00
Biomedical
Therapy
J o urnal o f
Integrating Homeopathy
and Conventional Medicine
Female
Disorders
Current Trends in Womens Health
Which Came First: Insulin Resistance or Inflammation?
Contents
I n Fo c u s
fixerOO/Fotolia.de
W h a t E l s e I s N e w ? . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 12
From the Practice
Re f r e s h Yo u r H o m o t ox i c o l o g y
iStockphoto.com/ DNY59
iStockphoto.com/RosemarieGearhart
iStockphoto.com/ Anatoliy Samara
Practical Protocols
20
Specialized Applications
E x p a n d Yo u r Re s e a r c h K n o wl e d g e
Re s e a r c h H i g h l i g h t s
)2
Published by/Verlegt durch: International Academy for Homotoxicology GmbH, Bahnackerstrae 16,
76532 Baden-Baden, Germany, www.iah-online.com, e-mail: journal@iah-online.com
Editor in Chief/verantwortlicher Redakteur: Dr. Alta A. Smit
Editor: Dr. David W. Lescheid
Managing Editor: Silvia Bartsch
Print/Druck: Dinner Druck GmbH, Schlehenweg 6, 77963 Schwanau, Germany
2011 International Academy for Homotoxicology GmbH, Baden-Baden, Germany
iStockphoto.com/Milena Lachowicz
References
1. Ron P. Daughters as caregivers of aging
parents: the shattering myth. J Gerontol Soc
Work. 2009;52(2):135-153.
2. Desvergne B, Feige JN, Casals-Casas C.
PPAR-mediated activity of phthalates: a link
to the obesity epidemic? Mol Cell Endocrinol.
2009;304(1-2):43-48.
3. Mendola P, Messer LC, Rappazzo K. Science
linking environmental contaminant exposures with fertility and reproductive health
impacts in the adult female. Fertil Steril.
2008;89(suppl 2):e81-e94.
4. Torres SJ, Nowson CA. Relationship between
stress, eating behavior, and obesity. Nutrition.
2007;23(11-12):887-894.
5. Elobeid MA, Padilla MA, Brock DW, Ruden
DM, Allison DB. Endocrine disruptors and
obesity: an examination of selected persistent
organic pollutants in the NHANES 19992002 data. Int J Environ Res Public Health.
2010;7(7):2988-3005.
6. Mllerov D, Kopeck J. White adipose tissue: storage and effector site for environmental pollutants. Physiol Res. 2007;56(4):375381.
)3
) I n Fo c u s
Current Trends
in Womens Health
By Michael E. Greer, MD
Obstetrician/Gynecologist
Introduction
)4
) I n Fo c u s
Uterus
fixerOO/Fotolia.de
Fallopian tube
Ovary
Cervix
Endometrial
(uterine) lining
Vagina
Myometrium
)5
http://en.wikipedia.org/wiki/File:Perforierte_
Endometriosezyste.jpg
) I n Fo c u s
)6
) I n Fo c u s
Adequate antibiotic coverage for anaerobic organisms is difficult to
achieve, with metronidazole appearing to have limited efficacy, possibly
because poor tolerability limits
compliance.16 Microbial resistance
to other antibiotics also is a problem.15-17
As a consequence of the prevalence
of antibiotic resistance, modulation
of the innate immune system to protect against infection has been discussed as an attractive alternative to
antibiotic therapies in the medical
literature.18 Study of the innate immune response has indicated that
there is variation in host immunity,
possibly because of genetic differences. Thus, a suboptimal innate immune response may result in a permissive environment for pathogen
colonization, whereas an excessive
response will result in disproportionate levels of inflammation and
tissue damage. An investigation of
modulation of the innate immune
response in the reproductive tract
could provide significant advances
in the management of PID and its
sequelae.18
Endometriosis
Endometriosis can have a profound
impact on a womans life, potentially affecting her education, career,
and ability to have children.19 The
cost of endometriosis to both the individual and society, including delayed diagnosis and ineffective treatments, is considerable and poorly
quantified.19 The results of a health
survey in the United States indicated
that half of women reporting endometriosis required at least a day of
bed rest within the past year, as a
consequence of the condition, with
the average number of days of bed
rest being 17.8.20 More than 8% of
women reported that endometriosis
limited their activity, and nearly 5%
reported that it limited them in their
)7
iStockphoto.com/Amanda Rohde
) I n Fo c u s
)8
) I n Fo c u s
Endometriosis
Bioregulatory therapy has a significant role to play in the treatment of
endometriosis because the condition
presents like a typical dysregulation
syndrome. The immune and neuroendocrine systems, and local tissue
cycles, are involved, making linear
intervention difficult; therefore, endometriosis lends itself to the multitargeted approach that is used in
homotoxicology.
The basic treatment for endometriosis is the inflammation-regulating
drug Traumeel. Ovarium compositum is added, along with Coenzyme
compositum for metabolic support.
Ovarium compositum also contains
hypophysis suis, which supports the
hypothalamic-pituitary-ovarian-adrenal axis. The immunomodulator,
Tonsilla compositum, is used to support the immune system. In addition, Tonsilla compositum contains
hypothalamus suis and glandula suprarenalis suis that further support
the hypothalamic-pituitary-adrenal
axis; and a primitive tissue, funiculus
umbilicalis suis, that is postulated to
support the connective tissue.28
Traumeel is given daily, whereas the
other medications are prescribed in
cycles of 5 weeks, with 4 weeks rest
in between (2 ampoules of each are
given orally or subcutaneously twice
a week). The number of cycles needed depends on the response of the
patient.
Metabolic Disorders:
Polycystic Ovary Syndrome
Polycystic ovary syndrome (PCOS)
is the most frequent endocrinopathy
in women of reproductive age,32 occurring in approximately 5% to 10%
of these women.33,34 The Rotterdam
criteria for the diagnosis of PCOS
require 2 of the following 3 criteria
to be met: irregular or no ovulation,
clinical/paraclinical
hyperandro-
)9
iStockphoto.com/ hartphotography1
) I n Fo c u s
Figure 4. Central obesity is common
in patients with polycystic ovary
syndrome. Increased visceral fat
is associated with a higher risk
of heart disease, hypertension,
) 10
) I n Fo c u s
References
1. Andersen A-MN, Wohlfahrt J, Christens P,
Olsen J, Melbye M. Maternal age and fetal
loss: population based register linkage study.
BMJ. 2000;320(7251):1708-1712.
2. Stein Z, Susser M. The risks of having
children in later life: social advantage may
make up for biological disadvantage. BMJ.
2000;320(7251):1681.
3. Shulman LP. Gynecological management of
premenstrual symptoms. Curr Pain Headache
Rep. 2010;14(5):367-375.
4. Vercellini P, Eskenazi B, Consonni D, et
al. Oral contraceptives and risk of endometriosis: a systematic review and metaanalysis [published online ahead of print
September 10, 2010]. Hum Reprod Update.
doi:10.1093/humupd/dmq042.
5. Cibula D, Gompel A, Mueck AO, et al. Hormonal contraception and risk of cancer.
Hum Reprod Update. 2010;16(6):631-650.
6. Tchaikovski SN, Rosing J. Mechanisms of
estrogen-induced venous thromboembolism.
Thromb Res. 2010;126(1):5-11.
7. Mass J, Watrin T, Laurent A, Deschamps S,
Guerrier D, Pellerin I. The developing female
genital tract: from genetics to epigenetics.
Int J Dev Biol. 2009;53(2-3):411-424.
8. Colborn T, vom Saal FS, Soto AM. Developmental effects of endocrine-disrupting chemicals in wildlife and humans. Environ Health
Perspect. 1993;101(5):378-384.
9. Martini AC, Vincenti LM, Santilln ME, et al.
Chronic administration of nonsteroidal-antiinflammatory drugs (NSAIDS): effects upon
mouse reproductive functions. Rev Fac Cien
Med Univ Nac Cordoba. 2008;65(2):47-59.
10. Biggs WS, Williams RM. Common gynaecologic infections. Prim Care Clin Office Pract.
2009;36(1):33-51.
11. Angotti LB, Lambert LC, Soper DE. Vaginitis: making sense of over-the-counter
treatment options. Infect Dis Obstet Gynecol.
2007;2007:97424.
12. Farage MA, Miller KW, Ledger WJ. Determining the cause of vulvovaginal symptoms.
Obstet Gynecol Surv. 2008;63(7):445-464.
13. Centers for Disease Control and Prevention,
Division of STD Prevention. STD Curriculum for Clinical Educatiors: Vaginitis Module, January 2010. http://www2.cdc.gov/
stdtraining/ready-to-use/Manuals/Vaginitis/vaginitis-notes-2010.doc. Accessed May
2, 2011.
) 11
Siggi/Fotolia.de
) 12
Melatonin Helps
Prevent Cancer in Women
Antihomotoxic Therapy
for Autoimmune Thyroiditis
Stroke. 2010;41(6):1243-1250.
iStockphoto.com/Don Bayley
iStockphoto.com/Karen Sarraga
Endometriosis and
Leiomyomata Linked to
Phthalate Exposure
F O R P RO F E S S I ONA L U S E ON LY
The information contained in this journal is meant for professional use only, is meant to convey general and/or specific worldwide scientific information relating to the
products or ingredients referred to for informational purposes only, is not intended to be a recommendation with respect to the use of or benefits derived from the
products and/or ingredients (which may be different depending on the regulatory environment in your country), and is not intended to diagnose any illness, nor is it
intended to replace competent medical advice and practice. IAH or anyone connected to, or participating in this publication does not accept nor will it be liable
for any medical or legal responsibility for the reliance upon or the misinterpretation or misuse of the scientific, informational and educational content of the
articles in this journal.
The purpose of the Journal of Biomedical Therapy is to share worldwide scientific information about successful protocols from orthodox and complementary practitioners. The intent of the scientific information contained in this journal is not to dispense recipes but to provide practitioners with practice information for a better
understanding of the possibilities and limits of complementary and integrative therapies.
Some of the products referred to in articles may not be available in all countries in which the journal is made available, with the formulation described in any article or
available for sale with the conditions of use and/or claims indicated in the articles. It is the practitioners responsibility to use this information as applicable
and in a manner that is permitted in his or her respective jurisdiction based on the applicable regulatory environment. We encourage our readers to share
their complementary therapies, as the purpose of the Journal of Biomedical Therapy is to join together like-minded practitioners from around the globe.
Written permission is required to reproduce any of the enclosed material. The articles contained herein are not independently verified for accuracy or truth. They have
been provided to the Journal of Biomedical Therapy by the author and represent the thoughts, views and opinions of the articles author.
) 13
Uterine Fibroids
By Olga Garca Domnguez, MD
Gynecologist
) 14
References
1. Stewart EA. Uterine fibroids. Lancet.
2001;357(9252):293-298.
2. Katz VL. Benign gynecologic lesions: vulva,
vagina, cervix, uterus, oviduct, ovary. In:
Katz VL, Lentz GM, Lobo RA, Gershenson
DM, eds. Comprehensive Gynecology. 5th ed.
Philadelphia, PA: Mosby Elsevier; 2007:chap
18.
3. Blake RE. Leiomyomata uteri: hormonal and
molecular determinants of growth. J Natl
Med Assoc. 2007;99(10):1170-1184.
4. Levy BS. Modern management of uterine fibroids. Acta Obstet Gynecol Scand.
2008;87(8):812-823.
5. Viswanathan M, Hartmann K, McKoy N, et
al. Management of uterine fibroids: an update
of the evidence. Evid Rep Technol Assess (Full
Rep). 2007;(154):1-122.
Further reading
1. Cnill Montobbio V. Tratado de Gine
cologa y de Tcnica Teraputica Gine
colgica. 5th ed. Barcelona, Spain: Labor; 1967.
2. Kushi M. Alimentacion Macrobiotica.
Madrid, Spain: EDAF; 2004.
3. Kyank H, Sommer K. Lehrbuch der
Gynkologie. 3rd ed. Leipzig, Germany: Thieme; 1978.
4. Ordinatio Antihomotoxica et Materia
Medica: Tratado Prctico de Terapia
Antihomotxica. 9th Rev ed. BadenBaden, Germany: Biologische Heilmittel Heel GmbH; 2007.
5. Pommier L. Diccionario Homeoptico
de Urgencia. 2nd ed. Barcelona, Spain:
Paidotribo; 2002.
6. Schmid F, Rimpler M, Wemmer U.
Medicina Antihomotxica: Principios,
Clnica, Prctica. Vol 1. 2nd ed. BadenBaden, Germany: Aurelia; 2004.
7. Vannier L. La Tpologia y sus Aplicacio
nes Teraputicas. Madrid, Spain: Mandala; 2001.
) 15
) Re f r e s h Yo u r H o m o t ox i c o l o g y
) 16
t is well established that persistently elevated levels of inflammatory cytokines play a significant role
in the development of chronic disease. For example, persistently high
levels of 1 or more of the proinflammatory cytokines (ie, interleukins 1
and 6 and tumor necrosis factor )
are common to the pathogenesis of
diseases such as cardiovascular disease, cancers, inflammatory bowel
disease, chronic fatigue syndrome,
and neurological disorders (eg, depression, Parkinson disease, and
Alzheimer disease).1
The elevation of these cytokines has
become such a common thread for
the development of these diseases
that the term sickness behavior2,3 has
recently been proposed to describe
the associated signs and symptoms
of fever, anorexia, fatigue, sleepiness, and social withdrawal. Additional support for the paramount
importance of inflammation in disease development has recently come
from the Justification for the Use of
Statins in Primary Prevention: An
Intervention Trial Evaluating Rosuvastatin (JUPITER). The results of
this trial suggest that the proposed
benefit of statin drugs in the prevention of cardiovascular disease was
more likely because of their ability
to reduce levels of high-sensitivity
C-reactive protein (a nonspecific inflammatory marker) than their effects on lowering cholesterol.4
mass, and in sex hormone and adipokine levels. These differences tend
to improve insulin sensitivity in
women compared with men8 and
suggest that sex differences must be
considered when preventing and
treating diseases associated with insulin resistance.
There is no question that obesity has
reached epidemic proportions in
many parts of the world. In many
countries, particularly those of industrialized and developed nations,
there is a regular excess intake of
calories from increasingly caloriedense but nutrient-poor foods and
drinks. The excess of calories, combined with an increasingly less
physically active society, creates a
daily energy surplus that eventually
leads to a dysregulation of the
bodys key storage hormone, insulin
(Figure).9 With cells no longer sensitive to insulin and a surplus of blood
glucose triggering the continued release of insulin from the pancreas,
hyperinsulinemia develops.
Adipose tissue is an endocrine organ
releasing many different signaling
molecules, some of which have direct localized and systemic inflammatory effects.10 The development
of adipose tissue is preceded by an
impairment of energy balance that is
primarily associated with the inability of the cells to respond to insulin,
either through inadequacy of insulin receptor signaling or some other
defect in the biochemical pathway.
iStockphoto.com/Martin McCarthy
) Re f r e s h Yo u r H o m o t ox i c o l o g y
Figure. Human
Insulin Molecule
Hyperinsulinemia
and Female Health
High insulin levels can modulate the
activity of gonadotropin-releasing
hormone in the hypothalamus (at
least in lean healthy controls) and,
therefore, interfere with the pattern
of release of luteinizing hormone
(LH).11 These data suggest that reproductive cycles, ovulation, and
fertility could be affected. Indeed,
recent evidence suggests that fasting
insulin levels, fasting serum levels of
sex hormonebinding globulin
(SHBG), and the free androgen index had strong negative influences
on the regularity of menstrual cycles
in young women.12 Furthermore,
women with insulin resistance and
hyperinsulinemia (and upper body
obesity, which is also termed android
or truncal obesity) had a greater risk
of anovulatory cycles13 that could be
reversed through the use of insulinsensitizing drugs.14
Glucose intolerance, including insulin resistance and impaired fasting
glucose level,15 is an important part
of the pathophysiological characteristics of polycystic ovary syndrome
(PCOS).16,17 However, insulin infusions to women with PCOS had no
effect on the secretion of LH, suggesting that the inappropriate secretion of LH observed in this disease
might not be directly due to insulin
resistance and hyperinsulinemia.18
Furthermore, there was no change
in the altered pattern of LH secretion in women with PCOS after insulin infusion despite an improvement in insulin sensitivity after
treatment with pioglitazone, a thiazolidinedione type of drug known
to modulate transcription of insulinsensitive genes in the muscle, liver,
and adipose tissue.19 This suggests
that the dysregulated gonadotropin
release in PCOS is caused by a
mechanism that is not directly related to insulin levels.
High insulin levels in the ovaries
help stimulate the production of steroid hormones, such as androstenedione and testosterone,20 that are
associated with some of the signs
and symptoms of disease in women
if they are in excess for a long time.
Higher levels of testosterone, but
not androstenedione, are correlated
with higher levels of insulin resistance in women (but not in men). In
particular, women with PCOS that
are also insulin resistant have the
highest circulating levels of testosterone, suggesting that their ovaries
are more sensitive to the testosterone-stimulating effects of insulin.21
Insulin is a key regulator of the synthesis of SHBG in the liver.22 Elevated levels of insulin down regulate
the production of SHBG and, therefore, increase the amount of bioavailable estrogen; this increases the
risk of diseases associated with estrogen excess. Furthermore, a decreased serum level of SHBG would
) 17
) Re f r e s h Yo u r H o m o t ox i c o l o g y
) 18
ple, both isoforms of estrogen receptor ( and ) are present in pancreatic beta cells. The insulin content
of pancreatic beta cells was increased
after long-term exposure to physiological levels of 17-estradiol, most
likely by binding with estrogen receptor .32
It is becoming increasingly evident
that environmental chemicals from
plastics and common household
products, such as bisphenol A (BPA)
and phthalates, have the potential to
trigger dysregulated metabolic
events that could lead to insulin resistance and contribute to the obesity epidemic.33 For example, there
is evidence that the environmental
estrogen mimetic BPA significantly
binds and activates estrogen receptor in pancreatic beta cells at serum levels that are plausible, suggesting that this could be one of the
early triggers of dysregulated insulin levels. The putative role of BPA
in disrupting the normal physiological regulation of glucose has been
reported and reviewed elsewhere.34,35 It is interesting to note
that in mouse models, when pregnant mice are exposed to environmentally relevant levels of BPA, glucose homeostasis is affected and
insulin resistance develops not only
in the mothers themselves, but also
in the male offspring. These negative effects initiated in utero persisted until adulthood, suggesting that
exposure to BPA early in development could influence the development of chronic disease later in
life.36
Phthalates, widely found in plastic
products, are additional environmental pollutants that disrupt cellular metabolism and, therefore, contribute to the development of insulin
resistance and obesity (at least in
men).37 This dysregulation of cell
metabolism was the result of the
ability of phthalates to interfere
) Re f r e s h Yo u r H o m o t ox i c o l o g y
References
1. Handschin C, Spiegelman BM. The
role of exercise and PGC1 in inflammation and chronic disease. Nature.
2008;454(7203):463-469.
2. Dantzer R, Kelley KW. Twenty years of research on cytokine-induced sickness behavior. Brain Behav Immun. 2007;21(2):153160.
3. Myers JS. Proinflammatory cytokines and
sickness behavior: implications for depression and cancer-related symptoms. Oncol
Nurs Forum. 2008;35(5):802-807.
4. Mora S, Ridker PM. Justification for the Use
of Statins in Primary Prevention: an Intervention Trial Evaluating Rosuvastatin (JUPITER): can C-reactive protein be used to
target statin therapy in primary prevention?
Am J Cardiol. 2006;97(2A):33A-41A.
5. Hotamisligil GS, Erbay E. Nutrient sensing
and inflammation in metabolic diseases. Nat
Rev Immunol. 2008;8(12):923-934.
6. Medzhitov R. Inflammation 2010: new adventures of an old flame. Cell. 2010;140(6):
771-776.
7. Hotamisligil GS. Inflammation and metabolic
disorders. Nature. 2006;444(7121):860867.
8. Geer EB, Shen W. Gender differences in insulin resistance, body composition and energy
balance. Gend Med. 2009;6(suppl 1):60-75.
9. Fair AM, Montgomery K. Energy balance,
physical activity, and cancer risk. In: Verma
M, ed. Cancer Epidemiology. New York, NY:
Humana Press; 2009. Methods in Molecular
Biology; vol 472.
10. Wozniak SE, Gee LL, Wachtel MS, Frezza EE.
Adipose tissue: the new endocrine organ? A
review article. Dig Dis Sci. 2009;54(9):18471856.
11. Moret M, Stettler R, Rodieux F, et al. Insulin
modulation of luteinizing hormone secretion
in normal female volunteers and lean polycystic ovary syndrome patients. Neuroendocri
nology. 2009;89(2):131-139.
12. Wei S, Schmidt MD, Dwyer T, Norman RJ,
Venn AJ. Obesity and menstrual irregularity:
associations with SHBG, testosterone, and
insulin. Obesity. 2009;17(5):1070-1076.
13. Morn C, Hernndez E, Ruz JE, Fonseca
ME, Bermdez JA, Zrate A. Upper body
obesity and hyperinsulinemia are associated with anovulation. Gynecol Obstet Invest.
1999;47(1):1-5.
14. Ibez L, Valls C, Ferrer A, Ong K, Dunger
DB, De Zegher F. Additive effects of insulin-sensitizing and anti-androgen treatment
in young, nonobese women with hyperinsulinism, hyperandrogenism, dyslipidemia,
and anovulation. J Clin Endocrinol Metab.
2002;87(6):2870-2874.
15. Salley KE, Wickham EP, Cheang KI, Essah
PA, Karjane NW, Nestler JE. Glucose intolerance in polycystic ovary syndrome: a position
statement of the Androgen Excess Society.
J Clin Endocrinol Metab. 2007;92(12):45464556.
29. Gunter MJ, Hoover DR, Yu H, et al. Insulin, insulin-like growth factor-I, and risk of
breast cancer in postmenopausal women.
J Natl Cancer Inst. 2009;101(1):48-60.
30. Gunter MJ, Hoover DR, Yu H, et al. A prospective evaluation of insulin and insulin-like
growth factor-I as risk factors for endometrial cancer. Cancer Epidemiol Biomarkers
Prev. 2008;17(4):921-929.
31. Kaaks R, Lukanova A, Kurzer MS. Obesity,
endogenous hormones, and endometrial cancer risk: a synthetic review. Cancer Epidemiol
Biomark Prev. 2002;11(12):1531-1543.
32. Alonso-Magdalena P, Ropero AB, Carrera
MP, et al. Pancreatic insulin content regulation by the estrogen receptor ER. PLoS One.
2008;3(4):e2069.
33. Desvergne B, Feige JN, Casals-Casas C.
PPAR-mediated activity of phthalates: a link
to the obesity epidemic? Mol Cell Endocrinol.
2009;304(1-2):43-48.
34. Alonso-Magdalena P, Morimoto S, Ripoll C,
Fuentes E, Nadal A. The estrogenic effect of
bisphenol A disrupts pancreatic -cell function in vivo and induces insulin resistance.
Environ Health Perspect. 2006;114(1):106112.
35. Alonso-Magdalena P, Ropero AB, Soriano
S, Quesada I, Nadal A. Bisphenol-A: a new
diabetogenic factor? Hormones (Athens).
2010;9(2):118-126.
36. Alonso-Magdalena P, Vieira E, Soriano S, et
al. Bisphenol A exposure during pregnancy
disrupts glucose homeostasis in mothers and
adult male offspring. Environ Health Perspect.
2010;118(9):1243-1250
37. Stahlhut RW, van Wijngaarden E, Dye TD,
Cook S, Swan SH. Concentrations of urinary
phthalate metabolites are associated with
increased waist circumference and insulin
resistance in adult US males. Environ Health
Perspect. 2007;115(6):876-882.
38. Hurst CH, Waxman DJ. Activation of PPAR
and PPAR by environmental phthalate
monoesters. Toxicol Sci. 2003;74(2):297308.
39. Gregor MF, Hotamisligil GS. Adipocyte
stress: the endoplasmic reticulum and metabolic disease. J Lipid Res. 2007;48(9):19051914.
40. Lamb RE, Goldstein BJ. Modulating an oxidative-inflammatory cascade: potential new
treatment strategy for improving glucose
metabolism, insulin resistance, and vascular
function. Int J Clin Pract. 2008;62(7):10871095.
) 19
) Practical Protocols
Genital Human
Papilloma Virus Infection
Bioregulatory Management
By Alta A. Smit, MD
) 20
References
1. Diaz ML. Human papilloma virus: prevention
and treatment. Obstet Gynecol Clin North Am.
2008;35(2):199-217, vii-viii.
2. Wheeler CM. Natural history of human papillomavirus infections, cytologic and histologic abnormalities, and cancer. Obstet Gyne
col Clin North Am. 2008;35(4):519-536, vii.
3. Garland SM, Hernandez-Avila M, Wheeler
CM, et al. Quadrivalent vaccine against human papillomavirus to prevent anogenital
diseases. N Engl J Med. 2007;356(19):19281943.
4. Steben M, Duarte-Franco E. Human papillomavirus infection: epidemiology and pathophysiology. Gynecol Oncol. 2007;107(2)
(suppl 1):S2-S5.
) Practical Protocols
Table. Three-Pillar Approach for the Treatment of HPV Infection
DET-Phase
Basic and/or
Symptomatic
Mucodermal
Urogenital
Gyncoheel
(inflammation)
Regulation Therapya
D&D
Impregnation
IM
Engystol
Tonsilla compositum
(if persistence is not cleared by
a regimen with Engystol only)
COS
Mucosa compositum
(vaginal and cervical)
Cutis compositum
(external genital warts)
Coenzyme compositum
Ubichinon compositum
(if not cleared by the initial regimen)
Note: Persistent HPV is classified as being in the impregnation phase and, therefore, should be addressed aggressively. Engystol has been
shown to have antiviral properties in several viruses, including the DNA viruses,13 and can increase interferon production.14 Thus, it is used
as a supportive measure. However, if the virus is still persistent at the first follow-up after initiating treatment, a course of Tonsilla compositum (supportive of the immune system) and Ubichinon compositum (for deep cellular detoxification) should be added (3 times a
week for 6 weeks) and Engystol should be continued after this period with follow-up.
In patients who are seen with persistence of the same strain for longer than 2 years, these 2 organ regulators should be the first intervention for the first cycle, followed by Engystol.
Dosages: Gyncoheel, 10 drops 3 times daily. Regulation therapy: tablets, 1 tablet 3 times daily; ampoules, 1 ampoule of each medication,
1 to 3 times per week; Detox-Kit, 30 drops of each medication in 1.5 L of water (drink throughout the day).
Abbreviations: COS, cell and organ support; D&D, detoxification and drainage; DET, Disease Evolution Table; HPV, human papilloma virus; IM,
immunomodulation.
a
Antihomotoxic regulation therapy consists of a 3-pillar approach: D&D, IM, and COS.
b
Advanced supportive detoxification and drainage consists of Hepar compositum (liver), Solidago compositum (kidney), and Thyreoidea
compositum (connective tissue).
c
The Detox-Kit consists of Lymphomyosot, Nux vomica-Homaccord, and Berberis-Homaccord.
12. Waxman AG, Zsemlye MM. Preventing cervical cancer: the Pap test and the HPV vaccine. Med Clin North Am. 2008;92(5):10591082, x.
13. Oberbaum M, Glatthaar-Saalmller B, Stolt
P, Weiser M. Antiviral activity of Engystol:
an in vitro analysis. J Altern Complement Med.
2005;11(5):855-862.
14. Roeska K, Seilheimer B. Antiviral activity of Engystol and Gripp-Heel: an in-vitro
assessment. J Immune Based Ther Vaccines.
2010;8:6. doi:10.1186/1476-8518-8-6.
) 21
) Specialized Applications
Contributions of
Biological Medicine in Infertility
10%
10%
30%
Uterotubal factors
Male factors
20%
3
Ovulatory factors
30%
) 22
Monart Design/Fotolia.de
) Specialized Applications
ly cause hyperprolactinemia,
should be examined.
4. Use of recreational drugs.
5. Nutrition.
The consumption of complex
car
abohydrates, which are rich
in fiber and have a low glycemic
index, should be recommended.9
There is increasing impor
tance
attributed to insulin in fertility.10,11
The consumption of proteins of
vegetable origin and white meat
is important. There is no need to
expand herein, but it is clear that
excessive amounts of arachidonic acid must be avoided. This ingredient is found in red meat and
contributes to the synthesis of
bad eicosanoids.12
For the same reasons, with a
view to recommend the good
eicosanoids,12 the use of extravirgin and cold-pressed vegetable oils should be emphasized.
) 23
) Specialized Applications
DET-Phase
Basic and/or
Symptomatic
Impregnation or
degeneration
Gyncoheel
Regulation Therapya
Optional
D&D
China-Homaccord
(if patient has a depressed mood)
IM
Traumeel
COS
Ovarium compositum
Placenta compositum
Aesculus compositum
Hepar compositum
Coenzyme compositum
Ubichinon compositum
Dosages: Gyncoheel, 10 drops 3 times daily. Regulation therapy: tablets, 1 tablet 3 times daily; ampoules, 1 ampoule of each medication, 1
to 3 times per week; Detox-Kit, 30 drops of each medication in 1.5 L of water (drink throughout the day). Optional therapy: ampoules, 1
ampoule 1 to 3 times per week; drops, 10 drops 3 times daily.
Abbreviations: COS, cell and organ support; D&D, detoxification and drainage; DET, Disease Evolution Table; IM, immunomodulation.
a
Antihomotoxic regulation therapy consists of a 3-pillar approach: D&D, IM, and COS.
The Detox-Kit consists of Lymphomyosot, Nux vomica-Homaccord, and Berberis-Homaccord.
) 24
References
1. Lim AS, Tsakok MF. Age-related decline in
fertility: a link to degenerative oocytes? Fertil
Steril. 1997;68(2):265-271.
2. Cruz JR, Gindoff PR. Age and reproduction.
Reprod Med Rev. 1999;7(1):61-69.
3. Edwards RG, Risquez F, eds. Modern Assisted
Conception. Cambridge, England: Reproductive Healthcare Ltd; 2003.
4. Ordinatio Antihomotoxica et Materia Medica:
Tratado Prctico de Terapia Antihomotxica.
6th Rev ed. Baden-Baden, Germany: Biologische Heilmittel Heel GmbH; 2002.
) 25
) E x p a n d Yo u r Re s e a r c h K n o w l e d g e
Purpose-Orientated
Clinical Research
In the previous article in this series, I provided an overview of the different medical study formats. Reference was
made to an evidence mosaic as a multifaceted evidence
base. In this article, I will delve a bit deeper into the role
of clinical research as part of the evidence base.
) 26
al studies are case series, case-control studies, and cohort studies. Cohorts can be defined in different
ways (eg, on the basis of exposure to
toxic substances, such as tobacco
smoke, or treatment[s] received).
The latter studies are sometimes referred to as postmarketing surveillance
studies. Such cohort studies are useful for collecting information on the
safety and effectiveness of particular
medicines or therapeutic approaches
in routine clinical practice. In summary, the key feature that distinguishes observational studies from
clinical trials is the absence of an
experimental intervention.
A postauthorization safety study (PASS)
is defined as a pharmacoepidemiological study performed in accordance with the terms of the marketing authorization, conducted with
the aim of identifying or quantifying a safety hazard related to an
authorized medicinal product.1
Therefore, a PASS is primarily characterized by its objective and not by
its design. For instance, there is a
PASS using an interventional design
that confirms the safety of Traumeel
Journal of Biomedical Therapy 2011 ) Vol. 5, No. 1
) E x p a n d Yo u r Re s e a r c h K n o w l e d g e
Table. Characteristics of Clinical Study Designs
Study Design
Characteristics
Randomized
This is an interventional study in which participants are randomly (ie, by chance) assigned to 1 of 2 or more
clinical trial
treatment arms. The reference treatment can be a placebo and/or an active treatment.
A pragmatic clinical trial aims to assess the effectiveness of a treatment as much as possible under realworld conditions (ie, Does it work?).
An explanatory clinical trial aims to assess the efficacy of a treatment under ideal conditions (ie, Can it
work?)
Postauthori
This is a pharmacoepidemiological study performed in accordance with the terms of the marketing authori-
study
medicinal product.
zation safety
Cohort study
zation, conducted with the aim of identifying or quantifying a safety hazard related to an authorized
This type of study involves the identification of 2 or more cohorts of patients, one receiving the exposure/
treatment of interest and the other(s) not, and following up these cohorts with regard to the outcome of
interest.
Case-control
study
This type of study involves the identification of patients who have the outcome of interest and control
patients who do not have the outcome of interest and then looking back to see if they had the exposure/
treatment of interest.
) 27
) E x p a n d Yo u r Re s e a r c h K n o w l e d g e
Ideal World
ts
ffec
te E
Hypothe
sis Confi
rmat
olu
Abs
ion
Cohort
Studies
Case
Control
Studies
Hypoth
esis Ge
neratio
n
Postauthorization
Safety Study:
Noninterventional
Case Series
ct
ffe
E
e
tiv
a
l
Re
Postauthorization
Safety Study:
Interventional
Real World
Clinical
Case Report
) 28
References
1. EudraLex - Volume 9 Pharmacovigilance
guidelines. European Commission Web site.
http://ec.europa.eu/health/documents/eudralex/vol-9/index_en.htm. Accessed May
2, 2011.
2. Arora S, Harris T, Scherer S. Clinical safety
of a homeopathic preparation. Biomed Ther.
2000;18(2):222-225.
3. Data on file. Baden-Baden, Germany: Biologische Heilmittel GmbH.
he International Congress on
Complementary Medicine Research in Troms, Norway, was an
intensive 4-day event involving 6
keynote, 160 oral, and 110 poster
presentations, as well as 5 symposia.
The International Congress on
Complementary Medicine Research
2010 was the fifth congress of the
International Society for Complementary Medicine Research; these
congresses take place on a yearly rotating basis in Europe, Australasia,
and the Americas. The fact that so
many complementary and alternative medicine (CAM) researchers
from throughout the world were
willing to travel such long distances
further underlined the rapid increase
of CAM research activity on a global scale. Dominant CAM treatment
modalities were Chinese medicine,
acupuncture, body-mind techniques,
and homeopathy.
Several basic research studies on homeopathy were presented, including
data from Kerstin Rska, PhD, suggesting that Engystol stimulates antiviral interferon type I production
in cells of the innate immune system
in vitro and that it might have a potent antiviral effect. Stephan
Baumgartner, PhD, presented studies that suggested there were biological effects of potentized substances, including rosy apple aphid
and Arsenicum album.
Jim Rogers gave an interesting presentation on the methods of homeo-
References
1. Nuhn T, Ldtke R, Geraedts M. Placebo
effect sizes in homeopathic compared to
conventional drugs: a systematic review of
randomised controlled trials. Homeopathy.
2010;99(1):7682.
2. ICCMR 2010 Abstract Book. Rev ed. ICCMR 2010 Web site. http://www.iccmr2010.
com/Media/Files/ICCMR-2010-AbstractBook-Revised-Edition. Accessed May 2,
2010.
) 29
) Re s e a r c h H i g h l i g h t s
) 30
Introduction
Breast cancer is a worldwide problem because of its high incidence.
The pain associated with breast cancer treatment, including surgery, radiotherapy, and chemotherapy, often
remains a long-term problem for
many patients. The pain can be a result of scars after surgery or the adverse effects of radiotherapy and
chemotherapy. This pain can definitely affect the quality of life of patients. Therefore, effective pain
treatments are important.
The World Health Organization
lists the following conventional
treatments for pain associated with
breast cancer: acetylsalicylic acid,
paracetamol, naproxen, metamizol,
and diclofenac (step 1 nonsteroidal
anti-inflammatory drugs); and tramadol, codeine, and dihydrocodeine
(step 2 opioid analgesic agents).
However, these conventional treatments may not be effective for all
patients who experience pain associated with breast cancer. Therefore,
the following complementary and
alternative therapies may also be
used (especially for short-term pain
relief ): acupuncture, hypnosis, relaxation/imagery, music, massage,
and herbal supplements. Finally, homotoxicological treatments, such as
Traumeel (Heel GmbH, BadenBaden, Germany), can be used to
treat resistant pain associated with
breast cancer.
In the study by Orellana Alvarellos
et al,1 a Traumeel injection was used
Results
Three months after the final Traumeel injection, the meanSD pain
score was 3.32.2 points (range,
1-7 points). This indicated a slight
overall increase in pain when compared with the level immediately
after the Traumeel injection. However, at 3 months after the final
treatment, the effects of Traumeel
injection therapy tended to vary
from patient to patient. For example,
1 patient experienced further pain
relief, from 4 to 2 points; 3 patients
maintained their pain relief (between 1 and 3 points); and 5 patients experienced increased levels
of pain (between 2 and 7 points).
Overall, all 9 women still had lower
levels of pain than they had before
the Traumeel injection was first administered.
Six months after the final Traumeel
injection, the meanSD pain score
was 4.12.5 points (range, 1-7
points). For 5 of the women, the
pain score remained the same; only
2 women experienced increased
pain (this increase did not require
treatment). Overall, the pain score
was lower than before treatment,
even after a lengthy period without
any further therapy. Finally, even 12
months after the last Traumeel injection, some of the women noted that
their pain had not been exacerbated.
In terms of physical disability, insomnia, and psychological distress
symptoms, all 9 women experienced
improvement after Traumeel injection therapy. At the 3-month obser-
iStockphoto.com/cunfek
iStockphoto.com/motorolka
) Re s e a r c h H i g h l i g h t s
The active ingredients of Traumeel
include two species of the purple
References
1. Orellana Alvarellos G, Ruiz de Viaspre
Alvear P, Kaszkin-Bettag M. A series of
case reports: clinical evaluation of a complex homeopathic injection therapy in the
management of pain in patients after breast
cancer treatment. Altern Ther Health Med.
2010;16(1):54-59.
2. Porozov S, Cahalon L, Weiser M, Branski
D, Lider O, Oberbaum M. Inhibition of IL1beta and TNF-alpha secretion from resting
and activated human immunocytes by the
homeopathic medication Traumeel S. Clin
Dev Immunol. 2004;11(2):143-149.
) 31
IAH Abbreviated
Course
An e-learning course leading to
certification in homotoxicology
from the International Academy for
Homotoxicology in just 40 hours.
Free of charge
) 32
www.iah-online.com