Re: Dr Pall: Nitric Oxide Cycle Theory: Will It Explain CFS, FM, and Other ‘Unexplained’ Illnesses?

[Guest guest]

The use of a cpap machine may be very beneficial in these conditions..

There's a cross over from sleep apnea and our conditions..

--- In infections , Penny Houle <pennyhoule@...>

wrote:

>

> Nitric Oxide Cycle Theory: Will It Explain CFS, FM, and Other

‘Unexplained’ Illnesses? - Q & A with L. Pall, PhD

>  

> http://www.prohealth.com//library/showArticle.cfm?libid=12896

>  

> First things first, I was glad to see that Dr. Pall says the origin of many

" unexplained " illnesses is probably viral and bacterial.

>  

> It feels like " deja vu all over again " ...like we're going in circles here.

But this theory does pique my interest because my tests with Dr. Gleuck,

identified a genetic inabily to process Nitric Oxide properly. This nitric

oxide dysregulation in my body is almost certainly a major cause of pain and

fatigue symptoms. 

>  

> Dr. Gleuck's recommendation for me was to supplement with Arginaid, a

supplement primarily used in hospitals. I take it off and on, and it seems to

help, but I find it difficult to be consistent with it. I'm not sure why he

doesn't recommend regular arginine supplements. I have heard mixed reports on

arginine. If you do think NO could be an issue for you and want to try

Arginaid, you can get it from Walgreen's on-line (I recommend the lemon

flavor). 

>  

> High Level athletes have trainers who use various therapies to deal with

nitric oxide buildup so that they can perform again quickly.  (I heard

one coach say that one of the reasons Phelps was able to accomplish all

those gold medals, was because he has very little difficulty with Nitric Oxide

the way other athletes do, and he doesn't need to rest between races the way

others do). Many athletes get daily massage (wouldn't that be great?) but I

doubt if most of us could afford it, and ice baths, right after they've finished

their sporting or athletic events. Tony talks about ice a lot but I don't think

I could handle ice baths at this stage. Would probably pass out.

>  

> Anyway, maybe we pwc should be looking into this a bit more. Dr. Pall seems

to think so, here's a link to his theory and protocol for reducing NO (near the

end of the article): 

>

http://chronicfatigue.about.com/gi/dynamic/offsite.htm?zi=1/XJ & sdn=chronicfatigu\

e & cdn=health & tm=108 & gps=375_1951_1219_568 & f=10 & su=p736.8.336.ip_ & tt=2 & bt=1 & bts=1\

& zu=http%3A//sprident.com/martin-pall/ 

>  

> A lot of his supplements sound familiar, but I also notice a number of them

I've taken in the past that have been somewhat beneficial.

>  

> penny

>  

> p.s. I also found another article which I'm pasting below. I'm not sure of the

source (newtreatments.org). It does explain a lot about nitric oxide

dysregulation in pwcs. Sounds very familiar, like the story of most of our

lives. I don't know if they're just making the theory fit the symptoms, or if

this really is a better understanding of how our illness works. Fingers crossed

some good will come of it.

>  

> http://www.newtreatments.org/Adrenals/ga/123

>  

> NITRIC OXIDE

>

> If the topic of nitric oxide is new to you, it will help a lot

>

> if you take the time to review some generalbackground on this toxic agent.

Click here for nitric oxide

> basics!

>

> An increase in nitric oxide during immune activation lowers

> overall adrenal output and, coupled withlow DHEA, will cause the same clinical

picture now evident in

> chronic fatigue syndrome andfibromyalgia (abstracts). Read a few of the

abstracts and you

> will see that increased levels of NO willnot only lower cortisol, but also

lower aldosterone, DHEA,

> pregnenolone and catecholaminesecretion.

>

> The most direct evidence that NO alter adrenal function comes

> from work with rats. Dr. CBCymeryng, et al, at the University of Buenos Aires

found that

> NO significantly decreasedcorticosterone (the same as cortisol in man)

production both

> in unstimulated and incorticotropin-stimulated zone fasciculate adrenal cells,

in a

> dose-dependent manner. The productionof pregnenolone from cholesterol was also

significantly

> reduced. This effect was reversed by ferroushemoglobin (abstract).

>

> But primary hypoadrenalism due to weakened adrenal glands is

> not as much in evidence in CFS andFM, as is secondary hypoadrenalism (defect

in

> pituitary-hypothalmus axis). The evidence in chronicfatigue syndrome and

fibromyalgia all point to a reduced ACTH

> response to CRH and vasopressin.

>

> But it does not matter in this theory whether you have primary

>

> or secondary hypoadrenalism!Upregulated nitric oxide due to hyperimmunity

(coupled with

> another toxic gas, carbon monoxide)also alters hypothalmus-pituitary function

and would create

> the exact same pattern now evidenced inthese illnesses (abstract).

>

> A vicious circle begins to form! Low cortisol and DHEA allows

> the immune system to becomehyper; hyper immune response (upregulated nitric

oxide and

> other cytokines) alters HPA axisfunction, resulting in low cortisol.

>

> If one were looking for a single factor that would completely

> explain chronic fatigue syndrome,including every single crazy symptoms known

to occur in this

> illness, you would need only look atupregulated nitric oxide (NO).

>

> Dr. AM Levin (Link) has examined this nitric oxide theory and

> is able to tie it in seamlessly with yeastinfections. I suspect that he is on

target, but I would also

> add that I believe many other pathogens canalso connect and cause the same

situation. Still, I do like

> his work in this area. He is the first MD tojump on the bandwagon of

upregulated NO as a major factor in

> CFS.

>

> As mentioned earlier, Tumor Necrosis Factor-alpha (TNF-a) is

> known to be increased in CFS.(Taking DHEA supplements helps down-regulates

TNF.

> (abstracts))

>

> Tumor necrosis factor-alpha and other Th1 cytokines

> upregulates the production of nitric oxide (NO)and nitric oxide synthase (NOS)

(abstracts) therefore, it is

> safe to say nitric oxide is upregulated inCFS (abstract).

>

> Even though no studies have been done to date about the strong

>

> connection between TNF-alpha(known to be increased in CFS) and NO, there is

evidence

> showing a strong possibility ofupregulated NO is CFS. As a matter of fact,

evidence suggest

> that autoimmune pathogenesis initiatedby inflammatory responses within the CNS

may result in part

> from a vicious cycle in whichTNF-alpha and NO mutually provoke each other's

production

> (abstract).

>

> Another important body of evidence is that fact that natural

> killer cell cytotoxicity, found low is CFS(abstract) (abstract), is also shown

dose-dependently low when

>

> chemical NO donors are addedduring afferent phase of NK stimulation with IL-12

and

> TNF-alpha. Conversely, when an inhibitor ofNO synthase was added, a subsequent

increase in the

> cytotoxicity of the effector cells towards theNK-sensitive target cells (K562)

was observed (abstract). In

> other words, upregulated nitric oxidelowers natural killer cell activity and

accounts for the

> evidence found in CFS.

>

> In support of this view of upregulated nitric oxide in CFS,

> other medical researchers are alsobeginning to suspect this simple gas in

playing a major role

> in CFS. One theory involvesN-methyl-D-aspartate (NMDA) receptors in the brain.

When brain

>

> function is balanced, GABA andNMDA receptor activity is balanced. In CFS,

however, NMDA

> receptors become substantiallymore active than GABA receptors. HealthComm

International

> feels that a key component in theupregulation of NMDA receptors in CFS

involves the

> overproduction of nitric oxide. They state, " This molecule, itself a

neurotransmitter, has been associated

>

> with stimulation of the NMDA receptorsystem when released into the nervous

system (Link).

> HealthComm is using an aspect of nitric oxide'sfunction in the brain to show

evidence of upregulation in CFS.

>

> It look's like they could be on to partof the problem in CFS--nitric oxide

does upregulate NMDA

> receptors (abstract). However, Isuggest this is a pattern that is more closely

associated with

>

> the symptoms of hypoadrenalism, than itis a single cause of CFS.

>

> Here is were the valium every 3 days can help. The drug

> enhances GABA binding and increasesGABA receptors (abstract), which, like a

see saw, will lower

> NMDA receptors, but tolerance doeshappen rapidly so dosing every third day is

mandatory in the

> benefit is to be continued.

>

> One might also try low dose trazodone every day as a way of

> down-regulating the NMDA receptors(abstract). This could also be the manner in

which low doses

> of selective serotonin reuptakeinhibitors (SSRIs) help some with CFS since

these drugs also

> down regulate NMDA receptors, atleast in the rat (abstract).

>

> Recent research also shows that the amino acid homocysteine is

>

> elevated in the spinal fluid and brainof PWC (abstract). This evidence

supports the view that nitric

>

> oxide is also elevated in CFS sincenitric oxide inhibits the enzyme that

breaks down

> homocysteine.

>

> Nitric oxide is the most potent vasodilator known. Excessive

> production of this simple moleculecauses the drastic fall in blood pressure

during shock. Nitric

>

> oxide is also now known to drasticallyreduce the pain threshold and to be

responsible for increased

> sensitivity to pain, especiallyfibromyalgia-like pain (references). Nitric

oxide is

> manufactured in cartilage cells (chondrocytes)(abstracts). Since nitric oxide

stimulates the reception of

> pain (abstracts), there can be little doubt thatNO is responsible for

fibromyalgia pain in CFS!

>

> NO also can stimulate insulin secretion by deenergizing

> mitochondria (abstract). Insulin also increasethe release of NO in the

vascular system (abstract)(abstract).

>

> Since NO is a potent vasodilator,insulin produced in response to a high

carbohydrate meal will

> cause increased vasodilation making aPWCs with neurally mediated hypotension

feel much worse. In

> other words, insulin and NO have aclose association that will lead to

hypoglycemic reactions in

> PWCs, making a high protein dietmandatory in treating CFS. The activated

immune system in

> chronic fatigue syndrome andfibromyalgia also reduces the manufacture of new

healthy red

> blood cells (erythropoiesis) (abstract).A strong connection exist between the

local activation of bone

>

> marrow T-lymphocytes, increasedproduction of cytokines, and reduced levels of

red blood

> cells.

>

> In additon, both inflammatory cytokines and nitric oxide (NO)

> interfere with the way the bodymetabolizes iron (references) (abstract). Not

only does NO

> cause problems with iron metabolism,but defects in iron utilization and

reutilization results in

> reduced performance of many iron-requiringenzymes and proteins (references).

>

> Research has found that when the immune system is activated

> the critical period in the developmentof nutritional iron deficiency occurs

after 30 to 40 days

> without iron supplementation. The person isunable to maintain hemoglobin

levels without endangering the

> iron-requiring enzyme groups which areessential for life (abstract). This

indicates that any single

> illness or combinations of factors that canstimulate the immune system and

increase nitric oxide

> production for longer than 30 to 40 days, couldprogress into CFS in selected

individuals.

>

> A similar iron metabolizing problem exist in AIDS. As HIV

> infection advances, progressive anemia isestablished. The study of iron

metabolism in these patients

> shows a pattern similar to that of theAnemia of Chronic Disease (see below). A

group of Spanish

> researchers think that these changes inAIDS might be due to iron sequestration

in phagocytic cells

> induced by release of cytokines from theimmune system (abstract).

>

> Red cell hemoglobin is the most important iron-requiring

> protein likely defective in CFS.Hemoglobin is the MAJOR scavenger of excessive

NO, therefore,

> an inability to remove this toxicimmune agent quickly before it vasodilates

blood vessels

> excessively and over reacts with healthycells can result in many of the

symptoms, particularly

> fatigue, neurally mediated hypotension, and jointpain. In addition, if nitric

oxide is not being properly

> scavenged, then problems with excessive NOcan occur even if NO is not

upregulated.

>

> As unbelievable as all this sounds, the very latest evidence

> indicates that nitric oxide also controls theamount of oxygen reaching the

cells. If you do not read any

> link in this article, you shouldstruggle to read this one (Link) . The

researchers found that

> the loss of oxygen flips a switch thatreleases nitric oxide in the arteries to

dilate blood vessels

> and increase blood flow so that theremaining oxygen can be delivered to

tissue. On the return

> trip to the lungs, the oxygen that was lostin the arteries is recaptured in

the veins, giving the

> appearance of inefficient oxygen delivery. Theresearchers measured blood flow

and oxygen concentration in

> several regions of rat brain while therats breathed air with varying oxygen

levels. They showed that

>

> hemoglobin releases a form of nitricoxide in the small arteries that regulate

blood flow, thus

> promoting oxygen delivery. When the animalsbreathed oxygen under higher air

pressure, oxygen levels

> increased in tissue, and hemoglobincompensated by halting NO release and

contracting blood

> vessels.

>

> The finding also clears up another puzzle. In test tube

> experiments, hemoglobin scavenges NO andconstricts blood vessels. Yet in the

body, hemoglobin does not

>

> have this effect under normalconditions. " This tendency to constrict blood

vessels seems to

>

> oppose hemoglobin's job of deliveringoxygen, " one researcher said. " Our

findings explain why

> hemoglobin doesn't constrict blood vesselsin the body. It releases NO in the

arteries to counteract the

> NO it scavenges. "

>

> But what if something goes wrong with this system? As

> mentioned above, cortisol reversesmacrophage activation, therefore, it can be

assumed that low

> cortisol will allow macrophages to bemore easily activated by stimuli. Since

these white cells dump

>

> loads of NO into the system when theyare activated, maybe one major problem

with chronic fatigue

> syndrome is activated macrophages.Release of NO from macrophages has been

visualized in the

> mouse (abstract). Their activation inchronic fatigue syndrome is theorized to

be similar to the

> manner in which a cancer drug (Taxol)primes macrophages in cancer patients

(abstract).

>

> Nitric oxide primed macrophages are ready to dump their NO at

> the least disturbance. This theorysuggest that increased stress of the faster

blood flow through

>

> the vessels, after isoproterenol isinjected in the TTT, releases this " primed "

nitric oxide,

> intensifying the effects of the drug causing theperson with activated

macrophages to go into syncope rather

> easily. The increased NO stimulates therelease of large amounts of

prostacylin, which causes

> bradycardia (slowing of heart rate)(references).

>

> Physical activity would increased the release of NO from

> primed macrophages simply because thestress of muscle activity would put

pressure on the primed

> macrophages causing them to dump theirNO. The action of the heart muscle would

also place

> alternating pressure on the macrophages. Flowstress of the blood flowing more

rapidly through the vascular

> system during exercise would alsorelease a lot of NO. So would a sudden drop

in barometric

> pressure. These factors would explainwhy chronic fatigue syndrome and

fibromyalgia are noted for an

>

> increase in symptoms after physicalactivity. Some with CFS and FM swear they

feel worse just

> before a weather front moves in, whichwould agree with the release of NO due

to a drop in

> atmospheric pressure.

>

> Hemoglobin is not the only iron-requiring enzyme likely

> defective in chronic fatigue syndrome andfibromyalgia. The cytochrome p450

liver enzyme system

> (abstract) is also likely defective. Theseenzymes are responsible for

metabolizing toxic chemicals and

> drugs (most antidepressants) intometabolites that can then be removed from the

body in the bile

>

> or by the kidneys (link).

>

> As mentioned earlier, inflammatory stimuli, such as TNF-alpha,

>

> are increased in chronic fatiguesyndrome. TNF-alpha increases nitric oxide

production and

> nitric oxide reacts with the ironcomplexes in the cytochrome p450 enzymes

thereby inhibiting

> the action of these important liverenzymes. (abstracts) (abstract).

>

> Defects in cytochrome p450 liver enzymes due to excessive

> nitric oxide (abstract) will result in abuild up of environmental chemicals in

the body and a

> super-sensitivity to certain drugs. (references)

>

> Most chemicals use in food processing do not cause problems

> for healthy people simply becausehealthy people have normal liver enzymes and

can metabolize

> these chemicals and flush them out ofthe body. But in people with defective

cytochrome p450

> enzymes, these chemicals can build up inthe body to the point where they

become toxic. Most chemicals

> can cause this toxicity. (link)

>

> The normal dosage of certain drugs can also cause toxic

> reactions if they are not being properlymetabolized due to a defect in the

p450 enzymes. (link) A

> person with this illness might have toreduce dosages of certain drugs to as

low as 1/10th of the

> normal dose to avoid reactions. Otherdrugs might not work simply because they

must be metabolized

> into their bioactive metabolite inorder to become effective.

>

> Fact is, the failure of the cytochrome p450 liver enzymes to

> detoxify the body is likely somewhatresponsible for multiple chemical

sensitivity and may even be

> related indirectly to what is now thoughtto be responsible for Gulf War

Syndrome. Researchers at the

> University of Texas believe they knowwhat causes Gulf War Syndrome. A long

term study of members of

>

> an Alabama Seabee unit thatserved in the Persian Gulf War strongly indicated

that many

> veterans who became ill do not carry aspecific gene that attempts to

neutralize the nerve gas Sarin.

>

> That lends more support to the claim thatsoldiers in the Gulf War were exposed

to small amounts of

> nerve gas. (link) The genetic defect couldexplain why some soldiers were

afflicted with the syndrome --

> which has a wide range of symptomsresembling chronic fatigue syndrome. The

biggest questions

> about Gulf War syndrome has been whyone person got sick when the person next

to him didn't. But

> now experts suspect a genetic reasonwhy some people got sick, linking the

illness to damage from

> certain chemicals.

>

> Writing in the journal Toxicology and Applied Pharmacology,

> the research team said a gene thatcontrols production of an enzyme known as

type Q paraoxonase,

> or PON-Q, which helps the bodydestroy toxins, might be responsible.

>

> It is highly specific for the chemical nerve agents sarin and

> soman as well as for the common pesticidediazinon. Fact is, several

organophosphorus insecticides are

> detoxified through the cytochromeP450/paraoxonase (PON1) pathway (abstract).

The reaserchers

> found strong statistical linksbetween Gulf War syndrome and veterans' reports

of exposure to

>

> combinations of chemicals likepesticides and low-level chemical nerve agents.

They predicted

>

> in 1997 that it might be due to aPON-Q deficiency, and now that's what they

have found. Human

> serum paraoxonase (PON 1)exists in 2 major forms (Q and R), which differ in

the amino

> acid glutamine and arginine, respectively.These PON allozymes hydrolyze

organophosphates and aromatic

> esters, and both also protect LDLfrom copper ion-induced oxidation.

>

> The group had linked three different neurological syndromes to

>

> the use of pesticide-containing fleacollars, highly concentrated insect

repellent and pills

> formulated with pyridostigmime bromide tocounteract the effects of nerve gas,

as well as exposure to

> low-level chemical nerve agents.

>

> Other researchers have theorized about a similar mechanism in

> chronic fatigue syndrome (abstract)involving toxicity through the GABAa

receptor. Corrigan, et

> al, discuss the possible involvement oforganochlorine compounds which are

widespread in the

> environment and may have similar toxiceffects through damaged cholinergic

input to the dentate gyrus

>

> of the hippocampus where cholinergicand GABAergic transmission are closely

linked.

>

> Researchers in Australia also found a close assoication

> between organochlorines and chronic fatiguesyndrome(abstract) (abstract).

>

> A defect in iron-requiring P450 liver enzymes might alter the

> cytochrome P450/paraoxonase(PON1) pathway, affecting paraoxonase-Q in people

with chronic

>

> fatigue syndrome, but it will likelytake decades before researchers answer

this question.

>

> Liver enzymes might also play the major role in many food

> allergies due to certain toxic compoundscontained naturally in some foods.

>

> Food allergies are also likely due to Leaky Gut Syndrome

> (link). In this illness, the stomach wall isweakened and allows tiny particles

of undigested food and food

>

> chemicals to enter into the bloodstream where they are picked up by immune

cells as pathogens.

> The immune reaction following theintrusion of food particles and food

chemicals can cause

> severe migraine type headaches, depressionand insomnia (link). The likely

cause of this problem in

> chronic fatigue syndrome is hyperimmunity,including upregulated IL-6 and

nitric oxide.

>

> The way it appears, anything that can activated the immune

> system over a long period of time canlead to cytochrome p450 liver enzyme

dysfunction and result in

>

> chronic fatigue syndrome andfibromyalgia!

>

> Since pregnenolone, progesterone, and DHEA are all

> biosynthesized from cholesterol by p450iron-requiring enzymes, the failure of

this enzyme system due

> to an iron metabolizing problem causedby hyperimmunity can lead to low levels

of these neurohormones

>

> (abstracts). Low levels of theseneurosteroids are know to cause brain fog,

especially

> pregnenolone.

>

> Problems with iron metabolism can also contribute to loss of

> energy, reduced oxygen utilization,reduced blood pressure control, altered

sleep, reduced brain

> perfusion, difficulty in concentration,and many other symptoms noted in CFS.

>

> At least one researcher is interested in the association

> between a defect in iron metabolism andincreased nitric oxide production.

(link)

>

> The secondary and/or primary hypoadrenalism found in CFS

> causes dehydration, decreasing thewater content in the blood by up to 40% in

some individuals

> (reference). When there is less water inthe body, there is an equal less

amount of water in the blood

> and the blood thickened! Since RBCand hemoglobin measurements are based on a

percentage of drawn

>

> blood, hemoconcentrated bloodis artificially increase in red cell numbers and

hemoglobin,

> causing an elevated reading in the drawnblood of a person with chronic fatigue

syndrome. This false

> increase in RDC indices prevents anyiron related blood problem from being

detected. People with

> chronic fatigue syndrome andfibromyalgia are anemic and neither they nor their

doctor are

> aware of it!

>

> The type of anemia is called, Anemia of Chronic Disease (ACD)

> (link) . ACD is common in patientswho have a long standing disease in which

the immune system is

>

> activated. The causes are complexand incompletely understood, but probably

involve inflammatory

>

> cytokines and nitric oxide. (link)

>

> In ACD the production of new red cells is insufficient for the

>

> degree of anemia and RBC length ofsurvival is shortened and there is an

impaired re-utilization

> of iron.

>

> ACD is fairly easy to diagnose if iron deficiency anemia (IDA)

>

> can be ruled out, and it is easy todiagnose IDA in an otherwise healthy

person. But the

> differential diagnosis of ACD and IDA in apatient who has a chronic disease

like chronic fatigue

> syndrome, who also has an iron metabolizingproblem, is extremely difficult.

The differential diagnosis

> requires assessment of iron status, but thatassessment is complicated by the

fact that ACD causes changes

> in the parameters of iron status.

>

> With chronic disease, Total Iron Binding Capacity (TIBC)

> decreases, counteracting the usualincrease due to iron deficiency. Serum iron

decreases,

> mimicking iron deficiency.

>

> The single most important diagnostic mark of iron deficiency

> is low serum ferritin, but ferritin ismarkedly elevated as an acute phase

protein in a chronic

> diseases, reaching many fold higher than thediagnostic point, even in clearly

iron deficient patients.

>

> Recent clinical studies demonstrate that serum transferrin

> receptor (sTfR), an independent parameterof iron status, adds to the power of

existing diagnostic tests

>

> in diagnosis of iron deficiency in patientswith chronic disease. It is, in

fact, comparable to marrow

> aspiration, the gold standard for irondeficiency, in evaluating iron status.

>

> Most doctors will not know how to diagnose borderline anemia

> in CFS, and may simply dismiss it asnot possible. To get iron status properly

evaluated, refer

> your doctor to this web site (click here).

>

> One other point should be made before leaving the subject of

> iron in chronic fatigue syndrome andfibromyalgia. Not only does dehydration

and low blood volume

> mask the presents of anemia, it alsoalters the flexibility of red blood cells

and their ability to

>

> deform and travel through the tiny capillariesin the brain. Dehydrated red

blood cells show signs of reduce

> elasticity (abstract) and could be thecause of reduced blood flow in the brain

noted in CFS. Tilt

> Table Test

>

> The results of Tilt Table Tests (TTT) in which 95% of CFS

> patients are positive for neurally mediatedhypotension is likely due to

increased nitric oxide production

>

> in CFS coupled with certain factorsduring the administration of the TTT. The

beta-adrenergic

> agonist, isoproterenol, is injected toincrease heart rate and decrease the

amount of time spent in

> the tilted position. In healthy folks withnormal nitric oxide levels, the drug

vasodilates the blood

> vessels and speeds the heart rate. But thisvasodilation is nitric oxide

dependent so that when NO is

> inhibited, the vasodilation is decreased(abstracts). Conversely, when NO is

upregulated as is

> theorized here, the response to isoproterenolis greatly exaggerated and

syncope can occur.

>

> Many PWCs complain that the TTT cause the same type of flare

> brought on by a period of intenseexercise. This is understandable since the

same release of NO

> by primed macrophages would occurwhen the heart rate increases during

exercise. The flare from

> post-exercise fatigue and a TTT wouldbe similar since they are both caused by

the same phenomena.

>

> The Aspirin Test High doses of aspirin is also known to

> relieve a severe flare in symptoms afterexercise. Aspirin not only inhibits

prostacylins, the drug is

> also a nitric oxide inhibitor (abstracts).Taking 3-4 aspirin during a severe

case of fatigue should

> cause you to recover about 30 minuteslater. The aspirin test should reveal to

you that your NO is

> upregulated and causing your fatigue.Taking aspirin when you feel fine will do

nothing so wait till

>

> you feel your worse to conduct this test.

>

> Taking aspirin before having a TTT would likely insure

> negative results for NMH. Aspirin can alsohelp you reduce post-exercise

fatigue.

>

> But one caution here: If you suffer a lot of headaches that

> seemed food related, you likely leaky gutsyndrome and taking aspirin can

aggravate this condition and

> bring on more headaches. Why AreSo Many Women Affected?

>

> Chronic Fatigue syndrome and fibromyalgia are predominately

> diseases of women because femalesnaturally have ~20% less red blood cells and

~20% less

> hemoglobin than men. They also suffer a fargreater iron loss than men due to

monthly blood loss. To make

> matters worse for women, recentresearch shows that whole-body production of

nitric oxide is

> 20+% greater in healthy women than inmen (abstract).

>

> Estrogen is the likely culprit because this hormone also

> stimulates nitric oxide production. Fact is,estrogen's upregulation of nitric

oxide, a potent vasodilator,

>

> is likely the reason estrogen preventsheart attacks. (abstracts) I don't know

how much comforting it

>

> is to tell a women with chronic fatiguesyndrome that she is less likely to

have a heart attack due to

>

> her illness. I would suppose that mostwould rather have the heat attack risk

and manage it with

> exercise.

>

> In support of this theory, a recent correlation of serum

> measures of nitric oxide production with lupusdisease activity has been

discovered (abstracts). Lupus is

> another mostly female illness, likely for thesame reasons above. Maybe a

nitric oxide study in CFS/FM is

> not far off? Certainly if Lupus wasshown to be associated with NO, some CFS

researcher will soon

> put two and two together.

>

> Blacks and CFS

>

> How many black people you know with CFS? None likely. Some

> researchers says this is becauseblacks don't complain to doctors, but that's

not true. Truth

> is, blacks do not suffer CFS and FMnearly as often as whites simply because

they respond much

> differently to increased levels of nitricoxide (Link) (abstract) (abstract).

Blacks also have higher

> blood pressure and generally have highercortisol levels.

>

> Serotonin

>

> People with chronic fatigue syndrome may or may not be

> deficient in serotonin. Upregulated nitricoxide does decreases serotonin

levels by inactivating

> tryptophan hydroxylase, the initial enzyme in thebiosynthesis of this

important neurotransmitter (abstract).

> And, since serotonin plays an importantrole in inhibiting the level of

TNF-alpha (abstract), reduced

> serotonin levels could explain the increasein this potent cytokine found in

some with CFS.

>

> But the serotonin picture is muddle. Many people with chronic

> fatigue syndrome respond negativelyto antidepressants taken to increase

serotonin levels. Several

>

> researchers have also found evidence ofhigh serotonin levels in chronic

fatigue syndrome. There is

> also minor evidence that an allergicreaction to serotonin could be going on in

some.

>

> Taking 5-HTP (link), the amino acid precursor to serotonin,

> might help restore serotonin and downregulate TNF-alpha is some PWCs. It

should also improve sleep

> and having a calming effect.Serotonin is an extremely important agent in

chronic fatigue

> syndrome and may or may not play a rolein many symptoms (link). This

hypothesis takes the view of

> individual need when it comes toserotonin. Try it, but don't hesitate to stop

taking serotonin

>

> boosters if you feel worse.

>

> Improving Red Cell Health

>

> Eating calves liver and/or taking various vitamins and

> supplements to improve red cell health after youhave been successful at

lowering cytokine/nitric oxide output

> with hydrocortisone (Every Third DayTherapy) will improve overall health.

However, one must first

> makes sure that they have controlledthe upregulated nitric oxide, before

taking iron supplements.

> The iron is sequestered away from nitricoxide in CFS for a reason. Iron forms

potent and dangerous

> oxygen radicals when exposed to highlevels of NO. Therefore, iron supplements

are not recommended

> until NO is brought under control.

>

> Dopamine

>

> Dopamine likely plays a big part in the symptoms of CFS

> because phentermine and other dopaminestimulates (ritalin, cylert) are know to

provide fantastic

> short term relief of chronic fatigue syndromeand fibromyalgia symptoms. But

this research effort has not

> yet try to unravel anything meaningfulfrom the study of dopamine in these

illnesses. Dopamine and

> nitric oxide are mentioned associatedwith each other in over 100 recent

medical abstracts so anyone

>

> interested in looking into this mightfind some great info.

>

> B-12

>

> Vitamin B-12, especially hydroxocobalamin (B-12a), is known to

>

> reduce the symptoms of chronicfatigue syndrome and fibromyalgia. B-12,

especially

> hydroxocobalamin, is also know as a nitric oxidescavenger (abstracts).

>

> In summary

>

> If you've got chronic fatigue syndrome, you have low cortisol

> and DHEA due to a blunted ACTHresponse to CRH. You also suffer from increased

cytokine

> production, upregulated nitric oxide, poorred cell health, defective

iron-requiring enzymes and proteins

>

> and low pregnenolone. Due to youractivated immunity and liver enzyme problems,

you also suffer

> from chemical exposure and selectivedeficiency of certain amino acids and

nutrients. These

> problems are collectively responsible for allyour symptoms.

>

> Since there are many different root causes, no particular

> drug, herb, or nutrient by itself can addressall the problems. This wide

variety of symptoms coming from

> many different aspects of the sameillness has also made this an extremely

difficult syndrome for

>

> the medical community and your friendsand relatives to accept. They will tend

to think you are

> faking it simply because you suffer from somany different, seemingly

unrelated, symptoms.

>

> The average person (and doctor) does not realize that

> dysregulated nitric oxide can cause so manydifferent medical problems!

>

> The best things you can do to recover is increase your

> cortisol bioactivity in order to lower cytokinesand nitric oxide, while at the

same time slowly addressing all

>

> the other medical problems. Not an easytask! You will need to go slow and by

extremely patient.

> Remember, you could begin one drug ornutrient to address one problem and, at

the same time, suffer

> an increase in symptoms from adifferent problem, causing you to think the new

nutrient you

> just started is not for you. Just theopposite could happen and likely has. You

could try a new

> product and have a natural reduction insymptoms not related to the new

product, causing you to think

> the new product is a wonder drug.

>

> Pay close attention to the nutrients that have a proven tract

> record for helping others. If you triedthem once and failed to improve--go

back and try them again.

>

> Spending the extra time to learn about the broad consequences

> of increased nitric oxide activity willhelp you to understand you illness and

accept this recovery

> program. Click here for more nitric oxideinfo and links.

>

>  http://www.newtreatments.org/

>  

>