Could Sulfur Deficiency be a Contributing Factor in Obesity, Heart Disease, Alzheimer's and Chronic...

8/12/2019 Could Sulfur Deficiency be a Contributing Factor in Obesity, Heart Disease, Alzheimer's and Chronic Fatigue Syndr

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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)eer,

& beliee 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 heaily

processed deriaties

of corn,


2/78

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)eer,

sulfur

has been consistently oerloo(ed in addressing

the issues

of nutritional deficiencies!

&n fact,

the American Food and Drug Administration

has not een

assigned

a minimum


3/78

daily reuirement 12D34

for sulfur!

One conseuence 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 conseuence,

it is assumed that almost any diet

)ould meet

the minimum

daily reuirements!

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 ourseles,

is found mainly in egg )hites


4/78

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 heaily processed foods!

Sulfur is lost

along the )ay,

and there is a lac( of a)areness

that this matters!

5/perts hae recently become a)are

that sulfur depletion

in the soil creates a serious deficiency

for plants 67ez$%%89,

brought about in part

by improed efficiency

in farming

and in part, ironically,

by successful attempts

to clean up air pollution!

Oer the last t)o decades,

the -!S! farming industry has steadily consolidated

into highly technologized

mega farms!


5/78

0he high yield

per acre

associated )ith these farms results

in greater depletion

of sulfur each year by the tall,

densely planted crops!

:lants

reuire sulfur

in the form

of the sulfate radical 1SO;+$4!


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Such accumulating organic matter

used to be

a ma>or source

of recyclable sulfur!

Ho)eer,

many modern machinery+based methods remoe

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 hae an increased ris(

to heart disease

compared to people

)ho drin( hard )ater

6Cra)ford"=@9!

2any possible reasons

hae been suggested for )hy

this might be true 1 :roposed theories

for soft )aterBhard

)ater differences in heart disease4,

and

>ust about eery trace metal

has been considered


8/78

as a possibility 6


9/78


10/78

to the *estern nations

are reece,

&taly and 7apan!

0hese three countries

also en>oy lo) rates of heart disease and obesity

and increased longeity!

&n South America,

a line

of olcanoes

trac(s the bac(bone

of Argentina!

Argentinians hae a much lo)er obesity rate

than their neighbors to the east

in


11/78

has

the lo)est childhood obesity

rates!

Significantly,

Ha)aii's youth are faring less )ell

than their parents

)hile Ha)aii ran(s as the fifth

from the bottom

in obesity rates,

its children aged "%+"

)eigh in at number "E!

As Ha)aii has recently become increasingly

dependent on food imports

from the mainland

to supply their needs,

they hae suffered accordingly

)ith increased obesity problems!

&n her recently

published boo(,

0he 7ungle 5ffect 62iller$%%=9, Dr! Daphne 2iller

deotes a full chapter

to &celand 1pp! "$+"@%4!

&n this chapter,

she struggles

to ans)er the uestion

of

)hy &celanders en>oy such remar(ably

lo) rates

of depression, despite liing

at a northern latitude,

)here one

)ould e/pect a high incidence


12/78

of Seasonal

Affectie Disorder 1SAD4!

She points out,

furthermore,

their e/cellent health record in other (ey areas

.*hen

compared to orth Americans,

they hae almost half

the death rate

from heart disease and diabetes, significantly less obesity,

and a greater life e/pectancy!

&n fact, the aerage 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

oer the fact

that former &celanders )ho moed

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),


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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/tensie olcanic eruptions

in the late "8%%'s that

blan(eted the highly cultiated

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 proiding

far more

sulfur to &celanders

than their counterparts

in the American diet proide!


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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!

o) comes the difficult uestion

)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


15/78

in many biological processes,

one

of )hich is metabolism!

Sulfur is present

in insulin,

the essential hormone that promotes

the utilization of sugar deried

from carbohydrates

for fuel in muscle and fat cells!

Ho)eer,

my e/tensie literature search has led me

to t)o mysterious molecules found in the blood stream

and in

many other parts of the body

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 conseuence,

it can trael freely

in the blood stream

rather than being pac(aged up

inside GDG 1the so+called .bad.

cholesterol4

for transport 6A/elsona"=8#9!


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0he form

of itamin D

that is present in both human mil(

6Ga(da)ala"=9

and ra) co)'s mil( 6


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from inasie

organisms 6Sandilands$%%=,

2crath$%%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 hae to be pac(aged up inside GDG

for deliery

to the tissues!


18/78

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 ineffectie for calcium transport,

the )ell+(no)n .primary. role

of itamin DE 63eee"=8"9!

Ho)eer,

itamin DE

clearly has many other positie effects

1it seems

that more and more

are being discoered eery day4,

and these include a role

in cancer protection,

increased immunity

against infectious disease, and protection

against heart disease

1 itamin D :rotects

against Cancer

and Autoimmune Diseases4!

3esearchers

don't yet understand

ho) it


19/78

achiees these benefits,

)hich hae been

obsered empirically but remain une/plained

physiologically!

Ho)eer,

& 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 agile 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 deeloping

a theory )hich

at its core

proposes an essential role for cholesterol sulfate

in the metabolism

of glucose for fuel

by these cells!


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also become too

disabled

to release their stored fats!

Fatty tissue

then accumulates on the body!

;! Sulfur and lucose 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 G-0;

is present

in the cytoplasm of muscle cells,

and it migrates

to the cell membrane

upon stimulation by insulin!

G-0; essentially acts

as a (ey

that unloc(s the door,

letting glucose

into the cell,

but,


22/78

li(e a (ey,

it only )or(s

)hen it's inserted

in the membrane!


23/78

in seeral distinct

o/idatie states,

ranging from I@

1in the sulfate radical4

to +$ 1in hydrogen sulfide4!

lucose, as a po)erful

reducing agent,

can cause

significant glycation damage to e/posed proteins,

leading

to the formation

of Adanced lycation 5nd :roducts 1A5's4

that are e/tremely destructie

to health

they are belieed to be a ma>or contributor

to heart disease ris(

6


24/78

hydrogen pero/ide,

to brea( do)n starch

into simple molecules, een in the absence

of any enzymes

to catalyze the reaction 6


25/78


26/78

& 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

proided

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, proided 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


27/78

from the sulfate radical

is pic(ed up

by the myoglobin, seuestered inside the molecule

for safe trael

to the mitochondria!

lucose brea(do)n products

and o/ygen are then deliered

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 proiding

the sulfate ion,

then this process brea(s do)n

miserably )hen cholesterol

sulfate

is not aailable!

First of all,

the lipid raft is not formed!

*ithout the lipid raft, the glucose

can not enter the cell!

&ntense physical e/ercise


28/78

can allo) glucose

to enter

the muscle cells een in the absence

of insulin 6O>u(a$%%$9!

Ho)eer,

this )ill lead

to dangerous e/posure of the cell's proteins

to glycation

1because

there is no iron sulfate to degrade the glucose4!

lycation

interferes )ith the proteins' ability

to perform their >obs, and leaes them more ulnerable

to o/idation damage!

One

of the important affected

proteins

)ould be myoglobin it )ould

no longer

be able to effectiely carry o/ygen


Furthermore,

o/idized myoglobin

released

into the blood stream by crippled muscle cells leads

to painful

and crippling rhabdomyolysis, and possible subseuent

(idney failure!

0his e/planation

accounts for

the obseration

that sulfur deficiency


29/78

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 leels of GDG,

particularly small dense GDG,

the )orst (ind,

1;4 lo) leels of HDG

1the .good. cholesterol4

and reduced cholesterol content )ithin the indiidual

HDG particles,

1#4 eleated blood pressure,

and 1@4

obesity,

particularly e/cess abdominal fat!

&

hae argued preiously that

this syndrome is brought on

by a diet that is high

in empty carbohydrates

1particularly fructose4

and lo)


30/78

in fats and cholesterol,

along )ith a poor itamin D

status 6Seneff$%"%9!

*hile &

still beliee that all of these

factors

are contributory, & )ould no) add another factor

as )ell

insufficient dietary sulfate!

& hae described

in a preious essay,

my interpretation

of obesity as being drien by a need

for abundant fat cells to conert 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 defectie

in glucose management they can't come up )ith

enough cholesterol sulfate

to seed

the lipid raft needed

to import

the glucose!

An alternatie )ay

to oecome a muscle cell's

defectie glucose metabolism

is

to e/ercise igorously,


31/78

so that the generated A2:J

1an indicator

of energy shortage4 induces

the G-0;

to migrate to the membrane

een in the absence

of insulin 6O>u(a$%%$9!

Once the glucose

is

inside the muscle cell, ho)eer,

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 intensie 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!


32/78

depleted

in cholesterol,

and this ma(es it

ulnerable

to future o/idatie damage!

Another )ay

to compensate for defectie glucose metabolism

in the muscle cells

is

to gain )eight!

Fat cells

must no) conert 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 aoid

glucose sources 1carbohydrates4

in the dietK

i!e! to adopt

a ery lo)+carb diet!

0hen

the fat

in the diet

can supply


33/78

the muscles

)ith fuel,

and the fat cells

are not burdened

)ith haing to store

up so much resere 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 leels

are lo),

i!e!, after prolonged periods

of fasting,

such

as oernight!

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 leels eleated,

and the release

of fats

from the fat cells is repressed!

As the dietary carbs

come in,


34/78

blood sugar

leels rise

dramatically because the muscle cells

can't utilize it!

0he lier

also processes e/cess glucose

into fat, and pac(ages it up

into GDG,

to further supply fuel

to the defectie muscle cells!


35/78

One

of the (ey proteins that gets damaged

is the apolipoprotein,

apo


36/78

conerting

glucose

to stored fats, the fat cells

are a)ash

in glucose, )hich damages

their apo5

through glycation 6Gi"==9!

Once their apo5

is damaged,

they can no longer transport cholesterol

to the membrane!

5/cess cholesterol accumulates

inside the fat cells and eentually destroys

their ability

to synthesize proteins!

Concurrently,

their cell membrane

becomes depleted

in cholesterol,

because they can no longer

delier it

to the membrane 6Seneff$%"%9!

A fat cell

that has deteriorated

to this degree has no choice

but to die

it sends out distress signals

that call

in macrophages!

0he macrophages

essentially consume

the dysfunctional fat cell,


37/78

)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 plaue build+up and heart disease!

&n a fascinating

set

of e/periments, 2a et al!

62a$%%89

hae sho)n that

the sulfate ion

attached to o/idized forms

of cholesterol

is highly protectie 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!


38/78

*hereas $#+HC present

in the medium causes

the macrophages to synthesize

and store

cholesterol and fatty acids, $#+HCES

has the e/act opposite effect

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!

! 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


39/78

in the ra) number

of elderly people 6*aldman$%%=9!


40/78

that amyloid beta

may actually be protectie

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 leels

of arious minerals

in the cells of a typical Alzheimer's

patient relatie

to the normal leel!

3emar(ably,

sulfur

is almost non+e/istent

in the Alzheimer's

patient's profile!

0o uote directly

from that site .*hile some drugs or antibiotics

may slo),

or if

it should happen,


41/78

halt

the progression

of Alzheimer's disease, sulfur supplementation

has

the potential of not only preenting,

but actually reersing

the condition, proided

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 oer the past years

has been

the bad reputation eggs hae been getting

in respect

to being a high source

of cholesterol, despite the fact

of dietary inta(e

of cholesterol haing 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!


42/78

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 plaue,

and is also present

in the Ge)y


43/78

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/idatie damage,

leading ultimately to the neuron's destruction!

&n my essay on Alzheimer's,

& argued

that biologically

pro+actie 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!


44/78

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 deelops an insensitiity

to insulin,

and,

as a conseuence, anaerobic metabolism

becomes

faored oer aerobic metabolism,

reducing

the chances for alpha+synuclein

to become o/idized!

O/idation


45/78

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 plaue4

6laser$%%#9 8!

&s

0he S(in a Solar+:o)ered


46/78

*hile

the obious biological factor

that )ould be impacted by sunlight

is itamin D,

studies conducted specifically

on itamin D status

hae been inconclusie, )ith some een sho)ing

a significant increased ris(

for heart disease

)ith increased inta(e of itamin D$ supplements

6Drolet$%%E9!

& beliee, 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!

itamin 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"=9


47/78

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 leels, they're not getting

at the crucial aspect

for heart protection, )hich

& thin(

is

the serum leel of itamin DE sulfate!

Furthermore, & beliee

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 een

the most important thing!

ien


and itamin DE sulfate are ery similar

in molecular structure,

& )ould imagine that

both molecules


48/78

are produced the same )ay!

And since itamin DE+sulfate synthesis

reuires sun e/posure,

& suspect that cholesterol sulfate

synthesis

may also e/ploit the sun's radiation energy!


49/78

the process

that produces

acid rain!

0he o/idation

of sulfide 1S+$4 to sulfate 1SO;+$4,

a strongly endothermic reaction

6Hoc(in$%%E9, conerts

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 conceiable

that )e rely on

bacteria in the s(in

to conert sulfide


50/78

to sulfate!

&t )ould not be the first time

that

humans hae 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 conert

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 conert

the light energy from the sun

into chemical energy

in the sulfate ion!

Another possibility

is

that )e hae specialized cells in the s(in,

possibly the (eratinocytes,

that are able to e/ploit sunlight

to conert sulfide

to sulfate,

using


51/78

a similar phototrophic mechanism

to C! tepidum!

0his seems uite plausible,

especially considering

that both human (eratinocytes and C! tepidum

can synthesize

an interesting -+< absorbing cofactor,

tetrahydrobioptin!

0his cofactor is found uniersally

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 -+light e/posure 6Costin$%%9!

Ho)eer,

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!


52/78

&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!

itamin 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"=9 so it must be

that sulfation

happens first, producing cholesterol

sulfate

or hydro/y+cholesterol sulfate,

)hich


53/78

is then optionally conerted

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

uniersally 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"=@9!

2elanin

is a potent -+light

absorber,

and


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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 conert it to ery useful chemical bonds

in the sulfate ion!

0he sulfate )ould eentually be

conerted bac( to sulfide

by a muscle cell

in the heart or a s(eletal muscle

1simultaneously recoering

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,


55/78

and

that is

a remar(able concept!

0he energy

in sunlight is conerted 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

delier the energy 1and the o/ygen4

.door+to+door. to the indiidual heart

and s(eletal muscle cells!

0oday's lifestyle,

especially in America,

seerely stresses this system!

First of all,

most Americans

beliee 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 hae been adised

to eat them sparingly!


56/78

Secondly,

as & discussed preiously,

natural food plant sources

of sulfur

are li(ely to be deficient due to

sulfur depletion

in the soil!

0hirdly,

)ater

softeners remoe sulfur

from our )ater supply,

)hich )ould other)ise be

a good source!

Fourthly, )e hae been discouraged

from eating

too much red meat, an e/cellent source

of sulfur+containing amino acids!

Finally, )e hae been instructed

by doctors

and other authoritarian sources to stay

out

of the sun and )ear high S:F sunscreen

)heneer )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 ineffectie

in deliering cholesterol


57/78

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"==9 )hich

deelops a persuasie theory that lo) blood serum

leels

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 adeuate nutrition!

0he authors

hae coined the term

.lo) C syndrome.

to represent this obsered profile!,

)here .C.

stands for the amino acid

.cysteine,.

and the tripeptide .glutathione,.

both of )hich

contain

a sulfhydryl radical .+S+H.


58/78

that is essential

to their function!

lutathione

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) C syndrome is surprising

and ery reealing

H& infection, cancer,

ma>or in>uries,

sepsis 1blood poisoning4,

Crohn's disea

se 1irritable bo)el syndrome4,

ulceratie colitis, chronic fatigue syndrome,

and athletic oer+training!

0he paper

6Drage"==9

is dense

but beautifully )ritten, and

it includes

informatie diagrams that e/plain the intricate feedbac( mechanisms

bet)een the lier

and the muscles that lead

to muscle )asting!

0his paper


59/78

fills

in some missing holes

in my theory, but the authors

neer suggest

that sulfur deficiency might actually be a precursor

to the deelopment

of lo) C syndrome!

& thin( that,

particularly )ith respect

to Crohn's disease, chronic fatigue syndrome,

and e/cessie e/ercise,

sulfur deficiency

may precede and proo(e

the muscle )asting phenomenon!

0he biochemistry

inoled 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 discussion

an inflammation

of the intestines,

associated )ith a )ide range of symptoms,

including

reduced appetite, lo)+grade feer,

bo)el inflammation,

diarrhea, s(in rashes,

mouth sores,

and s)ollen gums!


60/78

Seeral

of these symptoms

suggest problems )ith the interface

bet)een the body

and the e/ternal )orld

i!e!,

a ulnerability to inasie 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

eery)here there is an opportunity

for bacteria

to inade,

and certainly a prime opportunity

is aailable

at the endothelial barrier in the intestines!

0hus, & hypothesize that

the intestinal inflammation

and lo)+grade feer

are due to

an oeractie immune system,

necessitated by the fact that pathogens

hae

easier access )hen the endothelial cells

are deficient

in cholesterol sulfate!


61/78

0he s(in rashes

and mouth

and gum problems

are a manifestation

of inflammation else)here in the barrier!

Ordinarily, the lier

supplies cholesterol sulfate

to the gall bladder,

)here it is mi/ed

into bile acids,

and subseuently released

into the digestie system to assist

in the digestion of fats!

&f a person consistently eats

a lo)+fat diet,

the amount of cholesterol sulfate

deliered to the digestie system

from the lier

)ill be reduced!

0his )ill logically result

in a digestie system that is more ulnerable

to inasion

by pathogens!

0he sulfate

that's combined )ith cholesterol

in the lier is synthesized

from cysteine

1one of the t)o proteins

that are deficient

in lo) C syndome4!


62/78

So insufficient bioaailability

of cysteine

)ill lead to a reduced production

of cholesterol sulfate

by the lier!

0his )ill,

in turn, ma(e it difficult

to digest fats,

li(ely,

oer 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 infectie agents

in the intestines, )ith a conseuential

heightened immune response!

6DrNge"==9

further

discussses ho) a reduction

in the synthesis

of sulfate

from cysteine in the lier leads to

increased compensatory actiity

in another biological path)ay in the lier

that conerts glutamate

to arginine and urea!

lutamate

is highly significant

because it


63/78


64/78

As you

)ill recall,

& propose that cholesterol

SO;+$

accomplishes a number of important things

in muscle cells

it deliers 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 proides energy to the cell!

O 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 proides 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!

O

does not supply cholesterol,

so cholesterol


65/78

deficiency

remains a problem,

leaing the cell's proteins

and fats more ulnerable

to o/idatie damage!

Furthermore,

O 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 peril better

to reert

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"==9

further enhances

the need for the lier

to metabolize glutamate,

thus augmenting the feedbac( loop!

Furthermore,

as you'll recall,


66/78

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 leaes

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 lier

to shift from producing cholesterol

sulfate

to producing arginine

1and subseuently nitric o/ide4!

0his leaes

the intestines and muscle cells ulnerable

to o/idation damage,

)hich can e/plain

both

the intestinal inflammation

and


67/78

the muscle )asting

associated

)ith Crohn's disease!

0he immune system

depends upon abundant cholesterol

to defend

against seere stress!

& hae preiously argued

that high

serum cholesterol is protectie

against sepsis!

&t is )orth repeating here

the abstract from 6*ilson$%%E9,

)ho studied changes

in blood cholesterol leels follo)ing trauma,

infection,

and multiple organ failure

.Hypocholesterolemia

is an important obseration

follo)ing trauma!

&n a study

of critically ill trauma patients,

mean

cholesterol leels

)ere significantly lo)er 1""= ;; mgBdl4

than e/pected alues

1$%" " mgBdl4!

&n patients )ho died,

final cholesterol leels fell by EE

ersus a $8 increase

in suriors!


68/78

Cholesterol leels

)ere also adersely affected

by infection or organ system dysfunction!

Other studies hae illustrated

the clinical significance

of hypocholesterolemia!


69/78

So & thin(

it's plausible

that the muscle )asting

associated

)ith all of these conditions

is caused

by this same feedbac( mechanism!

&

hae discussed the role cysteine plays

in proiding sulfate

to the lier!


70/78


71/78

is perhaps hard

to say,

but proocatie 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 eidence 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 belieed


72/78

to hae first

made

their appearance seeral million years ago,

)ould hae been rich

)ith sulfur supplied by actie olcanism!

&t is stri(ing that people

liing today

in places

)here sulfur is abundantly proided

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 molecules cholesterol sulfate

and itamin DE sulfate!

3esearchers hae not yet determined

the role

that cholesterol sulfate plays

in the blood stream,

despite the fact that it is ubiuitous there!

3esearch e/periments

hae clearly sho)n that cholesterol sulfate

is protectie

against heart disease!

& hae deeloped

a theory proposing


is central

to the formation


73/78

of lipid rafts,

)hich,

in turn, are essential

for aerobic glucose metabolism!

& )ould predict

that deficiencies

in cholesterol sulfate lead

to seere defects

in muscle metabolism,

and this includes

the heart muscle!

2y theory )ould e/plain

the protectie role of cholesterol sulfate

in heart disease

and muscle )asting diseases!

& hae also argued


deliers o/ygen to myoglobin

in muscle cells,

resulting in safe o/ygen transport


& 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


74/78

in neurons

and muscle cells

from o/idatie damage, )hile maintaining

adeuate o/ygen supply


*hen muscles

become impaired in glucose metabolism

due to reduced

aailability

of cholesterol sulfate, proliferating fat cells

become inoled

in conerting glucose

to fat!

0his proides an alternatie fuel

for the muscle cells,

and replenishes the cholesterol supply

by storing

and refurbishing cholesterol

e/tracted from defectie 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 aailable

to ameliorate the situation!

Cholesterol sulfate

in the epithelium

protects

from inasion


75/78

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

proides a )ay for the s(in

to become

a solar+po)ered battery 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

inoled

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!


76/78

&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 achiees

these benefits

is not at all clear!

& strongly suspect

that it is itamin DE sulfate

that carries out

this aspect of itamin DE's

positie influence!

2odern lifestyle practices

conspire

to induce ma>or deficiencies

in cholesterol sulfate and itamin DE sulfate!

*e are encouraged to actiely aoid sun e/posure

and

to minimize dietary inta(e

of cholesterol+containing foods!

*e are encouraged


77/78

to consume

a high+carbohydrateBlo)+fat diet

)hich, as &

hae argued preiously

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 intensie

farming to )ater softeners,

deplete the supply of sulfur

in our food

and )ater!

Fortunately,

correcting

these deficiencies at the indiidual leel

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 liing a long and healthy life!

3eferences "!

A/elson"=8# 2agnus A/elson,

.$#+Hydro/yitamin DE E+sulphate is a ma>or

circulating form of itamin D

in man,.

F5


78/78

olume "=",

&ssue $,

$8 October, :ages ""+"#K

doi"%!"%"@B%%";+#=E

18#48%%%$+8

$! Cra)ford"=@ 0! Cra)ford

and 2argaret D! Cra)ford,

.:realence

and :athological Changes

of &schaemic Heart+Disease

in a Hard+)ater

and in a Soft+)ater Area,.

0he Gancet 1"=@4 Saturday ; Fe

Could Sulfur Deficiency be a Contributing Factor in Obesity, Heart Disease, Alzheimer's and Chronic...

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