finance, require large teams to coordinate the subjects compliance and
outcomes, and may have difficult ethical issues to resolve. Such RCTs typically result in correlation
statistics confirming or not associations of the variable(s) studied, rather than determining specific
causal pathways at a cellular or molecular level. In contrast, also demanding but relatively more
manageable and less costly for researchers are studies aimed at biochemical modeling, in vitro
cellular or in vivo animal studies, smaller cohort prospective and retrospective human longitudinal
studies, focused biochemical intervention pilot studies, research literature meta-analyses, case
studies, and self-reported or interviewer surveys.
In our newsletter we will be referring you to a variety of reports on nutritional supplements and other
preventive or restorative techniques. We encourage consumers of all allopathic pharmacological
products and complementary naturopathic supplement products, and related therapeutic
techniques, always to remain vigilant in assessing the type of scientific report upon which the
benefits of the drug, nutraceutical or cosmeceutical product, or alternative technique, is claimed to
rely. We, and you, our customers, want to know what works, what doesn't, and why. This is a task
we do not underestimate.
Edward J. Thorpe, Ph.D.
Editor, Kripps Healthy Lifestyles
(1) http://www.greatachievements.org/?id=2962,
http://en.wikipedia.org/wiki/History_of_chemistry,
http://www.chemheritage.org/explore/explore.html
http://www.aapm.org/medical_physicist/history.asp
(2) Richard P. Feynman, Cargo Cult Science, California
Institute of Technology commencement address, 1974
(3) http://www.emedicine.com/emerg/topic731.htm
(4)
http://www.mdanderson.org/patients_public/clinical_trials/displ
ay.cfm?id=7A230A82-7513- 11D4AEBD00508BDCCE3A&method=displayFull
(5)
http://www.jr2.ox.ac.uk/Bandolier/painres/download/whatis/
ebm.pdf
(6) http://emj.bmj.com/cgi/content/full/20/1/54

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May 2007

How to navigate our newsletter most usefully a note from our Managing Editor
Kripps Pharmacy is licensed by Health Canada as both a dispensary compounding pharmacy and
also a GMP manufacturer. Therefore, the company is experienced in both detailed formulations to
alleviate medical conditions, and also in sourcing high quality basic natural and synthesized
biochemicals in their granulated, powdered and extracts forms. These are the foundation chemicals
of all life on our planet. Kripps is an expert purchaser of these biochemicals, and a retail and bulk
supplier of the resulting quality products, as listed at our website. From this professional
perspective, we present the newsletter organized by two principles. Firstly, by the macronutrients
and micronutrients that are vital for human health. Excluding sunshine and water, these are:
A.
B.
C.
D.
E.

Proteins
Lipids
Carbohydrates
Vitamins-Minerals
Phytonutrients

Our second categorization principle (see the list below) selects those therapeutic topics derived
from traditional knowledge now focused in a modern light towards the basic choices constituting
healthy living. To do this, in each category we provide website links plus specific articles and
books. Kripps respects the struggle for knowledge comprising the history of medicine and
pharmacy. We appreciate the accumulated wisdom of much of the art and science of herbalism,
in the eastern and western traditions, as well as many of the holistic, prevention-focused
protocols based in non-allopathic, complementary medicine, to the extent these modalities can
be sufficiently verified by modern empirical techniques and their statistics. Hence, too, we
admire the creative work of the researchers and review writers whose articles we select, and we
gratefully acknowledge them for their achievements and professionalism. Thus, in our
newsletters we will be acting as a meta-site for this collection, creating a kind of anthology of
some of our favorite articles, books and sites.
We hope our readers will find this eclectic selection interesting and helpful, taken as they are
from laboratory and clinical research, review articles, meta-analyses, and popular science
journalism. Some articles give historical perspective that overlaps with other topics and articles
of greater or lesser currency. In any given newsletter issue, some of the nutrients-categories will
contain items of interest, and certain of the healthy-living topics will be addressed by relevant
articles. To manage the length of any issue of the newsletter, some nutrients and some topics
will not be addressed in detail. We welcome your suggestions respecting new topics and new
links, articles or books you think will be useful to our readers.
In this issue we begin with a focus on the nutrient Vitamin D and autoimmune disease, with a
review prepared by one of our favorite websites, plus other related reports. Research items on
other topics follow in that section. Please begin your selection at the bottom of page 4; for quick
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Volume 1, Issue 1,
May 2007
3

scrolling to the articles in this lengthy first issue, watch the PDF page-counter box on your
screen as you scroll.

1. Nutrition, Featured Research & Reviews,


pages 5-12
2. Nutrition & Related Biomedical Research &
Reviews, 13-28
3. Exercise, 29-34
4. Sleep, 34-37
5. Brain-Behavior, Stress & Distress, 38-44
6. Skin care, 44-45
7. Dental Oral health, 46
8. Weight Management, 46
9. Womens Health, 47-63
10. Longevity Research Developments, 64
11. How to Talk to Your Doctor, 65-71
12. Complementary Medicine, 71-74

Kripps Healthy Lifestyles

13. Herbalism & Aromatherapy, 75


14. Regulatory Topics,75
15. Legislative Developments, 76-79
16. Historical Articles of Interest, 80-108
17. Recent Popular Books of Interest, 109
18. Bibliography & Selected Meta-Lists, 110
19. Webwatch: links for your own pursuit of
health topics, 110-115
20. Biomedical FAQ; Myths & Facts,115-127
21. Community Calendar, 128-130
22. Kripps Current Special Sales, 131-134
23. You Tube,134
24. Archives, 134
25. Glossary of terms, 135
26. Feedback, 135
27. Disclaimer, 135

Volume 1, Issue 1,

May 2007

1. Nutrition, Featured Topic, Research & Review articles


Article from Vital Choices Newsletter (http://newsletter.vitalchoice.com/e_article000728662.cfm?x=b8M6Cmn,b2JyLGgM)
January 11, 2007

Low Vitamin D Levels Linked to MS, Lupus, and Fibromyalgia


Overlooked vitamin draws increasing scientific interest and is linked to more health conditions
by Craig Weatherby
As were reported in recent months, research results continue to underscore the importance of vitamin D: a onceoverlooked nutrient, among whose very few good food sources sockeye salmon ranks number one.
Fortunately, humans are hard-wired to generate ample amounts of vitamin D when UV sunrays strike their
skin. Unsurprisingly, people in northern temperate zones display vitamin D levels that range from sub-optimal to
decidedly deficient.
These shortages, which stem from poor sun exposure, arent severe enough to produce overt symptoms like rickets,
but appear to raise the risks of bone fractures and several common cancers (see Vitamin D vs. Cancer and Vitamin
D and Cancer: A Sunny Follow-Up Story).
And a Harvard study published late last year supports the conclusions of a 2004 Harvard investigation: the first
to reveal a connection between multiple sclerosis (MS) and low body levels of vitamin D.
In the 2004 study, researchers led by Harvard's Kassandra Munger used data from two large epidemiological studies
conducted in women: the Nurses' Health Study (92,253 women) and Nurses' Health Study II (95,310 women).
This earlier analysis showed that the risk of MS was 33 percent lower among the women whose total vitamin D intake
ranked in the highest fifth (quintile), compared with those in the lowest fifth.
And the authors also found that the risk of MS was 41 percent lower among women who took 400 IU or more of
supplemental per day, compared with women who reported taking no supplemental vitamin D. No association was
found between vitamin D from food and MS incidence, probably because the average American diet contains so little.
Multiple sclerosis (MS) afflicts some 350,000 people in the United States, making it among the most common
neurological diseases in young adults. Worldwide, MS affects 2 million people.
Significantly, rates of MS are higher in northern regions of the globe and lower in sunnier tropical climes.
Heres the scoop on the new Harvard study, followed by our report on some related research in lupus and
fibromyalgia.
Studies suggest vitamin D deficiency may play a role in MS
As we've noted, MS is more common in northern latitudes. In addition, vitamin D prevents MS from developing in
animals.
And two years ago, Finnish researchers reported intriguing findings that received little
attention (Soilu-Hanninen M et al 2005):

MS patients had lower tissue levels of vitamin D from June to September, compared
Harvard-based authors
with healthy controls. (Levels were the same in both groups during winter months.)
Kassandra Munger and
MS patients vitamin D stores were higher when their symptoms were in remission.
Dr. Alberto Ascherio
Last month, another team led by Harvard's Kassandra Munger published the results of a
study that seems to strengthen the connections between vitamin D and MS (Munger KL et al 2006).
Drawing on samples stored by the US Department of Defense, they examined blood from 257 military personnel
diagnosed with MS and 518 healthy controls, and divided the samples into five categories (quintiles), based on the
amounts of vitamin D in the blood (nanomoles per liter or nmol/L).

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The Harvard-led team found that the risk of MS among non-Hispanic Caucasians decreased as blood levels of
vitamin rose. Specifically, every 50-nmol/L increase in vitamin D (25-hydroxyvitamin D) cut the risk of MS by 41
percent.
And the people whose blood showed the highest levels of vitamin D enjoyed a 62 percent lower risk of developing
MS.
Further, the inverse correlation between high vitamin D levels and risk of multiple sclerosis was particularly strong
among personnel whose blood was drawn before the age of 20, suggesting that having high levels in early adulthood
may be particularly protective.
The relationship between vitamin D and MS was weaker among blacks and Hispanics. However, the researchers
noted that the smaller numbers of these individuals and their very low levels of vitamin D (due to having more UVblocking pigment in their skin) may have made a relationship between vitamin D and MS harder to detect.
It is important to note that this study does not prove a cause-effect relationship, although the researchers could
propose no other plausible explanation.
While the authors noted some unlikely possibilities, they came to the only logical conclusion: The results of our study
suggest that high circulating levels of vitamin D are associated with a lower risk of multiple sclerosis. (Munger KL et
al 2006)
Vitamin D in lupus and fibromyalgia
In addition to MS, there may be links between low body levels of vitamin D and these two conditions.
Let's take a look at two recent investigations.
Lupus study yields positive results
Systemic lupus erythematosus, better known as lupus, is an autoimmune condition that mostly afflicts women.
Researchers at the Medical University of South Carolina in Charleston knew that evidence from animal and clinical
studies suggest that vitamin D inadequacies plays a factor in other autoimmune diseases (rheumatoid arthritis,
multiple sclerosis, and type-1 diabetes), but this possible connection had never been well-studied in lupus.
After comparing vitamin D levels in 123 people with lupus and 240 healthy controls they detected a statistically
significant in trend toward lower vitamin D levels in Caucasian lupus patients.
Specifically, 67 percent of the lupus patients were vitamin D deficient, with African Americans showing about half as
much (15.9 ng/ml) compared to Caucasians (31.3 ng/ml).
As the Carolina team said (Kamen DL et al 2005), These results suggest vitamin D deficiency as a possible risk
factor for SLE [lupus] ....
Muscle pain linked to low vitamin D levels
Three years ago, researchers at the University of Minnesota Medical School in Minneapolis set out to measure the
prevalence of vitamin D deficiency in patients with persistent, nonspecific musculoskeletal pain syndromes
refractory to standard therapies (Plotnikoff GA, Quigley JM 2003).
This is a set of symptoms many physicians might diagnose as "fibromyalgia". This term simply means "pain in
muscles and fibers", and it refers to a mysterious condition characterized by patterns of pain in the muscles and
fascia (connective tissue bands) of the back, often accompanied by fatigue. Fibromyalgia has no certain cause or
cure.
The Minnesota team recruited 150 men and women patients aged 10 to 65, from six broad ethnic groups, and tested
their vitamin D levels.
All of the African American, East African, Hispanic, and American Indian patients had deficient levels of vitamin D:

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specifically, 20 ng/mL (nanograms per milliliter) of vitamin D or less.


And 93 percent of all the muscle-pain patients had deficient blood levels of vitamin D (12.08 ng/mL on average), with
no differences detected between non-immigrants and immigrants, or between men and women. The severity of
deficiency was greatest among young women, East Africans, and African Americans.
In addition, 28 percent of all patients were severely deficient in vitamin D (8 ng/mL or less).
Unsurprisingly, the researchers concluded that people with chronic, non-specific muscle pain are very likely to lack
sufficient vitamin D. And the deficiency was not limited to people normally considered at low risk for vitamin D
deficiency, such as elderly and housebound individuals.
While they could not conclude that vitamin D deficiency was causing the muscle pain, they wisely suggested that
doctors screen all patients with this kind of muscle pain for vitamin D status, if only to prevent its associated
problems, from weak bones to increased cancer risk.
Sources
Munger KL, Levin LI, Hollis BW, Howard NS, Ascherio A. Serum 25-hydroxyvitamin D levels and risk of
multiple sclerosis. JAMA. 2006 Dec 20;296(23):2832-8.
Grant WB. Epidemiology of disease risks in relation to vitamin D insufficiency. Prog Biophys Mol Biol. 2006
Sep;92(1):65-79. Epub 2006 Feb 28. Review.
Kamen DL, Cooper GS, Bouali H, Shaftman SR, Hollis BW, Gilkeson GS. Vitamin D deficiency in systemic
lupus erythematosus. Autoimmun Rev. 2006 Feb;5(2):114-7. Epub 2005 Jun 21. Review.
Soilu-Hanninen M, Airas L, Mononen I, Heikkila A, Viljanen M, Hanninen A. 25-Hydroxyvitamin D levels in
serum at the onset of multiple sclerosis. Mult Scler. 2005 Jun;11(3):266-71.
Plotnikoff GA, Quigley JM. Prevalence of severe hypovitaminosis D in patients with persistent, nonspecific
musculoskeletal pain. Mayo Clin Proc. 2003 Dec;78(12):1463-70.
Published by Vital Choice Seafood
Copyright 2007 Vital Choice Seafood, Inc.. All rights reserved.
Information in this newsletter is not meant to substitute for the advice provided by medical professionals, nor is it intended to diagnose,
treat, cure or prevent disease. Copyright is held by Vital Choice Seafood, to which all rights are reserved. Other than personal, noncommercial use or forwarding, no material in this newsletter may be copied, distributed, or published without the express permission of
Vital Choice Seafood.

Science & Technology: Bottled Sunshine ; Why Does Flu Break Out As the Nights Draw in?
Scientists Have Seen the Light - We Don't Get Enough of It. 09-15-06
Every winter, as the nights draw in and the weather grows cold, people start to cough, sniffle and
run a fever. Patients crowd doctors' surgeries and sales of painkillers, hot lemon drinks and cough
syrup soar. Flu is back.

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But why? What is it about flu that means outbreaks only occur in the winter? Isolated cases occur
throughout the year, as reported to the Royal College of GPs' Flu Monitoring Unit in Birmingham,
proving that the virus is in constant circulation year-round.
Now a group of researchers has come up with a novel answer to the conundrum. The "seasonal
stimulus" behind the annual winter flu epidemics is a lack of vitamin D due to shorter days and lack
of sunlight.
And they have even suggested that by taking a mega-dose of the vitamin at the first sign of the
illness, its worst symptoms might be alleviated - which could prove to be a potential life-saver in the
event of the threatened avian flu pandemic.
Flu kills 3,000 to 4,000 mainly elderly people in the UK in a mild year, 20,000 to 30,000 in an
epidemic year, and could kill tens or even hundreds of thousands more in the case of a pandemic.
The traditional explanation for the winter flu epidemics is that we tend to crowd indoors in the winter
months, which aids the spread of the virus. Fifty years ago, when millions of manual labourers
earned their living working outdoors, that may have been true.
But in the modern world, where most people work in offices and factories, travel on buses and
trains, and share the same indoor spaces in summer and winter, the explanation rings hollow. Some
of the people most vulnerable to flu - elderly people living in nursing homes - are there all year
round yet are at greatest risk from the virus in winter, much like everybody else.
The seasonal nature of flu has puzzled scientists for decades. Twenty-five years ago, a British
researcher called Edgar Hope- Simpson, who won fame after discovering the cause of shingles (he
was the first person to link the painful condition to the chickenpox virus) proposed that an unknown
seasonal factor lay behind the winter surfeit of flu.
He observed that countries lying on the same latitude, which have short winter days and long
summer ones, tended to experience flu outbreaks at the same time. Epidemics that took place in
Great Britain in the 17th and 18th centuries also occurred simultaneously across the country - long
before modern transportation could explain its rapid dissemination.
Dr Hope-Simpson published his findings in a book which suggested that the missing link could be
"solar radiation". Almost a quarter of a century later, in April 2005, an outbreak of influenza swept
through Atascadero State Hospital in California, which is a maximum- security institution for the
criminally insane similar to Broadmoor in England.
John Cannell, a psychiatrist at the hospital, watched as one ward after another ended up being
quarantined at the hospital and more and more inmates fell ill with the chills, aches and fever that
are typical of influenza. Then he noticed something unusual.
"First the ward below mine was infected, and then the ward on my right, left, and across the hall but no patients on my ward became ill," he said. "My patients had intermingled with patients from
infected wards before the quarantines. The nurses on my unit cross- covered on infected wards.
How did my patients escape infection?"
While pondering this puzzle, Dr Cannell came across a paper published in Nature by a team of
researchers from the University of California at Los Angeles showing that vitamin D stimulated the
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body's production of antimicrobial peptides which have been shown to attack bacteria, fungi and
viruses, including the influenza virus, and which play a key role in keeping the lungs free from
infection.
Dr Cannell had a long interest in vitamin D and had offered his patients large daily doses in the
belief that they would ward off a range of illnesses from cancer to depression. He believes, along
with a growing body of experts on the matter, that vitamin D deficiency is widespread and
unrecognised because current recommended levels are too low for optimum health.
"A single, 20-minute, full-body exposure to summer sun will trigger the delivery of about 20,000
units of vitamin D into the circulation of most people within about 48 hours. Compare that to the 100
units you get from a glass of milk or the several hundred daily units the US government
recommends as adequate intake," he said.
Throughout evolutionary history, humans obtained tens of thousands of units every day from the
sun. Even after migrating to temperate latitudes, where skin colour rapidly lightened to allow for
more rapid vitamin D production, humans worked outdoors. Only in recent decades as we have
increasingly lived and worked indoors, travelled in cars and lathered on sunblock have levels of
vitamin D sunk chronically low, according to Dr Cannell.
All the patients that were on Dr Cannell's ward were taking 2,000 units of vitamin D every day.
Could that be why they avoided getting the flu? Although unknown to Dr Hope-Simpson, vitamin D
not only increases production of antimicrobial peptides, helping the body fight infection, it
simultaneously acts to "damp down" the immune system, which prevents it from releasing too many
inflammatory cells - the cytokine response - into infected lung tissue.
Scientists who were studying the victims of the 1918 flu pandemic, the worst in history in which an
estimated 40 million people died around the world, were shocked to find that in some cases their
lungs were destroyed. Inflammatory cytokines triggered the complete destruction of the normal
epithelial cells which lined the respiratory tract. In effect, the flu virus triggered an overwhelming
response from the body's defences that ended in death. Vitamin D has since been found to prevent
this severe inflammatory reaction, Dr Cannell said.
"I subsequently did what physicians have done for centuries. I experimented, first on myself and
then on my family, trying different doses of vitamin D to see if it had any effect on viral respiratory
infections," Dr Cannell said. "Sev-eral of my medical colleagues experimented on themselves by
taking three-day courses of pharmacological doses (2,000 units per kilogram of body-weight per
day) of vitamin D at the first sign of flu. I also asked numerous colleagues and friends who were
taking physiological doses (which was 5,000 units per day in winter and fewer or none in summer) if
they ever got colds or flu and if so how severe the infections were."
The results of this personal research convinced Dr Cannell that vitamin D did indeed confer
protection against the virus. "Physiological doses reduce the incidence of viral respiratory infections
and pharmacological doses significantly ameliorate the symptoms if taken early in the course of the
illness," he said.
However, he added that the observations were too personal and anecdotal to qualify as scientific
evidence. Instead he contacted Professor Rhein-hold Vieth, from the Mount Sinai Hospital in
Toronto, and Ed Giovannucci from the Harvard School of Public Health and suggested his
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hypothesis that vitamin D could be the "seasonal stimulus" for winter flu that was first put forward 25
years ago by Dr Hope-Simpson.
Together with five other experts, who included Professor Michael Holick of Boston University and
Professor Cedric Garland of the University of California, they drew up the paper that was published
online last week in the journal titled Epidemiology and Infection, where Dr Hope-Simpson had
published most of his work three decades previously.
"We propose that annual fluctuations in vitamin D levels explain the seasonality of influenza.
Although our paper also discusses the possibility that [high] doses of vitamin might be useful in
treating some of the one million people in the world who die of influenza every year, this is only a
theory, like all theories it must betestedin well controlled scientific experiments.
However, as vitamin D deficiency has repeatedly been associated with many of the diseases of
civilisation, it is not too early for physicians to aggressively diagnose and adequately treat it."
Professor John Oxford, who is an expert on influenza and a professor of virology at Queen Mary
College, London, welcomed this theory. "This is a reasonable hypothesis with some scientific
underpinning but it needs putting to the test. Vitamin C has been discussed in relation to flu and had
its ups and downs for years. It is interesting to put vitamin D in the frame for people to take a look
at."
"However, I wouldn't advise anyone to rely on vitamin D to protect them-selves against flu. People
should think about anti-flu vaccination first, followed by anti-viral drugs, good personal hygiene and
then vitamin D," he said.
"We could test the theory by getting some young volunteers, whacking up their vitamin D levels in
one group while holding it down in the other and then giving both groups a dose of flu. It could be
carried out quite easily and it would not be a silly thing to do."
'A20-minute exposure to summer sun will trigger 20,000 units of vitamin D into the circulation within
48 hours'
Sunlight, skin and vitamin D: the facts
About 90 per cent of the body's supply of vitamin D comes from the action of sunlight on the skin,
but grey skies and short days between October and March mean that 60 per cent of the UK
population are deficient in the vitamin.
Vitamin D is essential for healthy bones and skin and protects against rickets in children and
osteoporosis in the elderly.
The vitamin cuts the risk of pancreatic cancer by almost half (43 per cent) when taken at the
recommended daily dose of 400IU (international units), according to a study of 46,000 men and
75,000 women by researchers from the University of Wisconsin that was published this week.
A daily dose of Vitamin D could cut the risk of cancers of the breast, colon and ovary by up to half, a
40-year review of research concluded last year.
Doctors writing in the American Journal of Public Health proposed a daily dose of 1,000
international units, two and a half times the current recommended dose in the UK.
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Countries around the world have begun to modify their warnings about the dangers of sunbathing,
as a
result
of the
growing research on vitamin D. The Cancer Council Australia said for the first time last year that
some exposure to the sun was healthy.
Vitamin D lowers insulin resistance which is one of the major factors leading to heart disease.
The vitamin influences the growth of a variety of cell types and plays a role in the repair and
remodelling of lung tissue.
It acts as an immunosuppressant and may help protect against the development of type 1 diabetes.
It influences production of a hormone that regulates calcium levels, in the body which in turn help to
regulate blood pressure.
Lack of vitamin D in the months before birth may affect the developing foetus in the womb and
increase the risk of schizophrenia.
Lack of the vitamin has been linked with the development of multiples sclerosis.

Experts call for vitamin D level hike


By Stephen Daniells

The tolerable upper intake level for oral vitamin D3 should be increased fivefold, experts from the US-based Council for Responsible Nutrition (CRN) has said after
a review of the science.

1/12/2007-

The risk assessment provides companies with a guide for safe upper levels for product
formulations, and consumers with vital information on safe dosage levels from products.
This risk assessment was needed to show that newer evidence supports the conclusion that
vitamin D is much safer then previously thought, particularly because of all the emergence
research that shows benefit for vitamin D at higher levels than consumers were traditionally
taking, lead author John Hathcock told NutraIngredients.com.
Currently, the tolerable upper intake level (UL) in Europe and the US is set at 2000 International
Units (IU), equivalent to 50 micrograms per day. However, recent research, particularly from
clinical trials, suggests that this should be raised. The CRN scientists state that this could be
raised to 10,000 IU (250 micrograms per day).
New data continue to emerge regarding the health benefits of vitamin D beyond its role in
bone, wrote the reviewers in the American Journal of Clinical Nutrition.
The intakes associated with those benefits suggest a need for levels of supplementation, food
fortification, or both that are higher than current levels.
The reviewers, from the CRN, Mount Sinai Hospital in Toronto and Crieghton University in
Nebraska, pooled data from 21 clinical trials using doses ranging from 10 to 2500 micrograms.

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The risk assessment also included data from animal studies, some of which used extraordinarily
high doses of vitamin D3.
The lack of adverse effects in clinical trials that used intake up to 1250 micrograms vitamin D
per day and the lack of adverse effects at lower doses inspires a high level of confidence in the
data from the strongly designed clinical trials that used 250 micrograms vitamin D per day, said
the reviewers.
The researchers also note that for practically all the reported cases of vitamin D toxicity have
involved doses that were in excess of those studied in the clinical trials.
Newer clinical trial data are sufficient to show that vitamin D is not toxic at intakes much higher
than previously considered unsafe, said the reviewers.
This demonstrated safety profile of vitamin D should safely permit increased intakes to achieve
additional benefits of this vitamin at higher levels than previously recognised.
Vitamin D is made by the body on exposure to sunshine, or can be consumed in small amounts in
milk, fish, liver and egg yolk. However because of the low amounts present in the diet, and lack
of sunshine in northern climates, with some estimates claiming that as much as 60 per cent of
northern populations may be vitamin D deficient.
And since dietary intakes are small, the best method for getting adequate levels of the vitamin
appears to be from supplements and/or fortified foods.
Indeed, the reviewers note that normal dietary sources provide about 2.5 micrograms per day,
while this can be increased up to 10 micrograms with fortified foods. Dietary supplements would
provide higher doses.
Unfortified foods, fortified foods, and most dietary supplements, combined, do not contribute to
a total exposure anywhere near the recommended vitamin D UL of 250 micrograms per day,
they said.
We applied the same method to our risk assessment as the Food and Nutrition Board had used
years ago, and our results concluded vitamin D could be safely taken in much higher amounts,
Hathcock told this website.
We hope that the Food and Nutrition Board along with health professionals and regulators will
take our assessment and recommendation seriously, he said.
Source: American Journal of Clinical Nutrition
January 2007, Volume85, Pages 6-18
Risk assessment for vitamin D
Authors: J.N. Hathcock, A. Shao, R. Vieth, R. Heaney

===========================================================================

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Ascorbic Acid, left to right:

Specimen: Recrystallized ascorbic acid (vitamin C)


Technique: Polarized Light
Vitamin C (ascorbic acid) crystals (125x)
Crossed Polarized Light Illumination
Vitamin C (ascorbic acid) crystals (20x)
Hoffman Modulation Contrast with crossed Polarized Light, and full wave plate

2. Nutrition, & Related Biomedical Research or Review articles

CANCER ON THE RISE WORLDWIDE


While the US recently celebrated the fact that there were approximately 3,000 fewer cancer deaths
in 2004 than there were the previous year, the world as a whole is facing a staggering 50 percent
increase in cancer incidence and deaths by the year 2020. The World Cancer Report, published by
a branch of the World Health Organization, predicts this increase and points out that this massive
spike in cancer incidence and deaths will be fueled in large part by preventable factors, such as
cigarette smoking, faulty diet and sedentary lifestyles.
In the year 2000, cancer was responsible for 12 per cent of the nearly 56 million deaths worldwide
from all causes: 5.3 million men and 4.7 million women developed cancer, and a total of 6.2 million
people died from the disease. But, according to the International Agency for Research on Cancer
(IARC), huge as this total already is, global cancer rates are set to increase even further.
Tobacco remains the single most important avoidable cancer risk. In the 20th century, tobacco killed
approximately 100 million people. It is sobering to realize that this is far more than the 60 million
soldiers and civilians who died in World War II plus the 20 million who died in World War I. Tobacco
is the single greatest health scourge of humanity.
The IARC emphasizes that a healthy lifestyle and diet can help reduce the cancer burden. In
particular, increased exercise and the frequent consumption of fruit and vegetables can make a
significant difference. Early detection through screening, particularly for cancer among women,
helps improve the outcome of treatment. But the predicted sharp increase in new cases - from 10
million to 15 million by 2020 - will be due not only to the steadily aging populations in both
developed and developing countries, but also reflects current trends in smoking and the growing
adoption of unhealthy sedentary lifestyles.
The IARC believes there is a strong justification for focusing cancer prevention on two main cancercausing factors - tobacco and diet, as well as certain infections that cause many cancers in the
developing world. These factors were responsible for 43 per cent of all cancer deaths in 2000 (i.e.,
2.7 million fatalities), and 40 per cent of all new diagnoses, (i.e., 4 million new cancer cases).
IARC is also preparing a Global Strategy on Diet, Physical Activity and Health. This strategy will
contain recommendations for governments on nutrition and physical activity goals and populationbased interventions to reduce the prevalence of chronic diseases including cancer.
However, the report underestimates the difficulty of reducing global tobacco consumption in the face
of the aggressive tactics used by transnational corporations to foster tobacco use, especially in the
developing world.
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Tobacco is the most avoidable cancer risk. Fifty percent of smokers are killed by their habit. Twenty
five percent of smokers will die prematurely during middle age (35 to 69 years). The lung cancer risk
for regular smokers is between 20- and 30-fold greater than that for non-smokers. Roughly 80 per
cent of lung cancers in both men and women are attributable to cigarette smoking. More than 50
percent of cancers of the bladder and renal pelvis are caused by smoking, and smokers are also at
elevated risk for many other malignancies, including pancreatic and colon cancer.
The prevalence of the deadly smoking habit in the developing world and in Central and Eastern
Europe is particularly worrying. I remember visiting Hungary in 1991, soon after the fall of the
Communist regime. The downtown area looked like a giant billboard for American brand cigarettes.
Hungary (like the rest of Europe) has since tried to crack down on this travesty.

Pictured above:
A cigarette advertisement from
Hungary
According to a recent report by Tibor Szelagyi of the Health 21 Hungarian Foundation, "The tobacco
companies not only invaded the Hungarian market by early participation in the privatization of the
former state tobacco monopoly, but also imported their sophisticated marketing experiences.
Evasion and violation of rules in force, creation of new partnerships, establishment and use of front
groups, finding effective ways for influencing decision makers were all parts of a well orchestrated
industry effort to avoid a strict marketing regulation for tobacco products." A similar situation
occurred in other Eastern European countries.
Once considered a Western disease, more than 50 per cent of the world's cancer burden now
occurs in developing countries, matching its effect in industrialized nations. While smoking is
undoubtedly the most familiar "culturally exported" plague, it is not the only one. The highly caloric
Western diet, rich in fat, refined carbohydrates and animal protein, coupled with an increasingly
sedentary lifestyle, results in an overall energy imbalance. This energy imbalance rapidly leads to
obesity, which is in turn associated with a number of serious and often deadly diseases, including
diabetes, cardiovascular disease, hypertension and various cancers, including cancers of the colon,
breast, uterus, kidney, esophagus and gall bladder.
Obesity is spreading as an epidemic throughout the world, fueled in part by the spread of fast-food
restaurants. If we are serious about reducing cancer deaths then tackling smoking and obesity
would be the obvious place to start.

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--Ralph W. Moss, Ph.D.


http://www.cancerdecisions.com/051307.html May 13, 2007
===========================================================

Green tea polyphenols reduce autoimmune symptoms in a murine model for human
Sjogren's syndrome and protect human salivary acinar cells from TNF- -induced
cytotoxicity 1
Authors: Stephen D. Hsu a; Douglas P. Dickinson a; Haiyan Qin a; James Borke a; Kalu U. E. Ogbureke a;
Julia N. Winger a; Amy M. Camba a; Wendy B. Bollag b; Hubert J. Stppler b; Mohamed M. Sharawy a;
George S. Schuster a
Affiliations: a Department of Oral Biology and Maxillofacial Pathology, School of Dentistry, Medical
College of Georgia. Augusta, GA. USA
b
Medical College of Georgia, Institute of Molecular Medicine and Genetics. Augusta, GA. USA
DOI: 10.1080/08916930601167343
Publication Frequency: 8 issues per year
Published in:
Autoimmunity, Volume 40, Issue 2 March 2007 , pages 138 - 147
Subject: Immunology;
Formats available: HTML (English) : PDF (English)

Abstract
Sjogren's syndrome (SS) is a relatively common autoimmune disorder. A key feature of SS is lymphocytic
infiltration of the salivary and lacrimal glands, associated with the destruction of secretory functions of these
glands. Current treatment of SS targets the symptoms but is unable to reduce or prevent the damage to the
glands. We reported previously that the major green tea polyphenol (GTP) epigallocatechin-3-gallate (EGCG)
inhibits autoantigen expression in normal human keratinocytes and immortalized normal human salivary
acinar cells (Hsu et al. 2005). However, it is not known whether GTPs have this effect in vivo, if they can
reduce lymphocytic infiltration, or protect salivary acinar cells from tumor necrosis factor- (TNF- )-induced
cytotoxicity. Here, we demonstrate that in the NOD mouse, a model for human SS, oral administration of
green tea extract reduced the serum total autoantibody levels and the autoimmune-induced lymphocytic
infiltration of the submandibular glands. Further, we show that EGCG protected normal human salivary acinar
cells from TNF- -induced cytotoxicity. This protection was associated with specific phosphorylation of p38
MAPK, and inhibitors of the p38 MAPK pathway blocked the protective effect. In conclusion, GTPs may
provide a degree of protection against autoimmune-induced tissue damage in SS, mediated in part through
activation of MAPK elements.
1 *This study was supported in part by funds from NIH grant CA097258, and Department of Oral Biology and
Maxillofacial Pathology, School of Dentistry to S.H. Data in this manuscript was presented in poster form at
the annual meeting of the American Association for Dental Research, 2006.
Keywords: Green tea polyphenols; EGCG; Sjogren's syndrome; acinar cells; MAPK
view references (53)
==================================================================================

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FOR IMMEDIATE RELEASE


Orthomolecular Medicine News Service, Jan 30, 2007
VITAMINS FIGHT DISEASE: Nutrients Effective but Overlooked
(OMNS Jan 30 2007) Vitamin supplementation fights disease. Although medical research has
repeatedly shown this, such has not always been the case in the news media. Recently, however,
the popular press is picking up more of the good news: Nutritional therapy is cheaper, safer, and
often more effective than pharmaceutical drugs.
NIACIN FIGHTS CARDIOVASCULAR DISEASE
The New York Times just reported (1) that inexpensive vitamin B-3, niacin, can increase HDL as
much as 35 percent when taken in high doses, usually about 2,000 milligrams per day. It also
lowers LDL, . . . (and) triglycerides as much as 50 percent. The Times quoted Steven E. Nissen,
M.D., president of the American College of Cardiology, as saying: "Niacin is really it. Nothing else
available is that effective."
Niacin was first used to successfully lower serum cholesterol in 1955. (2) Since then, placebocontrolled studies have confirmed that niacin prevents second heart attacks, and niacin also
reduced strokes. One study showed that after 15 years, men taking niacin had an 11 percent lower
death rate. Although a warm flush is a common side effect of niacin, the vitamin is safer than any
drug.
VITAMIN D PREVENTS MULTIPLE SCLEROSIS, CANCER
The Associated Press reports (3) that An abundance of vitamin D seems to help prevent multiple
sclerosis, according to a study in more than 7 million people that offers some of the strongest
evidence yet of the power of the sunshine vitamin against MS.
Multiple sclerosis is known to be more common among those persons living in northern latitudes.
But, says Harvard School of Public Healths Dr. Alberto Ascherio, "This is the first large prospective
study where blood levels are measured . . . (providing) much stronger evidence." (4,5)
AP adds that Other studies have linked high levels of vitamin D in the blood to lower risks of a
variety of cancers.
VITAMIN E EXTENDS LIFESPAN
People who have vitamin E in their bodies live longer, according to a 19-year study of 29,092 men.
National Cancer Institute researchers concluded that Higher circulating concentrations of alphatocopherol (vitamin E) within the normal range are associated with significantly lower total and
cause-specific mortality in older male smokers. (6) Vitamin E was found to reduce death from all
causes, including cancer and cardiovascular disease.
VITAMIN C PREVENTS STOMACH CANCER
(O)ne of the largest prospective analyses of the association of plasma and dietary vitamin C levels
with gastric cancer risk ever performed on Western European populations (7) indicates that having
more vitamin C in your blood plasma reduces your risk of stomach cancer.
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VITAMIN SAFETY
And best of all, vitamins are safe. There is not even one death per year from vitamin
supplementation. (American Journal of Emergency Medicine, Vol. 22, No. 5, September 2004.
http://www.aapcc.org/Annual%20Reports/03report/Annual%20Report%202003.pdf )
Nutritional Medicine is also known as Orthomolecular Medicine
Linus Pauling defined orthomolecular medicine as "the treatment of disease by the provision of the
optimum molecular environment, especially the optimum concentrations of substances normally
present in the human body." Orthomolecular medicine uses safe, effective nutritional therapy to fight
illness. For more information: http://www.orthomolecular.org
The peer-reviewed Orthomolecular Medicine News Service is a non-profit and non-commercial
informational resource.
Editorial Review Board:
Abram Hoffer, M.D., Ph.D.
Harold D. Foster, Ph.D.
Bradford Weeks, M.D.
Carolyn Dean, M.D., N.D.
Erik Paterson, M.D.
Thomas Levy, M.D., J.D.
Steve Hickey, Ph.D.
Andrew W. Saul, Editor and contact person. email: drsaul@doctoryourself.com .
References:
1. Mason M. An old cholesterol remedy is new again. NY Times, January 23, 2007.
http://www.nytimes.com/2007/01/23/health/23consume.html?_r=1&oref=slogin
2. Altschul R, Hoffer A & Stephen JD: Influence of nicotinic acid on serum cholesterol in man. Arch
Biochem Biophys 54:558-559, 1955.
3. Sunshine vitamin protects against MS: Huge study suggests vitamin D reduces risk of
debilitating disease. The Associated Press, Dec 19, 2006.
4. Munger KL, Levin LI, Hollis BW, Howard NS, Ascherio A. Serum 25-hydroxyvitamin D levels and
risk of multiple sclerosis. JAMA. 2006 Dec 20;296(23):2832-8.
5. Munger KL, Zhang SM, O'Reilly E, Hernan MA, Olek MJ, Willett WC, Ascherio A. Vitamin D
intake and incidence of multiple sclerosis. Neurology. 2004 Jan 13;62(1):60-5.
6. Wright ME, Lawson KA, Weinstein SJ, Pietinen P, Taylor PR, Virtamo J, Albanes D. Higher
baseline serum concentrations of vitamin E are associated with lower total and cause-specific
mortality in the Alpha-Tocopherol, Beta-Carotene Cancer Prevention Study. Am J Clin Nutr. 2006
Nov;84(5):1200-7.
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7. Jenab M, Riboli E, Ferrari P, et al. Plasma and dietary vitamin C levels and risk of gastric cancer
in the European Prospective Investigation into Cancer and Nutrition (EPIC-EURGAST).
Carcinogenesis. 2006 Nov;27(11):2250-7.
Read any previous OMNS release at: http://orthomolecular.org/resources/omns/index.shtml
To subscribe at no charge: http://orthomolecular.org/subscribe.html

Does Vitamin C Really Damage Your DNA?


http://www.mercola.com/display/PrintPage.aspx?docid=25407&PrintPage=yes
Vitamin C is an essential protector of body cells.
A newly published study says the vitamin can also play a "dual role" and, at times, actually
damages cells' genetic material. Investigators say their findings could help explain why high-dose
vitamin C has so far failed as an experimental cancer therapy.
The study showed that rancid fat molecules can react with vitamin C to form products that could
potentially harm DNA, although the reaction of these products with DNA was not demonstrated in
the study.
Hence, it was suggested that vitamin C can form genotoxins (DNA-damaging agents) from lipid
hydroperoxides, the implication being that vitamin C may enhance mutagenesis and the risk of
cancer.
Previous research has shown vitamin C can promote DNA damage, but this new research
demonstrates a different avenue the vitamin can take in doing harm.
In the average person, vitamin C may regularly act as both a cell's friend and foe, making a daily
megadose of vitamin C unlikely to fight illness.
This is a test tube experiment and here is "little evidence" that these harmful effects of
vitamin C are actually going on in the body.
What's more, a significant number of studies have shown vitamin C to either have no effect or a
positive impact on DNA.
As an antioxidant, vitamin C helps neutralize cell-damaging free radicals, which are byproducts
of metabolism found throughout the body. Because of this activity, some scientists have suggested
that high doses of vitamin C might help battle cancer by both protecting healthy cells from the
assaults of cancer treatment and by fighting tumor cells.
The free radicals that vitamin C normally combats can damage DNA directly or by converting certain
fatty acids into genotoxins. The researchers found that in the test tube, vitamin C can also give rise
to genotoxins by oxidizing these fats.
According to the researchers, these findings suggest it will be particularly important to be on guard

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for cell damage among participants in trials using vitamin C as a cancer combatant.
For healthy people the message echoes tried-and-true nutrition advice: eat a balanced diet rich in
fruits and vegetables rather than popping a high-dose vitamin C pill, since the vitamin is no "magic
bullet."
The popularity among health-conscious Americans for popping vitamin C pills was boosted by Linus
Pauling, a Nobel-prize-winning chemist who advocated large doses of the vitamin. He routinely took
15 grams daily and was 93 years old when he died in 1994.
However, a nutrient expert at the institution named for Pauling, said such large doses of vitamin C
have not been proven to be beneficial in clinical studies. The Linus Pauling Institute does not
currently endorse megadoses or promote vitamin C in preventing a cold.
They also only recommend taking 200 mg of vitamin C as a healthy body can only absorb about
that much a day and the surplus is carried away with the urine. Their advice is to eat a healthy diet
rich in fruits and vegetables.
The Institute of Medicine, an arm of the National Academy of Sciences, recommends that women
need 75 milligrams of vitamin C daily and 90 milligrams for men. Smokers need an additional 35
milligrams. These are levels easily achieved by a balanced diet.
Science June 15, 2001;292:2083-2086 and Washington Post June 14, 2001

Dr. Mercola's Comment:


The media has attempted to place a negative spin on vitamin C. If you want to understand
why this is, please review the excellent article I posted last year.
There are many reasons why this study is not supportive of the fear being suggested that
vitamin C will cause cancer. They will be reviewed further down in this response.
However, recent studies show that Americans only consume about 100 milligrams of vitamin
C from foods and that about 5% of Americans consume so little vitamin C that they exhibit
signs of scurvy.
So some of us need to increase our vitamin C intake. The solution is to obviously increase
your vegetables and fruits. If for some reason you can't do that, then you should consider a
vitamin C supplement that is balanced with bioflavanoids.
However, always remember, that whole foods are nearly always a better choice than
supplements.
It is interesting to note that the Linus Pauling Institute does not promote megavitamin
therapy for healthy adults and they are in agreement with lower doses as mentioned in the
story above.

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There are conditions, such as high levels of a certain substance called Lp(a) in which
megadoses of vitamin C may be useful.
They also posted a report on this study which does a wonderful job of breaking it down and
providing you with the truth behind the headlines.

To learn more, try the Linus Pauling Institute's Vitamin C information page.

COMMENT FROM LINUS PAULING INSTITUTE:


http://lpi.oregonstate.edu/
Let us remember that this study is a test tube experiment. The study does not describe
biochemistry or biology, and its relevance to reactions occurring in cells and tissues of the
human body is unknown. Many reactions of vitamin C occur in vitro (in the test tube) that will
not and cannot occur in vivo (in the living organism).
Why?
Because the physiological environment of the cell and the body contains thousands of
substances that also react with vitamin C and rancid fats thus derailing the chemistry
observed in a test tube system.
Rancid fats don't just wait around in vivo to bump into a vitamin C molecule, but instead are
very rapidly reduced to harmless "alcohols" by a number of enzymes.
Thus, the reaction rate of rancid fats with these enzymes compared to the reaction rate of
the rancid fats with vitamin C is of crucial importance and this was not measured in the
Science study.
From what we know from the study, incubations were done for two hours, an eternity in
biochemical terms. Enzymatic reactions as those indicated above to reduce rancid fats to
harmless alcohols that do not react with vitamin C usually take a fraction of a second, not
two hours!
It is interesting to note that vitamin C effectively inhibits the formation of rancid fats in the
first place. Thus, when your blood is exposed to oxidizing conditions, vitamin C forms the
first line of antioxidant defense, and no lipid rancid fats are formed.
Rancid fats begin to form only after vitamin C has been exhausted. Thus, in these
experiments rancid fats and vitamin C did not exist simultaneously in blood, and thus never
had the opportunity to react with each other.
What's more, the Science study used a concentration of rancid fats which in biochemical
terms was "a ton." Studies have shown that, in blood, rancid fats exist in concentrations
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which are 10,000-fold lower than what was used in the Science experiment. Again, this casts
serious doubt on the relevance of these results for living organisms.
To conclude from this study that vitamin C causes cancer would be as preposterous as to
say that we have found a cure for cancer based on a simple test tube experiment.
In fact, many animal studies and cell culture experiments have demonstrated anticancer
effects of vitamin C, and the vitamin has been used therapeutically in human cancer patients
with some apparent benefit.
Abstracted from Linus Pauling Institute Release
Related Articles:
Does Vitamin C Cause or Prevent Cancer?
Linus Pauling's Unified Theory and Therapy for Heart Disease
Vitamin C Foundation Rebuttal to Science Study

==========================================================================

http://cancerres.aacrjournals.org/cgi/content/abstract/0008-5472.CAN-06-3462v1
Published online first on January 9, 2007
[Cancer Research, 10.1158/0008-5472.CAN-06-3462]

Epidemiolohy and Prevention

Combinations of Tomato and Broccoli Enhance Antitumor Activity in Dunning


R3327-H Prostate Adenocarcinomas
Kirstie Canene-Adams 1, Brian L. Lindshield , Shihua Wang , Elizabeth H. Jeffery , Steven K. Clinton ,
John W. Erdman Jr.*
1 1

Division of Nutritional Sciences and Department of Food Science and Human Nutrition, University of Illinois, Urbana,
Illinois and 2Division of Hematology and Oncology, Department of Internal Medicine, James Cancer Hospital and Solove
Research Institute, The Ohio State University, Columbus, Ohio

To whom correspondence should be addressed. E-mail: jwerdman@uiuc.edu

Abstract
The consumption of diets containing 5 to 10 servings of fruits and vegetables daily is the foundation
of public health recommendations for cancer prevention, yet this concept has not been tested in
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experimental models of prostate cancer. We evaluated combinations of tomato and broccoli in the
Dunning R3327-H prostate adenocarcinoma model. Male Copenhagen rats (n = 206) were fed diets
containing 10% tomato, 10% broccoli, 5% tomato plus 5% broccoli (5:5 combination), 10% tomato
plus 10% broccoli (10:10 combination) powders, or lycopene (23 or 224 nmol/g diet) for 22 weeks
starting 1 month prior to receiving s.c. tumor implants. We compared the effects of diet to surgical
castration (2 weeks before termination) or finasteride (5 mg/kg body weight orally, 6 d/wk).
Castration reduced prostate weights, tumor areas, and tumor weight (62%, P < 0.001), whereas
finasteride reduced prostate weights (P < 0.0001), but had no effect on tumor area or weight.
Lycopene at 23 or 224 nmol/g of the diet insignificantly reduced tumor weights by 7% or 18%,
respectively, whereas tomato reduced tumor weight by 34% (P < 0.05). Broccoli decreased tumor
weights by 42% (P < 0.01) whereas the 10:10 combination caused a 52% decrease (P < 0.001).
Tumor growth reductions were associated with reduced proliferation and increased apoptosis, as
quantified by proliferating cell nuclear antigen immunohistochemistry and the ApopTag assay. The
combination of tomato and broccoli was more effective at slowing tumor growth than either tomato
or broccoli alone and supports the public health recommendations to increase the intake of a variety
of plant components. [Cancer Res 2007;67(2):836-43]
Key Words: Tomato, Lycopene, Broccoli, Prostate Cancer, finasteride
Source: Natural Environment Research Council
Date: May 11, 2007

Could Carrots Be The Secret To A Long Life And Sex Appeal?


Science Daily Researchers at the Universities of Glasgow and Exeter have found that eating certain
plant substances can slow down the rate of aging - and that females prefer mates that will be long-lived.

Colour variation in sticklebacks -- the lower fish had carotenoid supplements in its diet. (Credit: Image courtesy of
Natural Environment Research Council)

Carotenoids are naturally-occurring yellow and red pigments found in plants. Animals that eat those plants can then use
the pigments to make themselves colourful in order to attract mates. But carotenoids are also antioxidants, which
improve an animals ability to combat oxidative stress and strengthen its immune system.
This latest research has found for the first time that males eating more carotenoids were better able to protect their cells
from damage and so lived longer - and that females found these long-lived males particularly attractive.
The work was carried out on sticklebacks, and compared the fate of fish that all received the same basic diet but had
different amounts of carotenoid supplement. Male sticklebacks need carotenoids to produce the red throat patch that
they develop in the breeding season and display to females.
Dr Thomas Pike, researcher in Environmental and Evolutionary Biology at Glasgow University said: 'Males provided
with fewer carotenoids still tried to produce a bright red throat patch, but could only do so by diverting carotenoids away
from their role as antioxidants; so by trying to look as good as possible, these males aged faster.'

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In sticklebacks, the female lays her eggs in a males nest and then leaves, and it is the male alone who cares for the
eggs and young.
'It seems that females can tell if males haven't eaten many carotenoids, even if they do look quite red, and probably
found these males less attractive because they were more likely to die before they had finished looking after the young,'
said Dr Pike. 'The positive effects of a carotenoid-rich diet are likely to apply to many other animal species as well but
whether eating carrots makes humans longer-lived and more handsome remains to be seen!'
'The most brightly coloured males often get the girl, but why females prefer such show-offs hasn't been clear,' said Dr
Jon Blount, Research Fellow at the University of Exeter. 'Our study shows that redder males are more likely to be good
fathers, because they can survive the demands of parenting.'
Article: Carotenoids, oxidative stress and female mating preference for longer-lived males '
The study was carried out by the Fish Biology Research Group at the University of Glasgow, in collaboration with
researchers at the Akvaforsk Institute for Aquaculture Research in Norway and the University of Exeter, and will be
published in the scientific journal Proceedings of the Royal Society.
The study was funded by a grant from the Natural Environment Research Council.
Note: This story has been adapted from a news release issued by Natural Environment Research Council.
========================================================================================

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Eat healthy for life


http://www.hsph.harvard.edu/nutritionsource/pyramids.html
from EAT, DRINK, AND BE HEALTHY by Walter C. Willett, M.D. Copyright 2001, 2005
by the President and Fellows of Harvard College. Reprinted
by permission of Free Press/Simon & Schuster, Inc.

Forget your old ideas about healthy eating. Theres a different nutrition story now. This
story, based on evidence from rigorous scientific studies, is not about denying yourself the
foods you love or following a rigid diet plan. Its about choosing foods you like based on
the latest nutritional science and your own particular health concerns.
Research done since the 1990s
shows beyond all doubt that you
can lower your risk for the most
serious diseases of our time by
following a healthy diet. Healthy
eating, based on this science, can
prevent possibly 80% of cases of
heart disease and diabetes and help
ward off hypertension, osteoporosis,
and some forms of cancer.
Weve known for many years that
certain foods are healthy
especially fruits, vegetables, and
whole grains. But now we know why
theyre healthy. For the first time,
scientists can point to specific
nutrients and other substances in
foods that fight disease, including
vitamins, minerals, and plant
Healthy Eating Pyramid
chemicals. But while eat your
vegetables is a well-known refrain,
it may surprise you to know that you should eat fat, too. Thats right: Some of the
healthiest foods are fats. Maligned for many years as the bane of a healthy diet, some
types of fat mainly those from most plants and fish have been shown to keep arteries
clear, hearts beating normally, and to inhibit some forms of cancer.
This mounting evidence triggered a wholesale revision of the U.S. governments nutritional
recommendations in 2002 with the introduction of the new dietary reference intakes for
protein, carbohydrates, fats, and fiber. These guidelines shift the emphasis away from lowfat diets and instead urge people to eat unsaturated fats, vegetables, fruits, and whole
grains and to exercise daily. In 2003, the World Health Organization concurred and also
urged people to reduce salt consumption. And most recently, in 2005, the U.S. Department
of Agriculture (USDA) reworked its Dietary Guidelines for Americans to emphasize calorie
control and exercise. The same year, the USDA revised its famous food pyramid to reflect
the new emphasis on whole grains, healthy fats, and exercise.
The new government food pyramid is called My Pyramid because it has an interactive
Web site that allows you to customize it based on your age and level of activity. My
Pyramid is an improvement over the old USDA pyramid because it includes exercise as an
important factor in the equation and it offers 12 different eating plans. Still, it fails to
differentiate between different types of carbohydrates, fats, and proteins.
It used to be so simple. Fats were the villains, and carbohydrates were the heroes. More

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protein was good. But ongoing research on macronutrients has shifted the emphasis away
from white carbohydrates onto whole grains, good fats, and healthy sources of protein.
Macronutrients are the three basic categories of nutrients that humans need. They provide
the body with energy, and they enable the body to carry out many normal biological
functions. A healthy diet consists of a mix of foods from each of these categories, although
not in equal amounts.
Simple switches for healthy eating

Instead of:

Try:

Butter, solid margarine, or


lard

Olive oil, canola oil, or margarine without trans fats

Cream-based sauces

Tomato-based sauces

Corn flakes, Special K, or


other refined-grain cereal

Cheerios, Wheaties, or other whole-grain cereal

White pasta

Whole-wheat pasta

Smoked, cured, salted, or


canned meat or fish

Fresh or frozen meat or fish, without added salt

Sugared soda or juice

Water or juice mixed with sparkling water

Fries or onion rings

Roasted vegetables

Dips high in saturated fats

Hummus, peanut butter, or seasoned low-fat yogurt

Cookies

Graham crackers or oatmeal cookies

Fried foods

Grilled, broiled, steamed, poached, or roasted foods

Skipping breakfast

Eating oatmeal, whole-grain breads, or bran cereals

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Originally published February 7 2007

New Canadian food guide puts too much emphasis on red meat, dairy, say critics
by David Gutierrez

(NewsTarget) The Canadian government has released a revised food and nutrition guide for the first
time in more than 10 years but critics say that the guide overemphasizes unhealthier foods, including
red meat and dairy.
The food guide is Canada's second-most requested government document, after tax forms. The
government spent $1.5 million and four years revising it since the last version, with consultations from
more than 7,000 "stakeholders" including dairy, meat and egg producers. Approximately 2 million copies
are distributed yearly.
Some of the guide's revisions have been praised by health advocates. For example, it recommends
limiting trans fats and foods high in saturated fats and sugar. It encourages more consumption of fruits
and vegetables, along with 30 to 60 minutes of moderate exercise a day for adults.
Other recommendations have been more controversial. For example, the guide explicitly recommends
that people consume 2 to 3 tablespoons of unsaturated fat (such as from vegetable oil) per day. It also
suggests drinking two cups of milk to ensure adequate vitamin D intake, even though the body can
synthesize vitamin D with only a few minutes' daily exposure to sunlight. Critics point out that without
explicit calorie guidelines, following these recommendations could lead to weight gain in people of a
previously healthy weight.
Dr. Yoni Freedhoff, a specialist in obesity medicine, uses the example of a sedentary, middle-aged
woman of average height to highlight this problem:

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"[The new food guide] explicitly tells her to consume two glasses of 2 percent milk and three
tablespoons of unsaturated fat [per day]," he said. "Together those two choices would constitute over
one-third of her total daily calories."
Two cups of 2 percent milk contain 244 calories. Even skim milk contains 90 calories per cup.
"The new food guide is not a weight-loss tool of a diet system," said Dr. David Butler Jones, Canada's
Chief Public Health Officer. Instead, he said, the guide is intended to help people make healthy dietary
choices.
NewsTarget.com offers an unbiased, free, downloadable food guide at http://www.honestfoodguide.org .

Media
Contact:

Jennifer Johnson

03 May 2007

jennifer.johnson@emory.edu
(404) 727-5696

[ Print
| Email ]

Common Genetic Variation is Linked to Substantial Risk in Heart Attack


A common genetic variation on chromosome 9p21 is linked to a
substantial increase in risk for heart attack, according to a new
international research study. The findings are published today
in the online edition of Science, and will appear in an upcoming
printed edition of the journal.
Researchers found individuals with the variation have a 1.64fold greater risk of suffering a heart attack (myocardial
infarction) and a 2.02-fold greater risk of suffering a heart attack
early in life (before age 50 for men and before age 60 for women) than those
without the variation. Approximately 21 percent of individuals of European
descent carry two copies of the genetic variation (one from each parent), found
on chromosome 9p21.
The research project was led by the Icelandic genomics company deCODE
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Genetics, along with U.S. researchers at Emory University School of Medicine,


Duke University, and the University of Pennsylvania.
Myocardial infarction is the death of heart tissue that results when the blood
supply to the heart is cut off. It is the leading cause of death in the industrialized
world. Nearly half of men and one-third of women who reach the age of 40 will
suffer a heart attack in their lifetime.
The study led by deCODE Genetics uncovered the first common variant found to
be consistently linked to substantial risk of heart attack in multiple case-control
groups of European descent.
The researchers found a population-attributable risk for heart attack of 21
percent in general and of 31 percent for early onset cases. This means that were
the gene variant not present, there would potentially be 21 percent fewer heart
attacks overall in the population and 31 percent fewer early onset heart attacks.
"The gene variant we have linked to heart attack points us to a major biological
mechanism that substantially increases the risk," explains Emory cardiologist
Arshed A. Quyyumi, MD, one of the study authors. "Discoveries like this one
greatly heighten our understanding of the role genetics plays in heart disease."
Other Emory researchers involved in the study were Viola Vaccarino, MD, PhD,
professor of medicine (cardiology) and Allan I. Levey MD, PhD, professor and
chair of neurology.
Investigators enrolled 4,587 patients over the last eight years who suffered
myocardial infarctions, along with 12,769 control individuals. The study
participants in Atlanta were enrolled at Emory University Hospital, The Emory
Clinic and Grady Memorial Hospital through the Emory Genebank study and the
Clinical Registry in Neurology. The Emory Genebank studies the association of
biochemical and genetic factors to coronary artery disease in subjects
undergoing cardiac catheterization.
http://www.whsc.emory.edu/press_releases2.cfm?announcement_id_seq=10003

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3. Exercise
www.cbass.com
http://www.precisiontraining.com/
http://www.chekinstitute.com/index.cfm
http://www.bodytrends.com/default.asp
http://www.americanyogaassociation.org/contents.html
http://www.yogacanada.org/index_files/Page279.htm
=================================================================

Effect of Physical Activity on the Development of Knee Osteoarthritis


Posted 1/31/07
Felson DT, Niu J, Clancy M, Sack B, Aliabadi P, Zhang Y. Effect of recreational physical activities on the development of knee osteoarthritis in older adults of
different weights: The Framingham Study. Arthritis Rheum (Arthritis Care Res) 2007;57: .

What problem was studied?


Regular physical activity is recommended for all people. However, how exercise affects the development of
osteoarthritis (OA) is uncertain. One school of thought is that frequent load-bearing exercise causes cartilage
to become thicker, thereby preventing knee OA. Another school of thought is that the repetitive motions
associated with physical activity, particularly in overweight individuals, may contribute to the wear and tear
component of knee OA. David Felson, MD, and his team from Boston University School of Medicine and
Brigham and Womens Hospital in Boston performed a longitudinal, prospective study examining the effect
of recreational physical activity on the development of knee OA in people at risk for OA, many of whom were
overweight or obese. Although this particular study was funded by the National Institutes of Health and
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Boston University, Dr. Felson has received two research grants from the Arthritis Foundation, one to study
bone density and another to study the effects of vitamin K on OA.
What was done in the study?
Members of the Framingham Offspring study were recruited as part of a study of the inheritance of OA. Of
the subjects, 1,279 were included in an evaluation of physical activity and OA development. The participants
answered a questionnaire about physical activity, had knee X-rays taken and answered questions about knee
symptoms. They then had the same evaluation approximately nine years later. The participants included older
individuals (mean age, 53.2 years), many of whom were overweight (mean body mass index, 27.4), allowing
the scientists to evaluate the effects of activity on OA development and to test whether weight had any
influence on the results.
What were the study results?
Of the 2,259 knees evaluated at the end of nine years, 222 (9.8%) had narrowing of joint space evident in the
X-rays, 215 (9.5%) developed OA apparent by X-ray and 173 (7.2%) had knee symptoms (pain and stiffness).
Walking for exercise was the most commonly mentioned physical activity among the participants, and none
of the measured parameters were affected by walking -- risk of developing OA was neither increased nor
decreased by walking for exercise. Likewise, those exercising at a more vigorous intensity (enough to work
up a sweat) had no greater risk of developing OA than participants who did not exercise.
When analyzing the data separated by sex and body mass index, the results were the same. Those whose BMI
was above the median of the group and who performed regular physical activity had no greater risk of
developing knee OA than those whose BMI was below the median and engaged in regular exercise.
What is the relevance to people at risk of developing OA?
Patience White, MD, Chief Public Health Officer of the Arthritis Foundation pulls together the significance of
this research. The finding of Dr. Felsons study of middle aged and elderly peoples physical activity levels
and their risk of OA is welcome news for people who are at risk for developing osteoarthritis, the most
common form of arthritis in the US, affecting 21 million Americans and resulting in significant joint pain and
disability. This study reassures them that moderate to high intensity recreational physical activity with its
many health benefits will not result in increasing their risk of developing painful osteoarthritis. Now middleaged and older Americans at risk for osteoarthritis can act to improve their health by consulting their
physician about following the Centers for Disease Control and Prevention recommendations to undertake 30
minutes of physical activity of at least moderate intensity most days of the week.
http://www.arthritis.org/research/summaries/Felson_Framingham_Knee_OA.asp
============================================================================

A healthier, fitter YOU Simple strength training tips


www.health.harvard.edu
If youve never lifted weights in your life and many people havent why should you start now? The
answer is simple: Muscle tissue, bone density, and strength all dwindle over the years. So, too, does muscle
power. These changes open the door to accidents and injuries that can compromise your ability to lead an
independent, active life. Strength training is the most effective way to slow and possibly reverse much of this
decline.
Having smaller, weaker muscles doesnt just change the way people look or move. Muscle loss affects the body in
many ways. Strong muscles pluck oxygen and nutrients from the blood much more efficiently than weak ones.
That means any activity requires less cardiac work and puts less strain on your heart. Strong muscles are better at

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sopping up sugar in the blood and helping the body stay sensitive to insulin (which helps cells remove sugar from
the blood). In these ways, strong muscles can help keep blood sugar levels in check, which in turn helps prevent
or control type 2 diabetes and is good for the heart. Strong muscles also enhance weight control.
On the other hand, weak muscles hasten the loss of independence as everyday activities such as walking,
cleaning, shopping, and even dressing become more difficult. They also make it harder to balance your body
properly when moving or even standing still, or to catch yourself if you trip. The loss of power compounds this.
Perhaps its not so surprising that, by age 65, one in three people reports falls. Because bones also weaken over
time, 1 out of every 20 of these falls ends in fracture, usually of the hip, wrist, or leg. The good news is that the risk
of these problems can be reduced by an exercise and fitness routine that includes strength training.
Beginners simple strength boosting exercises
A sturdy chair with armrests and athletic shoes with non-skid soles are all you need for these simple strength
building exercises.

Seated bridge
Sit slightly forward in a chair with your hands on the armrests. Your feet should be flat on the
floor and slightly apart, and your upper body should be upright (dont lean forward). Using your
arms for balance only, slowly raise your buttocks off the chair until nearly standing with your
knees bent. Pause. Slowly sit back down. Aim for 812 repetitions. Rest and repeat the set.

Triceps dip
Put a chair with armrests up against a wall. Sit in the chair and put your feet together flat on
the floor. Lean forward a bit while keeping your shoulders and back straight. Bend your
elbows and place your hands on the armrests of the chair, so they are in line with your torso.
Pressing downward on your hands, try to lift yourself up a few inches by straightening out
your arms. Raise your upper body and thighs, but keep your feet in contact with the floor.
Pause. Slowly release until youre sitting back down again. Aim for 812 repetitions. Rest and
repeat the set.

Standing calf raise


Stand with your feet flat on the floor. Hold onto the back of your chair for balance. Raise yourself up on
tiptoe, as high as possible. Hold briefly, then lower yourself. Aim for 812 repetitions. Rest and repeat
the set.

====================================================================
Source: American Psychological Association
Posted: August 12, 2006

Exercise Helps Sustain Mental Activity As We Age, May Prevent Dementia-like


Illnesses
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Based on a review of studies on exercise and its effect on brain functioning in human and animal
populations, researchers find that physical exercise may slow aging's effects and help people maintain
cognitive abilities well into older age. Animals seem to benefit from exercise too and perform spatial
tasks better when they are active. Furthermore, fitness training -- an increased level of exercise -- may
improve some mental processes even more than moderate activity, say the authors of the review.
Findings from the review will be presented at the 114th Annual Convention of the American Psychological Association
(APA).
Varying opinions still exist on the benefits of exercise and activity, said authors Arthur F. Kramer, PhD, Kirk I. Erickson,
PhD and Stanley J. Colcombe of the University of Illinois at Urbana -- Champaign, "but our review of the last 40 years of
research does offer evidence that physical exercise can have
a positive influence on cognitive and brain functions in older animal and human subjects." Different methodologies were
examined to comprehensively study what effects exercise can have.
The researchers first examined the epidemiological literature of diseases to determine whether exercise and physical
activity can at certain points in a person's lifetime improve cognitive ability and decrease the likelihood of age-related
neurological diseases, like Alzheimer's. The authors then reviewed longitudinal randomized trial studies to see if specific
fitness training had an affect on cognition and brain function in older adults. Finally, animal studies were examined to
understand the molecular and cellular mechanisms responsible for exercise effects on the brain as well as on learning
and memory.
Based on a review of the epidemiological literature, the authors found a significant relationship between physical activity
and later cognitive function and decreased occurrence of dementia. And the benefits may last several decades. In a few
of the studies that examined men and women over 65 years old, the findings showed that those who exercised for at
least 15-30 minutes at a time three times a week were less likely to develop Alzheimer's Disease, even if they were
genetically predisposed to the disease.
By examining the human intervention studies, a relationship was also found between fitness training and improved
cognition, more efficient brain function and retained brain volume in older people, said Kramer. He cautions that
different fitness training regimens and aspects of mental functions need further study to solidify a causal relationship.
But, he added, there are some preliminary positive findings. In a four year study looking at the relationship between
physical activity on cognition and brain function in 62-70 year olds, "those who continued to work and retirees who
exercised showed sustained levels of cerebral blood flow and superior performance on general measures of cognition
as compared to the group of inactive retirees," said Kramer.
Other studies confirmed the evidence that fitness does have positive effects on brain function in older adults. A study of
older adults who were randomly assigned to either a walking group or a stretching and toning control group for six
months found that those in the walking group were better able to ignore distracting information in a distractibility task
than those in the control group. "Aerobically trained older adults showed increased neural activities in certain parts of
the brain that involved attention and reduced activity in other parts of the brain that are sensitive to behavioral conflict,"
said Kramer.
Animal studies also provide support for the aging benefits of physical activity. Analyzing the effects of exercise in animal
populations provides a unique window into learning about exercise-induced neurological and cognitive plasticity -- the
ability of parts of the brain to function in place of other parts of the brain, said Dr. Kramer. Some of the animal studies
reviewed used voluntary-wheel running experiments to show the existence of performance benefits of wheel running on
hippocampus-related spatial learning tasks. Moreover, a few studies found that aged rodents that exercised in a water
maze learned and retained information about a hidden platform better than age-matched controls.
Exercise also protected both young and aged animals from developing some age-related diseases as indicated by
increases in certain neurochemical levels that can offset or prevent certain pathological diseases.

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"From this review we have found that physical and aerobic exercise training can lower the risk for developing some
undesirable age-related changes in cognitive and brain functions," said Dr. Kramer, "and also help the brain maintain its
plasticity - ability to cover one function if another starts failing later in life."
More research is needed to know exactly how much and what types of exercise produce the most rapid and significant
effects on thinking and the brain; how long exercise effects last following the end of training; or how much exercise is
needed to get continued benefits, said Kramer.

Exercise Capacity: The Key To A Long And Healthy Life


If you were asked to name the most accurate predictor of a person's potential lifespan, what would you
say?
Smoking habits? Heart health? The presence of disease, like diabetes?
All good guesses. But according to new research, it's none of the above.
The miracle life extension therapy that's totally free
In this new study, published in this month's New England Journal of Medicine, researchers at Stanford
University clearly show that the most powerful predictor of lifespan is something completely different.
Something that is completely within our control, totally assessable, has no negative side effects - and is
totally free! So what is this miracle health cure?
The study's authors call it "exercise capacity". But what it really boils down to is fitness level - how much
can your body do and how much oxygen does it need to do it?
In this study, the researchers assessed the exercise capacities of 6,213 men (average age 59 years)
through a treadmill test. Each man walked on the treadmill at progressive speeds and inclines, while
sensors monitored his heart rate and a mask assessed oxygen and carbon dioxide flow. Each continued
walking or running until he was exhausted, reached maximum safe heart rate, or developed chest pain
or other symptoms. The researchers were able to estimate each man's maximal exercise capacity based
on a lifestyle questionnaire, and the treadmill programmes were adjusted accordingly, so most men
reached that point within 8 to 12 minutes.
Then the researchers translated each man's maximal exercise capacity into metabolic equivalents, or
METs. (One MET is considered roughly equal to the amount of oxygen used by the average seated
person. Two METs roughly equates to walking at a rate of less than two miles per hour, while eight METs
represents the oxygen used while jogging at a speed of six miles per hour.)
They also assessed each man's health history, taking note of existing cardiovascular disease, diabetes,
cigarette use, and hypertension.
A total of 3,678 men had existing cardiovascular disease, while 2,534 had no evidence of CVD.
Fitness cut the risk of death four-fold
The Stanford scientists followed up with each man years later (the average follow up period was six
years). And they found that, after adjustment for age, the man's exercise capacity was the best way to
predict which men would have died during follow up and which would live - and this held true for men
with and without cardiovascular disease. In both groups, the men with the lowest exercise capacities
(between 1.0 and 4.9 MET for people with cardiovascular disease) had about FOUR TIMES the risk of
death than men with the highest exercise capacities (10.7 MET or more for cardiovascular disease
patients).
If you're a beginning exerciser, this may seem like an intimidating goal. But take heart - even small
improvements in exercise capacity can reap big benefits. As the study's authors put it, "Among subjects

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with cardiovascular disease...we observed a near linear reduction in risk with increasing quintiles of
fitness." In other words, each improvement in fitness, no matter how slight it may seem, can help
lengthen your life. So even if you never get to "maximal exercise capacity" of 10.7 MET or more, you're
still doing something good for yourself.
And, according to researcher T. Edwin Atwood: "It's not how long you exercise...It doesn't take
marathons or running. Walking briskly every day for half an hour is a great risk modifier."
Obviously giving up smoking and following a healthy diet will help increase your MET score too.
20.07.2004
http://www.thehealthierlife.co.uk/article/3044/exercise-capacity.html
==============================================================

4. Sleep
http://www.sleepresearchsociety.org/
http://www.npi.ucla.edu/sleepresearch/
http://www.lboro.ac.uk/departments/hu/groups/sleep/
http://www.lboro.ac.uk/departments/hu/groups/sleep/article.htm
==========================================================================
FOODS FOR SLEEP
HTTP://WWW.ASKDRSEARS.COM/HTML/4/T042400.ASP

FOODS THAT HELP YOU SLEEP

What you eat affects how you sleep. One of the keys to a restful night's sleep is to get your brain
calmed rather than revved up. Some foods contribute to restful sleep; other foods keep you awake.
We call them sleepers and wakers. Sleepers are tryptophan-containing foods, because tryptophan
is the amino acid that the body uses to make serotonin, the neurotransmitter that slows down nerve
traffic so your brain isn't so busy. Wakers are foods that stimulate neurochemicals that perk up the
brain.

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Tryptophan is a precursor of the sleep-inducing substances serotonin and melatonin. This means
tryptophan is the raw material that the brain uses to build these relaxing neurotransmitters. Making
more tryptophan available, either by eating foods that contain this substance or by seeing to it that
more tryptophan gets to the brain, will help to make you sleepy. On the other hand, nutrients that
make tryptophan less available can disturb sleep.
Eating carbohydrates with tryptophan-containing foods makes this calming amino acid more
available to the brain. A high carbohydrate meal stimulates the release of insulin, which helps clear
from the bloodstream those amino acids that compete with tryptophan, allowing more of this natural
sleep-inducing amino acid to enter the brain and manufacture sleep- inducing substances, such as
serotonin and melatonin. Eating a high-protein meal without accompanying carbohydrates may
keep you awake, since protein-rich foods also contain the amino acid, tyrosine, which perks up the
brain.
To understand how tryptophan and carbohydrates work together to relax you, picture the various
amino acids from protein foods as passengers on a bus. A busload containing tryptophan and
tyrosine arrives at the brain cells. If more tyrosine "passengers" get off the bus and enter the brain
cells, neuroactivity will rev up. If more tryptophan amino acids get off the bus, the brain will calm
down. Along comes some insulin which has been stalking carbohydrates in the bloodstream. Insulin
keeps the tyrosine amino acids on the bus, allowing the brain-calming tryptophan effect to be higher
than the effect of the brain-revving tyrosine.
You can take advantage of this biochemical quirk by choosing protein or carbohydrate-rich meals,
depending on whether you want to perk up or slow down your brain. For students and working
adults, high protein, medium-carbohydrate meals are best eaten for breakfast and lunch. For dinner
and bedtime snacks, eat a meal or snack that is high in complex carbohydrates, with a small
amount of protein that contains just enough tryptophan to relax the brain. An all- carbohydrate
snack, especially one high in junk sugars, is less likely to help you sleep. You'll miss out on the
sleep-inducing effects of tryptophan, and you may set off the roller-coaster effect of plummeting
blood sugar followed by the release of stress hormones that will keep you awake. The best bedtime
snack is one that has both complex carbohydrates and protein, and perhaps some calcium. Calcium
helps the brain use the tryptophan to manufacture melatonin. This explains why dairy products,
which contain both tryptophan and calcium, are one of the top sleep-inducing foods.
SNOOZE FOODS

These are foods high in the sleep-inducing amino acid tryptophan:

Dairy products: cottage cheese, cheese, milk


Soy products: soy milk, tofu, soybean nuts
Seafood
Meats
Poultry
Whole grains
Beans
Rice
Hummus
Lentils
Hazelnuts, Peanuts

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Eggs
Sesame seeds, sunflower seeds
BEST BEDTIME SNACKS
Foods that are high in carbohydrates and calcium, and medium-to-low in protein also make ideal
sleep-inducing bedtime snacks. Some examples:
apple pie and ice cream (my favorite)
whole-grain cereal with milk
hazelnuts and tofu
oatmeal and raisin cookies, and a glass of milk
peanut butter sandwich, ground sesame seeds (It takes around one hour for the tryptophan in the
foods to reach the brain, so don't wait until right before bedtime to have your snack.)
BEST DINNERS FOR SLEEP
Meals that are high in carbohydrates and low-to-medium in protein will help you relax in the evening
and set you up for a good night's sleep. Try the following "dinners for sleep":
pasta with parmesan cheese
scrambled eggs and cheese
tofu stirfry
hummus with whole wheat pita bread
seafood, pasta, and cottage cheese
meats and poultry with veggies
tuna salad sandwich
chili with beans, not spicy
sesame seeds (rich in tryptophan) sprinkled on salad with tuna chunks, and whole wheat
crackers
Lighter meals are more likely to give you a restful night's sleep. High-fat meals and large servings
prolong the work your digestive system needs to do, and all the gas production and rumblings may
keep you awake. Some people find that highly-seasoned foods (e.g., hot peppers and garlic)
interfere with sleep, especially if you suffer from heartburn. (See gastroesophageal reflux). Going to
bed with a full stomach does not, for most people, promote a restful night's sleep. While you may
fall asleep faster, all the intestinal work required to digest a big meal is likely to cause frequent
waking and a poorer quality of sleep. Eat your evening meal early.
Heed the sleep wisdom: "Don't dine after nine."
FOODS THAT KEEP YOU AWAKE
Caffeine-containing foods top the list of foods that wake you up.
Here's why:
As a stimulant, caffeine speeds up the action of not only the nervous system, but of other major
body systems, too. Within fifteen minutes of downing a cup of coffee, the level of adrenaline in your
blood rises, which triggers an increase in heart rate, breathing rate, urinary output, and production
of stomach acids. Basically, caffeine's effects are the reverse of what you want to happen as you go
to sleep.
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Caffeine also prompts adrenal hormones to release sugar stored in the liver, which stimulates
sugar cravings to replenish the stores. Caffeine heightens the roller coaster effect of blood sugar
swings, producing a quick high after a morning cup of coffee, followed by a downturn in the
afternoon.
Caffeine's effects in the body are sort of like the law of gravity: what goes up must come down.
The morning jolt is often followed by afternoon doldrums. Caffeine also makes it difficult to sleep
well.
Know your caffeine quota. Some persons are more caffeine-sensitive than others. Many adults
can take up to 250 milligrams of caffeine a day (the average amount in 21/2 cups of coffee) and
experience no sleep problems. Others get jitters after one cola.
Time your caffeine boost. For most people, the effects of caffeine wear off within six hours, so
coffee in the morning will usually not interfere with sleep in the evening. Caffeine-containing
beverages at lunch may not affect your sleep, but coffee, tea, or cola in the evening is likely to keep
you awake.
CAFFEINE AND KIDS
Many school-age children get squirrelly following a jolt of caffeine-containing cola. Kids who are
already hyperactive may be bouncing off walls following a caffeine jolt. Best to limit children's
caffeine consumption to less than 50 milligrams a day, no more than one 12-ounce cola. Avoid
beverages that have added caffeine, touted for their energy-boosting effects. Children should not be
exposed to the addicting effects of to the caffeine buzz.
Know what foods contain the most caffeine. As you can see from the chart, coffee, colas, and
tea rank highest in caffeine content.
FOOD

CAFFEINE (mg.)

coffee, brewed, 6 ounces

105

coffee, instant, 6 ounces

55

Mountain Dew, 12 ounces 55


Colas, 12 ounces

35-45

Tea, 6 ounces

35

Contrary to what we are led to believe, chocolate is not high in caffeine. Two chocolate chip cookies
may contain less than 5 milligrams of caffeine, a packet of cocoa mix contains 5 milligrams, and one
chocolate candy bar contains around 10 milligrams. In fact, many people find chocolate desserts
that also contain dairy products to actually be a sleep inducer because of the combination of
tryptophan and carbohydrates.
To get the taste of tea with less of a caffeine jolt, recycle the tea bag. Discard the first cup of tea
made from the tea bag, which contains the most caffeine, and make another cup. Also, don't
squeeze the tea out of the tea bag, as these drops of tea contain more caffeine. Try grain-based hot
beverages and caffeine-free herbal teas as alternatives to coffee and tea.
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Some over-the-counter cold and headache remedies are high in caffeine. Check the label or ask the
pharmacist, especially if you are a caffeine-sensitive person.

5. Brain & Behavior, Stress & Distress


http://www.ourstolenfuture.org/newscience/behavior/behav.htm
http://serendip.brynmawr.edu/bb/
http://www.brainsource.com/neuropsy.htm
http://faculty.washington.edu/chudler/nutr.html

Nutrition, Brain Function, and Behavior


By Mike Espy |
Nutrition, Brain Function, and Behavior
It is widely accepted that a well-balanced diet and good nutrition are necessary to ensure
normal growth, prevent disease, and maintain physical performance. Despite much speculation and
some important early findings about general malnutrition, relatively little is known about how specific
nutrients affect the brain and other organ systems in relation to mental activities, emotional states,
and behavior in healthy individuals. With few exceptions (for example, vitamin B12 and iron), the
behavioral consequences of deficiency are not presently considered as criteria when establishing
recommended dietary allowances. However, the involvement of a broader range of disciplines and
recent methodological advances have led to the reemergence of studies on brain function and
behavior in relation to nutrition. This area of research represents a unique approach to assessing
the functional consequences of altered nutrition.
This chapter focuses on this nutrition research; describes current methods of assessing nutrition,
brain function, and behavior; highlights several interesting findings; and discusses future
challenges.
Why Study Brain Function and Behavior?
Among the public, there is a strong and persistent belief that what we eat affects our mental and
emotional states and, in general, our ability to perform day-to-day activities and to meet life's
demands. It seems we all have theories, or at least suspicions, about the functional importance of
this or that food or specific nutrient. In fact, some of us alter our diets and take supplements and
freely advise others to do likewise, with the firm belief that such changes will improve the way we
feel and our ability to perform.
This belief often creates a psychological environment amenable to food faddism and uncritical
acceptance of claims made by self-styled "nutritionists." Today's "smart" foods, promoted as a way
to increase "brain power" and enhance memory, are a recent example. Scientific evidence to
support most of these claims of the beneficial effects of specific nutrients or diets is at best
conflicting and, more typically, simply lacking. The study of nutrition, brain function, and behavior
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responds to public interest and will, with time, produce the experimental data needed to assess the
legitimacy of health claims and provide reliable criteria useful for evaluating nutritional status and
making recommendations for dietary intakes.
The consumption of nutrients (biologically active chemicals), in the form of foods or supplements,
affects body chemistry which, in turn, affects brain chemistry and function. Neural impulses are
largely the result of sodium and potassium exchange, but numerous other minerals, carbohydrates,
amino acids, proteins, and vitamins affect cell membrane permeability, neurotransmitter
metabolism, and the glial cells that provide structural and nutritional support to neurons.
The delicate chemical balance of the brain is somewhat protected by the blood-brain barrier, which
restricts entry of certain chemicals to the brain via the blood. Nevertheless, the brain is highly
susceptible to changes in body chemistry resulting from nutrient intake and deficiency.
The brain receives, stores, and integrates sensory information and initiates and controls motor
responses. These functions correspond to mental activities and form the basis for behavior. Thus,
theoretically, there is a direct connection between nutrition, brain function, and behavior.
Furthermore, behavior may be unique as a criterion for establishing nutritional adequacy, in that it
represents the functional integration of all biological systems, including homeostatic and other
compensatory mechanisms that determine the practical importance of a nutritional deficit or excess.
Who Studies Brain Function and Behavior?
In the United States, studies on nutrition and brain function are conducted at private laboratories
and hospitals, academic institutions, and government research laboratories. Government-supported
research in this area is concentrated in the Department of Defense (DOD), USDA, and the National
Institutes of Health (NIH). DOD nutrition programs focus on enhancing performance during combat
and in other stressful environments, while NIH nutrition programs focus on the brain and behavior
related to disease states and drugs used in treating disease. Only USDA addresses the
relationships among nutrition, brain function, and behavior in the population as a whole.
One of the six principal objectives stated in USDA's 1992-98 Agricultural Research Service (ARS)
Program Plan is to "develop the means for promoting optimal human health and well-being through
improved nutrition" and to "define adequate and safe ranges of intake for nutrients." To meet this
objective, the plan explicitly recognizes the need to acquire "information about the effects of foods
and nutritional adequacy on behavior and performance."
Within ARS, the Grand Forks Human Nutrition Research Center, in North Dakota, has been a
leader in studying the effects of nutrition on brain function and behavior in both humans and animals
for more than a decade. The human nutrition research centers located in San Francisco, CA,
Boston, MA, Beltsville, MD, and Houston, TX, have also conducted studies in this area.
The need for broad institutional support is clear because this research is truly multidisciplinary,
drawing heavily from the fields of biochemistry, physiology, neuroscience, psychology, and
medicine, and, less frequently, from epidemiology, sociology, and anthropology. Technological and
analytical advances have further involved the fields of biotechnology, computer science, and
multivariate statistics. Coordinating and integrating the activities of scientists from these diverse
fields is a significant challenge and key to successful research on nutrition, brain function, and

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behavior.
Important Issues To Consider
Several considerations are common to most studies of nutrition, including those on brain function
and behavior. Inadequate dietary intakes result in deficiency states that occur by degree, ranging
from suboptimal to marginal to severe. By definition, a severe clinical deficiency in any essential
nutrient is going to have profound effects, particularly during periods of early development.
However, cases of marginal or subclinical deficiencies are far more common (at least in the United
States) and thus probably merit greater attention by researchers and a larger share of experimental
resources.
Optimal intakes for all nutrients are difficult to determine and have not yet been established. This
issue of optimal intakes is particularly important to the study of brain function and behavior, and
interest arises in part from the increasing emphasis of medical and allied professionals on
promoting health rather than treating illness and in part from the belief that brain function and
behavior within the normal range can and should be improved.
The choice of an animal or human model is important. Animal studies permit greater control over
genetic and environmental variation, assessment of effects over an entire life span and even across
generations, and extensive analysis of brain chemistry and anatomy. They can also be useful in
assessing brain physiology, mental processes, and some emotional responses, such as anxiety.
However, there are often significant differences between humans and animals in nutrient
metabolism; human brain function and cognition are considerably more complex, and the behavioral
repertoire of humans, including speech, greatly exceeds that found in animals. Thus, the ability to
generalize findings from animal studies to humans is limited and many aspects of function simply
cannot be studied in animals.
Even within a healthy population, nutritional effects on brain function and behavior must be studied
separately in numerous distinct groups. These groups may be defined by characteristics such as
age, sex, body composition, exercise, stress, and dietary choices including consumption of
vegetarian and other restricted diets, caffeine, and alcohol. The overwhelming majority of existing
studies on nutrition, brain function, and behavior were conducted on children.
The diet contains both nutrients and non-nutrients. Examples of the latter are preservatives, artificial
sweeteners, and substances like caffeine and alcohol. Studies that assess the effects of excessive
amounts of either nutrients or non nutrients may be considered toxicological rather than nutritional
in nature. When nutrient intakes are manipulated by supplementation, amounts can be at either
physiologic (appropriate to the body's normal functioning) or pharmacologic amounts. Although
pharmacologic or therapeutic amounts may be required for a brief period to remedy a severe
deficiency, they are in excess of amounts that can be reasonably acquired from the typical diet.
Methods of Assessment
In experimental studies, nutrient intakes are manipulated, selected responses are measured, and
other potential factors are controlled. Intakes may be modified in an acute or chronic fashion.
Single-meal and short-term (weeks) supplement studies exemplify acute modifications, while longterm (months) supplement studies are examples of chronic approaches. In correlational studies,
nutritional intakes and status and response variables are measured and statistically interrelated.
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Because intakes and thus status are not under experimental control in these studies, other factors
that naturally change with intake and status may confound results and make them uninterpretable. It
is essential, therefore, that experimental studies be used in nutrition research on brain function and
behavior.
Nutritional status is determined by biochemical assay of biological samples (blood, urine, feces,
menses, sweat, and hair) to validate the effectiveness of manipulating nutrient intakes via the diet or
supplementation. In correlational studies, an estimate of intakes can be made using diaries of food
consumption or recall and, along with nutritional status, serve as a predictor variable.
Brain function is assessed biochemically, physiologically, and behaviorally. Biochemical assays of
blood and urine for carbohydrates, proteins, amino acids, and neurotransmitter precursors and
metabolites provide indices of changes in brain biochemistry relevant to nutritional intake and
status.
The electrical activity of the brain is measured by using the electroencephalogram (EEG) under
conditions of rest (the subject is given no explicit task demands) and while the subject is engaged in
some mental activity, such as counting backward by 7's. EEG data are long-latency responses of
the brain (greater than 1 second) and provide a measure of background rhythmic activity at rest and
during task performance.
Brain electrical activity is also measured in response to auditory, visual, and somatosensory
stimulation. Data collected in response to sensory stimulation are short-latency responses (less
than 1 second), referred to as evoked or event-related potentials (EPs), and they index how rapidly
the central nervous system responds to information-processing demands. If the subject is instructed
to respond (press a button) to some stimuli but not others, the EPs index the subject's expectation,
decisionmaking, and response preparation.
Behavior is assessed by measuring accuracy and response times during performance of cognitive
tasks. Cognition is simply the collection of psychological processes involved in sensing, attending
to, perceiving (attributing meaning), encoding, and retrieving information and using that information
to solve problems, make decisions, and execute controlled responses. Cognitive processes occur in
the context of and are affected by emotional or mood states, which are themselves the result of a
complex interaction between physiological activation and cognitive appraisal. Although performing
any activity involves most, if not all, cognitive processes, a well-designed task with multiple stimulus
or response conditions or both can emphasize a single process. Different cognitive processes are
associated with different patterns of electrical activity and with different regions of the brain.
Therefore, performance on cognitive tasks indirectly assesses brain function while providing a direct
assessment of behavior relevant to real-world activities.
Because of their subjective nature, mood states such as anger, anxiety, confusion, depression,
fatigue, and sleepiness are assessed by using self-report measures. Questionnaires and tests are
also used to assess nutritional effects on stress, intellectual achievement, and social behavior.
However, social behavior is most commonly measured by observing and recording the frequency,
quality, and intensity of contact with others.
Highlights From Human Studies
Studies of severe protein-calorie malnutrition in children have a long history and are by far the most
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common of any nutritional studies. They have reliably found that malnourished children have
abnormal EEG's, reduced activity levels, and impaired attention. A variety of other behavioral
consequences have been frequently, but not consistently, reported, including impaired or delayed
mental (particularly verbal) and motor development, impaired intersensory integration, reduced
academic performance, increased crying in infancy, hyperactivity, apathy, withdrawal, and impaired
social skills. With rare exceptions, however, these studies were correlational in design such that
brain and behavioral effects were confounded by an impaired interaction of the child with his or her
social and physical environment.
An ongoing series of experimental studies has repeatedly shown that eating a high-carbohydrate,
low-protein meal on an empty stomach increases the relative availability of the amino acid
tryptophan, and promotes synthesis of the neurotransmitter serotonin. Under these conditions,
several behavioral effects have been consistently observed: impaired attention and slowed reaction
times, increased fatigue and sleepiness, and reduced pain sensitivity.
Severe deficiencies in several B vitamins have profound effects for brain function and behavior,
including abnormal EEG's, impaired memory, anxiety, confusion, irritability, and depression.
Subclinical deficiencies in thiamin (B1), riboflavin (B2), niacin (B3), pyridoxine (B6), cobalamin
(B12), and folic acid are also commonly found in elderly and psychiatric populations. However,
experimental studies have not been done to determine the involvement of individual vitamins in
memory processes or in thought and affective (emotional) disorders. Experimental pyridoxine and
vitamin E deficiencies produce abnormal brain electrical activity in humans and animals, and vitamin
C supplementation in rather large doses (1-2 grams per day) seems to influence brain activity,
although in varying ways.
The relationship of iron to brain function and behavior has received considerable attention,
particularly in children. Iron deficiency reliably results in impaired attention and learning,
hyperactivity, and apathy, which are consistent with findings of reduced dopamine (a brain
neurotransmitter) in iron-deficient animals. In several studies with young adults, iron intake and
status were related to EEG and EP responses and to performance on tasks assessing short-term
memory; the findings indicate that low levels of iron result in reduced alertness and impaired
memory.
Supplementation and correlational studies have found increased brain and behavioral excitability
with low zinc intakes and status. Subclinical experimental magnesium depletion was also found to
increase brain electrical activity. Nutritional copper deficiency reduces brain excitability, consistent
with reported reductions in several neurotransmitters in copper-deficient animals. Behaviorally,
calcium supplementation has been related to relief of pain during menstruation.
Boron, a mineral not yet recognized as essential for humans, has shown effects on brain electrical
activity and cognitive performance in several studies with older adults. When compared with higher
boron intakes, EEG changes noted with low boron intake were in the direction of those found with
other forms of malnutrition. Low boron intake also increased reaction times on attention, perception,
memory, and motor tasks.
These highlights do not fully represent the numerous and varied studies conducted on nutrition,
brain function, and behavior in humans; however, they do represent the most consistent findings.
Experimental studies with animals are even more numerous, and there has been no attempt to
present the findings from studies of nutritional deficiencies during pregnancy and lactation, which
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have profound and often lasting effects on the developing nervous system. Likewise, space
limitations do not permit presentation of findings from studies on food additives, including
preservatives and sweeteners, or substances like caffeine and alcohol.
Future Research
The complexity of research on nutrition, brain function, and behavior is evident, but so too is its
potential to generate knowledge that has broad practical application and benefits. Future studies will
no doubt identify new relationships and better characterize existing ones, while attempting to
discover underlying mechanisms. Although the focus of early studies was on the effects of general
malnutrition in children, future studies will more likely focus on specific nutrients and their effects on
brain function and behavior in adults. Experimental (in contrast with correlational) studies offer the
best hope of distinguishing nutritional from nonnutritional effects on these critical aspects of
function.
It is also highly probable that future research will attempt to identify nutrient intakes that will result in
optimal performance (psychonutrition). To be sure, one challenge for researchers in this area will be
to present findings in a manner that tempers the public's tendency to uncritically embrace new
findings before they are replicated and refined and to overgeneralize highly specific findings
obtained under the controlled conditions of the laboratory.
Article Source: Health Guidance
http://www.healthguidance.org/entry/6266/1/Nutrition-Brain-Function-and-Behavior.html
Mike Espy
=========================================================================

Top 10 Practical and Positive Ways of Managing Stress and Distress


Stress is the body's reaction to a change that requires a physical, mental or emotional adjustment or response.
Distress is a negative stress response. It occurs when stress continues without relief. Distress disturbs the body's
internal balance causing physical and emotional symptoms: headache, elevated blood pressure, chest pain, insomnia,
depression, panic attack and anxiety.
Stress is a part of life. Knowing ways to manage stress can be beneficial.

1) Make Time to Relax.


Find ways of relaxing. Learn how to meditate or use relaxation exercises. Listen to soothing music. Take a bath. Do
whatever helps you relax. If needed learn stress management or biofeedback techniques from healthcare professionals,
as healthy ways to manage stress.

2) Maintain a Normal Routine.


As much as possible, try to stick to a normal daily routine. Limit additional responsibilities. Learn to say "No."

3) Eat a healthy Diet.


Focus on whole grains, fruits and vegetables. Avoid excessive sugar, fatty foods and caffeine. Use alcohol in
moderation and don't try and self-medicate which can make the distress worse.

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4) Include Exercise as Part of Your Day.


Participating in some kind of moderate exercise activity for at least 30 minutes on most days helps relieve stress, boost
energy levels, aid sleep and improve mood. Exercise is also good for the heart, lungs and mind. Activities include
walking, jogging, cycling, swimming, aerobics, hiking

5) Keep a Positive Attitude.


Holding positive thoughts, rather than succumbing to a negative one can help in maintaining a positive attitude. Think
positively about yourself. Surrounding yourself with positive and inspiring people can help elevate your mood.

6) Participate in Activities You Enjoy.


Make time for hobbies and other interests. Read a good book. Garden. Knit. Be part of a sports team. Keep a journal.
Work on Crafts. Volunteer your services. Assist someone in need.

7) Get Enough Sleep.


Getting 7 to 8 hours of sleep a night will make it easier to cope with stress and distress. A well-rested person is more
alert and quick thinking and less irritable, grouchy and tense.

8) Talk with a Trusted Person.


Talking with someone about intense feelings when distressed can be helpful. Share feelings with a trusted friend, family
member, healthcare professional or clergy. Sharing the distress helps to lessen the feelings of distress. Some find that
participating in a support group with others who have experienced similar situations or events can also be helpful in
easing distress.

9) Learn to Adapt Instead of Control.


Accept that there will be situations, events and people throughout life that you are unable to control. Learning to be
flexible, to roll with the punches and ride the waves can help in reducing stress.

10) Remember to Laugh.


Laughter is one of the best medicines; it releases chemicals into the brain that promote relaxation. People who are able
to find humor in life and are happier tend to be more productive live longer and have less physical problems. Maybe a
good laugh a day will help keep the stressors away.
http://dying.about.com/od/suddendeath/tp/manage_stress.htm?p=1
Image. Greek Golangco. A Distraught Woman. Royalty Free Use.

======================================================================
6. Skin Care
http://www.dermatology.ca/
http://www.skincarephysicians.com/
People still ignore skin cancer warnings
URL of this page: http://www.nlm.nih.gov/medlineplus/news/fullstory_49054.html (*this news item
will not be available after 06/09/2007)
Thursday, May 10, 2007
NEW YORK (Reuters Life!) - Many people still equate a tan with beauty and are not protecting
themselves from the sun's harmful rays, according to a new survey.
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Nearly one third of adults questioned in a national poll said they did not use sunscreen and 71
percent of people who used products to protect their skin do not apply them until after going out in
the sun.
"Despite all the messages about the importance of protecting from the sun, there is still a significant
subset of the population that doesn't use sunscreen and are exposed to the sun, which increases
the risk of skin cancers," said Dr. Craig Eichler, a skin cancer specialist in Naples, Florida.
Many people presume that it is only sun exposure early in life that can lead to skin cancer but
Eichler said it is not true.
"It is never too late to protect oneself. It can still decrease the risk of cancer," he added in an
interview.
The survey of 2,385 adults showed that nearly half of the people who applied sunscreen said they
were concerned about getting skin cancer.
"It is estimated that about one in five Americans will develop skin cancer," according to Eichler.
He added that although a tan is thought to be beautiful, it is damage to skin cells that induces a tan.
Cancer experts, researchers and doctors have been warning the public for years about the danger
of too much sun exposure and the link to skin cancer.
The majority of skin cancers are basal cell carcinomas, which are not considered life-threatening.
Malignant melanoma is the most serious type of skin cancer. It accounts for roughly 10 percent of
reported cases of the illness and can spread throughout the body, forming secondary tumors.
Doctors advise people to limit their exposure to the sun, to wear hats and clothing and to do outdoor
activities early or late in the day when the sun's rays are not as strong.
Eichler said typical sunscreen products need to be applied to the skin before going out because the
sun's rays can start damaging the skin in as little as 15 minutes.
"It is a good habit to apply sunscreen before starting an activity," he added.
http://www.nlm.nih.gov/medlineplus/news/fullstory_49054.html

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7. Dental-Oral Heath Care


http://www.cda-adc.ca/en/oral_health/index.asp
http://www.ada.org/
=====================================================================

8. Weight Management: There are countless sites and articles on this important topic, to
which we will return in later newsletters. We find the three sites below have rewarded us by
our close examination of all their detailed sections.
http://www.whfoods.com/index.html
http://www.nutritiondata.com/
http://www.thelifestylecompany.com/wloss/wm10thed.asp The LEARN PROGRAM

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9. Womens Health
http://www.4women.gov/
http://www.cdc.gov/women/
http://www.womens-health.com/
http://www.nlm.nih.gov/medlineplus/womenshealth.html
British Journal of Cancer (2007) 96, 11391146.
doi:10.1038/sj.bjc.6603689
Meat consumption and risk of breast cancer in the UK Women's Cohort Study
E F Taylor1, V J Burley1, D C Greenwood2 and J E Cade1
1

Nutritional Epidemiology Group, 3032 Hyde Terrace, University of Leeds, Leeds, LS2 9LN, UK

Biostatistics Unit, 3032 Hyde Terrace, University of Leeds, Leeds, LS2 9LN, UK

Correspondence to: Professor JE Cade, E-mail: j.e.cade@leeds.ac.uk


Received 16 November 2006; revised 19 February 2007; accepted 21 February 2007

We performed a survival analysis to assess the effect of meat consumption and meat type
on the risk of breast cancer in the UK Women's Cohort Study. Between 1995 and 1998 a
cohort of 35 372 women was recruited, aged between 35 and 69 years with a wide range of
dietary intakes, assessed by a 217-item food frequency questionnaire. Hazard ratios (HRs)
were estimated using Cox regression adjusted for known confounders. High consumption of
total meat compared with none was associated with premenopausal breast cancer, HR=1.20
(95% CI: 0.861.68), and high non-processed meat intake compared with none, HR=1.20 (95%
CI: 0.861.68). Larger effect sizes were found in postmenopausal women for all meat types,
with significant associations with total, processed and red meat consumption. Processed
meat showed the strongest HR=1.64 (95% CI: 1.142.37) for high consumption compared with
none. Women, both pre- and postmenopausal, who consumed the most meat had the
highest risk of breast cancer.
Keywords: prospective studies; breast neoplasms; meat; risk factors

Although evidence that links meat consumption with cancers of the stomach, colorectum and
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pancreas is increasing (Sandhu et al, 2001; Gonzalez et al, 2006; Larsson et al, 2006a, 2006b;
Lewin et al, 2006), studies of meat consumption and breast cancer have produced more conflicting
results. A meta-analysis of 31 casecontrol and cohort studies published before 2003 found a 17%
increase in risk associated with the highest category of meat intakes (Boyd et al, 2003). However, a
pooled analysis of the raw data from eight prospective cohort studies from North America, Canada
and Western Europe was unable to demonstrate such an association (Missmer et al, 2002).
Certain evidence suggests an interaction between cooking methods and diet in breast cancer
causation. Studies, however, are few and inconsistent. A casecontrol study of Chinese women in
Shanghai found that the positive association with red-meat intake was primarily restricted to those
who used deep-frying cooking methods, particularly among those who deep-fried foods to well-done
(Dai et al, 2002) suggesting an effect of heterocyclic amines or other carcinogens formed at high
temperatures. However, the Nurses' Health nested casecontrol study found no increase in risk with
cooking method or meat intake even for consumption of charred meat more than once a week in
rapid acetylators (Gertig et al, 1999).
Some of the inconsistency in findings may be owing to differences in definitions of total meat, red,
and processed meats and in the derivation of the meat content of meat dishes. Other
inconsistencies may arise owing to biases, errors and the homogeneity of diet within individual
population groups (Hankin, 1993; Kaaks and Riboli, 1997a). The UK Women's Cohort Study
(UKWCS), which was established in 1993 to investigate diet in relation to cancer and mortality from
selected causes, is well placed to examine meat consumption and breast cancer risk, the subject of
this paper.

MATERIALS AND METHODS


Study population
The UKWCS, described previously (Cade et al, 2004, 2007), was formed from 500 000 responders
to a direct mail survey of the World Cancer Research Fund (WCRF) after permission to carry out
the baseline study was obtained from 174 local research ethics committees (Woodhouse et al,
1997). Seventy-five percent of the responders agreed to take part in a more detailed survey; those
eligible for inclusion were women, aged between 35 and 69 years at the completion date of the
original mail survey. The 35 372 women who returned completed questionnaires formed the
UKWCS, this cohort being specifically designed to have a wide range of dietary intakes and
patterns to increase the potential power to detect statistically significant associations between
specific diets and disease; 28% are self-reported vegetarians.
Baseline data were gathered between 1995 and 1998 using a 217-item postal food frequency
questionnaire (FFQ), developed from that of the European Prospective Investigation into Cancer
and Nutrition (EPIC) study (Linseisen et al, 2002). This was validated in terms of nutrients, against a
semi-weighed 4-day food diary (Spence et al, 2002).
Details of women fulfilling the eligibility criteria were submitted to the UK Office of National Statistics
and subsequently flagged on the NHS central register. Incident cancers and cause of death were
coded according to the International Classification of Diseases 9 and 10. The investigation censor
date was 31st October 2004, with median follow-up of 8 years when a total of 1750 incident
malignant cancer cases had been recorded, including 283 premenopausal and 395
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postmenopausal breast cancers. Menopausal status was based on answers to the baseline
questionnaire regarding menstrual and obstetric history and the age at baseline. Power calculations
suggested 283 premenopausal breast cancer cases would give approximately 80% power to detect
a relative risk of 1.4 comparing two levels of a binary exposure with equal numbers in each group
(P<0.05), or more than 90% power for a relative risk of 1.5. In terms of postmenopausal breast
cancer, 395 cases would give approximately 90% power to detect a relative risk of 1.4 (P<0.05).
Analysing the exposure as a continuous variable would provide even more power.
Meat consumption
For the purpose of the study, meat types and meat dishes were grouped into the following
categories: red meat, poultry, offal and processed meat. Total meat was the sum of these four
categories. Non-processed was the sum of red meat, poultry and offal. Red meat consisted of beef,
pork, lamb and other red meats included in mixed dishes, for example, meat lasagne, moussaka,
ravioli and filled pasta with sauce; poultry included roast chicken, chicken slices, bread crumbed
chicken, chicken or turkey in a creamy sauce and chicken curry; meats considered as processed
were bacon, ham, corned beef, spam, luncheon meats, sausages, pies, pasties, sausage rolls, liver
pate, salami and meat pizza; offal (organ meats) existed as a single item on the FFQ.
Daily intakes of each of the four main meat types (red, poultry, offal and processed) were calculated
by summing the daily intakes of the individual food items within each meat type as described above.
Intakes of each item were determined by using the frequency categories to estimate the number of
daily portions. These were then converted into weights by referring to standard portion sizes for
each food item (Food Standards Agency, 2002). Intakes of each meat type were grouped into
consumption categories of 'none', 'low', 'medium' and 'high' by classing zero intakes as 'nonconsumers' and dividing non-zero intakes into tertiles. Consumption of offal tended to be more
limited and naturally fell into the three categories 'none', 'low' and 'high' consumption only, where
low consumption was defined as 2 g or less per day and high as over 2 g per day.
Statistical analysis
Exposures of interest were total meat consumption, non-processed vs processed meat consumption
and consumption of different meat types. Processed meat formed a separate category to be
compared against non-processed meat. Survival analyses were conducted in Stata version 9 using
Cox regression weighted by the inverse of the probability of being sampled to take into account the
large proportion of vegetarians in the cohort. The time variable used in the survival analysis was
time in the study (person years), calculated as the time from the date the questionnaire was filled in
until either a report of incident breast cancer, death or the censor date of the analysis, whichever
came first. Women with extremely high or low total energy intake (more than 6000 kcal and less
than 500 kcal) were excluded, as were women with prevalent breast cancer.
Two models were developed. Model 1 adjusted only for age (continuous) and energy intake by the
residuals method (split into quartiles) (Willett and Stampfer, 1986; Margetts and Nelson, 2000).
Model 2 adjusted for age, energy intake, body mass index (BMI) (continuous), physical activity
(continuous), parity (no children, 12 children, 34 children and 5+ children) and combined fruit and
vegetable consumption (split into quartiles). Smoking status, hormone replacement therapy use
(HRT) and oral contraceptive pill use were also included and all classed as present, past or never.
Additional confounders were included such as socioeconomic class (professional and managerial,
intermediate, and routine and manual), level of educational qualifications gained (none beyond age
14, O level, A level and degree level). Fractional polynomials were used to fit a smooth curve to the
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relationship between breast cancer and total meat intake using Model 2.
As breast cancer may represent different diseases in the two menopause status groups, an initial
analysis combined both groups, incorporating menopausal status as a confounder in the model. As
a test for interaction between meat consumption and menopausal status confirmed a potential
modifying effect of menopausal status, we have treated pre- and postmenopausal women
independently. The proportional hazards assumption was checked using graphical methods of
loglog curves and Schoenfeld goodness of fit tests (Schoenfeld, 1982), which confirmed the
hazards were proportional. Owing to the likelihood of differences in lifestyle characteristics between
vegetarians and meat eaters in addition to the absence of the meat component within their diet,
sensitivity analyses were undertaken excluding vegetarians. The sensitivity of results to excluding
women with any cancer incident within 1 year of entry to the study, and to the model building
strategy was assessed. Further analysis of sensitivity of results to the menopausal categorisation
was carried out by excluding women aged 4855 years whose menopausal status may have been
ambiguous. HRT users (past and present) were also excluded in a sensitivity analysis.

RESULTS
Basic characteristics and meat consumption in the cohort
Characteristics of the 33 725 women in the study are shown in Table 1. At baseline, the mean age
was 52 years and the average BMI 24.5 kg m-2. Cohort participants were relatively health
conscious, with low rates of smoking (11%) and alcohol consumption more than once per week
(52%). Most did not use full-fat milk (28 383, 88%), and a large proportion reported taking dietary
supplements (18 561, 58%). Meat eaters account for a higher percentage of present HRT users
than vegetarians, although it must be taken into consideration that vegetarians tend to be younger
and therefore less likely to be using HRT. In general, the cohort is well educated and middle class
where 8784 (27%) had been educated to degree level and 20 879 (63%) worked in professional or
managerial positions. More detail regarding the cohort women has been provided previously (Cade
et al, 2004).
Table 1
Baseline characteristics by
category of meat consumption

Table 1 shows that non-meat consumers were younger, more physically active, and had a lower
mean BMI than consumers. High meat consumers were more likely to be smokers, had the highest
total energy intake, highest mean BMI, highest proportion with no education beyond age 14 and
lowest proportion employed in professional or managerial occupations. Medium meat consumers
were most likely to be low fruit and vegetable consumers (less than 400 g daily). The lowest energy
intake was seen in the group with low meat consumption.
Meat consumption and breast cancer
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The initial analysis combining both pre- and postmenopausal women to test for effect modification
by menopausal status (Table 2) showed several significant interactions. Indeed, when independent
analyses were conducted for each menopausal status, trends were considerably different.
Table 2
Combined pre- and
postmenopausal breast cancer

The associations between meat consumption and premenopausal breast cancer are presented in
Table 3 for both Model 1 and Model 2. Use of the complex model showed risk of breast cancer to
increase with consumption of total meat, HR (hazard ratios)=1.20 (95% CI: 0.861.68) for high
consumers vs non-consumers. The estimated relative risk for an increase in total meat consumption
of 50 g day-1 (approximately half a portion) was 1.12 (95% CI: 1.021.23, Ptrend=0.02). Nonprocessed meat consumption was positively associated with risk, HR=1.20 (95% CI: 0.861.68) for
high consumers vs non-consumers with a relative risk per 50 g day-1 of 1.13 (95% CI: 1.011.26,
Ptrend=0.03). The association with processed meat was not statistically significant although the risk
in high consumers was similar to that observed in non-processed meat. The borderline nonsignificant association with red meat consumption tended to show the largest effect sizes of all meat
types, HR=1.32 (95% CI: 0.931.88) for high consumption vs the reference category with relative risk
per 50 g day-1 of 1.13 (95% CI: 0.991.29, Ptrend=0.08).
Table 3
Pre menopausal breast cancer

In postmenopausal women, slight positive trends were observed across the low, medium and high
meat categories with a more marked difference between those not consuming meat and those that
do. However, splitting the meat categories into more groups by dividing the low consumers into low
and very low consumers strengthened the dose response relationship with meat consumption.
There was a tendency for the point estimates to be somewhat larger in postmenopausal than in
premenopausal women (using Model 2), as shown in Table 4. Total meat intake was positively
associated with postmenopausal breast cancer, HR=1.63 (95% CI: 1.102.30) for high consumption
vs the reference category, and when treated as a continuous variable, resulted in a significant linear
trend and relative risk per 50 g day-1 of 1.10 (95% CI: 1.011.20, Ptrend =0.02). Relationships between
both processed meat and red meat and postmenopausal breast cancer were also significant. Risks
for the three meat types were similar when considering HRs of the categorical analysis, however,
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fitting meat in the model as a continuous predictor resulted in a much stronger relationship with
processed meat, giving a relative risk per 50 g day-1 of 1.64 (95% CI: 1.092.27, Ptrend=0.003).
Table 4
Postmenopausal breast cancer

Hazard ratios in the highest meat consumption category for Model 1 in premenopausal women were
slightly lower than for Model 2 for all meat types with the exception of offal (total meat: Model 1
HR=1.16, Model 2 HR=1.20). Tests for trend were more significant in Model 2. The opposite is true
for postmenopausal risk where HRs are lowered in the refined model and P-values become less
significant with greater adjustments. Figure 1 presents the fitted curve from fractional polynomials
for total meat intake showing similar increasing risk with increasing total meat intake for both preand postmenopausal women, apart from premenopausal women with low meat intake who appear
at lower risk than vegetarians.
Figure 1
Association between total meat
intake and breast cancer for preand postmenopausal women.

In the sensitivity results excluding vegetarians, estimates were broadly similar and conclusions
unchanged, emphasising a dose response across the consumption categories of meat in both preand postmenopausal women. Sensitivity analyses for ambiguous menopausal status and women
with cancer within 1 year of entry did not substantially alter HRs or overall trends. The links between
meat consumption, cooking methods (grilling, frying and casseroling of meat) and risk were
investigated by considering interactions within Model 2; there was no evidence of changes in risk.
Excluding HRT users from the analysis of postmenopausal women appeared to strengthen the
relationship with breast cancer.

DISCUSSION
The UKWCS is one of the largest cohorts investigating diet and cancer in women in the UK. It was
designed to include participants with a wide range of dietary exposures to optimise comparisons
between different levels of meat intake, as proposed previously (Kaaks and Riboli, 1997b; Schatzkin
et al, 2001). In our analysis, significant increased risks of incident premenopausal breast cancer in
relation to increased consumption of total meat and non-processed meat were observed. Borderline
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non-significant associations with red meat were also seen. We found positive associations between
postmenopausal breast cancer and total meat, processed meat and red meat consumption.
Relationships between both pre- and postmenopausal breast cancer and total and red meat
consumption confirm findings of a case control study among Chinese women in Shanghai where
positive associations were observed in pre- and postmenopausal breast cancers combined (Dai et
al, 2002). Although pre- and postmenopausal women were also considered separately, the full data
were not shown. Positive associations among those who usually deep-fried red meat until well
done, were found in both groups, although statistically significant only in premenopausal women.
The association with red meat intake and both pre- and postmenopausal breast cancer may be due
to a combination of nutritionally related factors, such as content of fat, protein and iron, andor meat
preparation (eg cooking or preserving methods) (Sinha, 2002). A comparison of high consumer HRs
for all meat types investigated showed that high consumers of red meat are most at risk of
premenopausal breast cancer when compared with non-consumers (HR=1.32, 95% CI: 0.931.88).
The association found between non-processed meat (red meat, poultry and offal) could also be
caused by the red meat component within the non-processed meat category.
Results of a large casecontrol study (10 149 cases and 7990 controls) in northern Italy between
1983 and 1996 also found significant positive associations of breast cancer (combined analysis of
pre- and post menopausal women) with red meat consumption (Tavani et al, 2000). In addition, a
meta-analysis of 12 casecontrol and five cohort studies published between 1966 and 1993 found
increased risks of breast cancer (combined pre- and postmenopausal) in high consumers, the
association with red meat (RR=1.54, 95% CI: 1.311.82) being stronger than that observed for total
meat (Boyd et al, 2003). However, a pooled analysis of eight previous cohort studies has shown no
significant association between consumption of total meat, red meat or white meat and risk of breast
cancer (Missmer et al, 2002) in both combined and separate analyses of pre- and postmenopausal
women. The pooled analysis was not able to correct for measurement error and there were
considerable differences in questionnaire design between studies limiting the power of specific food
analyses. Also, meat-cooking practices could not be taken into account.
Previous studies have tended to find inverse relationships with consumption of poultry (Delfino et al,
2000; Ronco et al, 2003) and have generally been statistically non-significant. Our findings do not
provide strong evidence of an association with poultry intake and breast cancer in either pre- or
postmenopausal women. However, another study showed statistically significant inverse trends
between consumption of poultry and postmenopausal breast cancer (Ambrosone et al, 1998). One
study found that risks were increased when chicken was consumed with skin suggesting that fat
rather than muscle meat may be the cause (Ronco et al, 2003). Other studies have suggested a link
between fat and breast cancer (Howe et al, 1991; Willett et al, 1992; Hunter et al, 1996; SmithWarner et al, 2001; Boyd et al, 2003; Cho et al, 2003).
Although HRs for pre menopausal breast cancer indicate a positive association with meat intake,
low consumers are at less risk than vegetarians. Low meat consumers also had the lowest energy
and fat intakes, but including the percentage of energy from fat as a confounder and also calculated
using the residuals method (Willett and Stampfer, 1986) did not significantly modify the risk
estimates. Vegetarians possess other characteristics other than not consuming meat and these may
influence the association with risk in some way. Although we adjusted for characteristics known to
be represented differently in meat eaters and vegetarians (Davey et al, 2003; Cade et al, 2004) and
performed various sensitivity analyses with the exclusion of the vegetarian group, some residual
confounding may remain.
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Genetic factors only account for a small proportion of breast cancers (approximately 510%). The
UKWCS are expected to have a higher proportion than this as family history of breast cancer may
have encouraged them to become WCRF supporters. In addition, some may have taken up a
vegetarian diet in the belief that it is protective against breast cancer. However, if these women are
also genetically predisposed to breast cancer, then the chances of developing breast cancer are
increased. This is more likely among the premenopausal women because genetic causes tend to
lead to early onset of breast cancer. This could explain why, in the premenopausal women,
vegetarians have a higher risk than others.
Risks for pre- and postmenopausal women were examined separately, based on variability in some
risk factors and because breast cancer may represent different diseases in these groups
(Ambrosone et al, 1998). Also, mean intakes of certain meats were found to differ significantly
between the two menopausal groups. In addition, after the menopause, increased deposition of
adipose tissue, the major site for oestrogen synthesis, will tend to elevate the level of endogenous
oestrogens (Siiteri, 1987). The association between intake of carcinogens from foods cooked at
high temperature and breast cancer risk may be modified by oestrogens and oestrogen-related
factors. Other analysis has found a difference in impact of dietary fibre on risk of breast cancer
between pre- and postmenopausal women (Cade et al, 2007).
There are several mechanisms whereby meat intake may contribute to breast cancer risk. Meat and
in particular processed meats can be a rich source of saturated fat. Although effect on mammary
carcinogenesis has been shown in animals, its human relevance is controversial (Ip, 1993). A
review of prospective studies has shown that dietary fat reduction can lower serum oestradiol levels
(Wu et al, 1999). Many established risk factors are linked to oestrogens such as early menarche,
late menopause and obesity in postmenopausal women (Key and Verkasalo, 1999). Other
mechanisms related to the formation of heterocyclic amines during cooking or nitroso compounds
found in processed meat (Willett, 2005) may be altered by inherited polymorphisms such as the
rapid variant of N-acetyltransferase 2 (Williamson et al, 2005). Red meat also contains high
biological-value protein and important micronutrients, all of which are essential for good health
throughout life.
In postmenopausal women, the largest effects were with processed meat and this was statistically
significant, HR=1.64 (95% CI: 1.142.37) for high vs non-consumers with relative risk per 50 g day-1
of 1.64 (95% CI: 1.192.27, Ptrend=0.003). Risks were increased by almost 50% for even low
consumers of processed meat. A casecontrol study in a subcohort of the Nurses' Health Study (466
cases) supports this, breast cancer (combined pre- and postmenopausal) being 40% more likely in
women consuming more than 0.07 portions of bacon daily in comparison with non-consumers
(Gertig et al, 1999). Although trends were statistically non-significant, non-processed meat and
poultry were both positively associated with postmenopausal breast cancer. Differences in outcome
trends for pre- and postmenopausal women may be owing to the fact that oestrogen metabolism
pathways differ according to menopausal status (Muti et al, 2000). If meat influences breast cancer
by affecting oestrogen metabolism, the effect may be relatively more important among women with
lower levels of circulating oestrogens.
The strength of this study was the wide range of meat intake within the cohort which reduces
measurement error (White et al, 1994; Kaaks and Riboli, 1997b; Schatzkin et al, 2001). Previous
studies have been limited in terms of the FFQs used which may not have been designed to capture
specific food groups in sufficient detail (Missmer et al, 2002). An analysis of EPIC-Norfolk data
concluded that dietary measurement error through the use of their FFQ may explain the absence of
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a significant association with dietary fat and breast cancer risk as well as some of the previously
reported inconsistencies on meat (Bingham et al, 2003).
In conclusion, women generally consuming most total meat, red and processed meat were at the
highest increased risk compared with non-meat consumers, though red and processed meat were
only statistically significant postmenopausally. Effect sizes were smaller in non-processed meat and
only statistically significant in premenopausal women. There were no statistically significant linear
associations with consumption of poultry or offal in either pre- or postmenopausal women. This
study indicates relationships with certain meats and breast cancer in both pre- and postmenopausal
women and merits further investigation in a larger study.

Acknowledgements
We thank the UK Women's Cohort Study steering group, and the women themselves who
participated in the study. We also thank the WCRF for their previous funding and support. An earlier
analysis of this study was funded by the Meat and Livestock Commission.
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Source: University Of
Michigan
Date: May 13, 2007

Deciding When To Have A Child, If Ever: The Impacts Later


In Life

Science Daily How does having children or not having them affect a
woman's happiness in later life? A new study examining nearly 6,000 women provides an unexpected
answer it's not so much whether you have children as when you have them.

Sociologist Amy Pienta (Credit: Image courtesy of University Of Michigan)

But even more important than when you become a mother is whether you have anyone else to love in your life.
"Whether a woman has had children or not isnt likely to affect her psychological well-being in later life," said University
of Michigan sociologist Amy Pienta. "What is more important is whether or not she has a husband, a significant other or
close social relationships in her life as she ages."
Pienta, a researcher at the U-M Institute for Social Research, is co-author of a study analyzing the implications of
childlessness, birth timing and marital status on women's psychological well-being in late midlife. University of Florida
researcher Tanya Koropeckyj-Cox is lead author of the study and University of North Carolina, Chapel Hill, graduate
student in Sociology Tyson Brown is a co-author of the study.
For the study, to be published in a forthcoming issue of the International Journal of Aging and Human Development, the
researchers analyzed data on women between the ages of 51 and 61 from two different national surveys. These women
were young adults in the 1950s, a time when most women married early and had first births between the ages of 19 and
24.
"These surveys included several widely used measures of psychological well-being," Pienta said. "The women were
asked about their levels of happiness, their depressive symptoms and loneliness, and about their satisfaction with family
life and life in general."
"If you just look at women who had kids compared to those who didn't, childless women reported being somewhat less
happy and more depressed," Pienta said. "But when we factored in socioeconomic characteristics and marital status,
there was no difference between the two groups."
Instead of just comparing childless women and mothers, the researchers examined how the late-life well-being of
childless women compared to that of three different groups of mothers who had their first children at different times
women who became mothers early (before age 19), "on-time" (between 19 and 24) or late (age 25 or later).
When they compared each group and controlled for sociodemographic factors as well, a more complex picture emerged
that suggests how much the timing of motherhood matters.

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Early mothers were the least satisfied and most depressed of all four groups, while delayed or late mothers were the
most satisfied with their lives and the happiest. All other things being equal, the childless women were about as satisfied
and happy with their lives as the on-time mothers.
"In mid-life, being married or having a partner has a greater impact on a woman's well-being than whether or not she
has children," Pienta said.
Early mothers were the most likely to be single and to have lower incomesfactors that largely explained their lower
psychological well-being. Delayed mothers tended to have more education and higher economic status than other
groups, and were much more likely than early mothers to be married.
"Most studies have shown that psychological well-being tends to decline when people have kids," Pienta said. "And it
only rebounds much later, when the children have left home. So it was surprising to find the highest level of well-being
among the group that was most likely to have children still living at home or still in college. It suggests that delaying
motherhood may have some benefits for womenprobably related to being more career focused and having higher
social standing."
Today's younger women are opting to remain childless at much higher rates than young women of the 1950s, Pienta
said. "Rates of childlessness among women in their 40s doubled between 1980 and 1998 from 10 percent to 19
percent," she said. This study suggests that the outlook for psychological well-being later in life for today's childless
women is quite good.
Todays women are also getting married and having children later, changes that.
Pientas research suggests may benefit womens psychological health in later life. Her personal experience suggests
that there may be earlier benefits as well. "My mom was 40 when I was born and my father was 45," Pienta said. "As a
consequence, I received Social Security benefits in high school, as a dependent of parents who were receiving Social
Security. I enjoyed being a late-life child."
Pienta, 38, married at age 30, a little later than todays norm, after finishing her doctoral degree. "We decided to have
children as soon as possible after marrying, but by the time my first daughter was born I was in my mid 30s. We have
two little girls, ages 2 and 4. My parents feel much younger than their same-age peers. They are enjoying being
grandparents to preschoolers when most of their friends have grandchildren in college. And living in a college town like
Ann Arbor, I see a lot of other late mothers. As long as you beat the biological clock, waiting to have children has a lot of
advantages."
Note: This story has been adapted from a news release issued by University Of Michigan.

http://www.sciencedaily.com/releases/2007/05/070511080340.htm

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Alcohol Fuels Growth of Breast Cancer


May 9, 2007

May 1, 2007/The Express -- Women who have just two alcoholic drinks a day massively
increase their risk of developing breast cancer, scientists warned yesterday.
Even as little as two small glasses of wine daily can fuel a tumour, doubling its size in a matter
of weeks.
The findings are particularly worrying for women in the U.K., where binge-drinking is rife and
alcohol-related deaths are soaring.
A third of all British women admit to drinking a moderate amount of alcohol or more each day.
Until now, consuming up to two units a day was considered to have certain health benefits,
helping to prevent heart disease and cut the risk of strokes.
However,the latest study by American scientists has found that the same quantity of alcohol
can rapidly increase the risk of breast cancer, a disease that kills 12,400 women a year in
Britain alone.
Experts last night described the research as worrying. Ed Yong, of Cancer Research UK, said,
"We have known for some time that alcohol increases the risk of breast cancer.
"But this research suggests it can also promote the growth of existing tumours. The results
reinforce the message that women can reduce their risk of breast cancer by cutting down on
how much they drink."
In the study, researchers at the University of Mississippi Medical Center gave female mice the
human equivalent of two drinks a day for four weeks, while a control group of mice was given
no alcohol at all. In the second week, mouse breast cancer cells were injected into each
animal's mammary glands. few weeks later, the tumours in the alcohol-fed mice weighed 1.4g
on average, almost twice the size of tumours in the control group.
The researchers believe alcohol resulted in the larger tumours due to an increased growth in
blood vessels. Without blood vessels to feed the tumour with oxygen and nutrients, it would
die. But when alcohol is consumed, cells go into overdrive to get rid of the toxins, sending out
a hormone called VEGF that stimulates the growth of blood vessels.

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The alcohol-fed mice had raised levels of VEGF as well as more blood vessels than the other
mice.
Jian-Wei Gu, who led the research, said, "This is the first study to use an animal model that
accurately mimics human breast cancer.
"Normal people produce cancer cells every day but, at the beginning, the cancer doesn't have
blood vessels, so it's easier for the immune system to fend them off. Once the cancerous cells
acquire a blood vessel lifeline, fostered by alcohol, the tumour growth takes off."
More than 42,000 women in Britain are diagnosed with breast cancer every year. The figures
mean that about one in nine British women will now develop breast cancer at some point in
their lives.
Drinking one unit of alcohol a day increases a woman's risk of breast cancer by about 6%,
claims Breakthrough Breast Cancer.
From the May 9, 2007, Prepared Foods e-Flash

Chemical Compounds Boost Breast Cancer Risk


Pollutants, food ingredients, solvents may all cause harm, researchers say

HealthDay
Monday, May 14, 2007

MONDAY, May 14 (HealthDay News) -- A detailed analysis of hundreds of completed


breast cancer studies has linked disease development with environmental exposure to more than 200 chemical
compounds.
The finding is part of an effort to build a free, online breast cancer database for researchers and the public.

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Described as "the most comprehensive of its kind," the database will highlight growing concern about environmental
carcinogens such as pollutants, food contaminants, and organic solvents. The scope of the project will also extend to
work that explores risk-related lifestyle factors such as diet, levels of physical activity, smoking/drinking habits and body
mass.
"This compilation is a great effort, because it summarizes all the evidence and gives us hints of what to look for next,"
explained researcher Leslie Bernstein, a professor of preventive medicine with the Keck School of Medicine at the
University of Southern California in Los Angeles.
The results are outlined in a supplement to the May 14th online issue of Cancer. The database is already accessible at
either www.silentspring.org/sciencereview or www.komen.org/environment.
According to the American Cancer Society (ACS), carcinogens are defined as agents that instigate abnormal cell
division or harmful changes in the structure of a cell's DNA. They include chemicals, radiation, or infectious agents,
among other things.
The ACS also notes that with the exception of skin cancer, breast cancer is the most common cancer among American
women. This year, almost 179,000 women in the United States will be diagnosed with the disease, and about 40,000
will die.
The International Agency of Research on Cancer has already classified 90 or so compounds as human carcinogens,
according to the ACS. But Bernstein's team said that most of the chemicals to which people are routinely exposed have
not undergone any testing for carcinogenic risk. An estimated 80,000 chemicals are registered in the United States for
commercial use, according to the researchers.
For more than two years, Bernstein worked alongside colleagues from Harvard University, the Roswell Park Cancer
Institute, and the Silent Spring Institute to amass and sort through approximately 900 national and international breast
cancer studies focused on carcinogens.
The team honed in on 460 human breast cancer studies, of which more than 150 looked at specific environmental
carcinogens among breast cancer patients. Most of those studies were conducted in the 1990s.
The remaining studies involved animal or laboratory research. The researchers pointed out that animal studies are valid
references, because all human carcinogens that have so far been tested in animals have also triggered tumors in
animal subjects.
In the animal studies alone, evidence surfaced that linked 216 chemicals to the onset of breast tumors. These included
36 industrial chemicals, 6 chlorinated solvents, 18 products of combustion, 10 pesticides, 18 dyes, four type of radiation,
47 pharmaceuticals, and 17 hormones.
Of these compounds, the researchers isolated 73 that can be found in either human food or consumer products.
They noted, for example, the lingering hazards associated with polychlorinated biphenyls (or PCBs), which were
typically used in the production of electrical equipment until federally banned in 1979. PCBs continue to pose a risk via
contaminated rivers, fish, and pre-existing building construction, the researchers warned.
In addition, the authors categorized 35 compounds as carcinogenic air pollutants, including polycyclic aromatic
hydrocarbons (or PAHs), which are byproducts of combustion.
The team also drew attention to another group of 25 organic compounds, including dioxins, which are produced by
waste incineration and manufacturing. These carcinogenic chemicals are present in many American workplaces and
place more than 5,000 women at an increased risk for breast cancer, the researchers said. These include women
working in machine shops, dry cleaners, hairdressers, glass manufacturers, and aircraft maintenance facilities, all of
which use harmful organic solvents.
Furthermore, among the identified carcinogens, 29 are produced in large amounts -- upwards of one million pounds or
more per year.

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The database project did not set strict guidelines as to how to limit exposure to carcinogens. But the authors said they
encouraged research and government oversight into the problem. They advised that people do try and limit their
exposure to PCB-contaminated fish, gasoline-generated air pollution, chlorinated tap water, non-stick coated cookware,
and detergents containing fluorescent whiteners.
Just how carcinogenic, in terms of breast cancer risk, are these and other compounds on the list? The jury is still out on
that question, Bernstein said.
"Women are terribly concerned about environmental causes of breast cancer," she said. "But it's really very difficult to
study. Often the only way we've been able to look at some of these things is during occupational exposures or accidents
-- what we usually call disasters."
"So, this work is a very useful tool for those of us who want to try to understand what we've missed in breast cancer.
Now, it's up to us to do something with all this information," Bernstein said.
Janet Gray, a professor of psychology and the director of the program in science, technology and society at Vassar
College in Poughkeepsie, N.Y., called the new database "an enormous contribution."
"Its greatest value is just the sheer comprehensive nature of the work, which allows both the public and researchers to
have access to huge amounts of information in one place," she said. "I think this effort will really move us forward."
=======================================================================================

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10. Longevity Research


http://www.nia.nih.gov/HealthInformation/Publications/
http://www.longevitymeme.org/

Small Italian town gains top health honor


CAGLIARI, Italy, Jan. 27 (UPI) -- A small Italian town in the Sardinian province of Nuoro has been
named by longevity expert Dan Buettner as one of healthiest places in the world.
The Daily Mail said that the America's National Institute on Aging expert tabbed the small Italian community as the site
for some of the world's healthiest people along with certain parts of Costa Rica, the Japanese island of Okinawa and a
Loma Linda, Calif.
Just as Buettner discovered during his longevity research, professor Luca Deiana of Sardinia's University of Sassari
confirmed that while life is simple in the Italian community, such simplicity has its advantages.
"There are also lifestyle and environmental factors which are very significant. These people have no stress in their lives
at all," he said of the Nuoro's residents. "They are simple country folk who have worked hard and lived off the land -mainly cereals, fresh fruit, vegetables, olive oil and meat."
Residents in the area offer similar recommendations regarding a healthy lifestyle, but many added that such efforts go
beyond the physical.
"The family is very important and we respect the old," Gigliola Congiu, a resident in the town of Silanus, told the
newspaper.

http://www.sciencedaily.com/upi/index.php?feed=Science&article=UPI-1-20070127-18125800-bc-italyoldage.xml
Copyright 2007 by United Press International. All Rights Reserved

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11. How to Talk to Your Doctor, or Choose Another To Whom You Can Talk
http://www.aarp.org/health/staying_healthy/prevention/a2003-03-13-talkdr.html
http://familydoctor.org/online/famdocen/home/pat-advocacy/healthcare/836.html
http://familydoctor.org/online/famdocen/home/pat-advocacy/healthcare/837.html
http://medicine.ucsd.edu/clinicalmed/index.htm
http://www.realage.com/news_features/tip.aspx?dat=8_2_2007
http://www.realage.com/srch/RASearch.aspx?query=choosing+doctor

HOW TO TALK TO DOCTORS


David Elfstrom
david@elfstrom.com

Be assertive and take an active role to improve your health care.


April 1997
Revised Feb 2000

As a person with chronic inflammatory arthritis, I have seen many physicians, surgeons and
specialists. Here's a few things I do to make appointments with my doctors run smoothly. Using
these strategies, my doctors have been more open to trying new treatments that I suggest. At the
same time, it's helped to identify other health problems that could have been overlooked. It's also
kept me from falling between cracks in the health care system and caught small mistakes made by
doctors. The end result is that my health has improved, going to see the doctor is no longer stressful
or alarming, and I find myself eagerly anticipating my next visit.

Keep a record of your health events.


Keep a daily log or journal of events related to your health care. You don't need to write down
something every day, just write down the important events related to your health. Here are
some suggestions:
blood test results -- make a table on the first page of your journal and fill it in at your
next visit..
o dates of corticosteroid injections
o dates and locations of diagnostic procedures (X-Rays, MRI, bone scan)
o dates starting and stopping a medication
o

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dates medication missed


stressful events in your life
unusual symptoms - quantify it: Instead of "I feel feverish today", write: "Today my
temperature was 101 degrees Fahrenheit". Instead of "I'm very thirsty", write "I drank
4 L of water today and I'm still thirsty".
o typical symptoms - quantify it: Rate your pain, stiffness, emotions on a 10-point
scale, where 1 = "Not noticable" and 10 = "Can't move!". Example: October 16: Back
pain=4, Knee swelling=7, Anxiety=2
o
o
o

Later, you will find this information invaluable when you see another doctor for the first time.
It's even great for your regular doctor. If you are like me, my regular doctors have a two-inch
thick folder of paperwork about me. When I want a corticosteroid injection, rather than
looking in the file, my rheumatologist asks me: "How many injections have you had in that
joint?". Do you think he wants to spend time looking through that huge file? No. But you
know the answer, because you've written it down in your journal.
Keeping the journal on a computer is a good idea. You can print a selection of it any time you need one. How to organize the diary is up to you, but
over time I have split up my journal into these sections:

1. Doctors. A list of doctors' full names, specialty, address, telephone numbers, fax
number, email (if you're lucky), receptionists' names, date of first visit, and even the
date of final visit if you are no longer a patient there. When I see a new doctor, I bring
this along because sometimes they want to contact a previous doctor. I print out two
copies of this list: one for my home phone book and one for my daily planner.
2. Blood Tests. Record your blood test results and the date the blood was drawn. By
recording a copy yourself, you can keep everything together and correlate changes in
your body with changes in your blood. In my journal, I include the lab's stated limits
for normal people and my doctor's interpretation of the test. I print out a copy of the
table and take it with me to each appointment to remind me to ask for the latest
blood test results.
3. Condensed Journal. Every month, summarize the regular journal in this section.
Just the facts. It's short, point form, one-line summaries. I send this to a new doctor
before the first appointment. To the doctor, this is a gold mine. It's a complete history
already prepared! She doesn't have to ask as many questions and I don't worry
about forgetting an important event in my medical history. Here is a sample:
March

Two weeks after the corticosteroid, my knee has filled up with fluid again.
High thirst (drinking 4 L of water daily) still continuting
1st visit with Dr. Lochnan
Dr. Lochnan: Blood test results: No calcium in blood
Radioactive iodine uptake thyroid scan done

April

Liver enzyme levels high (AST is 116)


Methotrexate and folic acid stopped
Second liver enzyme level test shows AST is down to 65
Dr. Lochnan's diagnosis: I have a hyper functioning thyroid nodule, NOT Grave's

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disease. Referral to Dr. Eisen.

4. Regular Journal. The gory details. Record how you felt, what your doctor said, exact
procedures that you had, including locations and dates. Remember, you'll be going
over it again to make the monthly summary. So be expressive. If you're experiencing
pain or other symptoms on a daily basis, you can keep track of your progress by using
the 10-point scale as mentioned above. Write down everything you feel is significant. I
keep this part private. Often just writing things down makes me feel better, because I
know I don't need to think about it anymore. If what I'm experiencing later turns out
to be an important symptom, it's down there in black and white so I don't have to
remember it weeks later at the doctor's office.

Read as much as you can about your illness and treatments.


Since you're reading this document, you're already on the right track! But you need a good
solid resource at your fingertips. Go to a bookstore and buy the following:
1. One of the latest guide to prescription drugs. If the one you have is three years
old, throw it out and get a new one. More than once I have been misled by an older
edition of this type of guide. I currently have three:
Long JW, Rybacki JJ: The Essential Guide To Prescription Drugs 2000. Harper
Resource, New York, 1999. Note that these books are post-dated for longer
bookstore shelf-life. From October onward, you can usually find next year's
edition.
Silverman HM, ed.: The Pill Book, 8th Edition. Bantam Books 1998.
Berner MS, Rotenberg GN: Canadian Medical Association new guide to
prescription and over-the-counter drugs. The Reader's Digest Association
(Canada) Ltd., Montreal, 1996. This is the best drug book I've ever seen. It's
much more than just drug listings. It's much cheaper and faster to order from
Canada directly than to special-order the book through Amazon.
I recommend that you avoid purchasing a pharmacist's book. It lists every single side
effect ever reported for each drug, easily leading you to attribute any little change in
your body to the medication you're taking.
2. A medical dictionary. I find the paperback book The Bantam Medical Dictionary
(Bantam Books, 1990) to be the best combination of price and readability. There are
other dictionaries with more terms, but the definitions are more complicated. The
cross-referencing in the Bantam Medical Dictionary is excellent. Later, if you outgrow
the basic medical dictionary and become interested in the Big Picture, I highly
recommend the following textbook: Totora GJ: Principles of Anatomy and Physiology,
9th ed. John Wiley & Sons, New York, 1999. If you're an information junkie like me,
move on up to Taber's Cyclopedic Medical Dictionary 18th ed. (F. A. Davis Company,
1997). However, some of you may be overwhelmed by Taber's graphic, full-color
photos of human diseases.

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Prioritize appointment objectives.


Before your appointment, type up a list of things that you wish to have addressed. Remember
that your doctor is busy and won't have a lot of time, often only 10 or 15 minutes. Put the list
in point form only, to keep you from reading directly off the sheet, and to prevent distracting
your doctor. Sort them by what you think the priority should be. Print out two copies, one for
yourself and one for your doctor. Keep it short and simple. Here's a sample:
Dr. Feelgood, March 1st 1997. 3pm
Current medications:
Cytotec 250 micrograms twice daily
Voltaren 50 mg slow release twice daily
[etc.]

Discuss: (most important first)

my occasional dizziness
stomach ache
obtain last session's blood test result
what are the symptoms of a yeast infection?
inquire about the risk of developing an ulcer
(if time) discuss the recent reports in the media that NSAID use can prevent
Alzheimer's.

It's important to give a copy to your doctor at the start of the appointment. There might be a
symptom that triggers a warning flag but you thought was unimportant. The priority of the
items on the list may change during your meeting, but as long as you have the list your doctor
will be able to cover the important ones.

Be Assertive.
When you're in the waiting room, resist the temptation to read your favorite magazine.
Instead, read over your agenda. Picture what you're going to say, and how you're going to say
it. Get the point where you know exactly what is on your list without looking at it. You want
the discussion to be natural and smooth.
When you are talking with your doctor, remember to avoid being passive AND avoid being aggressive. Instead, be assertive. There is a good
discussion with examples on being assertive at Mediconsult's web site.
Take a pen in with you and write down notes/answers to your questions next to your agenda items. If you can't write because of arthritis or other
reasons, ask your doctor to write down key words for you.

KEY POINT:

AVOID bringing published material and printouts to the appointment. (The only exception should be your little agenda
sheet). Such information is distracting for your doctor. They love paper! I end up feeling ignored. Don't keep it to the end of the appointment and
present it at the last minute, either. If you give it to him at the end of your appointment, the article may not get read, or it will distract the doctor from
his next patient. It takes time for your doctor to read and digest new information.
Instead, fax / mail / drop-off the information BEFOREHAND with a covering note saying that you'd "like to discuss this at our next appointment, on
March 23". I have never met a doctor who didn't appreciate this. However, when you do send them something, make certain that you READ it over
three times yourself. Look up words in your medical dictionary. Learn to pronounce and spell the hard words. My rheumatologist was very
impressed when I knew how to spell sulfasalazine, because he always got it wrong himself. If the words are very difficult, at least make your best
effort to understand the introduction and conclusion, the important parts. Later, you can ask your doctor to clear up any confusion.

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Doctors are people too, and anything you can do to make their task easier means they appreciate you more. You will earn their respect. The street
goes two ways. Remember in school when you talked about your teachers outside? Guess what... they talked about their students too. The same
applies to doctors. I've heard the receptionists and the doctors talk about their patients -- which ones they liked and which ones were annoying.
Treat the receptionists with respect too. They often get dumped on and can be real sticks in the mud at times. They have bad days just like everyone
else. Be very friendly with them. Never get angry at them for a long waiting period. If it's a big concern, write it down in your journal, and bring it up
with your doctor at the next appointment -- just don't be aggressive! Be assertive.

Avoiding the Power Struggle - Convincing a skeptical doctor to try


something new.
At times, a meeting with your doctor can feel like a battle. Perhaps you've read about a new
treatment on the news that sounds exciting. Who knows your body better than yourself?
You've read the drug information book, you know what symptoms to expect. You're being an
educated patient. And yet here's the doctor shooting holes in your arguments and resisting
your suggestions of new treatments to look into. What's gone wrong?
First of all, remember what I said about bringing paper into the meeting. DON'T bring in an article. Fax it a few days ahead of time with a small note.
But there is something else to consider: the medium itself, and how it is delivered, rather than the message. A printout from the web (even this web
page, I'm sorry to say) has less impact than a professionally-printed, multi-colored pamphlet. My doctors are well aware of the misinformation and
scams present on the web. In fact, they instantly turn off when I say the "Internet". So, I've stopped saying "Internet" or "the web". Now I say, "This
information is from a non-profit organization that specializes in ..."
Do all that you can to earn the respect of your doctor. To do this, you need to make your doctor's job easier. You've done that already by keeping a
diary, being educated, using an agenda and being assertive. One extra skill that takes a lot of practice is clearing a mental path for your doctor to
follow and allowing her to do her job. An example will help illustrate my point.
When I first started taking minocycline, I did not go to my doctor and say "I'm experiencing a Jarisch-Herxheimer Reaction". Leave the diagnosing to
them - it's their job. Instead, describe the symptoms. If they don't make the connection, give them a hint, but be subtle. Pretend you just thought of it.
Say "you know, I think I've heard about this type of thing before, only it was in people who had Lyme disease. They often get a fever after taking
antibiotics too, don't they?" By leaving the diagnosing to your doctors but helping them along, you can safely leverage their knowledge and earn
their respect at the same.
You see, it's entirely possible that you may be wrong. Once upon a time, I was convinced that the annoying thirst I was experiencing was due to
methotrexate. After all, the drug book recommended I drink lots of fluid with this drug. But when I told my doctor about this, he said the medication I
was taking could not cause me to be thirsty. The next time we met, I again told him that I was thirsty, and insisted it was the methotrexate. He
sidestepped the issue and quietly snuck in some extra blood tests that I wasn't aware of. As it turned out, he uncovered a problem in my thyroid
gland, something completely unexpected. I was correct to be assertive because the symptom turned out to be very important. But I was wrong to be
telling him what my diagnosis should be. If I had brought up the subject differently, he would have told me what tests he was running instead of being
secretive.
Always let doctors think of things for themselves. You're coming to the doctor to ask for their professional advice, not to tell them how to treat you. If
you want to try IV-delivered antibiotic therapy for inflammatory arthritis, you'll have to guide your doctor so he will conclude on his own that IV
antibiotic therapy will be beneficial. You can help by earning their respect and providing them with the information that they ask for. Sometimes it
will take two or three more appointments. Stick with it, be assertive, be patient.
Hopefully you have found these suggestions beneficial. Go to it!

Summary
Here's a summary in case you read like I do, skipping right to the end for the good parts:
Keep a medical diary of all significant health-related events.
Educate yourself: Seek out new treatments. Know everything about the medications
you are taking. Understand terminology using your medical dictionary.
o Write down a concise list of items to discuss before each appointment. Bring two
copies.
o Don't bring any other photocopies, Internet printouts, or newspaper clippings to the
meeting. Instead, fax them a few days ahead with a polite note saying that you'd like to
discuss them during your appointment. Be careful when using documents without
references and potentially misleading sources like the Internet.
o Be assertive rather than aggressive or passive.
o
o

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Be educated about your illness and symptoms, but leave the final diagnosing to your
doctor.

How to Talk to Your Doctor - The Doctor's Perspective


By: Patricia L. Raymond, MD, FACP, FACG, Norfolk, Virginia
(Reprinted from Participate, IFFGD, 1998)

http://www.aboutibs.org/

Functional gastrointestinal (GI) disorders, such as irritable bowel syndrome (IBS), have a wide variability in symptoms
and activity and require a lot of patient help in the management of the disorder. However, most physicians have been
forced by the economics of managed care to see more patients in less time than ever before. Patients with functional GI
disorders often tend to require more time than the average patient because multiple factors may be involved-time to
discuss things like diet, stress, or exercise, and their effects on this disorder.
Presently, a follow-up appointment in our office lasts for precisely 15 minutes. This includes the time it takes to clean the
room after the preceding patient, to have you change your clothes, and to make an entry on your chart. Certainly it is
important that you get the most out of the remaining 10 minutes when you can actually talk to your doctor.
Here are a few suggestions which can help improve the worth of the time that you do have with your physician.
Be Scientific - Functional GI disorders such as IBS require a lot of insight into dietary, stress, and behavioral variables.
My patients with the most success in managing their IBS tend to be scientific about their disorder. They record in a diary
(which may be obtained from IFFGD) things like stool patterns, diet, and activity. They bring the diary to my office where
we review and analyze it together.
For instance, together we may find trends in foods which cause more gas or bloating, unsuspected lactose intolerance
or sensitivity, or other hints to improve the management of this quite variable disorder.
Be Organized - Just as with the diary above, my most successful patient interactions include more time with me
because many baseline questions have already been answered by organized patients. Some patients routinely bring in
a list of what might be important medical information, such as medications with their frequency and dosage, a list of
allergies, or a list of current diagnoses for which they are being treated by other physicians.
Often, we find that a patient's medications are being taken too frequently or are not being taken with enough frequency
to improve the symptoms. Additionally, many drugs may cause side effects which mimic IBS. With a list of medications,
we can see any drug interactions (or possibly duplicate medications), cut the costs of medications, and improve side
effects.
Be Inquisitive - I am delighted when a patient brings with them a list of direct questions. That allows them to direct our
conversation and education to specific areas of interest or concern about their disorder. It is most disturbing to be
contacted by a patient, who has been seen in the office earlier that day, with questions that might have been asked face
to face for better understanding.
Be sure to ask your physician if there are new therapies available More from IFFGD - Guidelines on talking to your doctor and
Worksheet
or studies going on locally in the management of IBS such as
new drug studies, or behavioral management or hypnotherapy
studies. In addition, ask your physician whether there are any functional bowel disorder support groups locally. This may
prompt your physician to become the medical director of such a group.

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Be Interactive - The diagnosis of a functional GI disorder, once established, requires more partnership with your
physician and more personal responsibility than many other gastrointestinal disorders. Take charge of your disorder,
record your symptoms, be prepared for your doctor appointments with lists of medications and questions, and look for
other ways to manage your disorder, such as new therapies, diets, studies, stress control groups, and support groups. If
you have difficulty remembering the conversation and teaching of your physician, consider asking them if you could use
a tape recorder at your office appointments.
In Summary - Do your best to make the most of your all too brief interaction with your physician. Do not let your
appointment - for which you have prepared, driven to the physician's office (perhaps through rush-hour traffic), waited
for (yes, we know that we are generally late), and are then ushered into the office - deteriorate into a brief, "So how are
you doing," conversation. Make every moment count.

12. Complementary Medicine


http://nccam.nih.gov/
http://orthomolecular.org/index.shtml
http://altmedicine.about.com/library/bl_remedy_finder.htm

Save Your Heart


Dr. Michael Colgan

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When the first confirmed case of atherosclerosis was reported in the Journal of the
American Medical Association by Dr. James Herrick in 1912, the disease was so rare most
physicians could not find a single case. Seventy-seven years later, the same journal reported 60
million cases across America. We did it all to ourselves! The leading cause of death in
America is cardiovascular disease, responsible for some 40% of deaths. The next leading cause
of death is cancer at only 24%. Lets look at the major risk factors for cardiovascular disease.

Diet:
High saturated fats (over 25% of calories).
High trans-fats.
High sugar.
High glycemic (over 405 of calories).
High acid diet (regular use of antacids).
High salt diet (over 2 grams per day).
Low essential fats (under 20 grams per day)
Low fiber (under 30 grams per day).
Low B6, B12 and folic acid vitamins.
Low antioxidants.

Exercise:
Less than 30 minutes aerobic exercise five times per week.
Less than 30 minutes resistance/weight exercise three times per week.

Other Factors:
Smoking
Chewing tobacco
Exposure to second-hand smoke
Women with bodyfat over 23%
Men with bodyfat over 18%
Insulin resistance
Juvenile diabetes and adult-onset diabetes.
Stress
Depression
The more risk factors you have, the higher your chances are of having heart disease.
Combine these factors with the blood test indicators below and you could be on borrowed time.

Blood Test Indicators of Cardiovascular Risk Used at the Colgan Institute:


Total cholesterol above 168 mg/dl
LDL/HDL ratio over 3:1
Total cholesterol/HDL ratio above 3.5:1
Homocysteine above 12.0 umol/L
Blood pressure above 120/80 mmHg
Hemoglobin A1c above 5.5%
Triglycerides above 100 mg/dkl
Fibrinogen above 400 mg/dl
Insulin above 25 uU/ml
C-reactive protein above 0.5 mg/L
Albumin/globulin ratio below 1.1
So what can you do to help lower your risk. Dietary changes seem obvious and all follow
healthy eating practices. The exercise component is also straight forward, though it involves a
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greater time commitment. The other risk factors can be more difficult to eliminate or prevent.
Lets take a closer look at the mechanisms of atherosclerosis.

Atherosclerosis:
Most folk know that the typical American high-fat diet will raise cholesterol to high risk
levels within a month, and that a low-fat diet will lower them. This heart disease risk starts to rise
at a cholesterol level of 168 mg/dl. Regular exercise yields high levels of high-density
lipoproteins (HDL), the good cholesterol that scrubs and vacuums excess cholesterol off the
walls of your arteries. However, the major mechanism by which atherosclerosis takes hold is
oxidation. It starts with cells of your immune system called monocytes. These stick to the
arterial wall, then pass through it and transform into scavenger cells called macrophages that
gobble up wastes. This is what is supposed to happen. Problems arise when you subject the
system to excess free radicals, such as polluted city air, pesticide contamination or many
prescription drugs. Exercise is also a potent source of oxidation.
These excess free radicals begin to oxidize little particles of cholesterol called low-density
lipoproteins (LDL). The immune system macrophages in the arterial walls recognize the oxidized
LDLs as toxic to the body and gobble them up. If you have excess LDLs, the macrophages soon
become overstuffed with LDLs and breakdown into pathological cells called foam cells. These
foam cells form the fatty streaks on the arterial walls that are the beginning of atherosclerosis.
What can you do to inhibit the oxidation of LDL? Since 1988 seven cell and animal
studies have reported that vitamin E reduces LDL oxidation. Sixteen human studies have
reported that supplements of vitamin E reduced LDL in healthy subjects, smokers and diabetics.
The effective doses used were between 400-1600 iu per day, but supplementation had to
continue for a minimum of five months for changes to start to take place.
Fourteen animal studies since 1990 report that vitamin E, beta-carotene or combinations
of the two, with or without vitamin c, inhibit and even reverse induced atherosclerosis. A
representative study in monkeys reports regression of induced atherosclerosis from 33% to 8% in
eight months of supplementation.

Prevention of Heart Disease


Since 1989, 11 epidemiological studies have reported an inverse relationship between
plasma vitamin E and heart disease, including angina. Eight studies have reported the same
protective effects with beta-carotene and five studies report the same protective effect with
combinations of vitamin E, vitamin C and beta-carotene.
Media attention always focuses on those studies with poor results. The ATBC study in
Finland took 29,133 male smokers aged between 50 and 69 who had smoked an average of 21
cigarettes a day for an average of 36 years. All subjects continued to smoke. They were given
20 mg of synthetic beta-carotene and 50 mg of synthetic vitamin E for 5-8 years. There was no
effect. This study was a little like a flea trying to stomp an elephant. Much too little, and way too
late. The Physicians Health Study took 22,071 male physicians, aged between 40 and 84. They
were given 50 mg of beta-carotene on alternate days for 12 years. Overall there was no effect.
Again the dose was too small.
There have been a large number of studies showing positive trends. In the HOPE study
9541 high-risk patients aged 55+ with existing heart disease, diabetes or other health problems
were given 400 iu of natural source vitamin E for 4.5 years. These results showed a progressive
trend towards positive effects. The researchers report that in high-risk groups effects may take 5
years or more to show. In the GISSI study in Italy, 11,324 patients who had survived a heart
attack were given 300 iu of vitamin e, or 1 gram of omega-3 fish oil, or both for 3.5 years. There
was a 35% reduced risk of sudden death. And finally, in the CHAOS study in England, 2002
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patients with atherosclerosis were given 400-800 iu of vitamin E for 200 days. There was a 47%
reduced risk of myocardial infarction.
In 1997 a study reported in the Journal of the American Medical Association, showed that
1000 mg of vitamin C, plus 800 iu of vitamin E, (17 and 26 times the RDA), directly prevent
damage to arteries caused by high-fat food. An editorial in the same journal stated that The era
of nutrient supplements to support health and reduce illness is here to stay.
In April 1998, after 57 years of denial the RDA Committee of the National Academy of
Sciences finally admitted that the American diet does not contain sufficient nutrients for normal
health, and recommended that almost all Americans take vitamin supplements. And finally in
June 2002, after over 100 years of denial, the Journal of the American Medical Association
recommends daily vitamin supplements for Americans, tailored to the patients medical
profile, vitamin tests and lifestyle.
At the Colgan Institute we have been doing this since 1984. Our Daily Supplement Pak
formulas are designed by our computer matrix program that formulates for all our private clients,
using all the variables and physiological data from our testing procedures. We then provide our
private clients with their individual supplement program. To develop the Daily Supplement Paks,
we then set the computer program to design formulas for a specific set of variables to match, for
example, an average women over 50 (Womens 50+ Pak), a 30+ active lifestyle suburban man
and woman (Mens and Womens Active Paks) or a top competitive athlete (Athletes Pak). Our
Add-On Paks were then designed by giving the computer a set of variables with particular
problems (prostate, arthritis, vision, brain anti-aging, etc).
The specific nutrients that are directly involved in a healthy heart are:
Vitamin E (natural not synthetic): 400 1600 iu per day
Beta Carotene (natural not synthetic): 15 50 mg per day
Vitamin C: 1 4 grams per day
Omega-3 essential fats: 10 40 grams per day
As always these nutrients should only be taken in conjunction with a complete
supplement program. Individual nutrients do not work on their own, and for best effects you must
take all nutrients together. The amounts above would be the total amounts for the day. There
are no known toxic side-effects for these nutrients in this range.
American Heart Association, 19th Forum, 12th January 1992.
Verlangiari, J Am Coll Nutr, 1992;11:130-137.
New Engl J Med, 1993;328:1444-1456.
JAMA, 1997;278:1662-1686.
JAMA, 1997;277:1398-1399.
New Engl J Med, 9 Apr 1998.
JAMA, 2002;287:3127-3129.

Colgan Institute Canada


988 North End Road, Salt Spring Island, British Columbia, V8K 1L7, Canada
PH: 250-537-2069, Fax: 250-537-5824, Email: admin@colganinstitute.com
http://www.colganinstitute.com/

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These flowers (from left to right: San Martn spiral ginger, torch ginger,
Orchidantha and Heliconia) are all different species of ginger.

13. Herbalsim
http://www.herbalgram.org/default.asp
http://www.medicinehunter.com/index.html
http://www.rain-tree.com/index.html
http://www.herbmed.org/index.asp
The Green Pharmacy Herbal Handbook, James A Duke
http://www.mothernature.com/Library/Bookshelf/Books/41/1.cfm
Green Pharmacy, Barbara Griggs
The Herb Book: The Complete and Authoritative Guide to More Than 500 Herbs, John Lust
Holistic Herbal: A Safe and Practical Guide to Making and Using Herbal Remedies, David
Hoffman
===================================================

14. Regulatory Topics


http://www.fda.gov/
http://www.cfsan.fda.gov/~dms/ds-ind.html
http://www.hc-sc.gc.ca/
http://www.nih.gov/
http://www.quackwatch.org/05Links/othersites.html
http://www.ftc.gov/bcp/conline/pubs/buspubs/dietsupp.shtm
http://www.crnusa.org/
http://www.consumerlab.com/
==========================================================================
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15. Legislative Developments


Life Extension Foundation Legislative Action Center
http://www.LEF.org/lac/

FDA's CAM guidance ripe for misinterpretation, CRN


By Clarisse Douaud

The Council for Responsible Nutrition (CRN) has reported that the US Food &
Drug Administration's CAM guidance fosters misinformation that certain
Complementary and Alternative Medicine products should be regulated as drugs.

5/9/2007-

The trade association is the latest to join public discourse on FDA's draft "Guidance for industry
on complementary and alternative medicine products and their regulation by the food and drug
administration". In February, FDA opened a comment period and announced the availability of
the guidance, asserting it is just a point of reference and not in fact regulation.
But the dietary supplement industry has voiced its fear that the document will engender
confusion about which products apply, and who in fact regulates them.
"the draft guidance creates the misinterpretation that certain CAM products that are properly
regulated as dietary supplements should be regulated as drugs," wrote Andrew Shao, CRN vicepresident of scientific and regulatory affairs, in the comment addressed to FDA.
In the draft guidance, FDA uses the NCCAM (National Center for Complementary and Alternative
Medicine) definition for CAM: "a group of diverse medical and health care systems, practices, and
products that are not presently considered to be part of conventional medicine."
Of primary concern to CRN is the omission of qualifying language relating to how dietary
supplements are excluded from being a "drug" as defined in the Federal Food, Drug, and
Cosmetic Act (FD&CA).
For instance, says CRN, the guidance's definition of a drug excludes section 403 (r) of the Act,
which outlines how a food or dietary supplement with an FDA-approved health or
structure/function claim is not a drug.
In addition, CRN urges that the draft guidance include information on FDA-approved health
claims and qualified health claims in its discussion of dietary supplements. Health claims are
playing an increasingly crucial role for dietary supplement marketing and research.
Under FD&CA, use of claims implies a product is a drug. However, the Nutrition Labeling and
Education Act (NLEA) made labeling of packaged foods compulsory in 1993 and paved the way
for label claims that relating certain foods to disease risk reduction.
CRN also finds fault with FDA's supposition that bacteria in a probiotic product could run it into
the category of a 'biologic product' subject to the Public Health Service Act. The trade association
asserts probiotics are food components subject to FD&CA.
The American Herbal Products Association (AHPA) recently called on FDA to withdraw the CAM
draft guidance - stating it will only cause misunderstandings in the industry.
"The effect that the guidance has had on industry to date is to cause significant confusion," AHPA
president Michael McGuffin told NutraIngredients-USA recently. "Unless FDA either withdraws it
or corrects it and identifies the failure that it is attempting to address, it will continue to have
that effect."
AHPA said there is great potential for confusion surrounding what the guidance is for, what
products it refers to, and cited it as an example of federal resources badly spent.

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http://www.nutraingredients-usa.com/news/printNewsBis.asp?id=76400
DSHEA slightly strengthened.
The recently passed federal Dietary Supplement and Nonprescription Drug Consumer Protection
Act (S. 3546) will require manufacturers of dietary supplements and nonprescription drugs to notify
the FDA about serious adverse events related to their products.
http://www.nutriwatch.org/09Reg/s3546.pdf Beginning in December 2007, manufacturers must
report deaths; life-threatening experiences; inpatient hospitalizations; persistent or significant
disability or incapacity; birth defects; or the need for medical intervention to prevent any such
problems. Manufacturers will also have to place a telephone number or address on product labels
so consumers can contact them. The bill was passed in response to concerns about how difficult it
was for the FDA to ban ephedra sales even though thousands of people had adverse effects.
Congress reasoned that if notification could be increased, the FDA could do a better job of
identifying and dealing with dangerous products. However, public protection is only slightly
increased because other parts of DSHEA make it very cumbersome for the FDA to ban dietary
supplements and herbs. [Barrett S. How the Dietary Supplement Health and Education Act of 1994
weakened the FDA. Quackwatch, updated Feb 2, 2007]
http://www.quackwatch.org/02ConsumerProtection/dshea.html
Many prescription drugs ads are misleading.
Opponents argue that direct-to-consumer (DTC) ads mislead consumers and prompt requests for
products that are unnecessary or are more expensive than other equally effective drugs or
nonpharmacologic treatment options. Proponents counter that such ads educate people about
health conditions and available treatments and empower them to become more active participants
in their own care. Five researchers who studied DTC television ads for 24 prescription products
have
reported:
**82% of the ads made some factual claims, 86% made rational arguments for product use, but
nearly all (95%) included emotional appeals.
**Most ads framed their message in terms of losing (58%) and regaining control (85%) over some
aspect of life and as engendering social approval (78%).
**58% of the ads portrayed the product as a medical breakthrough.
**Only about 25% described the causes, risk factors, or prevalence of the conditions for which the
drugs might be useful.
**Lifestyle change was never mentioned as an alternative to products, but 19% portrayed it as an
adjunct to medication and 18% portrayed it as insufficient for controlling a condition.
The authors concluded:
"Despite claims that ads serve an educational purpose, they provide limited information about the
causes of a disease or who may be at risk; they show characters that have lost control over their
social, emotional, or physical lives without the medication; and they minimize the value of health
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promotion through lifestyle changes. The ads have limited educational value and may oversell the
benefits of drugs in ways that might conflict with promoting population health."
[Frosch DLL and others. Creating demand for prescription drugs: A content analysis of television
direct-to-consumer advertising. Annals of Family Medicine 5:6-13, 2007]
http://www.annfammed.org/cgi/reprint/5/1/6
An accompanying editorial by former FDA Commissioner David A.
Kessler, M.D. and a public-relations expert stated:
"Patients have always expected simple answers to complex questions, but direct-to-consumer
(DTC) advertising has elevated this problem to new heights, because patients in some ways now
rely on Madison Avenue as a provider of health information. There is nothing wrong with
pharmaceutical companies communicating directly with consumers, but they should adhere to the
standards and ethics of medicine, not the standards and ethics of selling soap or some other
consumer product that presents minimal risks. . . .
"Equally important is the possibility-the likelihood-that consumers who make health decisions based
on what they learn from television commercials ultimately take medicines they may not need, spend
money on brand medicines that may be no better than alternatives, or avoid healthy behaviors
because they falsely think a medicine is all they need." [Kessler DA, Levy DA. Direct-to-consumer
advertising: Is it too late to manage the risks? Annals of Family Medicine 5:4-5, 2007]
http://www.annfammed.org/cgi/reprint/5/1/4
The full text of both articles is available online free of charge.

GMPs on their way, White House tells Senator Hatch


By Clarisse Douaud

Senator Orrin Hatch's office received notice that FDA's Good Manufacturing
Practice (GMP) legislation has received final clearance from the White House Office of
Management and Budget, giving industry the signal to start preparing itself for the
impending changes.

5/10/2007-

Senator Hatch's office in Washington confirmed for NutraIngredients-USA that Senator Hatch
received a phone call from Rob Portman, the head of the White House Office of Management and
Budget, Wednesday. Portman informed Senator Hatch, a representative of Utah and frequent
advocate for the dietary supplement industry, that the legislation is likely to be published in five
weeks.
This development represents a ray of light for many parties within the dietary supplement
industry, which has been waiting for GMP legislation for twelve years.
A statute of the 1994 Dietary Supplements Health and Education Act (DSHEA), GMP legislation
has been referred to as the missing link in the overall governance of the dietary supplement
industry. The legislation will provide standards specific to this industry regarding purity, safety
and legality in manufacturing.
Republican senator Hatch, one of the principal authors of DHSEA, and Democrat senator Tom
Harkin from Iowa have been pushing for the legislation as a means to finalize the Act.
However, contrary to reports in the mainstream US media, industry stakeholders insist the
dietary supplement industry is in fact already regulated.

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"Sometimes you hear the mainstream media say this industry is not regulated," David Seckman,
executive director and CEO of the Natural Products Association, told NutraIngredients-USA. "They
will have to hang that statement with this mainstay regulation."
GMP regulation will provide the industry will further tangible evidence against "erroneous"
accusations, NPA vice president of scientific affairs Daniel Fabricant told NutraIngredients-USA.
In the coming weeks, it is not likely that trade associations will be able to answer many of their
members' questions on GMPs because they themselves will not see the document until it is
released online as part of FDA's (US Food & Drug Administration's) Federal Register. It
will subsequently be published in paper form.
Industry organizations and companies alike will then have their work cut out for them as the
document is set to be approximately 1300 pages in length. "Interpretation is the key," said
Seckman.
Trade organizations will then finalize educational sessions or workshops to inform industry on
how to comply with the regulations, which will depend on how the final draft of GMPs has turns
out.
"It's hard to tell until you see the final regulation," added Seckman.
The FDA draft of GMPs issued to industry for comment in 2003 allowed for a one- to three-year
implementation period for manufacturers to comply based on the size of the company.
NPA said it already has a lot of the elements in place for helping companies with Good
Manufacturing Practices and is plugging the third party GMP certification program it has run since
1999 as a means for companies to ensure they have the appropriate procedures in place.
"We think our certification program is a great way for companies to be prepared for this," said
Seckman.
The industry will also have the opportunity to comment to FDA on GMPs, which will be
categorized as an 'interim' final regulation and therefore subject to change. However, any desired
modifications could take a long time.
Trade associations will be waiting to see what changes have been made to the document since
2003 and to what extent their comments were taken into account. NPA was concerned at the
time that the GMPs were not as close to food GMPs as they had hoped and required more
stringent finished product testing.
The political advocates behind the regulation will also be going over it with a fine-tooth comb.
"Since it took an unusually long time to issue these final guidelines, I want to review the final
version very carefully to make certain they are good regulations," said Senator Hatch in a written
statement. "Every indication leads me to believe the Administration was very sensitive to the
impact the GMPs might have on the industry, especially on small businesses."
The Council for Responsible Nutrition reported to the media it is planning educational meetings
for members and non-members and that an announcement to this effect will be made in the
coming weeks. The United Natural Products Alliance has also been asking members to save
certain dates for yet-to-be finalized GMP workshops.

http://www.nutraingredients-usa.com/news/printNewsBis.asp?id=76457
=====================================================================

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16. Archives of Nutrition-Related Sciences: Selected interesting articles from the history of nutrition
and health-care.
_________________________________________________________________________________________
JOURNAL OF APPLIED NUTRITION, VOLUME 48, NUMBER 3, 1996
ORIGINAL
REPORT
Copyright - International Academy of Nutrition and Preventive Medicine
NUTRITIONAL SUPPLEMENT PROGRAM HALTS
PROGRESSION OF EARLY CORONARY ATHEROSCLEROSIS
DOCUMENTED BY ULTRAFAST COMPUTED TOMOGRAPHY
Matthias Rath, M.D. and Aleksandra Niedzwiecki, Ph.D.
ABSTRACT: The aim of this study was to determine the effect of a defined nutritional
supplement program on the natural progression of coronary artery disease. This nutritional
supplement program was composed of vitamins, amino acids, minerals, and trace elements,
including a combination of essential nutrients patented for use in the prevention and reversal of
cardiovascular disease. The study was designed as a prospective intervention before-after trial
over a 12 month period and included 55 patients (age 44-67) with various stages of coronary
heart disease. Changes in the progression of coronary artery calcification before and during the
nutritional supplement intervention were determined by Ultrafast Computed Tomography
(Ultrafast CT). The natural progression rate of coronary artery calcification before the
intervention averaged 44% per year. The progression of coronary artery calcification decreased
on average 15% over the course of one year of nutritional supplementation. In a subgroup of
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patients with early stages of coronary artery disease, a statistically significant decrease occurred,
and no further progression of coronary calcification was observed. In individual cases, reversal
and complete disappearance of previously existing coronary calcifications were documented.
This is the first clinical study documenting the effectiveness of a defined nutritional
supplement program in halting early forms of coronary artery disease within one year. The
nutritional supplement program tested here should be considered an effective and safe approach
to prevention and adjunct therapy of cardiovascular disease.
Key words: Coronary heart disease, Ultrafast Computed Tomography, nutritional
supplements

INTRODUCTION
According to the World-Health Organization,
over 12 million people die every year from heart
attacks, strokes and other forms of cardiovascular
disease (1). The direct and indirect costs for
treatment of cardiovascular disease are the single
largest health expense in every industrialized
country of the world. Despite modest success in
some countries in lowering the mortality rate from
heart attacks and strokes, the cardiovascular
epidemic is still expanding on a worldwide scale.
Current concepts of the pathogenesis of
cardiovascular disease focus on elevated plasma
risk factors damaging the vascular wall and thereby
initiating atherogenesis and cardiovascular disease
(2-4). Accordingly, drugs lowering cholesterol and
modulating other plasma risk factors have become a
predominant therapeutic approach in the prevention
of cardiovascular disease. A new scientific rationale
about the initiation of atherosclerosis and
cardiovascular disease was proposed by one of us
(5, 6). It can be summarized as follows:
cardiovascular disease is primarily caused by
chronic deficiencies of vitamins and other essential
nutrients with defined biochemical properties, such
as coenzymes, cellular energy carriers, and
antioxidants (7, 8). Chronic depletion of these
essential nutrients in endothelial and vascular
smooth muscle cells impairs their physiological
function. For example, chronic ascorbate
deficiency, similar to early scurvy, leads to
morphological impairment of the vascular wall and
endothelial microlesions, histological hallmarks of
early
atherosclerosis
(9-11).
Consequently,
atherosclerotic plaques develop as the result of an
overcompensating repair mechanism comprising
Kripps Healthy Lifestyles

deposition of systemic plasma factors as well local


cellular responses in the vascular wall (5, 6). This
repair mechanism is primarily exacerbated at sites
of
hemodynamic
stress,
explaining
the
predominantly local development of atherosclerotic
plaques in coronary arteries and myocardial
infarction as the most frequent clinical
manifestation of cardiovascular disease.
Animal studies have confirmed this scientific
rationale resulting in patents for the combination of
ascorbate with other essential nutrients in the
prevention and treatment of cardiovascular disease
(12). Based on this patented technology, we have
developed a nutritional supplement program, which
was tested in this study in patients with coronary
heart disease.
SUBJECTS AND METHODS
Subjects
A total of 55 patients, 50 men and 5 women, with
documented coronary artery disease assessed by
Ultrafast CT, were recruited for the study. The
inclusion criterion was the availability of a high
quality Ultrafast CT scan from a previous visit to
the Heart Scan facility in South San Francisco. At
the beginning of the study each patient completed a
comprehensive questionnaire, which was updated
after six months and after 12 months. This
questionnaire included medical history, previous
cardiac events, and cardiovascular risk factors, as
well as individual life style data. Specific questions
related to the patients' regular diet, (such as strictly
vegetarian diet, predominantly fruits and
vegetables, predominantly meat, fish or poultry; the
daily intake of different vitamins and other essential

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nutrients); and the frequency of physical exercise by


the patient. The laboratory tests available
documented a heterogeneous population with
respect to plasma cholesterol and triglycerides,
About half of the patients were taking different
types of prescription medication, including calcium
antagonists,
nitrates,
beta-blockers,
and
cholesterol-lowering drugs. Before entering the
study, the patients were instructed not to change
their diet or lifestyle other than adding the
nutritional supplement program tested. Any changes
were to be documented in their questionnaires.
Compliance with the nutritional supplement
program was monitored in the questionnaires,
through telephone calls and during the control
visits.

The extent of coronary calcification was


measured non-invasively with an Imatron C-100
Ultrafast CT scanner in the high resolution volume
mode, using a 100-millisecond exposure time. ECG
triggering was used so that each image was obtained
at the same point in the diastole, corresponding to
80% of the RR interval. In each scan, 30
consecutive images were obtained at 3-mm intervals
beginning 1 cm below the carina and progressing
caudally to include the entire length of the coronary
arteries. The scans at study entry and after 6 and 12
months of the study included a second scan
sequence of 30 images at 3 mm intervals across the
entire heart. The 30 images of the second scan were
taken between the 3 mm intervals of the first scan
resulting in a scanning of the heart at an interval of
1.5 mm. Total radiation exposure using this
Composition and Administration of Nutritional
technique was <I rad per patient (<. 0 1 Gy). The
Supplement Program
scan threshold was set at 130 Hounsfield units (Hu)
for identification of calcified lesions. The minimum
The following daily dosages of nutritional
area to differentiate calcified lesions from CT
supplements were taken for a period of one year:
artifact was 0.68 mm2. The lesion score, also
Vitamins: Vitamin C 2700 mg, Vitamin E (ddesignated Coronary Artery Scanning (CAS) score,
Alpha-Tocopherol) 600 IU, Vitamin A (as beta
was calculated by multiplying the lesion area by a
carotene) 7,500 IU, Vitamin B- I (Thiamine) 30 mg,
density factor derived from the maximal Hounsfield
Vitamin B-2 (Riboflavin) 30 mg, Vitamin B3 (as
unit within this area (13). The density factor was
Niacin and Niacinamide) 195 mg, Vitamin B-5
assigned in the following way: 1 for lesions with a
(Pantothenate) 180 mg, Vitamin B-6 (Pyridoxine)
maximal density with 130-199 Hu, 2 for lesions
45 mg, Vitamin B-12 (Cyanocobalamin) 90 mcg,
with 200-299 Hu, 3 for lesions with 300-399 Hu
Vitamin D (Cholecalciferol) 600 IU.
and 4 for lesions > 400 Hu. The total calcium areas
Minerals: Calcium 150 mg, Magnesium 180 mg,
and CAS scores of each Ultrafast CT scan were
Potassium 90 mg, Phosphate 60 mg, Zinc 30 mg,
determined by summing individual lesion areas or
Manganese 6 mg, Copper 1500 mcg, Selenium 90
scores from the left main, left anterior descending,
mcg, Chromium 45 mcg, Molybdenum 18 mcg.
circumflex and right coronary artery.
Amino acids: L-Proline 450 mg. L-Lysine 450
Several studies, have confirmed an excellent
mg, L-Carnitine 150 mg, L-Arginine 150 mg, and
correlation of the extent of coronary artery disease
L-Cysteine 150 mg.
as assessed by Ultrafast CT scanning when
Coenzymes and other nutrients: FolicAcid 390
compared to angiographic and histomorphometric
mcg, Biotin 300 mcg, Inositol 150 mg, Coenzyme
methods (13-15). Considering the accuracy and the
Q-10 30 mg, Pycnogenol 30 mg, and Citrus
non-invasive approach, Ultrafast CT was the
Bioflavonoids 450 mg.
method of choice for an intervention study that
included early, asymptomatic stages of coronary
artery disease.
Monitoring of Coronary Artery Disease
_______________________________________________________________________________________
Table 1. Clinical Characteristics of the Study Group as assessed from Patient Questionnaire
All Patients
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May 2007

82

n = 55

n = 21

Age:

40-49
5
(9%)
4
(8%)
50-59
24
(44%)
8
(40%)
60-69
26
(47%)
9
(52%)
Current Smoker
4
(7%)
1
(5%)
Past Smoker
36
(65%)
12
(57%)
Diabetes
4
(7%)
0
(0%)
Thyroid Dysfunction
3
(5%)
1
(5%)
Previous Cardiac Events
5
(9%)
0
(0%)
Previous Angioplasty
2
(4%)
1
(5%)
Currently on Medication
27
(49%)
7
(33%)
Previous Vitamin Intake
36
(65%)
15
(71%)
_______________________________________________________________________________________

Statistical Analysis
The growth rate of coronary calcifications was
calculated as the quotient of the differences in the
calcification areas or CAS scores between two
scans divided by the months between those scans
according to the formula (Area2-Area1):(Date2Datel), or (CAS score2-CAS score l):(Date2-Date
1) respectively. The data were analyzed using
standard formulas for means, medians, and standard

error of the means (SEM). Pearson's correlation


coefficient was used to determine the association
between continuous variables. One tailed Student ttest was used to analyze differences between mean
values, with a significance defined at <0.05.
Progression of calcification was predicted by linear

extrapolation. The distribution of the growth rate of


CAS scores was described by a smooth curve
resulting from a third order polynomial fit ( y - a +
bx3, where a= 0.9352959, b = 8.8235 x 105).
RESULTS
The aim of this study was to determine the effect
of a defined nutritional supplement program on the
natural progression of coronary artery calcification
particularly in its initial stages as measured by
Ultrafast CT. We therefore evaluated the results of
the entire study group (n=55) and of a subgroup of
21 patients with early coronary artery calcification,
as defined by a CAS score of <100.
Table I separately lists the characteristics of the
study population assessed by the questionnaire for
all patients and for a subgroup with early coronary
artery disease. This is the first intervention study

e per Month before Intervention

Figure 1. Distribution of monthly increase in CAS scores in relation to CAS scores at study entry. The data
represents all 55 patients individually. The calcification rate distribution pattern can be described by the
polynomial curve: y = a + W, where a = 0,9352959 and b = 8.8235 x 10-5.

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Using Imatron's Ultrafast CT technology: one of the


aims of this study was to determine the rate of
natural progression of coronary calcium deposits in
situ, without the intervention of the nutritional
supplement program. Figure I shows the
distribution of the monthly progression of
calcifications in the coronary arteries of all 55
patients in relation to their CAS score at study
entry.
We found that the higher the CAS score was
initially, without intervention, the faster the
coronary calcification progressed. Accordingly, the
average monthly growth rate of coronary
calcifications ranged from I CAS score per month in

patients with early coronary heart disease to more


than 15 CAS score per month in patients with
advanced stages of coronary calcifications. The
growth pattern of coronary calcifications can be
described as a third order polynomial fit curve. The
exponential shape of this curve signifies a first
quantification of the aggressive nature of coronary
atherosclerosis and emphasizes the importance of
early intervention. The changes in the natural
progression rate of coronary artery calcification
before the nutritional supplement program (-NS)
and after one year on this program (+NS) are shown
in Figure 2. The results are presented separately for
the calcified area and the CAS score. As presented

Change in Calcification
Score (CAS) per Month

Change in Calcification
Area per Month

Figure 2. Changes in the average monthly growth rate of calcified areas (2a, 2b) and CAS scores (2c, 2d) in all
study participants (n-55) and in a subgroup of patients with initial stages of coronary calcifications (CAS score
<100, n-21), before nutritional supplement intervention (-NS) and after one year of intervention (+NS). Data are
mean SEM, asterisk indicates significance at p < 0.05 (one tailed t-test ).

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in Figure 2a, the average monthly growth of


calcified areas for all 55 patients decreased from
1.24 mm2/month (SEM 0.3) before the nutritional
supplement program (-NS) to 1.05 mm2/month (
0.2) after one year on this program, (+NS). For
patients with early coronary artery disease (Figure
2b), the average monthly growth of the calcified
area decreased from 0.49 mm2/month ( 0. 16)
before taking the nutritional supplements (-NS) to
0.28 mm2/month (+0.09) after one year on this
program (+NS). As shown in Figure 2c, the
average monthly changes in the total CAS score
(calcified area X density of calcium deposits) for all

55 patients had decreased after one year on the


nutritional supplement program by 11%, from 4.8
CAS score/month (SEM 0.97) before the program
(-NS) to 4.27 CAS score/month ( 0.87) (+NS). In
patients with early coronary artery disease (Figure
2d) the average monthly growth of the total CAS
score decreased during the same time by as much as
65%, from 1.85 CAS score/month ( 0.49) before
the nutritional supplement program (-NS) to 0.65
CAS score/month ( 0.36) on this program (+NS).
The slow down in the progression of coronary

Figure 3. Actual progression of coronary calcification areas and CAS scores before and during one year of
nutritional supplement intervention in a subgroup of patients with initial stages of coronary calcification (CAS <
I00), compared to calculated progression without intervention (dotted line). Each data point represents the mean
value SEM.

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control scan after 6 months, allowing for additional


calcification during this nutritional supplement
insight into the time required for the nutritional
intervention for CAS scores of patients with early
supplements to exert their therapeutic effect This
coronary artery disease was statistically significant
additional evaluation was particularly important for
(p< 0.05) (Figure 2d). For the other three sets of
early forms of coronary artery disease, because any
data the decrease of coronary calcifications with the
therapeutic approach that can halt progression of
nutritional supplement program was evident;
however, largely due to the wide range of
early coronary calcification would ultimately
calcification values at study entry reflecting the
prevent myocardial infarctions.
Figure 3 shows the average coronary calcification
different stages of coronary artery disease it did not
reach statistical significance. It is noteworthy that
areas (Figure 3a) and total CAS scores
(Figure 3b) for patients with early coronary artery
the decrease in the CAS scores during intervention
with nutritional supplements was more pronounced
disease measured during different scanning dates
than for the calcified areas. This indicates a
before and during the course of the study. The
actual coronary calcification values for areas and
decrease in the density of calcium in addition to a
total, CAS scores during nutritional supplement
reduction in the area of coronary calcium deposits
during nutritional supplement intervention.
intervention are compared to the predicted values
Ultrafast CT scan at the beginning of the
obtained from linear extrapolation of the growth
rate without intervention. The letters A to D mark
study and after 12 months on the nutritional
supplement program were complemented by a
the different time points at which Ultrafast CT scans
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86

were performed. AB represents the changes in


coronary calcification before intervention with
nutritional supplement for the areas (Figure 3a) and
CAS scores (Figure 3b). Accordingly, BC
represents calcification changes during the first six
months on the nutritional supplement program and
CD changes during the second six months on the
program. The calculated progression rate for
coronary
calcifications
without
therapeutic
intervention by the nutritional supplement program
is marked by a dotted line, (B through F).
As seen in Figure 3a without the nutritional
supplement program the average area of coronary
calcifications in patients with early coronary artery
disease increased from 17.62 mm2 ( 1.0) at time
point A to 23.05 mm2 ( 1.8) at time point B. Thus,
the annual extension of calcified areas without
intervention was assessed at 31 %. At this
progression rate, the average calcified area would
reach 26.3 mm2 after six months (point E) and 29.8
mm2 after twelve months (point F). The nutritional
supplement intervention, resulted in an average
calcified area of 25.2 mm2 ( 2.2) after six months
and of 27.0 mm2 ( 1.7) after 12 months, reflecting
a 10% decrease compared to the predicted value.
Analogous observations were made for the total
CAS score before and during the nutritional
supplement program. Figure 3b shows that the
CAS score before the nutritional supplement
program increased by 44% per year, from 45.8 (
3.2) (point A) to 65.9 mm2 ( 5.2) (point B). At this
progression rate the total CAS score, without the
nutritional supplement program, would reach an
average of 77.9 after six months (point E) and of 91
(point F) after twelve months. In contrast to this
trend the actual CAS score values measured with

the nutritional supplement program were 75.8 (


6.2) after 6 months (point C) and 78.1 ( 5.1) after
12 months (point D). Thus, the progression of
coronary calcification as determined by the total
CAS scores decreased significantly during the
second six months of nutritional supplement
intervention (CD). The total score after twelve
months on the nutritional supplement program was
only 3% higher than after six months (CD), as
compared to the projected increase of 17% (EF),
indicating that during the second six months on the
nutritional supplement program the process of
coronary calcification has practically stopped.
Figure 4 shows the actual Ultrafast CT scans of a
51 year old patient with early, asymptomatic,
coronary artery disease. The patients' first Ultrafast
CT scan was performed in 1993 as part of an annual
routine check-up. The scan film revealed small
calcifications in the left anterior descending
coronary artery as well as in the right coronary
artery. The second CT scan was performed one
year later at which time the initial calcium deposits
had further increased. Figure 4a shows two
Ultrafast CT scan images taken before the
nutritional supplement program. Subsequently, the
patient started on the nutritional supplement
program. About one year later the patient received
control scans.
At this time point, coronary
calcifications were not found Figure 4b, indicating
the natural reversal of the coronary artery disease.

Figure 4a, 4b
Non-Reproducible

DISCUSSION

This

is the first study that provides quantifiable data from in situ measurements
about the natural progression rate of coronary artery disease. Although
atherosclerotic plaques have a complex histomorphological composition,
calcium dispersion within these plaques has been shown to be an excellent
marker for their advancement (11, 13). Our study determined that the calcified vascular areas expand at a rate
between 5 mm2 (early atherosclerotic lesions) and 40 mm2 (advanced atherosclerotic lesions). Before the
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nutritional supplement program the average annual increase of total coronary calcification was 44% (Figure 1).
Considering the exponential increase of coronary calcification, it is evident that the control of cardiovascular
disease has to focus on early diagnosis and early intervention.
Today, the diagnostic assessment of individual cardiovascular risk is largely confined to the measurement of
plasma cholesterol and other risk factors with little correlation to the extent of atherosclerotic plaques. More
accurate methods, such as coronary angiography, are confined to advanced, symptomatic, stages of coronary
artery disease. Ultrafast CT provides the diagnostic option to quantify coronary artery disease noninvasively in
its early stages (14, 15).
The most important finding of this study is that coronary artery disease can be effectively prevented and
treated by natural means. This nutritional supplement program was able to decrease the progression of coronary
artery disease within the relatively short time of one year, irrespective of the stage of this disease. Most
significantly, in patients with early coronary calcifications, this nutritional supplement program was able to
essentially stop its further progression. In individual cases with small calcified deposits, nutritional supplement
intervention led to their complete disappearance (Figure 4).
We postulate that the nutritional supplement program tested in this study initiates the reconstitution of the
vascular wall. Restructuring of the vascular matrix is facilitated by several nutrients tested, such as ascorbate
(vitamin C), pyridoxine (vitamin B-6), L-Lysine, and L-proline, as well as the trace element copper. Ascorbate
is essential for the synthesis and hydroxylation of collagen and other matrix components (16-18), and can be
directly and indirectly involved in a variety of regulatory mechanisms in the vascular wall from cell
differentiation to distribution of growth factors (19, 20). Pyridoxine and copper are essential for the proper
cross-linking of matrix components (8). L-Lysine and L-Proline are important substrates for the biosynthesis of
matrix proteins; they also competitively inhibit the binding of lipoprotein(a) to the vascular matrix, facilitating
the release of lipoprotein(a) and other lipoproteins from the vascular wall (5, 12, 21). Ascorbate and
a-tocopherol have been shown to inhibit the proliferation of vascular smooth muscle calls (22-24). Moreover,
tocopherols, beta-carotene, ascorbate, selenium and other antioxidants scavenge free radicals and protect plasma
constituents, as well as vascular tissue, from oxidative damage (25, 26). In addition, nicotinate, riboflavin,
pantothenate, carnitine, coenzyme Q-10, as well as many minerals and trace elements, function as cellular
cofactors in form of NADH, NADPH, FADH, Coenzyme A and other cellular energy carriers (8). The results of
this study confirm that maintaining the integrity and physiological function of the vascular wall is the key
therapeutic target in controlling cardiovascular disease. This also corroborates early angiographic findings that
supplemental vitamin C may halt the progression of atherosclerosis in femoral arteries (27).
These conclusions are even more relevant since deficiencies of essential nutrients are common (28, 29).
Moreover, many epidemiological and clinical studies have already documented the benefits of individual
nutrients in the prevention of cardiovascular disease (30-35). Compared to the high dosages of vitamins used in
some of these studies the amounts of nutrients used in this study are moderate, indicating the synergistic effect
of this program. In this context, it seems appropriate to critically review some of the approaches currently used
in the primary and secondary prevention of cardiovascular disease, including the extensive use of
cholesterol-lowering drugs. An intervention study including lovastatin was performed with a highly selected
group of hyperlipidemic patients, representing only an extremely narrow fraction of a normal population (36).
More recently, the reduction of myocardial infarctions and other cardiac events in patients taking simvastatin,
led to recommendations for its long-term use even by normolipidemic patients (37). However, because of their
potential side effects, the recommended use of these drugs has now been restricted to patients at high short-term
risk for coronary heart disease (38).
Similarly, certain natural approaches to prevention of cardiovascular disease deserve a critical review. A
program of rigorous diet and exercise claims to be able to reverse coronary heart disease (39). However, the
published study does not provide compelling evidence documenting the regression of coronary atherosclerosis.
Thus, the improved myocardial perfusion shown in that study was likely the result of the physical training
program, leading to an increased ventricular ejection fraction and an increased coronary perfusion pressure.
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Considering the urgent need for effective and safe public health measures towards the control of
cardiovascular disease, the validity of this study is of particular importance. In light of this, the following study
elements are noteworthy,
1. The patients in this study served as their own controls before and during nutritional supplement intervention,
thereby minimizing undesired co-variables such as age, gender, genetic predisposition, diet or medication.
2. Ultrafast CT has been extensively validated to assess the degree of coronary atherosclerosis, and it allowed
quantification of coronary atherosclerotic plaques in situ (13-15). This diagnostic technique also minimizes
errors as they occur in angiography studies in which vasospasms, formation or lysis of thrombi, and other
events cannot be differentiated from progression or regression of atherosclerotic plaques. Moreover,
Ultrafast CT provides valuable information about the morphological changes during progression and
regression of atherosclerotic plaques, by quantifying not only the area of coronary calcifications but also
their density. Furthermore, the automatic CT measurements of coronary calcifications eliminate human error
in the evaluation of the data.
In summary, the results of this study imply that coronary heart disease is a preventable and essentially
reversible condition. This study documents that coronary artery disease could be halted in its early stages by
following this nutritional supplement program. These results were achieved within one year, suggesting that
additional therapeutic benefits in patients with advanced coronary artery disease can be obtained by an extended
use of this program. The continuation of this study is currently under way to document these effects. This
nutritional supplement program signifies an effective and safe approach for the prevention and adjunct therapy
of cardiovascular disease. This study should encourage public health policy makers and health care providers to
redefine health strategies towards the control of cardiovascular disease.
ACKNOWLEDGMENTS
We are grateful to Jeffrey Kamradt for his dedicated help in coordinating this study; Douglas Boyd Ph.D.,
Lew Meyer Ph.D., and Dale Grant from Imatron/HeartScan, South San Francisco, for helping to plan the study
and providing the HeartScan facility; Lauranne Cox, Susan Brody, and Tom Caruso for their collaboration in
conducting the heart scans; Dr. Roger Barth and Bernard Murphy for their assistance in planning the study, and
to Martha Best for her secretarial assistance.

REFERENCES
1.

World Health Statistics, World Health Organization, Geneva, 1994.

2.

Brown MS, Goldstein JL. How LDL receptors influence cholesterol and atherosclerosis. Scientific American 1984;251:58-66.

3.

Steinberg D. Parthasarathy S. Carew TE, Wltztum JL. Modifications of low-density lipoprotein that increase its atherogenicity.
N Engl J Med. 1989;320:915-924.

4.

Ross R. The pathogenesis of atherosclerosis-an update. N Engl J Med. 1986;314:489-500.

5.

Rath M, Pauling L, A unified theory of human cardiovascular disease leading the way to the abolition of this disease as a cause
for human mortality. J Ortho Med, 1992;7:5-15.

6.

Rath M, Pauling L. Solution to the puzzle of human cardiovascular disease: Its primary cause is ascorbate deficiency, leading to
the deposition of lipoprotein(a) and fibrinogen/fibrin in the vascular wall. J Ortho Med. 1991;6:125-134.

7.

Rath M. Reducing the risk for cardiovascular disease with nutritional supplements. J Ortho Med 1992:3:1-6.

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8.

Stryer L. Biochemistry 3rd ed. New York: W.H. Freeman and Company; 1988.

9.

Stary HC. Evolution and progression of atherosclerotic lesions in coronary arteries of children and young adults. Atherosclerosis
(Suppl.) 1989:9:1-19-1-32.

10. Constantinides P. The role of arterial wall injury in atherogenesis and arterial thrombogenesis. Zentraibl alig Pathol pathol Anat.
1989:135:517-530.
11. Stolman JM, Goldman HM Gould BS. Ascorbic acid in blood vessels. Arch Pathol. 1961;72:59-68.
12. US Patent #5,278,189.
13. Agatsion AS, Janowitz WR, Kaplan G, Gasao J, Hildner F, Viamonte M. Ultrafast computed tomography -- detected coronary
calcium reflects the angiographic extent of coronary arterial atherosclerosis. Am J Cardiology. 1994;74:1272-1274.
14. Budoff MJ, Georgiou D, Brody A, ct aI. Ultrafast computed tomography as a diagnostic modality in
artery disease. Circulation, 1996; 93:898-904.

the detection of coronary

15. Maulner SI, Mautner CC, Froshlich J, et at. Coronary artery disease: prediction with in vitro electron beam CT Radiology.
1994;192:625-630.
16. Murad S, Grove D, Lindberg KA, Reynolds G, Sivarajah A, Pinnell SR. Regulation of collagen synthesis by ascorbic acid. Proc
Natl Acad Sci. 1981;78:2879-2882.
17. Do Clerck YA, Jones PA. The effect of ascorbic acid on the nature and production of collagen and elastin by rat smooth muscle
cells. Biochem J. 1980; 186:217-225.
18. Schwartz E, Bionkowski RS, Coltoff-Schiller B, Goldfisher S, Blumenfeld 00, Changes in the components of extracellular
matrix and in growth properties of cultured aortic smooth muscle cells upon ascorbate feeding. J Cell Biol. 1982;92:462-470.
19. Francheschi RT. The role of ascorbic acid in mesenchymal diffierentiation. Nutr Rev. 1992;50:65-70.
20. Dozin B, Quatro R, Campanile G. Cancedda R. In vitro diffierentiation of mouse embryo chondrocytcs: requirement for ascorbic
acid. Eur J Cell Biol. 1992;58:390-394.
21. Trieu VN, Zioncheck TF, Lawn RM, McConathy WJ. Interaction of apolipoprotein(a) with apolipoprotein B-containing
lipoproteins. J Biol Chem. 1991; 226:5480-5485.
22. Boscoboinik D, Szewczyk A, Hensey C, Azzi A. Inhibition of cell proliferation by a-tocopherol. Role of protein kinase C. J Biol
Chem. 1991; 266:6188-6194.
23. Ivanov V, Niedzwiecki A. Direct and extracellular matrix mediated effects of ascorbate on vascular smooth muscle cells
proliferation. 24th AAA (Age) and 9th Am Coll Clin Gerontol Meeting, Washington DC, 1994;Oct 14-18
24

Nunes GL, Sgoutas DS, Redden RA, Sigman SR, Gravanis MB. King SB, Berk BC. Combination of vitamins C and E alters
the response to coronary balloon injury in the pig. Arteriosclerosis, Thrombosis and Vascular Biology. 1995; 15:156-165.

25. Retsky KL, Freeman MW. Frei B. Ascorbic acid oxidation product(s) protect human low density lipoprotein against atherogenic
modification. Anti - rather than prooxidant. activity of vitamin C in the presence of transition metal ions. J Biol Chem.
1993;268:1304-1309.
26. Sies H, Stahl W. Vitamins B and C, beta-carotene and other carotenoids as antioxidants. Am J Clin Nutr.
1995;62(Suppl);I315S-l32IS.
27. Willis GC, Light AW, Gow WS. Serial arteriography in atherosclerosis. Can Med Ass J, 1954;71:562-568.
28. Levine M, Contry-Caritilena C, Wang Y, et al. Vitamin C pharmacokinetics in healthy volunteers: Evidence for a recommended
daily allowance. Proc Natl Acad Sci, 1996;93:3704-1709.

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29. Naurath HJ, Joosten E. Riezler R. Effects of vitamin B12. folate, and vitamin B6 supplements in elderly people with normal
serum vitamin concentrations. The Lancet. 1995;346:85-89.
30. Enstrom JE, Kanim LE, Klein MA.
Epidemiology, 1992;3:194-202.

Vitamin C intake and mortality among a sample of the United States population.

31. Riemersma RA, Wood DA, Macintyre CCA, Elton RA, Gey KF, Oliver MF. Risk of angina pectoris and plasma concentrations
of vitamin A, C, and E and carotene. The Lancet. 1991;337:1-5.
32. Hodis HN, Mack WJ, LaBree L, et al. Serial coronary angiographic evidence that antioxidant vitamin intake reduces progression
of coronary artery atherosclerosis. JAMA. 1995; 273:1849-1854.
33. Morriso n HI. Schaubel D, Desmcules M, Wigle DT. Serum folate and risk of fatal coronary heart disease. JAMA 1996; 275:
1993-1896.
34. Stephens NG, Parsons A, Schofield PM, et al. Randomized controlled trial of vitamin E in patients with coronary disease.
Cambridge Heart Antioxidant Study (CHAOS). The Lancet. 1996;347:781-786.
35.

Heitzer T, Just H, Menzel T.


1996;94:6-9.

Antioxidant vitamin C improves endothelial dysfunction in chronic smokers. Circulation.

36. Brown BG, Albers JJ, Fisher LD, Schafer SM, Lin J-T, et al. Regression of coronary artery disease as a result of intensive
lipid-lowering therapy in men with high levels of apolipoprotein B.
N Engl J Med. 1990;323:1289-1298.
37. Scandinavian Simvastatin Survival Study Group. Randomized trial of cholesterol lowering in 4444 patients with coronary heart
disease: the Scandinavian Simvastatin Survival Study (4S).
The Lancet 1994;344:1383-1389.
38. Newman TB, Hulley SB, Carcinogenicity of lipid-lowering drugs. JAMA. 1996;275:55-60.
38. Gould KL, Ornish D, Scherwitz L. et al. Changes in myocardial perfusion abnormalities by positron emission tomography after
long-term, intense risk factor modification. JAMA 1995;274:894-901.

Lipoprotein(a) Reduction by Ascorbate


Matthias Rath M.D. and Linus Pauling Ph.D.
Journal of Orthomolecular Medicine 7: 81-82.
Introduction
Lipoprotein(a) [Lp(a)] is associated with an increased risk of atherogenesis and thrombogenesis.
Recently it was proposed that Lp(a) is a surrogate for ascorbate.1 This proposal suggested a role of
ascorbate in the regulation of Lp(a) synthesis: namely, that increased intake of ascorbate, a strong
natural reducing agent, would lower Lp(a) plasma levels. N-Acetylcysteine (NAC) was then also
proposed to lower Lp(a) plasma levels and was reported to do this to a variable degree.2,3 The effect
of ascorbate in lowering Lp(a) plasma levels was studied in a clinical pilot study with the results
reported here.

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Patients, Materials and Methods


Eleven outpatients with coronary heart disease and elevated Lp(a) levels consented to participate in
this study. The patients received 9 grams of ascorbic acid (Bronson Pharmaceuticals, La Canada,
California) per day for a period of 14 weeks. Plasma Lp(a) levels were determined at the beginning
and at the end of the study. Lp(a) plasma levels were determined by a sandwich ELISA method with
monoclonal capture antibodies against apo(a) and monoclonal peroxidase-labeled antibodies against
the apoB-100 portion of the Lp(a) molecule. 4 The antibodies were a gift from Dr. J. C. Fruchart, Lille,
France.
Results
In this study ascorbate was found to lower Lp(a) plasma levels on average by 27% with a median
value also of 27% (Table 1). Two of the 11 patients showed no decrease of Lp(a) during this time
period. Lp(a) in the same plasma samples was also measured with immunological assays using
monoclonal antibodies against the apo(a) portion of the Lp(a) molecule for both, capturing and
revealing (radioimmunoassay[RIA], Pharmacia Diagnostics; anti-apo(a) sandwich ELISA). Changes in
Lp(a) plasma concentrations were measured for RIA mean +2%, median -7.5 % and for ELISA mean
-4%, median -12%. The mean values for vitamin C plasma levels were 48.6 uM at the beginning and
94.4 uM at the end of the study.

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Table 1.
Discussion
Two factors may account for the differences between the assay including an antibody against apoB
and the assays using exclusively anti-apo(a) antibodies. One factor could be the variation in epitopes
of the apo(a) molecule as a result of the variation of the molecular size determined by the genetic
isoforms. This factor was largely excluded in this study by determining the apo(a) isoforms by means
of SDS PAGE and subsequent immunoblotting with anti apo(a) antibodies.

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The second possible factor accounting for these differences is the effect of reducing agents on the
intramolecular disulfide bonds of the apo(a) molecule. This factor is discussed here in more detail.
Apo(a) has been proposed to function as a proteinthiol1 and the disulfide bonds of the repetitive
plasminogen kringle IV structure are known to have different dissociation constants. Elevated plasma
concentrations of reducing agents such as ascorbate or NAC could alter the epitope constellation of
the apo(a) molecule in vivo by reducing some of the many disulfide bonds to sulfhydryl groups.
Underthis condition, assays using only anti-apo(a) antibodies could give falsely positive results,
dependent on the specific epitopes they recognize in the repetitive kringle structures of the apo(a)
molecule.
In contrast, an assay measuring the apoB portion of the Lp(a) molecule should provide more reliable
results since apoB contains less disulfide bonds and in addition has a constant molecular size. This
conclusion could also explain the fact that the only two studies reporting a lowering of Lp(a) plasma
levels with reducing agents included assays using anti-apoB antibodies for detection (2, and this
paper). In contrast, assays exclusively based on antibodies against apo(a) gave variable results in the
presence of reducing agents. 2,3
From in vitro studies with NAC it was recently concluded that supraphysiological concentrations of
reducing agents above 1 mM decrease the immunoreactivity for Lp(a). 5 The extrapolation of these
results to the in vivo situation must, of course, be handled with care. The highest molar concentration
of ascorbate measured in the study reported here was 154 uM, a level that does not decrease the
immunoreactivity of apo(a) or Lp(a). The effect of physiological levels of ascorbate on the reduction of
disulfide bonds of the apo(a) molecule as well as the possible immunological implications need
further investigation
The results of the clinical study reported here, namely that dietary ascorbate supplementation
reduces Lp(a) plasma levels, was supported by in vitro studies in our laboratory with human liver cells
(HepG2, data not shown). In metabolic studies using S35 methionine increasing concentrations of
ascorbate in the cell culture medium decreased the amount of Lp(a) secreted by these cells.
Ascorbate concentrations up to 2.25 mM did not reveal any dissociation of apo(a) from apoB. It is,
therefore, concluded that the effect of ascorbate on Lp(a) plasma levels is the result of a decreased
rate of synthesis of Lp(a) particles in the liver.
In conclusion, ascorbate is a physiological reducing agent involved in the metabolic regulation of
Lp(a) synthesis. Dietary supplementation of ascorbate, as an adjunct to conventional therapy, should
contribute to reducing elevated Lp(a) plasma levels and the risk of cardiovascular disease. Prolonged
supplementation of ascorbate may be required to achieve these effects.
References
1. Rath M, Pauling L. Hypothesis: Lipoprotein(a) is a surrogate for ascorbate. Proceedings of the
National Academy of Sciences USA 1990; 87: 6204-6207.
2. Gavish D, Breslow J. Lipoprotein(a) reduction by N-acetylcysteine. Lancet 1991; 337:203-204.
3. Stalenhoef AFH, Kroon A, Demacker PNM. N-acetylcysteine and lipoprotein. Lancet 1991; 337:
491.

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4. Vu Dac N, Mezdour H, Parra HJ, Luc G, Luyeye I, Fruchart JC. A selective bi-site
immunoenzymatic procedure for human Lp(a) lipoprotein quantification using monclonal antibodies
against apo(a) and apoB. Journal of Lipid Research 1989; 30: 1437-1443.

5. Scanu AM, Pfaffinger D, Fless GM, Makino K, Eisenbart J, Hinman J. Attenuation of immunologic
reactivity of lipoprotein(a) by thiols and cysteine-containing compounds. Arteriosclerosis and
Thrombosis 1992; 12: 424-429

=============================================================================================

December 17, 2002

Rebuilding the Food Pyramid


The dietary guide introduced a decade ago has led people astray. Some fats are healthy for the heart,
and many carbohydrates clearly are not
By Walter C. Willett and Meir J. Stampfer

In 1992 the U.S. Department of Agriculture officially released the Food Guide
Pyramid, which was intended to help the American public make dietary choices
that would maintain good health and reduce the risk of chronic disease. The
recommendations embodied in the pyramid soon became well known: people
should minimize their consumption of fats and oils but should eat six to 11
servings a day of foods rich in complex carbohydrates--bread, cereal, rice, pasta
and so on. The food pyramid also recommended generous amounts of vegetables
(including potatoes, another plentiful source of complex carbohydrates), fruit and
dairy products, and at least two servings a day from the meat and beans group,
which lumped together red meat with poultry, fish, nuts, legumes and eggs.
Even when the pyramid was being developed, though, nutritionists had long
known that some types of fat are essential to health and can reduce the risk of
cardiovascular disease. Furthermore, scientists had found little evidence that a
high intake of carbohydrates is beneficial. Since 1992 more and more research
has shown that the USDA pyramid is grossly flawed. By promoting the
consumption of all complex carbohydrates and eschewing all fats and oils, the
pyramid provides misleading guidance. In short, not all fats are bad for you, and by
no means are all complex carbohydrates good for you. The USDA's Center for
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Nutrition Policy and Promotion is now reassessing the pyramid, but this effort is
not expected to be completed until 2004. In the meantime, we have drawn up a
new pyramid that better reflects the current understanding of the relation between
diet and health. Studies indicate that adherence to the recommendations in the
revised pyramid can signif- icantly reduce the risk of cardiovascular disease for
both men and women.
How did the original USDA pyramid go so wrong? In part, nutritionists fell victim to
a desire to simplify their dietary recommendations. Researchers had known for
decades that saturated fat--found in abundance in red meat and dairy products-raises cholesterol levels in the blood. High cholesterol levels, in turn, are
associated with a high risk of coronary heart disease (heart attacks and other
ailments caused by the blockage of the arteries to the heart). In the 1960s
controlled feeding studies, in which the participants eat carefully prescribed diets
for several weeks, substantiated that saturated fat increases cholesterol levels.
But the studies also showed that polyunsaturated fat--found in vegetable oils and
fish--reduces cholesterol. Thus, dietary advice during the 1960s and 1970s
emphasized the replacement of saturated fat with polyunsaturated fat, not total fat
reduction. (The subsequent doubling of polyunsaturated fat consumption among
Americans probably contributed greatly to the halving of coronary heart disease
rates in the U.S. during the 1970s and 1980s.)
The notion that fat in general is to be avoided stems mainly from observations that
affluent Western countries have both high intakes of fat and high rates of coronary
heart disease. This correlation, however, is limited to saturated fat. Societies in
which people eat relatively large portions of monounsaturated and polyunsaturated
fat tend to have lower rates of heart disease. On the Greek island of Crete, for
example, the traditional diet contained much olive oil (a rich source of
monounsaturated fat) and fish (a source of polyunsaturated fat). Although fat
constituted 40 percent of the calories in this diet, the rate of heart disease for
those who followed it was lower than the rate for those who followed the traditional
diets of Japan, in which fat made up only 8 to 10 percent of the calories.
Furthermore, international comparisons can be misleading: many negative
influences on health, such as smoking, physical inactivity and high amounts of
body fat, are also correlated with Western affluence.
Unfortunately, many nutritionists decided it would be too difficult to educate the
public about these subtleties. Instead they put out a clear, simple message: "Fat is
bad." Because saturated fat represents about 40 percent of all fat consumed in the
U.S., the rationale of the USDA was that advocating a low-fat diet would naturally
reduce the intake of saturated fat. This recommendation was soon reinforced by
the food industry, which began selling cookies, chips and other products that were
low in fat but often high in sweeteners such as high-fructose corn syrup.
When the food pyramid was being developed, the typical American got about 40
percent of his or her calories from fat, about 15 percent from protein and about 45
percent from carbohydrates. Nutritionists did not want to suggest eating more
protein, because many sources of protein (red meat, for example) are also heavy
in saturated fat. So the "Fat is bad" mantra led to the corollary "Carbs are good."
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Dietary guidelines from the American Heart Association and other groups
recommended that people get at least half their calories from carbohydrates and
no more than 30 percent from fat. This 30 percent limit has become so entrenched
among nutritionists that even the sophisticated observer could be forgiven for
thinking that many studies must show that individuals with that level of fat intake
enjoyed better health than those with higher levels. But no study has
demonstrated long-term health benefits that can be directly attributed to a low-fat
diet. The 30 percent limit on fat was essentially drawn from thin air.
The wisdom of this direction became even more questionable after researchers
found that the two main cholesterol-carrying chemicals--low-density lipoprotein
(LDL), popularly known as "bad cholesterol," and high-density lipoprotein (HDL),
known as "good cholesterol"--have very different effects on the risk of coronary
heart disease. Increasing the ratio of LDL to HDL in the blood raises the risk,
whereas decreasing the ratio lowers it. By the early 1990s controlled feeding
studies had shown that when a person replaces calories from saturated fat with an
equal amount of calories from carbohydrates the levels of LDL and total
cholesterol fall, but the level of HDL also falls. Because the ratio of LDL to HDL
does not change, there is only a small reduction in the person's risk of heart
disease. Moreover, the switch to carbohydrates boosts the blood levels of
triglycerides, the component molecules of fat, probably because of effects on the
body's endocrine system. High triglyceride levels are also associated with a high
risk of heart disease.
The effects are more grievous when a person switches from either
monounsaturated or polyunsaturated fat to carbohydrates. LDL levels rise and
HDL levels drop, making the cholesterol ratio worse. In contrast, replacing
saturated fat with either monounsaturated or polyunsaturated fat improves this
ratio and would be expected to reduce heart disease. The only fats that are
significantly more deleterious than carbohydrates are the trans-unsaturated fatty
acids; these are produced by the partial hydrogenation of liquid vegetable oil,
which causes it to solidify. Found in many margarines, baked goods and fried
foods, trans fats are uniquely bad for you because they raise LDL and triglycerides
while reducing HDL.
The Big Picture
To evaluate fully the health effects of diet, though, one must look beyond
cholesterol ratios and triglyceride levels. The foods we eat can cause heart
disease through many other pathways, including raising blood pressure or
boosting the tendency of blood to clot. And other foods can prevent heart disease
in surprising ways; for instance, omega-3 fatty acids (found in fish and some plant
oils) can reduce the likelihood of ventricular fibrillation, a heart rhythm disturbance
that causes sudden death.
The ideal method for assessing all these adverse and beneficial effects would be
to conduct large-scale trials in which individuals are randomly assigned to one diet
or another and followed for many years. Because of practical constraints and cost,
few such studies have been conducted, and most of these have focused on
patients who already suffer from heart disease. Though limited, these studies have
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supported the benefits of replacing saturated fat with polyunsaturated fat, but not
with carbohydrates.
The best alternative is to conduct large epidemiological studies in which the diets
of many people are periodically assessed and the participants are monitored for
the development of heart disease and other conditions. One of the best-known
examples of this research is the Nurses' Health Study, which was begun in 1976 to
evaluate the effects of oral contraceptives but was soon extended to nutrition as
well. Our group at Harvard University has followed nearly 90,000 women in this
study who first completed detailed questionnaires on diet in 1980, as well as more
than 50,000 men who were enrolled in the Health Professionals Follow-Up Study
in 1986.
After adjusting the analysis to account for smoking, physical activity and other
recognized risk factors, we found that a participant's risk of heart disease was
strongly influenced by the type of dietary fat consumed. Eating trans fat increased
the risk substantially, and eating saturated fat increased it slightly. In contrast,
eating monounsaturated and polyunsaturated fats decreased the risk--just as the
controlled feeding studies predicted. Because these two effects counterbalanced
each other, higher overall consumption of fat did not lead to higher rates of
coronary heart disease. This finding reinforced a 1989 report by the National
Academy of Sciences that concluded that total fat intake alone was not associated
with heart disease risk.
But what about illnesses besides coronary heart disease? High rates of breast,
colon and prostate cancers in affluent Western countries have led to the belief that
the consumption of fat, particularly animal fat, may be a risk factor. But large
epidemiological studies have shown little evidence that total fat consumption or
intakes of specific types of fat during midlife affect the risks of breast or colon
cancer. Some studies have indicated that prostate cancer and the consumption of
animal fat may be associated, but reassuringly there is no suggestion that
vegetable oils increase any cancer risk. Indeed, some studies have suggested that
vegetable oils may slightly reduce such risks. Thus, it is reasonable to make
decisions about dietary fat on the basis of its effects on cardiovascular disease,
not cancer.
Finally, one must consider the impact of fat consumption on obesity, the most
serious nutritional problem in the U.S. Obesity is a major risk factor for several
diseases, including type 2 diabetes (also called adult-onset diabetes), coronary
heart disease, and cancers of the breast, colon, kidney and esophagus. Many
nutritionists believe that eating fat can contribute to weight gain because fat
contains more calories per gram than protein or carbohydrates. Also, the process
of storing dietary fat in the body may be more efficient than the conversion of
carbohydrates to body fat. But recent controlled feeding studies have shown that
these considerations are not practically important. The best way to avoid obesity is
to limit your total calories, not just the fat calories. So the critical issue is whether
the fat composition of a diet can influence one's ability to control caloric intake. In
other words, does eating fat leave you more or less hungry than eating protein or
carbohydrates? There are various theories about why one diet should be better
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than another, but few long-term studies have been done. In randomized trials,
individuals assigned to low-fat diets tend to lose a few pounds during the first
months but then regain the weight. In studies lasting a year or longer, low-fat diets
have consistently not led to greater weight loss.
Carbo-Loading
Now let's look at the health effects of carbohydrates. Complex carbohydrates
consist of long chains of sugar units such as glucose and fructose; sugars contain
only one or two units. Because of concerns that sugars offer nothing but "empty
calories"--that is, no vitamins, minerals or other nutrients--complex carbohydrates
form the base of the USDA food pyramid. But refined carbohydrates, such as
white bread and white rice, can be very quickly broken down to glucose, the
primary fuel for the body. The refining process produces an easily absorbed form
of starch--which is defined as glucose molecules bound together--and also
removes many vitamins and minerals and fiber. Thus, these carbohydrates
increase glucose levels in the blood more than whole grains do. (Whole grains
have not been milled into fine flour.)
Or consider potatoes. Eating a boiled potato raises blood sugar levels higher than
eating the same amount of calories from table sugar. Because potatoes are mostly
starch, they can be rapidly metabolized to glucose. In contrast, table sugar
(sucrose) is a disaccharide consisting of one molecule of glucose and one
molecule of fructose. Fructose takes longer to convert to glucose, hence the
slower rise in blood glucose levels.
A rapid increase in blood sugar stimulates a large release of insulin, the hormone
that directs glucose to the muscles and liver. As a result, blood sugar plummets,
sometimes even going below the baseline. High levels of glucose and insulin can
have negative effects on cardiovascular health, raising triglycerides and lowering
HDL (the good cholesterol). The precipitous decline in glucose can also lead to
more hunger after a carbohydrate-rich meal and thus contribute to overeating and
obesity.
In our epidemiological studies, we have found that a high intake of starch from
refined grains and potatoes is associated with a high risk of type 2 diabetes and
coronary heart disease. Conversely, a greater intake of fiber is related to a lower
risk of these illnesses. Interestingly, though, the consumption of fiber did not lower
the risk of colon cancer, as had been hypothesized earlier.
Overweight, inactive people can become resistant to insulin's effects and therefore
require more of the hormone to regulate their blood sugar. Recent evidence
indicates that the adverse metabolic response to carbohydrates is substantially
worse among people who already have insulin resistance. This finding may
account for the ability of peasant farmers in Asia and elsewhere, who are
extremely lean and active, to consume large amounts of refined carbohydrates
without experiencing diabetes or heart disease, whereas the same diet in a more
sedentary population can have devastating effects.
Eat Your Veggies
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High intake of fruits and vegetables is perhaps the least controversial aspect of the
food pyramid. A reduction in cancer risk has been a widely promoted benefit. But
most of the evidence for this benefit has come from case-control studies, in which
patients with cancer and selected control subjects are asked about their earlier
diets. These retrospective studies are susceptible to numerous biases, and recent
findings from large prospective studies (including our own) have tended to show
little relation between overall fruit and vegetable consumption and cancer
incidence. (Specific nutrients in fruits and vegetables may offer benefits, though;
for instance, the folic acid in green leafy vegetables may reduce the risk of colon
cancer, and the lycopene found in tomatoes may lower the risk of prostate
cancer.)

The best way to avoid obesity is to LIMIT YOUR TOTAL CALORIES, not just
the fat calories.
The real value of eating fruits and vegetables may be in reducing the risk of
cardiovascular disease. Folic acid and potassium appear to contribute to this
effect, which has been seen in several epidemiological studies. Inadequate
consumption of folic acid is responsible for higher risks of serious birth defects as
well, and low intake of lutein, a pigment in green leafy vegetables, has been
associated with greater risks of cataracts and degeneration of the retina. Fruits
and vegetables are also the primary source of many vitamins needed for good
health. Thus, there are good reasons to consume the recommended five servings
a day, even if doing so has little impact on cancer risk. The inclusion of potatoes
as a vegetable in the USDA pyramid has little justification, however; being mainly
starch, potatoes do not confer the benefits seen for other vegetables.
Another flaw in the USDA pyramid is its failure to recognize the important health
differences between red meat (beef, pork and lamb) and the other foods in the
meat and beans group (poultry, fish, legumes, nuts and eggs). High consumption
of red meat has been associated with an increased risk of coronary heart disease,
probably because of its high content of saturated fat and cholesterol. Red meat
also raises the risk of type 2 diabetes and colon cancer. The elevated risk of colon
cancer may be related in part to the carcinogens produced during cooking and the
chemicals found in processed meats such as salami and bologna.
Poultry and fish, in contrast, contain less saturated fat and more unsaturated fat
than red meat does. Fish is a rich source of the essential omega-3 fatty acids as
well. Not surprisingly, studies have shown that people who replace red meat with
chicken and fish have a lower risk of coronary heart disease and colon cancer.
Eggs are high in cholesterol, but consumption of up to one a day does not appear
to have adverse effects on heart disease risk (except among diabetics), probably
because the effects of a slightly higher cholesterol level are counterbalanced by
other nutritional benefits. Many people have avoided nuts because of their high fat
content, but the fat in nuts, including peanuts, is mainly unsaturated, and walnuts
in particular are a good source of omega-3 fatty acids. Controlled feeding studies
show that nuts improve blood cholesterol ratios, and epidemiological studies
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indicate that they lower the risk of heart disease and diabetes. Also, people who
eat nuts are actually less likely to be obese; perhaps because nuts are more
satisfying to the appetite, eating them seems to have the effect of significantly
reducing the intake of other foods.
Yet another concern regarding the USDA pyramid is that it promotes
overconsumption of dairy products, recommending the equivalent of two or three
glasses of milk a day. This advice is usually justified by dairy's calcium content,
which is believed to prevent osteoporosis and bone fractures. But the highest rates
of fractures are found in countries with high dairy consumption, and large
prospective studies have not shown a lower risk of fractures among those who eat
plenty of dairy products. Calcium is an essential nutrient, but the requirements for
bone health have probably been overstated. What is more, we cannot assume that
high dairy consumption is safe: in several studies, men who consumed large
amounts of dairy products experienced an increased risk of prostate cancer, and
in some studies, women with high intakes had elevated rates of ovarian cancer.
Although fat was initially assumed to be the responsible factor, this has not been
supported in more detailed analyses. High calcium intake itself seemed most
clearly related to the risk of prostate cancer.

Men and women eating in accordance with THE NEW PYRAMID had a lower
risk of major chronic disease.
More research is needed to determine the health effects of dairy products, but at
the moment it seems imprudent to recommend high consumption. Most adults who
are following a good overall diet can get the necessary amount of calcium by
consuming the equivalent of one glass of milk a day. Under certain circumstances,
such as after menopause, people may need more calcium than usual, but it can be
obtained at lower cost and without saturated fat or calories by taking a
supplement.
A Healthier Pyramid
Although the usda's food pyramid has become an icon of nutrition over the past
decade, until recently no studies had evaluated the health of individuals who
followed its guidelines. It very likely has some benefits, especially from a high
intake of fruits and vegetables. And a decrease in total fat intake would tend to
reduce the consumption of harmful saturated and trans fats. But the pyramid could
also lead people to eat fewer of the healthy unsaturated fats and more refined
starches, so the benefits might be negated by the harm.
To evaluate the overall impact, we used the Healthy Eating Index (HEI), a score
developed by the USDA to measure adherence to the pyramid and its
accompanying dietary guidelines in federal nutrition programs. From the data
collected in our large epidemiological studies, we calculated each participant's HEI
score and then examined the relation of these scores to subsequent risk of major
chronic disease (defined as heart attack, stroke, cancer or nontraumatic death
from any cause). When we compared people in the same age groups, women and
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men with the highest HEI scores did have a lower risk of major chronic disease.
But these individuals also smoked less, exercised more and had generally
healthier lifestyles than the other participants. After adjusting for these variables,
we found that participants with the highest HEI scores did not experience
significantly better overall health outcomes. As predicted, the pyramid's harms
counterbalanced its benefits.
Because the goal of the pyramid was a worthy one--to encourage healthy dietary
choices--we have tried to develop an alternative derived from the best available
knowledge. Our revised pyramid emphasizes weight control through exercising
daily and avoiding an excessive total intake of calories. This pyramid recommends
that the bulk of one's diet should consist of healthy fats (liquid vegetable oils such
as olive, canola, soy, corn, sunflower and peanut) and healthy carbohydrates
(whole grain foods such as whole wheat bread, oatmeal and brown rice). If both
the fats and carbohydrates in your diet are healthy, you probably do not have to
worry too much about the percentages of total calories coming from each.
Vegetables and fruits should also be eaten in abundance. Moderate amounts of
healthy sources of protein (nuts, legumes, fish, poultry and eggs) are encouraged,
but dairy consumption should be limited to one to two servings a day. The revised
pyramid recommends minimizing the consumption of red meat, butter, refined
grains (including white bread, white rice and white pasta), potatoes and sugar.
Trans fat does not appear at all in the pyramid, because it has no place in a
healthy diet. A multiple vitamin is suggested for most people, and moderate
alcohol consumption can be a worthwhile option (if not contraindicated by specific
health conditions or medications). This last recommendation comes with a caveat:
drinking no alcohol is clearly better than drinking too much. But more and more
studies are showing the benefits of moderate alcohol consumption (in any form:
wine, beer or spirits) to the cardiovascular system.
Can we show that our pyramid is healthier than the USDA's? We created a new
Healthy Eating Index that measured how closely a person's diet followed our
recommendations. Applying this revised index to our epidemiological studies, we
found that men and women who were eating in accordance with the new pyramid
had a lower risk of major chronic disease. This benefit resulted almost entirely
from significant reductions in the risk of cardiovascular disease--up to 30 percent
for women and 40 percent for men. Following the new pyramid's guidelines did
not, however, lower the risk of cancer. Weight control and physical activity, rather
than specific food choices, are associated with a reduced risk of many cancers.
Of course, uncertainties still cloud our understanding of the relation between diet
and health. More research is needed to examine the role of dairy products, the
health effects of specific fruits and vegetables, the risks and benefits of vitamin
supplements, and the long-term effects of diet during childhood and early adult life.
The interaction of dietary factors with genetic predisposition should also be
investigated, although its importance remains to be determined.
Another challenge will be to ensure that the information about nutrition given to the
public is based strictly on scientific evidence. The USDA may not be the best
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government agency to develop objective nutritional guidelines, because it may be


too closely linked to the agricultural industry. The food pyramid should be rebuilt in
a setting that is well insulated from political and economic interests.
Walter C. Willett and Meir J. Stampfer are professors of epidemiology and nutrition
at the Harvard School of Public Health. Willett chairs the school's department of
nutrition, and Stampfer heads the department of epidemiology. Willett and
Stampfer are also professors of medicine at Harvard Medical School. Both of them
practice what they preach by eating well and exercising regularly.
1996-2007 Scientific American, Inc. All rights reserved.

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Pre-Hippocratic Medicine: The Philosopher-Scientist


By Albert S. Lyons
Pre-Hippocratic Medicine: The Philosopher-Scientist
Greek secular, rational medicine, which reached its summit in the time of Hippocrates, was
undoubtedly preceded by a long tradition. But we do not know precisely the nature of medicine, or
even science, in the centuries between the Homeric period of the ninth or eighth century B.C. and
the advent of the philosopher-scientists in the sixth century. Interchanges among Crete, Mycenae,
Egypt, and Asia had always contained interlacings of religious and empiric healing methods, so it
is likely that this cross-fertilization continued. A few bits of information from Hesiod's Works and
Days of the eighth century suggest the prevalence of a kind of folk medicine which combined
basic hygienic rules with pragmatic use of foods and plants, but it also included religious and
magical associations. Therefore, when one comes upon the sixth centuryabout which we have
direct and indirect information on the philosopher-scientistsone is impressed by what appears to
be a sudden new approach: an attempt to give all phenomena natural rather than supernatural
explanations.
By the time of Thales (640? -546 B.C.), the first true scientist-philosopher of the Greeks, his
birthplace Miletos on the Aegean west coast of Asia Minor had become a great port of trade, with
an international population and exceptional thinkers and teachers. It was on the periphery of the
Greek world, and in that sense typical of the areas in which the new philosophies seem to have
developed: the Aegean islands, the Asiatic coast, and Italy and Sicily, in centers which must have
been growing over centuries.
Meanwhile, the practice of medicine was probably carried on by itinerant craftsmen, as in Homer's
time. Information was transmitted orally from generation to generation, and by the time of
Hippocrates (mid-fifth century B.C.) practitioners were engaged in a variety of methods of differing
effectiveness. At the same time, medical teaching groups, or "schools," were developing
throughout the Greek world and were heirs of both the empiric tradition and the philosophic
inquiries of the philosopher-scientists.
Our information about Thales is based on what others wrote about him and quoted from his
teachings. ("What is difficult? To know thyself. What is easy? To advise another.") The man who
emerges from these accounts had an extraordinarily wide range of interests and a profound effect
on his contemporaries and followers. It is no wonder that he was considered among the seven
greatest sages.
Thales believed that the basic element in all animal and plant life was water, from which came
earth and air. He made many contributions to mathematics, astronomy, navigation, and geometry,
and is said to have developed several of the geometric theorems later used by Euclid. The most
significant attribute of his work, for which he has been called the "Father of Science," is that his
explanations of phenomena did not fall back on supernatural agency. Although he accepted the
idea of a God, he did not use religious means to seek or establish the natural processes of the
universe or of humans.
At Miletos, two especially influential thinkers followed Thales: Anaximander (fl. c. 560 B.C.) and
Anaximenes (fl. c. 546 B.C.). Anaximander (extending the rational views of Thales) taught that all
living creatures had their beginnings in water. Even man originally came from a water organism.
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Anaximander also espoused the doctrine that the universe was constituted of opposite forces in
balance and that it was governed by universal laws. His pupil Anaximenes considered air rather
than water the primary element and therefore the essential requirement for life.
Heraclitos (fl. c. 500 B.C.), the outstanding philosopher of Ephesos, to the north of Miletos,
considered fire rather than water or air as the principal element, but he underlined Anaximander's
concept of opposites by suggesting that tensions between opposing forces were essential to the
universe and to life. Change was the only constant.
By the sixth century B.C., four basic elements had become generally accepted as the components
of all substances: water, earth, fire, and air, each of which had its corresponding characteristic
wet, dry, hot, cold. This doctrine of the four elements and their qualities (later projected into the
four humors) continued to affect medical theory for many centuries, even into recent times.
There were many other leaders of what was referred to as the Ionian school because it sprang
from the islands and territories to which the ancient mainland Ionians had migrated. Each inquired
rationally into the makeup of humans as well as the cosmic environment.
At the western borders of the Greek world in the sixth century, an Italic "school" of philosophers
was centered in Sicily and southern Italy. The most famous group was at Crotona, where
Pythagoras came to teach. A center of philosophy may have been there before he arrived, but the
influence of Pythagoras and the teachings of his followers were to have a profound effect on
medicine.
Pythagoras (fl. c. 530 B.C.) was born on the island of Samos just off the coast of Asia Minor, but
he emigrated west to Crotona in southern Italy because of his opposition to the tyrant Polycrates.
He and his followers formed not only a school of philosophy but also a religious cult that allied
itself with the ancient mystical teachings of Orpheos.
The Pythagoreans in the west focused principally on the soul and the spiritual universe, whereas
Thales in the east was concerned with matter. Humans were fallen gods eventually capable of
returning to divinity, for although the body decayed the soul was continually reborneven in
animals. All life was therefore sacred, and surgical procedures were forbidden since they might
interfere with the soul. Their belief in reincarnation resembles some religious ideas developing in
India (where the Buddha also lived in the sixth century B.C.).
The basic principle of the Pythagorean universe was not any of the elemental substances but
rather the science of numbers, which determined what happened in living creatures as well as in
the cosmos. Each number had a special significance beyond its own function in mathematical
process. For instance, I represented God, 2 stood for matter. Therefore 12 was the universe,
divisible by 4 three times. The Pythagoreans also established scientific theories of sound and of
musical octaves. Furthermore, as proponents of the mythical teachings of Orpheos, they felt that
music should play an important role in their discipline.
Balance in all things was the goal of correct behavior. Opposite pairs of substances and qualities
achieved the balance; therefore the number 4 was important to health, and the concept of four
elements with four qualities received further impetus, particularly when supported by so influential
a school.

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As a logical concomitant of Pythagorean beliefs, diet was vegetarian and frugal, but there were a
few curious prohibitions against some foods, such as beans. The explanation given by Diogenes
Laertius (third century A.D.) was that in mythical times the bean had been a symbol of the head
and therefore of the mind, which might have made it taboo to this sect. Cabbage, anise, and squill
were recommended to maintain health and treat illness, and external applications of plant
substances were also permissible, but the chief Pythagorean therapy consisted of diet, exercise,
music, and meditation.
Other "schools" of medicine (that is, associations of philosophers, medical teachers, practitioners,
and students) had been developing nearby in Sicily, in Cyrene on the African coast, and in
Rhodes, Cnidos, and Cos at the eastern periphery of the Greek world. But Crotona was the most
famous of philosophic centers according to Herodotos. Democedes, one of the best-known
practitioners among the Greeks, was educated at Crotona, and his reputation increased after he
went to Aegina and to Athens. He was persuaded to come to Samos by its ruler Polycrates, but
when Samos was taken by the Persians Democedes was brought along to the court of Darius.
There chance brought him to the attention of the king, whose ankle injury he was able to treat
successfully, as well as his daughter's abscessed breast. We do not know his method of
treatment, but Egyptian physicians had previously been unsuccessful in relieving the king's
difficulties.
A younger member of the Crotona school (possibly of the fifth century B.C.) was Alcmaeon,
whose principal focus was on man, not the cosmos. His book Concerning Nature may be the
beginning of Greek medical literature, but only a few fragments survive. Works by a number of
later writersespecially Aristotleare the principal sources for what was contained in Alcmaeon's
teachings. He held a general philosophic attitude: health is harmony; disease is a disturbance of
the harmony. But he also believed that investigation (including dissection), not just philosophy,
was needed in order to understand the body. His combination of direct observation and
experimental testing stands out as unique in his time.
Although many remarkable facts emerged from his dissections (probably on animals), his most
striking contribution was to establish the connection between the sense organs and the brain.
Even the optic nerves and their chiasm (crossing) were clearly delineated. Going further he
concluded that the brain was the organ of the mind, not only perceiving sensations but also
responsible for thought and memory. About a century later, Aristotle, one of the greatest
philosopher-scientists in history, disagreed entirely with Alcmaeon, believing instead that the heart
was the center of sensation.
Alcmaeon was also a hostage of his age. For instance, he speculated that sleep occurred when
the blood vessels in the brain were filled; withdrawal of blood from the brain caused waking. Along
with his careful dissections of the eye and demonstrations of the pathways connecting the brain
and the eye, he reported that the eye contains both water and fire. However, he condemned the
commonly accepted belief of the time that semen originated in the brain. His doctrine of the
balancing of opposite qualities and its effect on health were in agreement with Pythagorean
teachings. But the breadth of his detailed examinations and rational concepts opened a new view
on the acquisition of medical knowledge. He can be called virtually the first medical scientist.
Further south in Sicily another Greek Italic center of medicine flourished. The best-known member
of this group was Empedocles (c. 493-c. 433 B.C.). Many fragments of his writings survive, and
much other information about him is contained in later commentaries. From these sources
historians have obtained a picture of an aristocratic leader of enormous egotism but also of
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exceptional knowledge and ability. He went about dressed in purple finery and decorated with
flowers, boasting in verse of his own godlike nature and power of accomplishment. Yet, he did
work prodigious feats for his city and its citizens. During a time when it was as still possible for one
person to encompass many fields he seemed to outdistance anyone else in being many-sided.
Poet, statesman, priest, philosopher, scientist, physicianhe excelled in all.
His treatises were written in verse, a common practice, and he preached the Pythagorean
doctrines concerning purity of mind, body, and behavior, as well as the virtues of regulated,
temperate diet and exercise. His teaching that gained the widest influence was the concept that all
things inanimate and animate were comprised of four basic elements: water, air, fire, and earth.
Although this belief was accepted before Empedocles, he is often credited with its origination.
The elements according to Empedocles are joined together during life and separate after death.
Substances are formed by attraction and repulsion of the elements in different proportions. He
saw that the element air had substance and could exert pressure. The flow of blood through the
body was connected in some way with propulsion by air. Respiration occurred not only through
the nose and mouth but also through respiratory pores in the skin; after Hippocrates, a system of
medicine called Methodist was developed from this idea. Even today some speak of the opening
of the pores in hot weather and their closing in the cold.
The theories espoused by the followers of Empedocles led to further elaboration and were a step
toward the concept that matter is composed of atoms. For instance, Anaxagoras (c. 500-c. 428
B.C.) held that each element was composed of many small invisible particles or seeds which were
released from a food by digestion and then reconstituted into components of the bodysuch as
bone and muscle. However, it was Democritos and Leucippos later in the fifth century B.C. who
advanced the fully developed theory that all matter is made up of atoms of different size, weight,
shape, and position. All animate and inanimate objects were originally created by the collisions
and combinations of atoms. Democritos also dealt with diet, health and illness, and his speculative
writings had a great influence on medical as well as scientific thought.
Of the other philosopher-scientist groups flourishing in the sixth and fifth centuries, two of the most
important in influence were at Cnidos on the Asia Minor shore, and at Cos on an island off the
coast. However, their fame may have come late in the fifth century B.C. because the historian
Herodotos, who wrote in the mid-fifth century, spoke of the "schools" at Cyrene in Africa and
Crotona in Italy but made no mention of either Cnidos or Cos.
It was on Cos that Hippocrates lived and taught. The writings of the Coan teachers, presumably
by Hippocrates or by others of his time, are called the Corpus Hippocraticum and will be
considered in a later section.
Neighboring Cnidos on the mainland was the location of a group of teachers and students that
was probably as important as Cos and slightly older. The "Cnidian Sentences" was a collection of
medical treatises which has not survived and is only known to us by mention in the Corpus
Hippocraticum and through later commentators on Hippocrates, especially Galen in the second
century A.D. Scholars consider it probable that some writings attributed to Hippocrates actually
came from Cnidos.
For a long time historians have assumed that Cos and Cnidos were rival centers, but more recent
analysis suggests that the two groups may not have been much different or even competitive.
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Nevertheless, a summary of the attitudes which scholars heretofore have believed were prevalent
at the two locations may help clarify medical principles in the Greek world.
In Cnidos diseases were supposed to have been elaborately categorized according to the organ
affected, a system with some resemblance to the practice in the Mesopotamian lands east of
Cnidos. Treatments which were linked with and listed with each disease were simple and sparse.
In contrast, the Hippocratists, it was assumed, made virtually no classifications and used empiric
rather than theoretical bases for the management of patients. With respect to treatment, however,
Hippocratic methods were not much different from the Cnidian.
In addition, according to Galen, the system at Cnidos emphasized elaborate diagnosis based on
symptoms, so that virtually every symptom was a disease. For instance, there were seven
diseases of the bile, twelve of the bladder, and four types of consumption (which usually meant
the spitting of blood). Although descriptions of the patient's history were complete and clear, the
accent was on the disease rather than the patient (Hippocratic methods emphasized the patient
rather than the disease, with great attention paid to observing and evaluating the physical
findings). Wherever these Cnidian characteristics are found in the body of the Hippocratic works,
they have been attributed by some scholars to Cnidian origin. Two treatises, On Diet and Acute
Diseases and On Diseases, have been particularly singled out as probable contributions from
Cnidos.
Some of the outstanding leaders of that school were Euryphon, Ctesias, Chrysippos, Polycrates,
Endoxos, and Nichomachos, the father of Aristotle. According to Galen, Euryphon, a great
anatomist, was one of the most famous physicians of his time and made many contributions to the
"Cnidian Sentences." Ctesias, a younger contemporary of Hippocrates, attained fame as a
physician in the Persian court of Artaxerxes Mnemon, and he wrote a commentary on Hippocrates
which contained a number of disagreements with the methods and conclusions.
However, the most famous name that has come down to us is Hippocrates of Cos. Whether the
teachings with which he has been associated are the work of one man or of many is not known.
When the Hippocratic writings were collected in the great library of Alexandria in the fourth century
B.C., the works of others were presumably also attributed to Hippocrates. So when we speak of
Hippocrates we are probably referring to more than one man. Nevertheless, there is some
evidence that he did exist and that he may indeed have been the extraordinary person later
generations considered him. In any case, he typifies in his teachings, his life, and his behavior the
ideal to which all healers strive and which all patients seek in their doctors.
Before considering the principles and methods of Hippocrates, it is appropriate to describe the
common medical practices of his time.
Article Source: Health Guidance
http://www.healthguidance.org/entry/6336/1/Pre-Hippocratic-Medicine-The-Philosopher-Scientist.html

Albert S. Lyons
==========================================================================

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17. Recent Popular Books of Interest.

Mindbody Toolkit: Experience Self Healing With Clinically Proven Techniques


Dr. Andrew Weil
Discover Your Own Self-Healing Powers with Mind-Body Tools from Dr. Andrew Weil. Andrew
Weil, M.D. The evidence is overwhelming: you can tap the power of your mind to directly influence
your health, using clinically proven tools that anyone can master. With Dr. Andrew Weils MindBody Tool Kit, listeners join the best-selling author of Spontaneous Healing (Ballantine, 1996)
along with three renowned colleagues and friendsall leading specialists in alternative
medicineto experience a potent prescription of self-healing practices. This information-packed
"integrative medicine chest" includes an in-depth 52-page interactive workbook and 25 MindTraining Cards designed to support a daily practice. Step by step, users will learn an empowering
four-part series of mind-body techniques: BreathingDr. Weil reveals "the master key to self
healing" MeditationDr. Jon Kabat-Zinn introduces listeners to the oldest and most effective
system for calming the mind Guided ImageryDr. Martin Rossman invites us to heal the body
with this effective and easy-to-learn skill Sound TherapyPioneering music therapist Kimba
Arem leads a complete sound-healing journey to rejuvenate and balance our physiology and mind
states "Your mind can elicit a healing response when even conventional medicine has proven
ineffective," explains Dr. Weil. Here are the self-healing mind-body tools to start optimizing your
health today and for the rest of your lifewith Dr. Andrew Weils Mind-Body Tool Kit. Note:
Includes material from Breathing, Meditation for Optimum Health, Self-Healing with Guided
Imagery, and Self-Healing with Sound and Music.
Read full review at Amazon.com.
You On A Diet; Dr. M.F. Roizen, Dr. M.C. Oz
http://www.realage.com/doctorCenter/YouOnADiet/entry1.aspx

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18. Bibliography, and Selected Meta-lists


Biochemical Individuality, Roger J. Williams
Present Knowledge Nutrition in Nutrition, 9th Edition, by International Life Sciences InstituteNutrition Foundation (Corporate Author), Ekhard E. Ziegler (Editor), L. J., Jr Filer (Editor),
Lloyd J. Filer (Editor)
http://www.vitalchoice.com/readings.cfm
========================================================================
19. Webwatch: Favorite websites of interest for daily scientific, regulatory or institutional generalhealth news.
http://medlineplus.gov/

Start here with over 700 topics on conditions, diseases and wellness
About your prescription and over-the-counter medicines, herbs and supplements
Includes pictures and diagrams
Spellings and definitions of medical words
Current health news and press announcements
Find doctors, dentists and hospitals
A service for finding local resources for health-related issues
Local health services, libraries, organizations, international sites and more

http://www.hc-sc.gc.ca/

About Health Canada


Consumer Product Safety
Diseases & Conditions
Drugs & Health Products
Emergencies & Disasters
Environmental & Workplace Health
First Nations & Inuit Health
3

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Food & Nutrition


Health Care System
Healthy Living
Science & Research
Government
Health Partners

http://www.sciencedaily.com/health/
Science Daily, Health
http://www.crnusa.org/index.html
Council for Responsible Nutrition: the science behind the supplements
http://news.bbc.co.uk/1/hi/health/default.stm
BBC Health News
http://www.eatright.org/cps/rde/xchg/ada/hs.xsl/index.html
American Dietetic Association: discover daily nutrition tips, nutrition fact sheets, child nutrition,
Find a referral to a Dietitian, plus easy access to other food and nutrition web sites.
http://www.orthomolecular.org
Journal of Orthomolecular Medicine
http://www.mypyramid.gov/
My Pyramid: food pyramid
http://www.phoenixdatacenter.org/foodsites.html
Phoenix Data: links to a variety of nutrition and related web sites.
http://www.ars.usda.gov/main/site_main.htm?modecode=12354500
USDA Agriculture Research Service: Nutrition Data Laboratory.
Search the extensive database for nutrition values and the composition of over 6,200 foods. This
site allows the user the opportunity to submit ones own data as well. See FAQs and Glossary
sections + links to other sites that are related to Food Composition and Nutrition for both the U.S.
and other countries.
http://fnic.nal.usda.gov/nal_display/index.php?tax_level=1&info_center=4
Food and Nutrition Information Center (FNIC)
The Food and Nutrition Information Center, affiliated with the National Agriculture Library & the
USDAs Agriculture Research Service, offers databases, resource lists, and other related links.
Discover informative data related to healthy school meals, food safety, dietary supplements, food
composition, dietary guidelines, food guide pyramid, reports & studies, as well as topics from A-Z.
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http://www.ift.org/cms/
Institute of Food Technologists
Publications, news, policy activities, science & technology, information source, latest products and
services, learning and career opportunities.
http://www.fdli.org/
Food and Drug Law Institute
A non-profit institute dedicated to advancing the public health by providing a neutral forum for
critical examination of the laws, regulations, and policies related to drugs, medical devices, other
healthcare technologies, and foods
http://www.ifst.org/site/cms/contentChapterView.asp?chapter=1
Institute of Food Science & Technology ( IFST)
Food Science & Technology, answers to FAQs about food quality & safety, & other food related
resources on the web & hot topics, find a consultant, and conduct a personalized search.!
http://www.aad.org/default.htm
American Academy of Dermatology
http://www.netwellness.org/default.cfm#feature
University consumer wellness resource
http://www.realage.com/index.aspx
RealAge: Topics to improve healthy aging
http://www.newsrx.com/
NewsRX: large database health news
http://www.alzheimersupport.com/
Pro Health: Alzheimer Support
http://www.everydaychoices.org/tools.html
Healthy Choices: The American Cancer Society, American Diabetes Association and American
Heart Association
http://nihseniorhealth.gov/
National Institute of Health, Seniors Health
http://www.jhsph.edu/clf/index.html
Center for a Livable Future: sustainable nutrition, agriculture & living
http://www.sciencedaily.com/
Science Daily, Health & Medicine
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http://www.cspinet.org/
Center for Science in the Public Interest: Independent consumer-protection advocate, combining
nutrition science and political action.
www.consumerlab.com
Consumer Lab: independent testing of health and nutrition products
http://www.cookingforengineers.com/
Interesting recipes, tools, references
Cookingforengineers
http://www.whfoods.com/
Worlds Healthiest Foods; excellent range of data, information, and guidance
http://www.cookinglight.com/cooking/hl/0,14270,,00.html
Cooking Light, healthy lifestyle features
http://www.epicurious.com/shop/healthy
Epicurious: quality cooking tools, organic foods, cookbooks, and gifts for the healthy gourmet.
http://www.nytimes.com/pages/health/index.html ,
NYTimes, health , health news, trends, business, and innovations.
http://www.nutrition.gov/
USA, Department of Agriculture, Voluminous nutrition information and resources from the
U.S.D.A, Department of Health and Human Services, the Food and Nutrition Information Center,
and the National Agricultural Library.
http://www.nutritionj.com/start.asp
Nutrition Journal: free-access, peer-reviewed nutrition research journal that focuses exclusively
on human nutrition research
http://www.my-calorie-counter.com/calorie_counter.asp
My Calorie Counter: free online exercise & diet support
http://www.slowfoodusa.org/
Slow Food Movement: combines an appreciation for fine food with ecological awareness,
emphasizing wholesome, locally-produced foods, healthy cuisine and community.
http://www.webmd.com/
WEBMD: Daily review of health news and research
http://www.OrganicConsumers.org
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Organic Consumers Association (OCA), OCA monitors and reports on important issues
impacting all things organic:
http://www.CommercialAlert.org , http://www.StopDrugAds.org)
Commercial Alert (CA). Investigates direct-to-consumer drug advertising
http://www.PRwatch.org
PR Watch, Intended to expose and counter corporate and government public relations spin.
http://www.plos.org/index.php, http://medicine.plosjournals.org
PLoS Medicine, Technical biomedical original reports, independent open-sourced

http://www.EWG.org
Environmental Working Group, Focuses on the environment, educating readers with articles
about toxic chemicals in foods and consumer products, threats to the environment, and possible
problems of corruption between commercial interests and government regulators.

http://www.abc.net.au/health/library/default.htm
ABC Health Matters
American Heart Association
http://www.americanheart.org/presenter.jhtml?identifier=1200000
Dedicated to reducing disability and deaths from heart attack and stroke through education,
research, and advocacy.

American Diabetes Association

http://www.diabetes.org/home.jsp
Providing education, resources, and hope to those with living with diabetes as well as those who
want to reduce their risk.
New York Times Health Section
http://www.nytimes.com/
In-depth and wide-ranging coverage of health news, trends, business, and innovations
Nutrition.gov
http://nutrition.gov/
Nutrition information and resources from the U.S.D.A, Department of Health and Human Services,
the Food and Nutrition Information Center, and the National Agricultural Library.
Nutrition Journal
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http://www.nutritionj.com/
A free-access, peer-reviewed nutrition research journal that focuses exclusively on human
nutrition research.

20. BioMedical / Nutritional FAQ, + Myths & Facts


http://www.foodinfoquest.com/
http://www.quackwatch.org/
http://www.quackwatch.org/05Links/othersites.html

Fluorescence micrographs of
cyanobacteria. About 2 billion
years ago, oxygen-producing
photosynthetic prokaryotes that
used to be called blue-green
algae were responsible for
launching the process that
increased the concentration of
atmospheric oxygen from less
than 1 percent to about 20
percent today, making possible
the evolution of humans and
other animals. Credit: Mary
Sarcina University College

Some related books:


Quack!: Tales of Medical Fraud from the Museum of Questionable Medical Devices, Bob McCoy
Quack, Quack, Quack: The Sellers of Nostrums in Prints, Posters, Ephemera, and Books, William,
H. Helfand
Quacks: Fakers and Charlatans in Medicine Roy Porter
Snake Oil, Hustlers and Hambones: The American Medicine Show Ann Anderson
The Great American Medicine Show: Being an Illustrated History of Hucksters, Healers, Health
Evangelists, and Heroes from Plymouth Rock to the Present, David Armstrong
===================================================
MAGICAL THINKING AND THE "ANTI-AGING" MARKETPLACE
Trying to establish an understanding of the world - and in particular, our bodies and aging without using the scientific method is a hopeless task.
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You'll wind up somewhere, but it certainly won't be anywhere useful or productive; we humans are
just too good at seeing patterns where there are none, and rationalizing success in the midst of
abject failure. Sadly, the "anti-aging" marketplace is chock full of buyers and sellers who are doing
just this:
"To distinguish causal from fortuitous improvements that might follow any intervention, a set of
objective procedures has evolved for testing putative remedies. Unless a technique, ritual, drug, or
surgical procedure can meet these requirements, it is ethically questionable to offer it to the public,
especially if money is to change hands. Since most 'alternative' therapies (i.e., ones not accepted
by scientific biomedicine) fall into this category, one must ask why so many customers who would
not purchase a toaster without consulting Consumer Reports shell out, with trusting naivete, large
sums for unproven, possibly dangerous, health remedies.
"Some people will believe enough in any new such proposal to spend resources, and other,
better-educated people rightly estimate that they'll make money from investing in the beliefs of the
first group. Once it all gets going, you'll see a self-sustaining industry with the resources to expand
the pool of consumers through (mis)education, and which comes to employ more and more true
believers in key positions."
None of which will do any good for our health and life spans - it's all castles in the sky and dogged
determination to avoid the work, understanding and sacrifice necessary to gain real results. There
will always be buyers when "incorrect" is cheaper than "correct," and the consequences of a bad
choice slow to materialize.
ENGINEERING AND REAL ANTI-AGING MEDICINE
If magical thinking is the abuse of certain aspects of human intelligence, then engineering is the
gainful use of those very same aspects. The work of the medical engineer is to take the output of
the scientific method - truth and understanding, carefully sifted - and fit the pieces together in new
ways. In other words, to make the leap of invention that results in new therapies and better,
healthier, longer lives. Good engineering does not have to wait for all the facts to be known, in
medicine or any other field:
http://www.fightaging.org/archives/001068.php
"Bridges and monuments were built well before the formalism of physics, materials science and
architecture; the 'how' was common practice long before the 'why'. Humans excel at operating in
an environment of less than perfect understanding, deciphering complex and poorly understood
systems - and a good thing too.
"In this era of biotechnology, the eager engineering mindset is turned towards genes, cells and
biochemistry. If there's one thing better than engineering, it's engineering during the exploration of
an enormously intricate system. Each new fact carved out from the unknown by researchers is a
puzzle piece to be set with all the others, turned about and around, compared for new and
interesting fits. The medical engineers take those pieces and gleefully work to build wonderful,
effective new medical technologies."
Real anti-aging medicine - biotechnologies of repair that can be envisaged today, but do not yet
exist outside the laboratory - is the province of scientists and engineers. The shrill marketing of
supplements and look and feel products will not help you live a much longer, healthier life, so why
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pay it any attention? Focus on the scientific method, on the engineers who work with the resulting
fruits of science, for that is the path to the future. These scientists and engineers need your
support to move forward at a faster pace; consider lending a hand to help out.
http://www.fightaging.org/archives/001072.php

Religion, spirituality, and medicine


R P Sloan, E Bagiella, T Powell
THE LANCET Vol 353 February 20, 1999
Lancet 1999; 353: 66467
Behavioral Medicine Program, Columbia-Presbyterian Medical
Center (R P Sloan , PhD, E Bagiella , PhD. and Department of
Psychiatry, Columbia University (R P Sloan, T Powell ,MD; New
York State Psychiatric Institute (R P Sloan); Division of
Biostatistics, School of Public Health, Columbia University
(E Bagiella); and Center for the Study of Society and Medicine,
Columbia University (T Powell), New York NY 10032, USA
Correspondence to: Dr Richard P Sloan, Columbia University,
Box 427, 622 West 168th St, New York 10032
(e-mail rps7@columbia.edu)
Religion and science share a complex history as well as a
complex present. At various times worldwide, medical
and spiritual care was dispensed by the same person. At
other times, passionate (even violent) conflicts
characterised the association between religion and
medicine and science. As interest in alternative and
complementary medicine has grown, the notion of linking
religious and medical interventions has become widely
popular, especially in the USA. For many people,
religious and spiritual activities provide comfort in the
face of illness. However, as US medical schools
increasingly offer courses in religion and spirituality1and
as reports continue to indicate interest in this subject
among both physicians and the general public, it is
essential to examine how, if at all, medicine should
address these issues. Here, in a comprehensive, though
not systematic, review of the empirical evidence and
ethical issues we make an initial attempt at such an
examination. Interest in connecting religion and medicine
In a recent poll of 1000 US adults, 79% of the
respondents believed that spiritual faith can help people
recover from disease, and 63% believed that physicians
should talk to patients about spiritual faith.2. Recent
articles in such US national newspapers as the Atlanta
Constitution, Washington Post, Chicago Tribune, and USA
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Today report that religion can be good for your health. A


new magazine, Spirituality and Health, edited by the
former editor of Harvard Business Review, has begun
publication. Eisenberg and colleagues, in a widely cited
article on unconventional therapies, noted that 25% of
all respondents reported using prayer as medical therapy.3. King and Bushwick 4
reported that 48% of hospital inpatients wanted their physicians to pray with
them.4. Within the medical community, there is also
considerable interest. Meetings sponsored by the US
National Institute of Aging, the National Center for
Medical Rehabilitation Research,5 and the Mind/Body
Medical Institute, Beth Israel Deaconess Hospital,
Boston, have drawn large, enthusiastic audiences. Nearly
30 US medical schools include in their curricula courses
on religion, spirituality, and health.1 Of 296 physicians
surveyed during the October, 1996, meeting of the
American Academy of Family Physicians, 99% were
convinced that religious beliefs can heal, and 75%
believed that prayers of others could promote a patients
recovery. Benson writes that faith in God has a healthpromoting effect. 6 . Larson and Matthews argue for
spiritual and religious interventions in medical practice,
hope that the wall of separation between medicine and
religion will be torn down,7
and assert that the medicine of the future is going to be prayer and Prozac (ref 8, p85). In an
American Medical Association publication,
Matthews and colleagues recommend that clinicians ask
what can I do to support your faith or religious
commitment? to patients who respond favourably to
questions about whether religion or faith are helpful in
handling your illness.9. Empirical evidence
In many studies, religion, as a putative antecedent to
health outcomes, has been measured in several wayseg,
assessment of religious behaviours, such as frequency of
Religion and science share a complex history as well as a
complex present. At various times worldwide, medical
and spiritual care was dispensed by the same person. At
other times, passionate (even violent) conflicts
characterised the association between religion and
medicine and science. As interest in alternative and
complementary medicine has grown, the notion of linking
religious and medical interventions has become widely
popular, especially in the USA. For many people,
religious and spiritual activities provide comfort in the
face of illness. However, as US medical schools
increasingly offer courses in religion and spirituality1 and
as reports continue to indicate interest in this subject
among both physicians and the general public, it is
essential to examine how, if at all, medicine should
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118

address these issues. Here, in a comprehensive, though


not systematic, review of the empirical evidence and
ethical issues we make an initial attempt at such an examination.
Interest in connecting religion and medicine
In a recent poll of 1000 US adults, 79% of the
respondents believed that spiritual faith can help people
recover from disease, and 63% believed that physicians
should talk to patients about spiritual faith.2, Recent
articles in such US national newspapers as the Atlanta
Constitution, Washington Post, Chicago Tribune, and USA
church attendance or prayer; dimensions of religious
experience, such as the comfort it may provide; and
health differences as a function of differences in religious
denomination or degree of religious orthodoxy.
In addition, health outcomes vary considerablyeg,
physical disease outcomes, mental health outcomes, and
health behaviours. Here, we consider methodological
issues that pertain to studies of physical disease
outcomes. Control for confounding variables and other covariates
Confounders such as behavioural and genetic differences
and stratification variables such as age, sex, education,
ethnicity, socioeconomic status, and health status may
have an important role in the association between religion
and health. Failure to control for these factors can lead to
a biased estimation of this association. Multivariate
methods allow estimation of the magnitude of the
association between religious variables and health
outcomes while controlling for the effects of other
variables. However, use of these methods requires
complete presentation of the resultsat least the
coefficients and corresponding confidence intervals for all
the variables in the statistical model. Reports that fail to
do this are incomplete and may be misleading.
Attempts to assess the effect of degree of religiousness
on health outcomes show this. Increased religious
devotion, assessed as service as a Roman Catholic priest,10,nun,11
Morman priest,12, or Trappist or Benedictine monk,13
is associated with reductions in morbidity and
mortality. These cases, however, were selected for study
precisely because they are inclined to stricter adherence
to codes of conduct that proscribe behaviours associated
with risk (eg, smoking, alcohol consumption, sexual
activity, psychosocial stress, and in some cases, consumption of meat).
In a series of studies from Israel,1416 religiousness,
measured as religious orthodoxy, was also shown to
confer health benefits. However, one of these 14 was a
case-control study, the deficiencies of which are widely
known. In another,15 a multivariate model that predicted
mortality from coronary heart disease included standard
risk factors but omitted religion, and no information on
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risk-ratio or confidence intervals or even level of statistical


significance was provided. Finally, in a study matching
secular and religious Kibbutzim according to location,
use of the same regional hospital, and members older
than 40 years, all-cause mortality was significantly greater
among members of the secular Kibbutzim. However, the
strategy of matching ensures equivalence of groups only
on the matched variables. As a consequence, the groups
differed with respect to dietary habits, smoking, blood
cholesterol concentrations, and marital status, with the
secular group having greater risk, as the authors
themselves report. The multivariate analysis of mortality
did not control for these factors.
Control for confounding and other covariates also
affects studies that report that religious behaviours and
experiences influence health outcomes. In some studies
with large databases, this problem can be addressed. Both
the Alameda County Study and the Tecumseh
Community Health Study showed that frequency of
attendance at religious services was inversely associated
with mortality.17,18. However, after control for all relevant
covariates, this relation held only for women. In another
large study, attendance at religious services was
associated with increased functional capacity in the
elderly19 but after control for appropriate covariates, this
relation held for only 3 of the 7 years in which outcome
data were collected. There was no effect on mortality.
20. In a smaller study, religiousness predicted mortality in the
elderly poor but only among those in poor health.21
In many other studies, inadequate control for
important covariates points to significant findings when
none may exist. For example, Pressman and colleagues
22 reported that among elderly women after surgical repair
of broken hips, religiousness was associated with better
ambulation status at discharge. Although the analysis
controlled for severity of health condition, it did not
control for age, a critical variable when studying
functional capacity in the elderly.
In some cases, problems of interpretation arise not so
much in the original research but rather in secondary
sources. A case in point is a report by Comstock and
Partridge 23 frequently cited as showing a positive
association between church attendance and health.
However, as Comstock himself later reported, this finding
was probably due to failure to control for the important
covariate of functional capacity: people with reduced
capacity (and poorer health) were less likely to go to
church.24. This latter study is rarely cited. Similarly,
Koenig reports that a study by Colantonio and
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Colleagues 25found lower rates of stroke in persons who


attended religious services at least once per week . . ..26
However, this was only the case for the univariate analysis
and the effect disappeared after covariates such as levels
of physical function were added to the analysis. Levin, in
a review of a review, reported that 22 of 27 studies of
religious attendance and health showed a significant
positive relation, 27 despite his own previous assertion that
associations between attendance and health are highly
questionable because this research is characterised by
numerous methodological problems including the failure
to adjust for confounders and covariates. 28
Finally, many studies evaluate differences in health
indicators as a function of religious denomination (eg, ref
2931). However, they are generally conducted precisely
because religious groups differ on risk behaviours such as
smoking and alcohol consumption or on genetic heritage.
Failure to control for multiple comparisons
Many studies on religion and health fail to make an
adjustment for the greater likelihood of finding a
statistically significant result when conducting multiple
statistical tests. For example, one study reported that
religious attendance was inversely associated with high
concentrations of interleukin-6 in the elderly.32
However,interleukin-6 was one of eight outcome variables and
there was no attempt to control for multiple comparisons,
as the authors themselves reported. In a retrospective
study,33 the associations between frequency of prayer and
six items measuring subjective health were examined.
Analyses of variance were conducted on each of these six
perceptions of health and three revealed effects of
frequency of prayer at the 005 level of statistical
significance. In such studies, adjustments of
levels to control for such multiple comparisons would render these
findings non-significant. There are similar problems in the only published
randomised clinical trial. 34 In this double-blind study,
patients in a coronary-care unit (CCU) were assigned
randomly either to standard care or to daily intercessory
THE LANCET Vol 353 February 20, 1999
665 prayer ministered by three to seven born-again
Christians. 29 outcome variables were measured, and on
six the prayer group had fewer newly diagnosed ailments.
However, the six significant outcomes were not
independent: the prayer group had fewer cases of newly
diagnosed heart failure and of newly prescribed diuretics
and fewer cases of newly diagnosed pneumonia and of
newly prescribed antibiotics. There was no control for
multiple comparisons, a fact recognised by the author. To
address this issue, multivariant analysis was conducted
but the results were not presented, except for a p value
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for overall model.


Conflicting findings
Published work on religion and health lacks consistency,
even among well-conducted studies. For example, while
Idler and Kasl found some effects of religious attendance
on functional capacity in the elderly, measures of
religious involvement, an index of the private,
reflective aspects of religion, were not associated with
any health outcome. Neither church attendance nor
religious involvement was associated with lower
mortality.20 However, in two other large studies,17,18
church attendance was associated with lower mortality,
but only in women. Inconsistencies also arise within studies not based on
large epidemiological samples. For instance, when each
individual item from the scale of religiousness used by
Idler and Kasl, was used in another study, religious
comfort and strength was significantly associated with
lower mortality after cardiac surgery in the elderly even
after control for relevant confounders. 35 However, the
other items from this scale, including religious
attendance, did not predict mortality. Moreover, when
the entire scale was used, the relation between religion
and mortality failed to reach significance. Byrd 34 reported
an advantage in hospital course for the group receiving
prayer compared with the control group. However, the
groups did not differ in days in the CCU, length of stay
in hospital, and number of discharge medications. While
total cholesterol concentrations were lower across all age
groups for a cohort of Seventh Day Adventists (SDAs)
than in age-matched healthy New York City men and
women, suggesting a lower risk of coronary heart disease
among SDAs, serum triglycerides of the SDA men in the
coronary-prone age range (>32 years) were 19% higher
than in the controls, which suggests the opposite. 29
To some degree, lack of consistency is characteristic of
an evolving field and may be the product of differences in
study design, definitions of religious and spiritual
variables, and outcome variables. The absence of specific
definitions of religious and spiritual activity is an
important problem, since many of the studies to which
we refer define these activities differently. Published
research would be substantially improved with better
definitions of these terms. However, inconsistency in the
empirical findings makes it difficult to support
recommendations for clinical interventions.
Ethical issues
Health professionals, even in these days of consumer
advocacy, influence patients by virtue of their medical
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expertise. When doctors depart from areas of established


expertise to promote a non-medical agenda, they abuse
their status as professionals. Thus, we question inquiries
into a patients spiritual life in the service of making
recommendations that link religious practice with better
health outcomes. Is it really appropriate, as Matthews
and colleagues 9 recommend, for a physician to ask
patients what he or she can do to support their faith or
religious commitment?
A second ethical consideration involves the limits of
medical intervention. If religious or spiritual factors were
shown convincingly to be related to health outcomes,
they would join such factors as socioeconomic status and
marital status, 38 already well established as significantly
associated with health. Although physicans may choose to
engage patients in discussions of these matters to
understand them better, we would consider it
unacceptable for a physician to advise an unmarried
patient to marry because the data show that marriage is
associated with lower mortality.38 This is because we
generally regard financial and marital matters as private
and personal, not the business of medicine, even if they
have health implications. There is an important difference
between taking into account marital, financial, or
religious factors and taking them on as the objects of
interventions.
A third ethical problem concerns the possibility of
doing harm. Linking religious activities and better health
outcomes can be harmful to patients, who already must
confront age-old folk wisdom that illness is due to their
own moral failure.37 Within any individual religion, are
the more devout adherents better people, more
deserving of health than others? If evidence showed
health advantages of some religious denominations over
others, should physicians be guided by this evidence to
counsel conversion? Attempts to link religious and
spiritual activities to health are reminiscent of the now
discredited research suggesting that different ethnic
groups show differing levels of moral probity, intelligence,
or other measures of social worth. 37 Since all human
beings, devout or profane, ultimately will succumb to
illness, we wish to avoid the additional burden of guilt for
moral failure to those whose physical health fails before
our own.
Some practitioners who link faith and medical practice
do so appropriately, and in ways that do not depend on
utilitarian expectations of better health. For instance,
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devout health professionals may view their work as an


extension of their religious beliefs. Such physicians may
or may not choose to share their opinions with patients.
However, some patients and doctors may be aware of a
common faith. There is no ethical objection to coworshippers discussing medical issues in the context of a
shared faith. Indeed, a thorough understanding of a
patients religious values can be extremely important in
discussing critical medical issues, such as care at the end
of life. Irrespective of the practitioners religion, respectful
attention must be paid to the impact of religion on the
patients decisions about health care. 38
An especially poignant example of the devout
practitioner who appropriately notes connections between
illness, recovery, and prayers of thanks is provided by
Prager, in describing a serious illness in his son. 41 Prager
does not suggest that his son recovers function because
he is faithful, but rather teaches how the faithful may give
thanks for recovery. Such connections between faith and
health are valuable because they are sensitive to all
aspects of the patients experience, yet in no way depend
on spurious claims about scientific data. 666
THE LANCET Vol 353 February 20, 1999
Conclusions
Even in the best studies, the evidence of an association
between religion, spirituality, and health is weak and
inconsistent.
We believe therefore that it is premature to promote
faith and religion as adjunctive medical treatments.
However, between the extremes of rejecting the idea that
religion and faith can bring comfort to some people
coping with illness and endorsing the view that physicians
should actively promote religious activity among patients
lies a vast uncharted territory in which guidelines for
appropriate behaviour are needed urgently.
Nonetheless, caution is required. There is a temptation
to conclude that this matter can be resolved as soon as
methodologically sound empirical research becomes
available. Even the existence of convincing evidence of a
relation between religious activity (however defined) and
beneficial health outcomes may not eliminate the ethical
concerns that we raise here. Religious pursuits, such as
decisions to marry or have children, are qualitatively
different from health behaviours such as quitting smoking
or eating a low-fat diet, even if they are linked
unequivocally to health benefits.
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No-one can object to respectful support for patients


who draw upon religious faith in times of illness.
However, until these ethical issues are resolved,
suggestions that religious activity will promote health,
that illness is the result of insufficient faith, are
unwarranted.
We gratefully acknowledge the contributions of the many colleagues and
friends who reviewed this manuscript.
References
1 Levin JS, Larson DN, Puchalski CM. Religion and spirituality in
medicine: research and education. JAMA 1997; 278: 79293.
2 McNichol T. The new faith in medicine. USA Today. April 7,
1996: 4.
3 Eisenberg DM, Kessler RC, Foster C, Norlock FE, Calkins DR,
Delbanco TL. Unconventional medicine in the United States:
prevalence, costs, and patterns of use. N Engl J Med 1993; 328:
24652.
4 King DE, Bushwick B. Beliefs and attitudes of hospital inpatients
about faith healing and prayer. J Family Practice 1994; 39: 34952.
5 Marwick C. Should physicians prescribe prayer for health? Spiritual
aspects of well-being considered. JAMA 1995; 273: 156162.
6 Benson H. Timeless Healing. New York: Fireside, 1996.
7 Matthews DA, Larson DB. Faith and medicine: reconciling the twin
traditions of healing. Mind/Body Medicine 1997; 2: 36.
8 Sides H. The calibration of belief. New York Times Magazine 1997;
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9 Matthews DA, McCullough ME, Larson DB, Koenig HG, Swyers JP,
Milano MG. Religious commitment and health status. Arch Family
Medicine 1998; 7: 11824.
10 Michalek AM, Mettlin C, Priore RL. Prostate cancer mortality among
Catholic priests. J Surg Oncol 1981; 17: 12933.
11 Timio M, Lippi G, Venanzi S, et al. Blood pressure trend and
cardiovascular events in nuns in a secluded order: a 30-year follow-up
study. Blood Pressure 1997; 6: 8187.
12 Gardner JW, Lyon JL. Cancer in Utah Mormon men by lay
priesthood level. Am J Epidemiol 1982; 116: 24357.
13 de Gouw HWFM, Westndrop RGJ, Kunst AE, Mackenbach JP,
Vandenbrouke JP. Decreased mortality among contemplative monks
in the Netherlands. Am J Epidemiol 1996; 141: 77175.
14 Friedlander Y, Kark JD, Stein Y. Religious orthodoxy and myocardial
infarction in Jerusalem: a case control study. Int J Cardiol 1986; 10:
3341.
15 Goldbourt U, Yaari S, Medalie JH. Factors predictive of long-term
coronary heart disease mortality among 10 059 male Israeli civil
servants and municipal employees. Cardiology 1993; 82: 10021.
16 Kark JD, Shemi G, Friedlander Y, Martin O, Manor O, Blondheim
SH. Does religious observance promote health? Mortality in secular
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and religious kibbutzim in Israel. AJPH 1996; 86: 34146.


17 House JS, Robbins C, Metzner HL. The association of social
relationships and activities with mortality: prospective evidence from
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18 Strawbridge WJ, Cohen RD, Shema SJ, Kaplan GA. Frequent
attendance at religious services and mortality over 28 years. AJPH
1997; 87: 95761.
19 Idler EL, Kasl SV. Religion among disabled and nondisabled persons
II: Attendance at religious services as a predictor of the course of
disability. J Gerontol 1997; 52B: S306S316.
20 Idler EL, Kasl SV. Religion, disability, depression, and the timing of
death. Am J Sociol 1992; 97: 10521079.
21 Zuckerman DM, Kasl SV, Ostfeld AM. Psychosocial predictors of
mortality among the elderly poor. Am J Epidemiol 1984; 119: 41023.
22 Pressman P, Lyons JS, Larson DB, Strain JJ. Religious belief,
depression and ambulation status in elderly women with broken hips.
Am J Psychiatry 1990; 147: 75860.
23 Comstock GW, Partidge KB. Church attendance and health. J Chronic
Dis 1972; 225: 66572.
24 Comstock GW, Tonascia JA. Education and mortality in Washington
County, Maryland. J Health Soc Behav 1977; 18: 5461.
25 Colantonio A, Kask SV, Ostfeld AM. Depressive symptoms and other
psychosocial factors as predictors of stroke in the elderly. Am J
Epidemiol 1992; 136: 88494.
26 Koenig HG. Is religion good for your health? Binghamton, NY:
Haworth Pastoral Press, 1997.
27 Levin JS. Religion and health: is there an association, is it valid, and is
it causal? Soc Sci Med 1994; 38: 147582.
28 Levin JS, Vanderpool HY. Is frequent religious attendance really
conducive to better health?: toward an epidemiology of religion. Soc
Sci Med 1987; 24: 589600.
29 Walden RT, Schaefer LE, Lemon FR, Sunshine A, Wynder EL. Effect
of environment on the serum cholesterol-triglyceride distribution
among Seventh-day Adventists. Am J Med 1964; 36: 26976.
30 Rasanen J, Kauhanen J, Lakka TA, Kaplan GA, Salonen JT. Religious
affiliation and all-cause mortality: a prospective population study in
middle-aged men in eastern Finland. Int J Epidemiol 1996; 25:
124449.
31 Lyon JL, Gardner K, Gress RE. Cancer incidence among Mormons
and non-Mormons in Utah (United States) 197185. Cancer Causes
Control 1994; 5: 14956.
32 Koenig HG, Cohen HG, George LK, Hays JC, Larson DB, Blazer
DG. Attendance at religious services, interleukin-6, and other
biological parameters of immune function in older adults. Int J
Psychiatry Med 1997; 27: 23350.
33 Levin JS, Lyons JS, Larson DB. Prayer and health during pregnancy:
Findings from the Galveston Low birthweight Survey. Southern Med J
1993; 86: 102227.
34 Byrd RC. Positive therapeutic effects of intercessory prayer in a
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coronary care unit population. Southern Med J 1988; 81: 82629.


35 Oxman TE, Freeman DH, Manheimer ED. Lack of social
participation or religious strength and comfort as risk factors after
cardiac surgery in the elderly. Psychosomatic Med 1995; 57: 515.
36 Sorlie PD, Backlund E, Keller JB. US mortality by economic,
demographic, and social characteristics: the National Longitudinal
Mortality Study. AJPH 1995; 85: 94956.
37 Gould SJ. The mismeasure of man. New York: Norton, 1981.
38 Powell T. Regligion, race, and reason. J Clin Ethics 1995; 6: 7377.
39 Prager K. For everything a blessing. JAMA 1997; 277: 1589.
THE LANCET Vol 353 February 20, 1999, 667

Melittosphex burmensis, which has been trapped in amber for the past hundred million years,
is the oldest bee fossil ever discovered. It lived in northern Myanmar (Burma) in Southeast Asia
about 35 million to 45 million years earlier than the next oldest specimens known to science.

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21. Community Calendar, Seasonal / Institutional announcements


http://www.hc-sc.gc.ca/ahc-asc/conferences/calend/index_e.html
http://www.pohly.com/dates.html
http://www.psqh.com/calendar.html
http://www.hopehealth.com/calendar.asp
http://www.medem.com/medlb/article_detaillb.cfm?article_ID=ZZZZG27SWAC&sub_cat=58
===================================================================

News From the AAP:

Summer Safety Tips


May 4, 2007 Keep your family safe this summer by following these tips:
Fun in the Sun

Babies Under 6 Months: Avoiding sun exposure and dressing infants in lightweight long
pants, long-sleeved shirts and brimmed hats that shade the neck are still the top
recommendations from the AAP to prevent sunburn. However when adequate clothing and
shade are not available, parents can apply a minimal amount of sunscreen with a sun
protection factor (SPF) of at least 15 to small areas, such as the infant's face and the back of
the hands.
For Young Children: Apply sunscreen at least 30 minutes before going outside, and use
sunscreen even on cloudy days. The SPF should be at least 15.
For Older Children: The first, and best, line of defense against the sun is covering up. Wear a
hat with a three-inch brim or a bill facing forward, sunglasses (look for sunglasses that block 99
percent to 100 percent of ultraviolet rays), and cotton clothing with a tight weave. Stay in the
shade whenever possible, and limit sun exposure during the peak intensity hours between 10
a.m. and 4 p.m.
Use a sunscreen with an SPF of 15 or greater. Be sure to apply enough sunscreen about one ounce
per sitting for a young adult. Reapply sunscreen every two hours, or after swimming or sweating. Use
extra caution near water, snow and sand as they reflect UV rays and may result in sunburn more
quickly.
Heat Stress in Exercising Children

The intensity of activities that last 15 minutes or more should be reduced whenever high heat
and humidity reach critical levels.
At the beginning of a strenuous exercise program or after traveling to a warmer climate, the
intensity and duration of exercise should be limited initially and then gradually increased during
a period of 10 to 14 days to accomplish acclimatization to the heat. Before prolonged physical

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activity, the child should be well-hydrated. During the activity, periodic drinking should be
enforced, for example, each 20 minutes, 5 oz. of cold tap water or a flavored sports drink for a
child weighing 90 lbs., and 9 oz. for an adolescent weighing 130 lbs., even if the child does not
feel thirsty.
Clothing should be light-colored and lightweight and limited to one layer of absorbent material
to facilitate evaporation of sweat. Sweat-saturated garments should be replaced by dry
garments.
Practices and games played in the heat should be shortened and more frequent water/hydration
breaks should be instituted.
Pool Safety

Install a fence at least four-feet high around all four sides of the pool. The fence should not
have openings or protrusions that a young child could use to get over, under or through.
Make sure pool gates open out from the pool, and self-close and self-latch at a height children
can't reach.
Never leave children alone in or near the pool, even for a moment.
Keep rescue equipment (a shepherd's hook a long pole with a hook on the end and life
preserver) and a portable telephone near the pool.
Avoid inflatable swimming aids such as "floaties." They are not a substitute for approved life
vests and can give children a false sense of security.
Children may not be developmentally ready for swim lessons until after their fourth birthday.
Swim programs for children under 4 should not be seen as a way to decrease the risk of
drowning.
Whenever infants or toddlers are in or around water, an adult should be within arm's length,
providing "touch supervision."
Bug Safety
Don't use scented soaps, perfumes or hair sprays on your child.
Avoid areas where insects nest or congregate, such as stagnant pools of water, uncovered
foods and gardens where flowers are in bloom.
Avoid dressing your child in clothing with bright colors or flowery prints.
To remove a visible stinger from skin, gently scrape it off horizontally with a credit card or your
fingernail.
Combination sunscreen/insect repellent products should be avoided because sunscreen needs
to be reapplied every two hours, but the insect repellent should not be reapplied.
Insect repellents containing DEET are most effective against ticks and mosquitoes, and can
prevent Lyme Disease.
The concentration of DEET in products may range from less than 10 percent to over 30 percent.
The benefits of DEET reach a peak at a concentration of 30 percent, the maximum
concentration currently recommended for infants and children. DEET should not be used on
children under 2 months of age.
The concentration of DEET varies significantly from product to product, so read the label of any
product you purchase.

Playground Safety

The playground should have safety-tested mats or loose-fill materials (shredded rubber, sand,
wood chips or bark) maintained to a depth of at least 9 inches. The protective surface should be
installed at least 6 feet (more for swings and slides) in all directions from the equipment.
Equipment should be carefully maintained. Open "S" hooks or protruding bolt ends can be
hazardous.
Swing seats should be made of soft materials such as rubber, plastic or canvas.
Make sure children cannot reach any moving parts that might pinch or trap any body part.

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Never attach or allow children to attach ropes, jump ropes, leashes or similar items to
play equipment; children can strangle on these.
Make sure metal slides are cool to prevent children's legs from getting burned.
Parents should never purchase a home trampoline or allow children to use home trampolines.
Parents should supervise children on play equipment to make sure they are safe.
Bicycle Safety

Do not push your child to ride a two-wheeled bike until he or she is ready, at about age 5 or 6.
Consider the child's coordination and desire to learn to ride. Stick with coaster (foot) brakes until your
child is older and more experienced for hand brakes.

Take your child with you when you shop for the bike, so that he or she can try it out. The value
of a properly fitting bike far outweighs the value of surprising your child with a new one.
Buy a bike that is the right size, not one your child has to "grow into." Oversized bikes are
especially dangerous.
Your child needs to wear a helmet on every bike ride, no matter how short or how close to
home. Many accidents happen in driveways, on sidewalks and on bike paths, not just on
streets. Children learn best by observing you. Whenever you ride, put on your helmet.
When purchasing a helmet, look for a label or sticker that says the helmet meets the CPSC
safety standard.
A helmet protects your child from serious injury, and should always be worn. And remember,
wearing a helmet at all times helps children develop the helmet habit.
A helmet should be worn so that it is level on the head, not tipped forwards or backwards. The
strap should be securely fastened, and you should not be able to move the helmet in any
direction. If needed, the helmet's sizing pads can help improve the fit.
Skateboard and Scooter Safety
Children should never ride skateboards or scooters in or near traffic.
All skateboarders and scooter-riders should wear a helmet and other protective gear.
Communities should continue to develop skateboard parks, which are more likely to be
monitored for safety than ramps and jumps constructed by children at home.
Lawn Mower Safety

Try to use a mower with a control that stops the mower from moving forward if the handle is let
go.
Children younger than 16 years should not be allowed to use ride-on mowers.
Children younger than 12 years should not use walk-behind mowers.
Make sure that sturdy shoes (not sandals or sneakers) are worn while mowing.
Prevent injuries from flying objects, such as stones or toys, by picking up objects from the lawn
before mowing begins. Have anyone who uses a mower wear hearing and eye protection.
Do not pull the mower backward or mow in reverse unless absolutely necessary, and carefully
look for children behind you when you mow in reverse.
Always turn off the mower and wait for the blades to stop completely before removing the grass
catcher; unclogging the discharge chute; or crossing gravel paths, roads or other areas.
Do not allow children to ride as passengers on ride-on mowers.

======================================================

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22. Kripps Special Sales: See our Catalogue for


Vitamin D Transdermal Cream.

MEDICAL RESEARCH

Vitamin D
casts cancer
prevention in new light
Bombshell U.S. study will tie incidence rate to lack of
sunshine rather than pollutants
MARTIN MITTELSTAEDT
ENVIRONMENT REPORTER

For decades, researchers have puzzled over why rich


northern countries have cancer rates many times higher than
those in developing countries -- and many have laid the
blame on dangerous pollutants spewed out by industry.
But research into vitamin D is suggesting both a plausible
answer to this medical puzzle and a heretical notion: that
cancers and other disorders in rich countries aren't caused
mainly by pollutants but by a vitamin deficiency known to be
less acute or even non-existent in poor nations.
Those trying to brand contaminants as the key factor behind cancer in the West are
"looking for a bogeyman that doesn't exist," argues Reinhold Vieth, professor at the
Department of Nutritional Sciences at the University of Toronto and one of the
world's top vitamin D experts. Instead, he says, the critical factor "is more likely a
lack of vitamin D."
What's more, researchers are linking low vitamin D status to a host of other serious
ailments, including multiple sclerosis, juvenile diabetes, influenza, osteoporosis and
bone fractures among the elderly.
Not everyone is willing to jump on the vitamin D bandwagon just yet. Smoking and some
pollutants, such as benzene and asbestos, irrefutably cause many cancers.
But perhaps the biggest bombshell about vitamin D's effects is about to go off. In June, U.S.
researchers will announce the first direct link between cancer prevention and the sunshine
vitamin. Their results are nothing short of astounding.
A four-year clinical trial involving 1,200 women found those taking the vitamin had about a 60-percent reduction in cancer incidence, compared with those who didn't take it, a drop so large -- twice
the impact on cancer attributed to smoking -- it almost looks like a typographical error.
And in an era of pricey medical advances, the reduction seems even more remarkable because it
was achieved with an over-the-counter supplement costing pennies a day.
One of the researchers who made the discovery, professor of medicine Robert Heaney of
Creighton University in Nebraska, says vitamin D deficiency is showing up in so many illnesses
Kripps Healthy Lifestyles
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May 2007
131

besides cancer that nearly all disease figures in Canada and the U.S. will need to be re-evaluated.
"We don't really know what the status of chronic disease is in the North American population," he
said, "until we normalize vitamin D status."
Sunshine vitamin
For decades, vitamin D has been the Rodney Dangerfield of the supplement world. It's the vitamin
most Canadians never give a second thought to because it was assumed the only thing it did was
prevent childhood rickets, a debilitating bone disease. But the days of no respect could be
numbered. If vitamin D deficiency becomes accepted as the major cause of cancer and other
serious illnesses, it will ignite the medical equivalent of a five-alarm blaze on the Canadian health
front.
For many reasons, Canadians are among the people most at risk of not having enough vitamin D.
This is due to a quirk of geography, to modern lifestyles and to the country's health authorities,
who have unwittingly, if with the best of intentions, played a role in creating the vitamin deficiency.
Authorities are implicated because the main way humans achieve healthy levels of vitamin D isn't
through diet but through sun exposure. People make vitamin D whenever naked skin is exposed
to bright sunshine. By an unfortunate coincidence, the strong sunshine able to produce vitamin D
is the same ultraviolet B light that can also causes sunburns and, eventually, skin cancer.
Only brief full-body exposures to bright summer sunshine - of 10 or 15 minutes a day - are needed
to make high amounts of the vitamin. But most authorities, including Health Canada, have urged a
total avoidance of strong sunlight or, alternatively, heavy use of sunscreen. Both
recommendations will block almost all vitamin D synthesis.
Those studying the vitamin say the hide-from-sunlight advice has amounted to the health
equivalent of a foolish poker trade. Anyone practising sun avoidance has traded the benefit of a
reduced risk of skin cancer - which is easy to detect and treat and seldom fatal - for an increased
risk of the scary, high-body-count cancers, such as breast, prostate and colon, that appear linked
to vitamin D shortages.
he sun advice has been misguided information "of just breathtaking proportions," said John
Cannell, head of the Vitamin D Council, a non-profit, California-based organization.
"Fifteen hundred Americans die every year from [skin cancers]. Fifteen hundred Americans die
every day from the serious cancers."
Health Canada denies its advice might be dangerous. In an e-mailed statement, it said that most
people don't apply sunscreen thoroughly, leaving some skin exposed, and that people spend
enough time outside without skin protection to make adequate amounts of vitamin D.
However, the Canadian Cancer Society last year quietly tweaked its recommendation to recognize
that limited amounts of sun exposure are essential for vitamin D levels.
Avoiding most bright sunlight wouldn't be so serious if it weren't for a second factor: The main
determinant of whether sunshine is strong enough to make vitamin D is latitude. Living in the north
is bad, the south is better, and near the equator is best of all.
Canadians have drawn the short straw on the world's latitude lottery: From October to March,
sunlight is too feeble for vitamin D production. During this time, our bodies draw down stores built
by summer sunshine, and whatever is acquired from supplements or diet.
Government regulations require foods such as milk and margarine to have small amounts of
added vitamin D to prevent rickets.
Other foods, such as salmon, naturally contain some, as does the cod liver oil once commonly
given to children in the days before milk fortification. But the amounts from food are minuscule
compared to what is needed for cancer prevention and what humans naturally can make in their
skin.
Vitamin D levels in Canada are also being compromised by a lifestyle change. Unlike previous
generations that farmed or otherwise worked outside, most people now spend little time outdoors.
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One survey published in 2001 estimated office- and homebound Canadians and Americans spend
93 per cent of waking time in buildings or cars, both of which block ultraviolet light.
Consequently, by mid-winter most Canadians have depleted vitamin D status. "We're all a bit
abnormal in terms of our vitamin D," said Dr. Vieth, who has tested scores of Canadians,
something done with a simple blood test.
How much is enough?
Just how much vitamin D is required for optimum health is the subject of intense scientific inquiry.
Dr. Vieth has approached the matter by asking: What vitamin D level would humans have if they
were still living outside, in the wild, near the equator, with its attendant year-round bright
sunshine? "Picture the natural human as a nudist in environments south of Florida," he says.
He estimates humans in a state of nature probably had about 125 to 150 nanomoles/litre of
vitamin D in their blood all year long - levels now achieved for only a few months a year by the
minority of adult Canadians who spend a lot of time in the sun, such as lifeguards or farmers.
For the rest of the population, vitamin D levels tend to be lower, and crash in winter. In testing
office workers in Toronto in winter, Dr. Vieth found the average was only about 40 nanomoles/L,
or about one-quarter to one-third of what humans would have in the wild.
The avalanche of surprising research on the beneficial effects of vitamin D could affect dietary
recommendations as well. Health Canada says that, in light of the findings, it intends to study
whether recommended dietary levels need to be revised, although the review is likely to be years
away.
A joint Canadian-U.S. health panel last studied vitamin D levels in 1997, concluding the relatively
low amounts in people's blood were normal. At the time, there was speculation vitamin D had an
anti-cancer effect, but more conclusive evidence has only emerged since.
"There needs to be a comprehensive review undertaken and that is planned," says Mary Bush,
director general of Health Canada's office of nutrition policy and promotion.
But Ms. Bush said the government doesn't want to move hastily, out of concern that there may be
unknown risks associated with taking more of the vitamin.
Those who worry about low vitamin D, however, say this stand is too conservative - that the
government's caution may itself be a health hazard.
To achieve the vitamin D doses used for cancer prevention through foods, people would need to drink about three litres of milk a day, which is
unrealistic.

If health authorities accept the new research, they would have to order a substantial increase in
food fortification or supplement-taking to affect disease trends. As it is, the 400 IU dosage
included in most multivitamins is too low to be an effective cancer fighter.
Dr. Vieth said any new recommendations will also have to reflect the racial and cultural factors
connected to vitamin D. Blacks, South Asians and women who wear veils are at far higher risks of
vitamin D deficiencies than are whites.
Although humans carry a lot of cultural baggage on the subject of skin hue, colour is the way
nature dealt with the vagaries of high or low vitamin D production by latitude.
Those with very dark skins, whose ancestors originated in tropical, light-rich environments, have
pigmentation that filters out more of the sunshine responsible for vitamin D; in northern latitudes,
they need more sun exposure - often 10 times as much - to produce the same amount of the
vitamin as whites.
Dr. Vieth says it is urgent to provide information about the need for extra vitamin D in Canada's
growing non-white population to avoid a future of high illness rates in this group.
Researchers suspect vitamin D plays such a crucial role in diseases as unrelated as cancer and
osteoporosis because the chemical originated in the early days of animal evolution as a way for
cells to signal that they were being exposed to daylight.
Even though living things have evolved since then, almost all cells, even those deep in our bodies,
have kept this primitive light-signalling system.
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In the body, vitamin D is converted into a steroid hormone, and genes responding to it play a
crucial role in fixing damaged cells and maintaining good cell health. "There is no better anticancer agent than activated vitamin D. I mean, it does everything you'd want," said Dr. Cannell of
the Vitamin D Council.
Some may view the sunshine-vitamin story as too good to be true, particularly given that the
number of previous claims of vitamin cure-alls that subsequently flopped. "The floor of modern
medicine is littered with the claims of vitamins that didn't turn out," Dr. Cannell allowed.
But the big difference is that vitamin D, unlike other vitamins, is turned into a hormone, making it
far more biologically active. As well, it is "operating independently in hundreds of tissues in your
body," Dr. Cannell said.
Referring to Linus Pauling, the famous U.S. advocate of vitamin C use as a cure for many
illnesses, he said: "Basically, Linus Pauling was right, but he was off by one letter."

Ribbon representations of two orthogonal views of the DBP-actin complex.

Actin - Orange subdomain 1, Green subdomain 2, Yellow subdomain 3, Red subdomain 4


DBP - Blue domain 1, Magenta domain 2, Cyan domain 3 - (color-coded as in reference 29).
ATP and Ca2+ (green) are shown as space-filling representations.

http://biophysics.bumc.bu.edu/faculty/head/index.html

=========================================================================
23. YouTube: See Dr. Thorpe on YouTube.
http://www.youtube.com/results?search_query=vitamin+d3+cream&search=Search
24. Archives: Past Kripps Healthy Lifestyles newsletters: none exist yet; this is Volume 1, Issue 1.

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25. Glossary of Terms: See the following links.


http://www.wikipedia.org/
http://www.nlm.nih.gov/medlineplus/mplusdictionary.html
http://medical-dictionary.thefreedictionary.com/
http://www.medterms.com/script/main/hp.asp
http://cancerweb.ncl.ac.uk/omd/
26. Feedback: This is Volume 1, Issue 1 of the Kripps newsletter. The newsletter will be a work in
progress and will evolve. We welcome your feedback for improving the newsletter. Please email
our managing editor, Steve: sbripley@shaw.ca, placing in the subject box the word newsletter.
27. Disclaimer & Permitted Uses
A. Kripps Healthy Lifestyles newsletter is intended solely for general educational purposes.
Kripps Pharmacy Ltd., and its affiliates and personnel, do not purport to diagnose or prescribe for
medical conditions of specific individual readers of the newsletter, and can take no responsibility
for the use or misuse of the data and opinions expressed in these articles. As always, readers are
encouraged to seek the opinion of their physician before employing any information contained in
the articles.
B. The use of Kripps Healthy Lifestyles for commercial purposes is prohibited without written
permission from Kripps Pharmacy ltd. Copyright is held by Kripps, to which all rights are reserved.
The newsletter may be copied or forwarded for personal, non-commercial use, with appropriate
individual credits acknowledged.

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