Could

Sulfur Deficiency
be a Contributing Factor
in Obesity,
Heart Disease,
Alzheimer's
and Chronic Fatigue Syndrome?
by Stephanie Seneff
seneffcsail!mit!edu
September "#, $%"%
"! &ntroduction
Obesity
is
'uic(ly becoming
the number one health
issue
confronting America today,
and has also risen
to epidemic proportions )orld)ide!
&ts spread
has been associated
)ith the adoption
of a *estern+style diet!
Ho)e,er,
& belie,e
that
the )idespread consumption
of food imports
produced by -!S! companies
plays
a crucial role
in the rise
in obesity )orld)ide!
Specifically,
these .fast foods.
typically include hea,ily
processed deri,ati,es
of corn,
soybeans,
and grains,
gro)n
on highly efficient mega+farms!
Furthermore,
& )ill argue
in this
essay
that one
of the core underlying causes
of obesity
may be sulfur deficiency!
Sulfur
is
the eighth most common element
by mass
in the human body,
behind o/ygen,
carbon,
hydrogen,
nitrogen,
calcium,
phosphorus,
and potassium!
0he t)o
sulfur+containing amino acids,
methionine and cysteine,
play essential physiological roles
throughout the body!
Ho)e,er,
sulfur
has been consistently o,erloo(ed
in addressing
the issues
of nutritional deficiencies!
&n fact,
the American Food
and Drug Administration
has not e,en
assigned
a minimum
daily re'uirement 12D34
for sulfur!
One conse'uence of sulfur's
limbo nutritional status
is
that it
is omitted
from the long list
of supplements
that
are commonly artificially added
to popular foods
li(e cereal!
Sulfur
is found
in a large number
of foods,
and,
as a conse'uence,
it is assumed
that almost any diet
)ould meet
the minimum
daily re'uirements!
5/cellent sources
are eggs,
onions,
garlic,
and leafy dar(
green ,egetables
li(e (ale and broccoli!
2eats,
nuts,
and seafood
also contain sulfur!
2ethionine,
an essential amino acid,
in that
)e are unable
to synthesize it oursel,es,
is found mainly in egg )hites
and fish!
A diet high
in grains
li(e bread and cereal
is li(ely
to be deficient
in sulfur!
&ncreasingly,
)hole foods such
as corn and soybeans
are disassembled
into component parts
)ith chemical names,
and then reassembled
into hea,ily processed foods!
Sulfur
is lost
along the )ay,
and there is
a lac( of a)areness
that this matters!
5/perts
ha,e recently become a)are
that sulfur depletion
in the soil
creates a serious deficiency
for plants 67ez$%%89,
brought
about in part
by impro,ed efficiency
in farming
and in part,
ironically,
by successful attempts
to clean up air pollution!
O,er the last t)o decades,
the -!S! farming industry
has steadily consolidated
into highly technologized
mega farms!
0he high yield
per acre
associated
)ith these farms results
in greater depletion
of sulfur each year
by the tall,
densely planted crops!
:lants
re'uire sulfur
in the form
of the sulfate
radical 1SO;+$4!
<acteria
in )ell aerated soil,
similar
to nitrogen
fi/ing bacteria,
can con,ert elemental sulfur
into sulfate
through an o/idation process!
Coal contains
a significant amount of sulfur,
and factories
that
burn coal
for energy release sulfur dio/ide
into the air!
O,er time,
sun e/posure
con,erts
the sulfur dio/ide
to sulfate,
a significant contributor
to acid rain!
Acid rain
is a serious pollutant,
in that hydrogen sulfate,
a potent acid,
penetrates la(es,
ma(ing them too acidic
for lifeforms
to thri,e!
0he Clean Air Act,
enacted by congress
in "=8%,
has led
to substantial decreases
in the amount of acid rain
released
into the atmosphere!
Factories
ha,e introduced highly effecti,e
scrubbing
technologies
to comply
)ith the la),
and,
as a conse'uence,
less sulfate
ma(es its )ay
bac(
into the soil!
2odern farmers
apply highly
concentrated fertilizer
to their soil,
but this fertilizer
is typically enriched
in phosphates
and often contains no sulfur!
5/cess phosphates
interfere
)ith sulfur absorption!
&n the past,
organic matter
and plant residues
remained
after the fruit
and
grain
)ere har,ested!
Such accumulating organic matter
used
to be
a ma>or source
of recyclable sulfur!
Ho)e,er,
many modern machinery+based
methods remo,e
a great deal more
of the organic matter
in addition
to the edible portions
of the plant!
So the sulfur
in the decaying organic matter
is also lost!
&t is estimated that
humans
obtain about "%?
of their sulfur supply
from drin(ing )ater!
3emar(ably,
people )ho
drin( soft )ater
ha,e an increased ris(
to heart disease
compared
to people
)ho drin( hard )ater
6Cra)ford"=@A9!
2any possible reasons
ha,e been suggested for )hy
this might be true
1 :roposed theories
for soft )aterBhard
)ater differences
in heart disease4,
and
>ust about e,ery trace metal
has been considered
as a possibility 6<iorc("=@#9!
Ho)e,er,
& belie,e that
the real reason
may simply be
that hard )ater
is more li(ely
to contain sulfur!
0he sulfate ion
is
the most useful form
of sulfur for humans
to ingest!
*ater softeners
pro,ide a con,enient en,ironment
for sulfur+reducing bacteria,
)hich con,ert sulfate 1SO;+$4
into sulfide 1S+$4,
emitting hydrogen sulfide gas!
Hydrogen sulfide gas
is a poison
that has been (no)n
to cause nausea,
illness
and,
in e/treme cases,
death!
*hen the bacteria
are thri,ing,
the gas
)ill diffuse
into the air
and gi,e
off a foul odor!
Ob,iously,
it is rare
that
the concentration
is sufficiently high
to cause se,ere problems!
<ut the sulfate ion
is lost
through the process!
*ater that
is naturally soft,
such as )ater
collected from rain run+off,
also contains
little or no sulfur,
because it
has gone
through an
e,aporation+condensation cycle,
)hich
lea,es behind
all
the hea,ier molecules,
including sulfur!
$! Sulfur A,ailability
and Obesity 3ates
0he ultimate source
of sulfur
is ,olcanic roc(,
mainly basalt,
spe)ed up
from the earth's core
during ,olcanic eruptions!
&t is generally belie,ed
that humans first e,ol,ed
from a common ape ancestor
in the African rift zone,
a region
that )ould ha,e en>oyed
an abundance
of sulfur
due to the hea,y ,olcanic
acti,ity
there!
0he three principle suppliers
of sulfur
to the *estern nations
are Creece,
&taly and 7apan!
0hese three countries
also en>oy lo) rates
of heart disease and obesity
and increased longe,ity!
&n South America,
a line
of ,olcanoes
trac(s
the bac(bone
of Argentina!
Argentinians
ha,e a much lo)er obesity rate
than their neighbors
to the east
in <razil!
&n the -nited States,
Oregon and Ha)aii,
t)o states
)ith significant ,olcanic
acti,ity,
ha,e
among the lo)est obesity rates
in the country!
<y contrast,
the highest obesity rates
are found
in the mid)est
and southern farm countryD
the epicenter
of the modern
agricultural practices
1mega farms4
that lead
to sulfur depletion
in the soil!
Among all fifty states,
Oregon
has
the lo)est childhood obesity
rates!
Significantly,
Ha)aii's youth
are faring less )ell
than their parentsD
)hile Ha)aii ran(s
as the fifth
from the bottom
in obesity rates,
its children
aged "%+"A
)eigh in at number "E!
As Ha)aii
has recently become increasingly
dependent
on food imports
from the mainland
to supply
their needs,
they ha,e suffered accordingly
)ith increased obesity problems!
&n her recently
published boo(,
0he 7ungle 5ffect 62iller$%%=9,
Dr! Daphne 2iller
de,otes a full chapter
to &celand 1pp! "$A+"@%4!
&n this chapter,
she struggles
to ans)er
the 'uestion
of
)hy &celanders
en>oy such remar(ably
lo) rates
of depression,
despite li,ing
at a northern latitude,
)here one
)ould e/pect a high incidence
of Seasonal
Affecti,e Disorder 1SAD4!
She points out,
furthermore,
their e/cellent health record
in other (ey areasD
.*hen
compared
to Forth Americans,
they ha,e almost half
the death rate
from heart disease and diabetes,
significantly less obesity,
and a greater life e/pectancy!
&n fact,
the a,erage life span
for &celanders
is
amongst the longest
in the )orld!.
1:! "EE4!
*hile she
proposes that
their high
fish consumption,
)ith associated high inta(e
of omega three fats,
may plausibly be
the main beneficial source,
she puzzles
o,er the fact
that former &celanders
)ho mo,ed
to Canada
and also eat lots
of fish
do not also en>oy
the same decreased rate
of depression
and heart disease!
&n my ,ie),
the (ey
to &celanders' good health lies
in the string
of ,olcanoes
that ma(e up
the bac(bone
of the island,
)hich
sits
atop the mid+Atlantic
ridge crest!
Dr! 2iller
pointed
out 1p! "E@4
that
the mass e/odus to Canada
)as due to
e/tensi,e ,olcanic
eruptions
in the late "8%%'s that
blan(eted
the highly culti,ated
southeast region
of the country!
0his means,
of course,
that
the soils
are highly enriched
in sulfur!
0he cabbage,
beets,
and potatoes that
are
staples
of the &celandic diet
are li(ely pro,iding
far more
sulfur
to &celanders
than their counterparts
in the American diet pro,ide!
E! *hy Does
Sulfur Deficiency
Gead
to Obesity?
0o summarize
)hat
has been said thus far,
1"4 foods
are becoming
depleted
in sulfur,
and 1$4
locations
)ith naturally high sulfur
deposits
en>oy protection against obesity!
Fo) comes
the difficult 'uestionD
)hy does sulfur
deficiency
lead
to obesity?
0he ans)er,
li(e much
of biology,
is complicated,
and part of )hat
& theorize
is con>ecture!
Sulfur
is (no)n
as a healing mineral,
and
a sulfur deficiency
often leads
to pain and inflammation
associated
)ith ,arious muscle
and s(eletal disorders!
Sulfur
plays a role
in many biological processes,
one
of )hich
is metabolism!
Sulfur
is present
in insulin,
the essential hormone
that promotes
the utilization of sugar deri,ed
from carbohydrates
for fuel
in muscle and fat cells!
Ho)e,er,
my e/tensi,e literature search
has led me
to t)o mysterious molecules
found in the blood stream
and in
many other parts
of the bodyD
,itamin DE sulfate
and cholesterol
sulfate 6Strott$%%E9!
-pon e/posure
to the sun,
the s(in
synthesizes ,itamin DE sulfate,
a form
of ,itamin D that,
unli(e unsulfated ,itamin DE,
is )ater soluble!
As a conse'uence,
it can tra,el freely
in the blood
stream
rather than being pac(aged up
inside GDG
1the so+called .bad.
cholesterol4
for transport 6A/elsona"=8#9!
0he form
of ,itamin D
that is
present in both human mil(
6Ga(da)ala"=AA9
and ra) co)'s mil(
6<aulch"=8$9
is ,itamin DE sulfate
1pasteurization
destroys it
in co)'s mil(,
and
the mil(
is then artificially enriched
)ith ,itamin D$,
an unsulfated plant+deri,ed form
of the ,itamin4!
Cholesterol sulfate
is also synthesized
in the s(in,
)here it
forms a crucial part
of the barrier
that (eeps
out harmful bacteria
and other microorganisms
such
as fungi 6Strott$%%E9!
Cholesterol sulfate
regulates
the gene
for a protein
called profilaggrin,
by interacting li(e a hormone
)ith the nuclear
receptor 3O3+alpha!
:rofilaggrin
is
the precursor
to filaggrin,
)hich
protects
the s(in
from in,asi,e
organisms 6Sandilands$%%=,
2cCrath$%%89!
A deficiency
in filaggrin
is associated
)ith asthma and arthritis!
0herefore,
cholesterol sulfate
plays
an important role
in protection
from asthma and arthritis!
0his e/plains
)hy sulfur
is a healing agent!
Gi(e ,itamin DE sulfate,
cholesterol sulfate
is also )ater+soluble,
and it too,
unli(e cholesterol,
does not ha,e
to be pac(aged up inside GDG
for deli,ery
to the tissues!
<y the )ay,
,itamin DE
is synthesized through a couple
of simple steps
from cholesterol,
and
its chemical structure is,
as a conse'uence,
nearly identical to that
of cholesterol!
Here &
pose the interesting 'uestionD
)here do
,itamin DE sulfate
and cholesterol sulfate
go once
they are
in the blood stream,
and
)hat role
do
they play
in the cells?
Surprisingly,
as far as
& can tell,
nobody
(no)s!
&t has been determined that
the sulfated form
of ,itamin DE
is stri(ingly ineffecti,e
for calcium transport,
the )ell+(no)n .primary. role
of ,itamin DE 63ee,e"=8"9!
Ho)e,er,
,itamin DE
clearly has many other
positi,e effects
1it seems
that more
and more
are being disco,ered e,ery day4,
and these
include a role
in cancer protection,
increased immunity
against infectious disease,
and protection
against heart disease
1 Hitamin D
:rotects
against Cancer
and Autoimmune Diseases4!
3esearchers
don't yet understand
ho) it
achie,es these benefits,
)hich ha,e been
obser,ed empirically
but remain une/plained
physiologically!
Ho)e,er,
& strongly suspect
it is
the sulfated form
of the ,itamin
that instantiates
these benefits,
and
my reasons
for this belief
)ill become clearer
in a moment!
One ,ery special feature
of cholesterol sulfate,
as opposed
to cholesterol itself,
is
that it
is ,ery agileD
due to its polarity
it can freely pass
through cell membranes
almost
li(e a ghost 63odriguez"==#9!
0his means
that cholesterol sulfate
can easily enter
a fat or muscle cell!
& am de,eloping
a theory
)hich
at its core
proposes an essential role
for cholesterol sulfate
in the metabolism
of glucose for fuel
by these cells!
<elo),
& )ill sho)
ho) cholesterol
sulfate
may be able
to protect
fat and muscle cells
from damage
due to e/posure
to glucose,
a dangerous reducing agent,
and
to o/ygen,
a dangerous o/idizing agent!
& )ill further argue that,
)ith insufficient
cholesterol sulfate,
muscle and fat cells
become damaged,
and
as a conse'uence
become glucose intolerantD
unable
to process glucose
as a fuel!
0his happens first
to muscle cells
but e,entually to fat cells,
as )ell!
Fat cells
become storage bins
for fats
to supply
fuel
to the muscles,
because the muscles
are unable
to utilize glucose
as fuel!
5,entually,
fat cells
also become too
disabled
to release their stored fats!
Fatty tissue
then accumulates
on the body!
;! Sulfur
and Clucose 2etabolism
&n order
to understand my theory,
you )ill need
to (no) more
about glucose metabolism!
S(eletal muscle cells
and fat cells
brea( do)n glucose
in the presence of o/ygen
in their mitochondria,
and
in the process
they produce A0:,
the basic energy currency
of all cells!
A glucose transporter
called CG-0;
is present
in the cytoplasm
of muscle cells,
and it migrates
to the cell membrane
upon stimulation
by insulin!
CG-0;
essentially acts
as a (ey
that unloc(s
the door,
letting glucose
into the cell,
but,
li(e a (ey,
it only )or(s
)hen
it's inserted
in the membrane!
<oth glucose and o/ygen,
unless they are carefully managed,
can cause harm
to the cell's proteins
and fats!
0he glucose
enters
the cell
)ithin special cholesterol
rich sites
in the cell )all
called lipid rafts 6&noue$%%@9!
0his is li(ely orchestrated
to protect
the cell )all
from damage,
because e/tra cholesterol
allo)s
the ,ulnerable lipoproteins
in the cell )all
to pac( more tightly
and reduce
their ris(
of e/posure!
&n muscle cells,
myoglobin
is able
to store additional o/ygen,
bound
to an iron molecule
safely se'uestered
in an interior ca,ity
)ithin the myoglobin protein!
Sulfur
is a ,ery ,ersatile molecule,
because it can e/ist
in se,eral distinct
o/idati,e states,
ranging
from I@
1in the sulfate radical4
to +$
1in hydrogen sulfide4!
Clucose,
as a po)erful
reducing agent,
can cause
significant glycation damage
to e/posed proteins,
leading
to the formation
of Ad,anced Clycation 5nd
:roducts 1AC5's4
that
are e/tremely destructi,e
to healthD
they are belie,ed
to be a ma>or contributor
to heart disease ris(
6<ro)nlee"=889!
So,
& hypothesize that,
if sulfur 1I@4
is made a,ailable
to glucose
as a decoy,
the glucose
)ill be di,erted into reducing
the sulfur
rather than glycating
some ,ulnerable protein such
as myoglobin!
&n searching the *eb,
& came across an article
)ritten in the "=E%'s
about the stri(ing ability
of iron sulfate,
in the presence
of the o/idizing agent
hydrogen pero/ide,
to brea( do)n starch
into simple molecules,
e,en in the absence
of any enzymes
to catalyze
the reaction 6<ro)n"=E@9!
0he article
pointedly mentioned
that iron )or(s much better
than other metals,
and sulfate )or(s much better
than other anions!
&n the human body,
starch
is first con,erted
to glucose
in the digesti,e system!
0he muscle
and fat cells only need
to brea( do)n glucose!
0hus,
their tas(
is easier,
because the iron sulfate
is no) starting
from
an intermediate brea(do)n product
of starch
rather than from
starch itself!
*here )ould
the iron sulfate
come from?
&t seems
to me
that
the cholesterol sulfate,
ha,ing hopped
across the cell membrane,
could transfer
its sulfate radical
to the myoglobin,
)hose iron molecule
could pro,ide
the other half
of the formula!
&n the process,
the sulfur molecule's charge
)ould be dri,en do)n
from I@
to +$,
releasing energy
and absorbing
the impact
of the reducing
effects
of glucose,
and therefore ser,ing
as a decoy
to protect
the proteins
in the cell
from glycation damage!
*hen the cell
is e/posed
to insulin,
its mitochondria
are triggered
to start
pumping both hydrogen pero/ide
and hydrogen ions
into the cytoplasm,
essentially gearing up
for the assault
by glucose!
&f cholesterol sulfate
enters
the cell
alongside the glucose,
then all
the players
are a,ailable!
& con>ecture
that cholesterol sulfate
is
the catalyst
that seeds
the lipid raft!
&ron sulfate
is then formed
by bonding
the iron
in the heme unit
in myoglobin
to a sulfate ion
pro,ided
by cholesterol sulfate!
0he cholesterol
is left behind
in the cell )all,
thus enriching
the ne)ly forming lipid raft
)ith cholesterol!
0he hydrogen pero/ide,
pro,ided by the mitochondria
upon insulin stimulation,
catalyzes
the dissolution
of glucose
by the iron sulfate!
0he pumped hydrogen
can pair
up )ith the reduced
sulfur 1S+$4
to form hydrogen sulfide,
a gas
that can easily
diffuse bac(
across the membrane
for a repeat cycle!
0he o/ygen
that is released
from the sulfate radical
is pic(ed up
by the myoglobin,
se'uestered inside the molecule
for safe tra,el
to the mitochondria!
Clucose brea(do)n products
and o/ygen
are then deli,ered
to the mitochondria
to complete
the process
that ends
)ith )ater,
carbon dio/ide,
and A0:
++ all
)hile (eeping
the cell's cytoplasmic
proteins safe
from glucose
and o/ygen e/posure!
&f &'m
right about this role
for cholesterol sulfate both
in seeding
the lipid raft
and in pro,iding
the sulfate ion,
then this process
brea(s do)n
miserably )hen cholesterol
sulfate
is not a,ailable!
First of all,
the lipid raft
is not formed!
*ithout the lipid raft,
the glucose
can not enter the cell!
&ntense physical e/ercise
can allo) glucose
to enter
the muscle cells
e,en in the absence
of insulin 6O>u(a$%%$9!
Ho)e,er,
this )ill lead
to dangerous e/posure
of the cell's proteins
to glycation
1because
there is no iron sulfate
to degrade the glucose4!
Clycation
interferes
)ith the proteins' ability
to perform their >obs,
and lea,es them more ,ulnerable
to o/idation damage!
One
of the important affected
proteins
)ould be myoglobinD
it )ould
no longer
be able
to effecti,ely carry o/ygen
to the mitochondria!
Furthermore,
o/idized myoglobin
released
into the blood stream
by crippled muscle cells leads
to painful
and crippling rhabdomyolysis,
and possible subse'uent
(idney failure!
0his e/planation
accounts for
the obser,ation
that sulfur deficiency
leads
to muscle pain and inflammation!
#! 0he 2etabolic Syndrome
0he metabolic syndrome
is a term
used
to encapsulate a comple/ set
of mar(ers associated
)ith increased ris(
to heart disease!
0he profile
includes 1"4
insulin resistance
and dysfunctional
glucose metabolism
in muscle cells,
1$4 e/cess triglycerides
in the blood serum,
1E4 high le,els
of GDG,
particularly small dense GDG,
the )orst (ind,
1;4 lo) le,els
of HDG
1the .good. cholesterol4
and reduced cholesterol content
)ithin the indi,idual
HDG particles,
1#4
ele,ated blood pressure,
and 1@4
obesity,
particularly e/cess abdominal fat!
&
ha,e argued pre,iously
that
this syndrome is brought on
by a diet
that is high
in empty carbohydrates
1particularly fructose4
and lo)
in fats and cholesterol,
along )ith a poor ,itamin D
status 6Seneff$%"%9!
*hile &
still belie,e
that all of these
factors
are contributory,
& )ould no) add another factor
as )ellD
insufficient dietary sulfate!
& ha,e described
in a pre,ious essay,
my interpretation
of obesity as being dri,en
by a need
for abundant fat cells
to con,ert glucose
to fat
because the muscle cells
are unable
to efficiently utilize glucose
as fuel!
*ith sulfur deficiency
comes
the ans)er as to
)hy muscle cells
)ould be defecti,e
in glucose managementD
they can't come up )ith
enough cholesterol sulfate
to seed
the lipid raft
needed
to import
the glucose!
An alternati,e )ay
to o,ecome
a muscle cell's
defecti,e glucose metabolism
is
to e/ercise ,igorously,
so that the generated A2:J
1an indicator
of energy shortage4
induces
the CG-0;
to migrate
to the membrane
e,en in the absence
of insulin 6O>u(a$%%$9!
Once the glucose
is
inside the muscle cell,
ho)e,er,
the iron+sulfate mechanism
>ust described
is dysfunctional,
both
because
there's no cholesterol sulfate
and
because
there's no hydrogen pero/ide!
Additionally,
)ith intensi,e e/ercise
there's also a reduced supply
of o/ygen,
so the glucose
must be processed anaerobically
in the cytoplasm
to produce lactate!
0he lactate
is released
into the blood stream
and shipped
to the heart
and brain,
both of )hich
are able
to use it
as fuel!
<ut the cell membrane
remains
depleted
in cholesterol,
and
this ma(es it
,ulnerable
to future o/idati,e damage!
Another )ay
to compensate
for defecti,e glucose metabolism
in the muscle cells
is
to gain )eight!
Fat cells
must no) con,ert glucose
into fat
and release it
into the blood stream
as triglycerides,
to fuel
the muscle cells!
&n the conte/t
of a lo) fat diet,
sulfur deficiency
becomes
that much )orse a problem!
Sulfur deficiency
interferes
)ith glucose metabolism,
so
it's a much healthier choice
to simply a,oid
glucose
sources 1carbohydrates4
in the dietK
i!e!
to adopt
a ,ery lo)+carb diet!
0hen
the fat
in the diet
can supply
the muscles
)ith fuel,
and
the fat cells
are not burdened
)ith ha,ing
to store
up so much reser,e fat!
&nsulin suppresses
the release
of fats
from fat cells 6Scappola"==#9!
0his forces
the fat cells
to flood
the bloodstream
)ith triglycerides
)hen insulin le,els
are lo),
i!e!,
after prolonged periods
of fasting,
such
as o,ernight!
0he fat cells
must dump
enough triglycerides
into the bloodstream
during fasting periods
to fuel
the muscles
)hen
the dietary supply
of carbohydrates
(eeps insulin le,els ele,ated,
and
the release
of fats
from the fat cells
is repressed!
As the dietary carbs
come in,
blood sugar
le,els rise
dramatically because
the muscle cells
can't utilize it!
0he li,er
also processes e/cess glucose
into fat,
and pac(ages it up
into GDG,
to further supply fuel
to the defecti,e muscle cells!
<ecause the li,er
is so preoccupied
)ith processing
glucose and fructose
into GDG,
it falls behind
on the generation
of HDG,
the .good. cholesterol!
So the result
is ele,ated le,els
of GDG,
triglycerides,
and blood sugar,
and reduced le,els
of HDG,
four (ey components
of the metabolic syndrome!
0he chronic presence
of e/cess glucose
and fructose
in the blood stream leads
to a host
of problems,
all
related
to glycation damage
of
blood stream proteins
by glucose e/posure!
One
of the (ey proteins
that gets damaged
is the apolipoprotein,
apo<,
that's encased in the membrane
of the GDG particles!
Damaged apo<
inhibits
the ability of GDG
to efficiently
deli,er its contents
1fat and cholesterol4
to the tissues!
Fat cells
again come
to the rescue,
by sca,enging
the bro(en
GDG particles
1through a mechanism
that does not re'uire apo<
to be healthy4,
ta(ing them apart,
and e/tracting
and refurbishing
their cholesterol!
&n order
to function properly,
the fat cells
must ha,e intact Apo5,
an antio/idant that cleans up
o/idized cholesterol
and transports it
to the cell membrane
for deli,ery
to HDG particles!
@! Fat Cells,
2acrophages and Atherosclerosis
*hile diligently
con,erting
glucose
to stored fats,
the fat cells
are a)ash
in glucose,
)hich damages
their apo5
through glycation 6Gi"==A9!
Once their apo5
is damaged,
they can
no longer transport cholesterol
to the membrane!
5/cess cholesterol
accumulates
inside the fat cells
and e,entually destroys
their ability
to synthesize proteins!
Concurrently,
their cell membrane
becomes
depleted
in cholesterol,
because they
can no longer
deli,er it
to the membrane 6Seneff$%"%9!
A fat cell
that has deteriorated
to this degree
has no choice
but to dieD
it sends
out distress signals
that call
in macrophages!
0he macrophages
essentially consume
the dysfunctional fat cell,
)rapping
their o)n membrane
around the fat cell's membrane
that is no) barely able
to hold
its contents inside 6Cinti$%%#9!
2acrophages are also
principle players
in the fatty strea(s
that
appear
along the sides
of ma>or arteries leading
to the heart,
and are associated
)ith pla'ue build+up
and heart disease!
&n a fascinating
set
of e/periments, 2a et
al!
62a$%%89
ha,e sho)n
that
the sulfate ion
attached
to o/idized forms
of cholesterol
is highly protecti,e
against fatty strea(s
and atherosclerosis!
&n a set
of in+,itro e/periments,
they demonstrated diametrically
opposite reactions
from macrophages
to $#+hydro/yl cholesterol
1$#+HC4
,ersus its sulfocon>ugate
$#+hydro/yl cholesterol sulfate
1$#+HCES4!
*hereas $#+HC present
in the medium causes
the macrophages
to synthesize
and store
cholesterol and fatty acids,
$#+HCES
has the e/act opposite effectD
it promotes
the release of cholesterol
to the medium
and causes fat
stores
to shrin(!
Furthermore,
)hile $#+HC
added
to the medium
led to apoptosis
and cell death,
$#+HCES
did not!
& suggest that
the sulfate radical
is essential
for the process
that feeds
cholesterol
and o/ygen
to the heart muscle!
A! Sulfur and Alzheimer's
*ith an aging population,
Alzheimer's disease
is
on the rise,
and
it has been argued that
the rate
of increase
is disproportionately high
compared
to the increase
in the ra) number
of elderly people 6*aldman$%%=9!
<ecause
of a con,iction
that
the amyloid beta pla'ue
that is
a signature
of Alzheimer's
is also
the cause,
the pharmaceutical industry
has spent hundreds of millions,
if
not billions,
of dollars
pursuing drugs
that reduce
the amount of pla'ue
accumulating
in the brain!
0hus far,
drug trials
ha,e been
so disappointing
that many
are beginning
to belie,e
that amyloid beta
is not
the cause
after all!
3ecent drug trials
ha,e sho)n
not only no impro,ement,
but actually
a further decline
in cogniti,e function,
compared
to placebo
1 Fe) Lor( 0imes Article4!
& ha,e argued else)here
that amyloid beta
may actually be protecti,e
against Alzheimer's,
and
that problems
)ith glucose metabolism
are
the true culprit
in the disease!
Once &
began
to suspect sulfur deficiency
as a ma>or factor
in Americans' health,
& loo(ed into
the relationship
bet)een sulfur deficiency
and Alzheimer's!
&magine
my surprise
)hen & came upon a )eb page
posted
by 3onald 3oth,
)hich sho)s a plot
of the le,els
of ,arious minerals
in the cells
of a typical Alzheimer's
patient relati,e
to the normal le,el!
3emar(ably,
sulfur
is
almost non+e/istent
in the Alzheimer's
patient's profile!
0o 'uote directly
from that siteD
.*hile some drugs or antibiotics
may slo),
or if
it should happen,
halt
the progression
of Alzheimer's disease,
sulfur supplementation
has
the potential of
not only pre,enting,
but actually re,ersing
the condition,
pro,ided
it has not progressed
to a stage
)here much damage
has been done
to the brain!.
.One ma>or reason
for the increase
in Alzheimer's disease
o,er the past years
has been
the bad reputation eggs
ha,e been getting
in respect
to being a high source
of cholesterol,
despite the fact
of dietary inta(e
of cholesterol
ha,ing little impact
on serum cholesterol
++ )hich
is no) also finally ac(no)ledged
by mainstream medicine!
&n the meantime,
a large percentage of
the population lost out
on an e/cellent source
of sulfur and a host
of other essential nutrients
by follo)ing
the nutritional misinformation
spread
on eggs!
Of course,
onions and garlic
are another rich source
of sulfur,
but ,olume+)ise,
they cannot duplicate
the amounts
obtained
from regularly consuming eggs!.
*hy should sulfur
deficiency
be so important
for the brain?
& suspect
that
the ans)er lies
in the mysterious molecule
alpha+synuclein,
)hich sho)s
up alongside amyloid+beta
in the pla'ue,
and is also present
in the Ge)y <odies
that are a signature
of :ar(inson'
s disease 6Oli,ares$%%=9!
0he alpha+synuclein molecule
contains four methionine residues,
and all four
of the sulfur molecules
in the methionine residues
are con,erted
to sulfo/ides
in the presence of o/idizing
agents
such
as hydrogen pero/ide
6Claser$%%#9!
7ust
as in the muscle cells,
insulin
)ould cause
the mitochondria of
neurons
to release hydrogen pero/ide,
)hich
)ould then allo)
the alpha+synuclein
to ta(e up o/ygen,
in a )ay
that is
,ery reminiscent
of )hat
myoglobin
can do
in muscle cells!
0he lac( of sufficient sulfur
should directly impact
the neuron's ability
to safely carry o/ygen,
again paralleling
the situation
in muscle cells!
0his )ould mean that
other proteins and fats
in the neuron
)ould suffer
from o/idati,e damage,
leading ultimately
to the neuron's destruction!
&n my essay
on Alzheimer's,
& argued
that biologically
pro+acti,e restriction
in glucose metabolism
in the brain
1a so+called type+&&& diabetes
and a precursor
to Alzheimer's disease4
is triggered
by a deficiency
in cholesterol
in the neuron cell membrane!
Again,
as in muscle cells,
glucose entry
depends
upon cholesterol+rich lipid rafts,
and,
)hen the cell
is deficient
in cholesterol,
the brain
goes into a mode
of metabolism
that prefers
other nutrients besides glucose!
& suspect
that a deficiency
in cholesterol
)ould come about
if there is
insufficient cholesterol sulfate,
because cholesterol
sulfate
li(ely plays an important role
in seeding
lipid rafts,
)hile
concurrently enriching
the cell )all
in cholesterol!
0he cell
also de,elops an insensiti,ity
to insulin,
and,
as a conse'uence,
anaerobic metabolism
becomes
fa,ored
o,er aerobic metabolism,
reducing
the chances
for alpha+synuclein
to become o/idized!
O/idation
actually protects alpha+synuclein
from fibrillation,
a necessary structural change
for the accumulation
of Ge)y bodies
in :ar(inson's disease
1and li(ely
also Alzheimer's pla'ue4
6Claser$%%#9 8!
&s
0he S(in a Solar+:o)ered <attery
for the Heart?
0he e,idence
is 'uite compelling
that sunny places
afford protection
from heart disease!
A study
described
in 6Crimes"==@9
pro,ides
an in
depth anaylsis of data
from
around the )orld
sho)ing an in,erse relationship
bet)een heart disease rates
and sunny climateBlo) latitude!
For instance,
the cardio,ascular+related
death rate
for men
bet)een the ages
of ##
and @;
)as A@" per "%%,%%% men
in <elfast,
Forthern &reland,
but only "A#
in 0oulouse,
France!
*hile
the ob,ious biological factor
that )ould be impacted
by sunlight
is ,itamin D,
studies
conducted specifically
on ,itamin D status
ha,e been inconclusi,e,
)ith some e,en sho)ing
a significant increased ris(
for heart disease
)ith increased inta(e
of ,itamin D$ supplements
6Drolet$%%E9!
& belie,e,
first of all,
that
the distinction
bet)een ,itamin DE
and ,itamin DE+sulfate
really matters,
and also
that
the distinction
bet)een ,itamin D$
and ,itamin DE
really matters!
Hitamin D$
is
the plant form
of the ,itamin
++ it )or(s similarly to DE
)ith respect
to calcium transport,
but it
cannot be sulfated!
Furthermore,
apparently the body
is unable
to produce ,itamin DE sulfate
directly from unsulfated
,itamin DE 6Ga(da)ala"=AA9
1)hich
implies
that
it produces
,itamin DE sulfate
directly from cholesterol sulfate4!
& am not a)are
of any
other food source besides ra)
mil( that
contains ,itamin DE
in the sulfated form!
So,
)hen studies
monitor
either ,itamin D supplements
or ,itamin D serum le,els,
they're not getting
at the crucial aspect
for heart protection,
)hich
& thin(
is
the serum le,el
of ,itamin DE sulfate!
Furthermore,
& belie,e
it is e/tremely li(ely
that ,itamin DE sulfate
is not
the only thing
that's impacted
by greater sun e/posure,
and maybe not e,en
the most important thing!
Ci,en
that cholesterol sulfate
and ,itamin DE sulfate
are ,ery similar
in molecular structure,
& )ould imagine that
both molecules
are produced the same )ay!
And since ,itamin DE+sulfate
synthesis
re'uires sun e/posure,
& suspect
that cholesterol sulfate
synthesis
may also e/ploit
the sun's radiation energy!
<oth cholesterol and sulfur
afford protection
in the s(in
from radiation damage
to the cell's DFA,
the (ind
of damage
that can lead
to s(in cancer!
Cholesterol and sulfur
become o/idized upon e/posure
to the high fre'uency rays
in sunlight,
thus acting as antio/idants to
.ta(e
the heat,.
so to spea(!
O/idation
of cholesterol
is
the first step
in the process
by )hich cholesterol
transforms itself
into ,itamin DE!
Sulfur dio/ide
in the air
is con,erted nonenzymatically
to the sulfate ion
upon sun e/posure!
0his is
the process
that produces
acid rain!
0he o/idation
of sulfide 1S+$4
to sulfate 1SO;+$4,
a strongly endothermic reaction
6Hoc(in$%%E9,
con,erts
the sun's energy
into chemical energy
contained
in the sulfur+o/ygen bonds,
)hile simultaneously pic(ing up
four o/ygen molecules!
Attaching
the sulfate ion
to cholesterol
or ,itamin DE
is an ingenious step,
because it
ma(es
these molecules
)ater+soluble
and
therefore easily transportable
through the blood stream!
Hydrogen sulfide 1H$S4
is consistently found
in the blood stream
in small amounts!
As a gas,
it can diffuse
into the air from
capillaries
close
to the s(in's surface!
So it is concei,able
that )e rely on
bacteria in the s(in
to con,ert sulfide
to sulfate!
&t )ould not be
the first time
that
humans
ha,e struc( up
a symbiotic relationship
)ith bacteria!
&f this is true,
then )ashing
the s(in
)ith antibiotic soap
is a bad idea!
:hototrophic bacteria,
such
as Chlorobium tepidum,
that can con,ert
H$S to H$SO;
e/ist
in nature 6Mer(le$%%=, *ahlund"=="9,
for e/ample
in
sulfur hot springs
in Lello)stone :ar(!
0hese
highly specialized bacteria
can con,ert
the light energy
from the sun
into chemical energy
in the sulfate ion!
Another possibility
is
that )e ha,e specialized cells
in the s(in,
possibly the (eratinocytes,
that are able
to e/ploit sunlight
to con,ert sulfide
to sulfate,
using
a similar phototrophic mechanism
to C! tepidum!
0his seems 'uite plausible,
especially considering
that both human (eratinocytes
and C! tepidum
can synthesize
an interesting -H+<
absorbing cofactor,
tetrahydrobioptin!
0his cofactor
is found uni,ersally
in mammalian cells,
and
one
of its roles
is to regulate
the synthesis
of melanin 6Schallreut=;9,
the s(in
pigment that
is associated
)ith a tan
and protects
the s(in
from damage
by -H+light e/posure 6Costin$%%A9!
Ho)e,er,
tetrahydrobiopsin
is ,ery rare
in the bacterial (ingdom,
and C!
tepidum is
one
of the ,ery fe) bacteria
that can synthesize it
6Cho==9!
Get me
summarize at this point
)here &'m on solid ground
and )here
&'m speculating!
&t is undisputed
that
the s(in
synthesizes cholesterol sulfate
in large amounts,
and
it has been suggested that
the s(in
is
the ma>or supplier
of cholesterol sulfate
to
the blood stream 6Strott$%%E9!
0he s(in
also synthesizes
,itamin DE sulfate,
upon e/posure
to sunlight!
Hitamin DE
is synthesized
from cholesterol,
)ith o/ysterols
1created from sun e/posure4
as an intermediate step
1o/ysterols
are
forms of cholesterol
)ith hydro/yl groups
attached
at ,arious places
in the carbon chain4!
0he body
can't synthesize
,itamin DE sulfate
from ,itamin DE 6Ga(da)ala"=AA9
so it must be
that sulfation
happens first,
producing cholesterol
sulfate
or hydro/y+cholesterol sulfate,
)hich
is then optionally con,erted
to ,itamin DE sulfate
or shipped out
.as is!.
Another highly
significant feature
of s(in cells
is that
the s(in
stores sulfate ions
attached
to molecules
that are
uni,ersally present
in the intracellular matri/,
such
as heparan sulfate,
chondroitin sulfate,
and (eratin sulfate 62ilstone"==;9!
Furthermore,
it has been sho)n
that e/posure
of the melanin
producing
cells 1melanocytes4
to molecules
containing
reduced sulfur 1+$4 leads
to suppression
of melanin synthesis 6Chu$%%=9,
)hereas e/posure
to molecules
li(e chondroitin sulfate
that
contain
o/idized sulfur 1I@4
leads
to enhancement
of melanin synthesis 6Jatz"=A@9!
2elanin
is a potent -H+light
absorber,
and
it )ould compete
)ith reduced sulfur
for the opportunity
to become
o/idized!
&t is therefore logical that,
)hen sulfur is reduced,
melanin synthesis
should be suppressed,
so that sulfur
can absorb the solar energy
and con,ert it
to ,ery useful chemical bonds
in the sulfate ion!
0he sulfate
)ould e,entually be
con,erted bac(
to sulfide
by a muscle cell
in the heart
or a s(eletal muscle
1simultaneously reco,ering
the energy
to fuel
the cell
and unloc(ing
the o/ygen
to support aerobic metabolism
of glucose4,
and
the cycle
)ould continually repeat!
*hy am
& spending
so much time tal(ing
about all of this?
*ell,
if &'m right,
then the s(in
can be ,ie)ed
as a solar+po)ered battery
for the heart,
and
that is
a remar(able concept!
0he energy
in sunlight
is con,erted into chemical energy
in the o/ygen+sulfur bonds,
and then transported
through the blood ,essels
to the heart
and s(eletal muscles!
0he cholesterol sulfate
and ,itamin DE sufate
are carriers that
deli,er the energy
1and the o/ygen4
.door+to+door.
to the indi,idual heart
and s(eletal muscle cells!
0oday's lifestyle,
especially in America,
se,erely stresses this system!
First of all,
most Americans
belie,e
that any food
containing
cholesterol
is unhealthy,
so the diet
is e/tremely lo)
in cholesterol!
5ggs are
an e/cellent source
of sulfur,
but
because
of their high cholesterol content
)e ha,e been ad,ised
to eat them sparingly!
Secondly,
as & discussed pre,iously,
natural food plant
sources
of sulfur
are li(ely to be
deficient due to
sulfur depletion
in the soil!
0hirdly,
)ater
softeners
remo,e sulfur
from our )ater supply,
)hich )ould other)ise be
a good source!
Fourthly,
)e ha,e been discouraged
from eating
too much red meat,
an e/cellent source
of sulfur+containing amino acids!
Finally,
)e ha,e been instructed
by doctors
and other authoritarian sources
to stay
out
of the sun
and )ear high S:F sunscreen
)hene,er )e
do get sun e/posure!
Another significant contributor
is the high carbohydrate,
lo) fat diet,
)hich leads
to e/cess glucose
in the blood
stream that
glycates GDG particles
and renders them ineffecti,e
in deli,ering cholesterol
to the tissues!
One of those
tissues
is the s(in,
so s(in
becomes further
depleted in cholesterol
due to glycation damage
to GDG!
=! Sulfur Deficiency
and 2uscle *asting Diseases
&n bro)sing the *eb,
& recently came upon
a remar(able article 6DrNge"==A9
)hich
de,elops a persuasi,e theory
that lo) blood serum
le,els
of t)o sulfur+containing molecules
are a characteristic feature
of a number
of diseasesBconditions!
All of these
diseases
are associated
)ith muscle )asting,
despite ade'uate nutrition!
0he authors
ha,e coined the term
.lo) CC syndrome.
to represent
this obser,ed profile!,
)here .CC.
stands for
the amino acid
.cysteine,.
and
the tripeptide .glutathione,.
both of )hich
contain
a sulfhydryl radical .+S+H.
that is essential
to their function!
Clutathione
is synthesized
from the amino acids cysteine,
glutamate,
and glycine,
and glutamate deficiency
figures
into the disease process
as )ell,
as &
)ill discuss later!
0he list
of diseasesBconditions
associated
)ith lo) CC syndrome
is surprising
and ,ery re,ealingD
H&H infection,
cancer,
ma>or in>uries,
sepsis 1blood poisoning4,
Crohn's
disea
se 1irritable bo)el syndrome4,
ulcerati,e colitis,
chronic fatigue syndrome,
and athletic o,er+training!
0he paper
6Drage"==A9
is dense
but beautifully )ritten,
and
it includes
informati,e diagrams that e/plain
the intricate feedbac( mechanisms
bet)een the li,er
and the muscles
that lead
to muscle )asting!
0his paper
fills
in some missing holes
in my theory,
but the authors
ne,er suggest
that sulfur deficiency
might actually be a precursor
to the de,elopment
of lo) CC syndrome!
& thin( that,
particularly )ith respect
to Crohn's disease,
chronic fatigue syndrome,
and e/cessi,e e/ercise,
sulfur deficiency
may precede
and pro,o(e
the muscle )asting phenomenon!
0he biochemistry
in,ol,ed
is complicated,
but &
)ill try
to e/plain it
in
as simple terms as possible!
& )ill use
Crohn's disease
as my primary focus
for discussionD
an inflammation
of the intestines,
associated )ith a )ide range
of symptoms,
including
reduced appetite,
lo)+grade fe,er,
bo)el inflammation,
diarrhea,
s(in rashes,
mouth sores,
and s)ollen gums!
Se,eral
of these symptoms
suggest
problems )ith the interface
bet)een the body
and
the e/ternal )orldD
i!e!,
a ,ulnerability
to in,asi,e pathogens!
& mentioned
before that cholesterol sulfate
plays a crucial role
in the barrier
that (eeps
pathogens from penetrating
the s(in!
&t logically plays
a similar role
e,ery)here there is
an opportunity
for bacteria
to in,ade,
and certainly
a prime opportunity
is a,ailable
at the endothelial barrier
in the intestines!
0hus,
& hypothesize that
the intestinal inflammation
and lo)+grade fe,er
are
due to
an o,eracti,e immune system,
necessitated
by the fact that pathogens
ha,e
easier access
)hen the endothelial cells
are deficient
in cholesterol sulfate!
0he s(in rashes
and mouth
and gum
problems
are a manifestation
of inflammation
else)here in the barrier!
Ordinarily,
the li,er
supplies cholesterol sulfate
to the gall bladder,
)here it
is mi/ed
into bile acids,
and subse'uently released
into the digesti,e system
to assist
in the digestion
of fats!
&f a person
consistently eats
a lo)+fat diet,
the amount of cholesterol sulfate
deli,ered
to the digesti,e system
from the li,er
)ill be reduced!
0his )ill logically result
in a digesti,e system
that is more ,ulnerable
to in,asion
by pathogens!
0he sulfate
that's combined )ith cholesterol
in the li,er
is synthesized
from cysteine
1one
of the t)o proteins
that are deficient
in lo) CC syndome4!
So insufficient bioa,ailability
of cysteine
)ill lead
to a reduced production
of cholesterol sulfate
by the li,er!
0his )ill,
in turn,
ma(e it difficult
to digest fats,
li(ely,
o,er time,
compelling
the person
to adhere
to a lo)+fat diet!
*hether lo)+fat diet
or sulfur
deficiency
comes first,
the end result
is a ,ulnerability
to infecti,e agents
in the intestines,
)ith a conse'uential
heightened immune response!
6DrNge"==A9
further
discussses
ho) a reduction
in the synthesis
of sulfate
from cysteine
in the li,er leads to
increased compensatory acti,ity
in another biological path)ay
in the li,er
that con,erts glutamate
to arginine and urea!
Clutamate
is highly significant
because it
is produced mainly
by the brea(do)n
of amino acids
1proteins in the muscles4K
i!e!,
by muscle )asting!
0he muscle cells
are triggered
to cannibalize themsel,es
in order
to pro,ide ade'uate glutamate
to the li,er,
mainly,
in my ,ie),
in order
to generate enough arginine
to replace
the role of sulfate
in muscle glucose metabolism
1i!e!,
these acti,ities
in the li,er
and muscles
are circular
and mutually supporti,e4!
Arginine
is
the ma>or source
of nitric o/ide 1FO4
and FO
is
the ne/t best thing
for muscle glucose metabolism
in the absence
of cholesterol sulfate!
FO
is a poor substitue
for SO;+$,
but it
can function
in some
of the missing roles!
As you
)ill recall,
& propose
that cholesterol
SO;+$
accomplishes a number
of important things
in muscle cellsD
it deli,ers o/ygen
to myoglobin,
it supplies cholesterol
to the cell membrane,
it helps
brea( do)n glucose,
protects
the cell's proteins
from glycation
and o/idation damage,
and pro,ides energy
to the cell!
FO can help
in reducing glycation damage,
as nitrogen
can be reduced
from I$
to %
1)hereas sulfur
)as reduced from I@
to +$4!
&t also pro,ides
o/ygen,
but it
is unable
to transfer
the o/ygen directly to myoglobin
by binding
)ith the iron molecule,
as )as
the case
for sulfate!
FO
does not supply cholesterol,
so cholesterol
deficiency
remains a problem,
lea,ing
the cell's proteins
and fats more ,ulnerable
to o/idati,e damage!
Furthermore,
FO itself
is an o/idizing agent,
so myoglobin
becomes
disabled,
due to both o/idation
and glycation damage!
0he muscle cell,
therefore,
engages
in mitochondrial o/idation
of glucose
at its o)n perilD
better
to re,ert
to anaerobic metabolism
of glucose
to decrease
the ris(
of damage!
Anaerobic metabolism
of glucose results
in a build+up
of lactic acid,
)hich,
as e/plained
in 6DrNge"==A9
further enhances
the need
for the li,er
to metabolize glutamate,
thus augmenting
the feedbac( loop!
Furthermore,
as you'll recall,
if &'m
right about
cholesterol sulfate seeding
lipid rafts,
then,
)ith a cholesterol sulfate
deficiency,
the entry
of both glucose and fat
into the muscle cell
are compromised!
0his situation
lea,es
the cell
)ith little choice
but
to e/ploit
its internal proteins
as fuel,
manifested
as muscle )asting!
&n summary,
a number
of different arguments
lead
to the hypothesis
that sulfur deficiency
causes
the li,er
to shift
from producing cholesterol
sulfate
to producing arginine
1and subse'uently nitric o/ide4!
0his lea,es
the intestines
and muscle cells ,ulnerable
to o/idation damage,
)hich
can e/plain
both
the intestinal inflammation
and
the muscle )asting
associated
)ith Crohn's disease!
0he immune system
depends
upon abundant cholesterol
to defend
against se,ere stress!
& ha,e pre,iously argued
that high
serum cholesterol
is protecti,e
against sepsis!
&t is )orth
repeating here
the abstract
from 6*ilson$%%E9,
)ho studied changes
in blood cholesterol le,els
follo)ing trauma,
infection,
and multiple organ failureD
.Hypocholesterolemia
is an important obser,ation
follo)ing trauma!
&n a study
of critically ill
trauma patients,
mean
cholesterol le,els
)ere significantly lo)er
1""= O ;; mgBdl4
than e/pected ,alues
1$%" O "A mgBdl4!
&n patients )ho died,
final cholesterol le,els
fell by EE?
,ersus a $8? increase
in sur,i,ors!
Cholesterol le,els
)ere also ad,ersely affected
by infection
or organ system dysfunction!
Other studies
ha,e illustrated
the clinical significance
of hypocholesterolemia!
<ecause lipoproteins
can bind
and neutralize
lipopolysaccharide,
hypocholesterolemia
can negati,ely impact outcome!
Fe) therapies
directed
at increasing
lo) cholesterol le,els
may become
important options
for the treatment
of sepsis!.
0hus,
many
of these conditionsBdiseases
that lead
to muscle )asting
may do so
because cholesterol
1and
therefore cholesterol sulfate4
is depleted
from the blood serum!
0his results
in the same feedbac( loop
bet)een the li,er
and
the muscles that &
discussed
)ith regard to Crohn's disease!
So & thin(
it's plausible
that
the muscle )asting
associated
)ith all of these
conditions
is caused
by this
same feedbac( mechanism!
&
ha,e discussed
the role cysteine plays
in pro,iding sulfate
to the li,er!
<ut )hat
is
the role
of glutathione,
the other sulfur+containing
protein
that's depleted
in lo) CC syndrome?
2uscle cells
ordinarily contain
significant le,els
of glutathione,
and its depletion leads
to mitochondrial damage
62artensson"=8=9!
:atients
undergoing
surgical trauma
ha,e been found
to e/hibit reduced
glutathione le,els
in their s(eletal
muscles 6Guo"==@9!
&t is tempting
to speculate
that cholesterol sulfate
pro,ides
the sulfur
needed
for glutathione synthesis,
so that the deficiency
)ould be e/plained
by the reduced a,ailability
of cholesterol
follo)ing
the immune system's
heightened response
to surgical trauma!
Clutathione
is a potent antio/idant,
so its deficiency
)ill further contribute
to dysfunction
of the muscle cell's
mitochondria,
therefore greatly impairing
its energy supply!
0here is a gro)ing a)areness
that glutathione deficiency
may play a role
in many diseases!
Lou
may )ant
to chec( out this *eb site
describing
a long list
of diseases
that may be impacted
by glutathione deficiency!
*hether the problems
arise >ust
due to insufficient supply
of the glutathione molecule itself,
or
)hether
a more general
sulfur deficiency
is the root cause,
is perhaps hard
to say,
but pro,ocati,e nonetheless!
"%! Summary
Although sulfur
is an essential element
in human biology,
)e hear surprisingly little
about sulfur in discussions
on health!
Sulfur
binds strongly
)ith o/ygen,
and is able
to stably carry
a charge
ranging from I@
to +$,
and is therefore ,ery ,ersatile
in supporting
aerobic metabolism!
0here is strong e,idence
that sulfur deficiency
plays a role in diseases
ranging from Alzheimer's
to cancer
to heart disease!
:articularly intriguing
is
the relationship
bet)een sulfur deficiency
and muscle )asting,
a signature
of end+stage cancer,
A&DS,
Crohn's disease,
and chronic fatigue syndrome!
0he African rift zone,
)here humans
are belie,ed
to ha,e first
made
their appearance se,eral
million years ago,
)ould ha,e been rich
)ith sulfur supplied
by acti,e ,olcanism!
&t is stri(ing
that people
li,ing today
in places
)here sulfur
is abundantly pro,ided
by recent ,olcanism
en>oy a lo) ris(
for heart disease and obesity!
&n my research
on sulfur,
& )as dra)n
to t)o mysterious moleculesD
cholesterol sulfate
and ,itamin DE sulfate!
3esearchers
ha,e not yet determined
the role
that cholesterol sulfate
plays
in the blood stream,
despite the fact that it
is ubi'uitous there!
3esearch e/periments
ha,e clearly sho)n
that cholesterol sulfate
is protecti,e
against heart disease!
& ha,e de,eloped
a theory
proposing
that cholesterol sulfate
is central
to the formation
of lipid rafts,
)hich,
in turn,
are essential
for aerobic glucose metabolism!
& )ould predict
that deficiencies
in cholesterol sulfate
lead
to se,ere defects
in muscle metabolism,
and
this includes
the heart muscle!
2y theory
)ould e/plain
the protecti,e role
of cholesterol sulfate
in heart disease
and muscle )asting diseases!
& ha,e also argued
that cholesterol sulfate
deli,ers o/ygen
to myoglobin
in muscle cells,
resulting
in safe o/ygen transport
to the mitochondria!
& argue
a similar role
for alpha+synuclein
in the brain!
0here is a stri(ing relationship
bet)een Alzheimer's
and sulfur depletion
in neurons
in the brain!
Sulfur
plays a (ey role
in protectiing proteins
in neurons
and muscle cells
from o/idati,e damage,
)hile maintaining
ade'uate o/ygen supply
to the mitochondria!
*hen muscles
become
impaired in glucose metabolism
due to reduced
a,ailability
of cholesterol sulfate,
proliferating fat cells
become in,ol,ed
in con,erting glucose
to fat!
0his pro,ides
an alternati,e fuel
for the muscle cells,
and replenishes
the cholesterol supply
by storing
and refurbishing cholesterol
e/tracted
from defecti,e GDG!
0hin people
)ith cholesterol and sulfur
deficiency
are ,ulnerable
to a )ide range
of problems,
such
as Crohn's disease,
chronic fatigue syndrome,
and muscle )asting,
because fat cells
are not a,ailable
to ameliorate the situation!
Cholesterol sulfate
in the epithelium
protects
from in,asion
of pathogens
through the s(in,
)hich
greatly reduces
the burden
placed
on the immune system!
:erhaps
the most intriguing possibility
presented here
is
the idea
that sulfur
pro,ides a )ay for the s(in
to become
a solar+po)ered batteryD
to store
the energy
from sunlight as chemical energy
in the sulfate molecule!
0his seems
li(e a ,ery sensible
and practical scheme,
and
the biochemistry
in,ol,ed
has been demonstrated
to )or(
in
phototrophic sulfur+metabolizing
bacteria
found
in sulfur hot springs!
0he s(in
produces ,itamin DE sulfate
upon e/posure
to sunlight,
and
the ,itamin DE
found
in breast mil(
is also sulfated!
&n light of
these facts,
it is 'uite surprising
to me
that
so little research
has been directed
to)ards understanding
)hat role sulfated
,itamin DE plays
in the body!
&t is recently becoming apparent
that
,itamin DE
promotes a strong immune system
and offers protection
against cancer,
yet ho) it
achie,es
these benefits
is not
at all clear!
& strongly suspect
that it
is ,itamin DE sulfate
that carries out
this aspect
of ,itamin DE's
positi,e influence!
2odern lifestyle practices
conspire
to induce ma>or deficiencies
in cholesterol sulfate
and ,itamin DE sulfate!
*e are encouraged
to acti,ely a,oid sun e/posure
and
to minimize
dietary inta(e
of cholesterol+containing foods!
*e are encouraged
to consume
a high+carbohydrateBlo)+fat diet
)hich,
as &
ha,e argued pre,iously
1Seneff$%"%4,
leads
to impaired cholesterol upta(e
in cells!
*e are told nothing
about sulfur,
yet many factors,
ranging
from the Clean Air Act
to intensi,e
farming
to )ater softeners,
deplete
the supply of sulfur
in our food
and )ater!
Fortunately,
correcting
these deficiencies
at the indi,idual le,el
is easy
and straightfor)ard!
&f you >ust
thro) a)ay the sunscreen
and eat more eggs,
those t)o steps alone
may greatly increase your chances
of li,ing
a long and healthy life!
3eferences "!
A/elson"=8# 2agnus A/elson,
.$#+Hydro/y,itamin DE E+sulphate
is a ma>or
circulating form of ,itamin D
in man,.
F5<S Getters 1"=8#4,
Holume "=",
&ssue $,
$8 October,
:ages "A"+"A#K
doiD"%!"%"@B%%";+#A=E
18#48%%%$+8
$! Cra)ford"=@A 0! Cra)ford
and
2argaret D! Cra)ford,
.:re,alence
and :athological Changes
of &schaemic
Heart+Disease
in a Hard+)ater
and in a Soft+)ater Area,.
0he Gancet 1"=@A4
Saturday ; Fe