I have studied your questionnaire responses and the lab test results
you sent me. The bottom line is that I agree that you do have chronic
fatigue syndrome, and I think there is good evidence that the
glutathione depletion”methylation cycle block hypothesis does fit
your
case. I think that you will benefit from the simplified treatment
protocol that I have suggested. You may also benefit from some
additional supplements to deal with particular issues. Here are the
results of my analysis:

Genetics:

According to my hypothesis, in order to develop a sporadic case of CFS
(in contrast to the epidemic cluster cases) a person must have some
genetic predisposition. Your Nutrigenomic panel results show ACE
deletion (+/+), no CBS SNPs, very slow COMT, very slow MAO A, MTHFR
C677T (+/-), MTRR S175L (+/-), MTRR A66G (+/-), NOS (+/-), SUOX (+/-),
VDR Bsm/Taq (+/-), and VDR Fok (+/-).

I think that you are already pretty familiar with what these mean,
since you have a Genetic Analysis Report from Dr. Amy Yasko, but I will

comment on them briefly.

The ACE deletion has the effect of raising the concentration of
angiotensin converting enzyme, which increases the rate of conversion
of angiotensin I to angiotensin II. The latter normally causes the
adrenals to increase their secretion of aldosterone, which causes the
kidneys to retain more sodium in the blood, and to dump more potassium
into the urine. However, in CFS it seems that in many cases this
effect is countered by the blunting of the HPA
(hypothalamus-pituitary-adrenal) axis earlier on, so that the
aldosterone secretion is actually not elevated. We dont have enough

data to determine what the situation is in your case completely, but we

do have some. We have a red blood cell potassium level that is low.
We dont have a sodium level, and we dont have an aldosterone
measurement.

We have some other information about your adrenal function: We have a
one-time blood measurement of cortisol at 11 a.m. that is within the
normal range, but we dont know how it is behaving around the clock.

DHEA-sulfate is low, but we dont have a straight DHEA measurement,
so
we cant tell whether this low value results from low DHEA secretion
by
the adrenals, or because of low sulfation of DHEA to form DHEA-sulfate.

There is evidence for the latter in your case (see the discussion of
SUOX below), so that may be the whole cause. We know that your
flashlight-pupils test indicated adrenal fatigue. We know that you
suffer from mild reactive hypoglycemia, which implicates the HPA axis.

We know that Cortef was overstimulating to you (however, you didnt
report the dosage, so its difficult to interpret this), and we know
that adrenal extract was helpful to you. One of your Spectracell tests

showed low pantothenic acid (vitamin B5), and the adrenals have a high
need for that.

According to my hypothesis, the HPA axis blunting that occurs in CFS
results from low production of ACTH by the pituitary as a result of
glutathione depletion there. You have other evidence for glutathione
depletion (see below), so I suspect that you do in fact have low ACTH
production. We dont have an ACTH measurement for you, so cant
check
that, but I suspect that that is what accounts for much of the HPA
dysfunction evidenced by the above mentioned abnormalities in your
case.

It is very good to see that you do not have CBS upregulating SNPs. I
think that this will enable you to recover faster than those who do.

You have very slow COMT as a result of the most extreme combination of
COMT SNPs: H62H (+/+), V158M (+/+), and L136L (-/-). The VDR Bsm/Taq
(+/-) modifies this only slightly. The result is that you are not able

to metabolize (break down) your catecholamines (dopamine,
norepinephrine, and epinephrine (or adrenaline)) nearly as rapidly as
normal. This accounts for both your sensitivity to epinephrine
injections by the dentist and at least partially for your fainting on
the tilt table test when epinephrine was administered. When you are
given epinephrine, it will rise to higher concentrations and stay in
your body longer than normal, and thus will give you potentiated
effects.

In CFS, there is also a decreased rate of production of dopamine
because of lowered levels of tetrahydrobiopterin, which is coupled to
the folate system, which is blocked. So your genetically slow
breakdown of dopamine may be compensating somewhat for your low rate of

production of it, thus keeping the levels nearer to normal than they
would otherwise be.

Your very slow COMT also means that you are not be able to use methyl
groups as fast as normal, and that means that you should avoid
supplements that contain methyl groups. You reported that
methylcobalamin was overstimulating to you, but that hydroxocobalamin
is very helpful. I think your slow COMT explains why you dont
tolerate methylcobalamin well. The benefit from hydroxocobalamin is
further evidence that you have a methylation cycle block, and also
evidence that you are able to convert hydroxocobalamin to
methylcobalamin.

You also have very slow metabolism (breakdown) of serotonin, because of

your MAO A (+/+). Since the low BH4 in CFS also slows the production
of serotonin, this SNP may be partially compensating for the low rate
of production, and thus keeping the serotonin levels more nearly normal

than they would otherwise be, as in the case of dopamine discussed
above. You reported that both SSRIs and SAMe made you feel
œspacy.
SSRIs raise the levels of serotonin in the synapses by blocking their
normal reuptake. SAMe increases the rate of production of serotonin,
among its other effects. I think that your slow MAO A accounts for
this response to both SSRIs and SAMe, as they both probably cause the
serotonin levels to rise too high in the presence of the very slow
breakdown rate.

The heterozygous SNP in your MTHFR C677T gene means that you are not
able to convert methylene tetrahydrofolate to 5-methyl tetrahydrofolate

(same as FolaPro) as rapidly as normal. As you probably know, the
latter is the active form of folate that is needed by the enzyme
methionine synthase, which is blocked in many cases of CFS, including
yours, in my opinion, based on the evidence you have reported. I think

this is consistent with your experience of receiving benefit from
taking FolaPro, and I do think that FolaPro should be part of your
treatment, because of this SNP.

Its good to see that you dont have the other MTHFR SNP.

Its also good to see that you dont have the MTR SNP.

You have two MTRR SNPs, but they have opposite effects on the rate of
the MTRR reaction. So you will need some B12, but not as much as the
PWCs who have more serious issues with MTR and MTRR. And the form of
B12 that would be best for you, as you have already found, is
hydroxocobalamin, because of your very slow COMT.

You have NOS D298E (+/-). This slows the ability of your epithelial
nitric oxide synthase to convert arginine to citrulline and nitric
oxide. When the BH4 deficiency that results from the low production of

5-methyltetrahydrofolate is included in the picture, this could be
causing production of some oxidizing species from this reaction
(superoxide and peroxynitrite), which will contribute to oxidative
stress.

You also have the SUOX S370S (+/-) heterozygous SNP. As you may know,
the normal (also called œwild-type) version of this SNP is
actually
(+/+), in contrast to all the others in this panel. So the homozygous
situation with this one would be (-/-) instead of (+/+). (Its just
the result of a mistaken choice of what was the population norm for
this SNP when it was assigned.) In any case, Dr. Yasko, as you may
know, has never seen the homozygous allele in this case, and that
suggests that humans are probably not able to live if they inherit it,
which further suggests that even the heterozygous SUOX SNP is very
severe. In your case, we have measurements of your plasma cysteine and

plasma sulfate, and the former is above normal, while the latter is
below normal, giving you a very abnormal ratio of the two. This is
consistent with having a very slow SUOX reaction, which is the reaction

that converts sulfite to sulfate. This reaction is downstreatm of
cysteine in the sulfur metabolism, so that most of the sulfate normally

in the blood has originated as cysteine (though some comes in from the
diet). I think this can have important consequences for you. For one
thing, if cysteine rises too high, it can become a neurotoxin. On the
other hand, if sulfate goes too low, its normal jobs dont get done.

Three of them are to produce DHEA-sulfate from DHEA, as mentioned
above, to supply sulfate to the glycosaminoglycans in the cartilage of
the joints to help them to hold water, and to provide one of the main
phase II detox pathways for disposing of a variety of toxins. Note
that your sulfation pathway was low normal on your comprehensive detox
profile. Im somewhat surprised that you didnt report joint
problems.
You could boost your sulfate by taking supplements of Epsom salt
(magnesium sulfate) or glucosamine sulfate, or by taking baths in Epsom

salts with baking soda. Some people do not respond well to sulfate
supplementation, so you could try it, and if it helps continue it, but
if it causes problems, stop. In cases where there are problems, I
suspect its because of the presence of sulfate reducing bacteria in
the gut, and these convert sulfate to hydrogen sulfide (the Å“rotten
egg
gas), which has some toxicity. I know that you have some dysbiosis,

so you may have sulfate-reducing bacteria in your gut, and I think you
would just have to try this to see if it helps or causes problems.

There are a couple of things that puzzle me from what youve
reported.
One is that you reported that you dont have a history of sulfite
sensitivity, such as from dried fruits or wines. I would have expected

that you would, since you have the SUOX SNP. A common symptom of
elevated sulfite is headaches. The other puzzling thing to me is that
you find that NAC is beneficial to you, and you actually take 2 grams
per day of it. Thats a fairly high dosage for NAC, since going
higher
than 1 gram per day has been reported to produce pro-oxidant effects
rather than antioxidant effects. And since your pathway for disposing
of excess cysteine would appear to be slowed by the SUOX SNP, Im
surprised that you find this beneficial. When cysteine goes too high,
it produces neurological symptoms.

A couple of supplements that may be helpful to you because of the SUOX
SNP are thiamine (vitamin B1) and molybdenum. Sulfite tends to break
down thiamine (though your Spectracell test didnt show a deficiency
in
it). Your red blood cell elements test showed that you were a little
low in molybdenum, so taking more (perhaps 500 micrograms per day)
would be a good idea. You were also low in copper, and copper and
molybdenum are competitive, so supplementing with a little copper would

probably be a good idea, too, but it should not be overdone (perhaps 2
milligrams per day). It would be a good idea to measure these levels
again after some time of supplementing, to see how they are doing.

The effect of the VDR (Bsm/Taq) SNP was discussed above. The VDR Fok
SNP will mean that you will have some difficulty in regulating your
blood sugar levels, and that is also consistent with your history of
mild reactive hypoglycemia.

These are all the genetic results that we have on you. There are three

other categories of genetic results that I have found to be relevant in

various cases of CFS. The first is genetic polymorphisms in the detox
enzymes, as evaluated by the Genovations Detoxigenomics panel. I think

that this might be a helpful panel for you to have, for a couple of
reasons. First, you reported that you have been very sensitive to
pharmaceuticals. That suggests that you might have SNPs in one or more

of the cytochrome P450 enzymes that detox pharmaceuticals, such as the
CYP3A4 enzyme or one of the others. Knowing which specific ones have
SNPs would give you a list of pharmaceuticals that you would know you
need to avoid or to take smaller than normal dosages if you do take
them. The other reason is that you have Spectracell test results that
show normal functional response of your lymphocytes to addition of
glutathione, but low total antioxidant function. I think Ive seen
only three cases like that in the past, and my data are not complete,
but I suspect that this means that there are SNPs in the enzymes that
utilize glutathione in conjugating toxins and in quenching lipid
peroxides, i.e. the glutathione transferase (GST) enzymes, which are
also characterized in the Detoxigenomic panel. Another possible
contributor to this situation would be low activity of the glutathione
peroxidase enzyme, an enzyme which requires selenium. Your
glutathione peroxidase activity came out at the low end of the normal
range, and your red blood cell test showed that you were more deficient

in selenium than in any other essential element. (Im a little
puzzled
why you did not also have a lower T3 level on your thyroid panel,
because the enzyme that converts T4 to T3 also requires selenium.
There must have been enough to supply this enzyme.) Knowing the status

of your GST polymorphisms would help to explain the Spectracell
results. Im still trying to figure out what to do about GST
polymorphisms. Boosting glutathione is one thing that can be done,
because it works without the help of these enzymes to some extent.
Boosting selenium is another, because glutathione peroxidase can take
some of the lipid peroxide load off the glutathione transferases.

The other pertinent genetics involve the blood coagulation system and
the HLA (human leukocyte antigen) system. From your questionnaire
responses, I dont see much evidence that you have a hypercoagulation

problem, so I wont suggest the Hemex tests for you. If you could
have
an erythrocyte sedimentation rate test run (its a very inexpensive
blood test), it would shed some light on this. If it came out below 5
mm per hour, and if you always have cold hands and feet, those would
suggest a possible hypercoagulation problem, and the next step would be

to have a soluble fibrin monomer test run by Hemex Lab. If not, it
probably isnt an issue for you.

The final type of genetic information that is pertinent for some PWCs
is the HLA panel offered by LabCorp, which is recommended by Dr.
Shoemaker. This one is important for people who may have a mold
susceptibility problem or chronic Lyme disease. I dont see evidence

that those are likely in your questionnaire responses. I realize that
you did not pass the visual contrast sensitivity test, but I suspect
that the reason may have been your blurry vision rather than the
presence of biotoxins from mold or Lyme disease. So I wont suggest
pursuing this for now, either.

Onset:

You reported that you had two onsets of CFS, the first at age 18 and
the second at age 23. According to my current hypothesis, in order for

a person who has the genetic predisposition toward CFS to actually
develop a case of it, the person must be subjected to some combination
of long-term stressors that tend to lower glutathione or bring on a
methylation cycle block. Either of these will will bring on the other
chronically, by a vicious circle mechanism. You reported that at age
18 you had a case of the flu, and that the CFS symptoms followed from
that. You reported that prior to your second, more severe onset of
CFS at age 23, you had been taking antibiotics (Ampicillin) for several

years to treat acne. There may have been some other factors involved
as well, including diet, since you reported that your diet was low in
vitamins, minerals and essential fatty acids, and included significant
amounts of fast foods and soft drinks. I think that antioxidants and
animal-based protein are particularly important in protecting against
glutathione depletion and methylation cycle block, so if your diet was
low in either or both, I think that could have contributed. You also
reported consuming significant amounts of alcohol on the weekends, and
the metabolism of alcohol generates oxidizing free radicals, putting a
load on glutathione, which lies at the basis of the bodys
antioxidant
enzyme system. The immune system presents a large demand for
glutathione when fighting viral infections such as flu, so that could
certainly have been a contributor to lowering your glutathione status.

The disruption of the normal bacterial flora in your gut from the
multi-year use of oral antibiotics might have interfered with
absorption of vitamin B12 in the ileum (lower small intestine). Over
the course of several years, this may have depleted your B12 stores to
the point that there was not enough available to form sufficient
methylcobalamin to operate your methionine synthase, which would have
brought on a methylation cycle block. Since glutathione depletion and
the methylation cycle block are bound together in a vicious circle
mechanism in my hypothesis, I think both these scenarios could have
brought on CFS in your case.

Evidence for glutathione depletion:

The most direct evidence you have for glutathione depletion is that the

plasma reduced glutathione level was measured to be below the normal
range on a sample given on Sept. 19, 2003. I think there is also some
indirect evidence. First, you report abnormally high daily urine
volume, high frequency of urination, and arising from sleep to urinate.

Although you do not report constant thirst, I think it is possible
that you have a mild case of central diabetes insipidus (not to be
confused with diabetes mellitus, which involves blood glucose and
insulin). Central diabetes insipidus is common in CFS, and it is caused by
insufficient production of antidiuretic hormone (arginine vasopressin)
by the hypothalamus/pituitary. In my hypothesis, this is
caused by glutathione depletion. You also have evidence for HPA axis
dysfunction, as discussed earlier. In my hypothesis, in CFS this is
caused by glutathione depletion in the pituitary, which leads to
insufficient production of ACTH. You also have physical fatigue, and
in my hypothesis, this is caused in CFS by glutathione depletion in the

skeletal muscles. I suspect that the long recovery time you require
after alcohol ingestion is a result of additional glutathione depletion

in the detox of the alcohol, which as I mentioned above produces
oxidizing free radicals.

Evidence for methylation cycle block:

The most direct evidence you have for this is your abnormally high
homocysteine level. While not all PWCs or autistic children who have a

methylation cycle block have high homocysteine, nevertheless when this
is present, it does indicate that there is a methylation cycle block.
I suspect that the reason yours is so high is that you have been
pushing your blocked methylation cycle with a high dosage of methionine

(more on this below). Correcting high homocysteine can often by
accomplished in the general population using conventional folic acid,
conventional cyanocobalamin, conventional vitamin B6, and
trimethylglycine (betaine), and this is what many clinicians suggest.
However, if a person has certain genetic polymorphisms, more active
forms of folate and B12 may be necessary, because the person is not
able to properly utilize the conventional supplemental forms, and this
seems to be true for many PWCs.

Indirect evidence for a methylation cycle block in your case comes from

the fact that you have experienced benefit from taking supplements that

impact the methylation cycle.

Endocrine issues:

I have already discussed your HPA axis function above. It appears that

you also have some issues with your HPG (gonadal) and HPT (thyroid)
axes. Your free testosterone is low, and your TSH is below the normal
mean value. I suspect that both are due to problems in the
hypothalamus/pituitary that result from low glutathione there, though I

dont have detailed biochemical mechanisms worked out for them.
Im
hopeful that getting glutathione levels up will correct these problems.

Complete blood counts:

Your white cell count was low-normal, and your red cell count was low.

Your mean corpuscular volume was above the normal mean value. Your red

cell volume distribution width was below normal, but this parameter is
not very specific. Your hemoglobin and hematocrit were both
low-normal. I think these values are consistent with vitamin B12 or
folate deficiency, as they are tending toward a macrocytic anemia.
This would be consistent with a methylation cycle block, which
necessarily involves a folate cycle block and thus decreases the
ability to produce DNA and RNA to make new blood cells. Lifting the
methylation cycle block should help this, but you could also take
supplementary nucleotides in the meantime. There are some in the HHC
Complete Vitamin.

Brain function and vision:

You reported brain fog and problems with cognition, as well as
blurriness of your vision. You also reported that these occur
together, and that your SPECT and PET scans indicate low blood
perfusion of the brain. I suspect that low blood supply to the brain
is a major cause of this problem. You also reported problems with
fainting and failing the tilt table test. I think these are also
consistent with problems in sufficient blood supply to the brain. We
dont have a measurement of your total blood volume or of your
cardiac
output. I suspect from the evidence for diabetes insipidus, discussed
above, that you do have low blood volume. This in turn can cause low
venous return to the heart and can result in low cardiac output, which
can affect blood supply to the brain. Im hopeful that getting your
glutathione levels up will correct these problems.

Gut:

You have evidence for dysbiosis, and that is to be expected from the
chronic use of oral antibiotics (Ampicillin). Im somewhat surprised

that you did not report any symptoms of gut dysfunction, such as
motility problems. Perhaps this means that your gut serotonin levels
are being held high enough because of your MAO A (+/+) SNP that your
peristalsis is normal. Thats a very good thing. I note that you
are
taking digestive enzymes and probiotics, and that may help with the
dysbiosis. Ive found that human-derived probiotics are more
effective
than those from other sources. I suggest a product by Pharmax, called HLC high potency capsules.

Contracted muscles:

I suspect that this results from a low rate of ATP production in the
mitochondria of the skeletal muscle cells, resulting from glutathione
depletion there. ATP is necessary to relax the muscle fibers. Getting
glutathione up should help this.

Twitching eyelids:

This is a symptom of low magnesium, which was also found in your red
blood cell elements test. I believe that low intracellular magnesium
is caused by glutathione depletion. There is evidence in the medical
literature for this mechanism in red blood cells. Supplementing
magnesium orally and/or by injections can help this, but ultimately
getting the glutathione levels up is the answer, in my opinion.

Sleep apnea:

You suggested that you may have developed this within the past year. I

suspect that in CFS, sleep apnea develops because of mitochondrial
dysfunction due to glutathione depletion. The result is a lower rate
of carbon dioxide production by the cells, and hence a lower carbon
dioxide concentration in the blood. The respiratory center in the
brain stem controls the rate and depth of breathing based on carbon
dioxide and pH in the blood it receives. Low carbon dioxide will cause

a reduction in the rate and depth of breathing to the point that
breathing actually stops during sleep until the low oxygen trip point
is reached, which results in arousal and gasping, and this process
continues over and over during sleep. If your doctor would give you a
trial with an APAP machine, you could see if this would help. An APAP
machine is like a CPAP machine, except that it automatically adjusts
the pressure to the patients needs. Thus, you dont need to have
a
fixed pressure determined in a sleep lab test. Of course, you have to
have a doctor who is willing to write you an order for one of these
machines. I sleep with an APAP machine myself, because I have
obstructive sleep apnea, which is the more common type in the general
population (especially in older men!)

Supplements:

I suspect that in the past you have been compensating for your
methylation cycle block and your glutathione depletion by sort of a brute force approach. In the case of the methylation cycle
block,
you have been taking a high daily dosage of methionine (4.5 grams). I
suspect that this was partially overwhelming your methylation cycle
block by raising homocysteine to a high level, thus pushing the BHMT
alternate pathway by the mass action principle of chemistry. This
would not have corrected the block in methionine synthase, but it would

have given you more methylation capacity via increased levels of SAMe
and return of homocysteine to methionine via BHMT. I think you were
able to get away with this because you dont have CBS
upregulations.
The problem with this approach is that it raises the level of
homocysteine, and that is associated with heart disease. So I dont
recommend that you continue such a high dosage of methionine. I think
there is a smaller amount in the HHC Complete Vitamin. You took a high
dosage of folic acid, and because you apparently dont have
polymorphisms in your dihydrofolate reducase (DHFR, not measured in the

Yasko panel), you were able to make use of ordinary folic acid to
supply enough tetrahydrofolate and other folate forms (not including
5-methyltetrahydrofolate, which you couldnt make very well because
of
your MTHFR SNP) in order to prevent a major macrocytic anemia from
developing, though your complete blood count shows that you have a
tendency in that direction. To top this off, since you have the SUOX
SNP, which would slow the flow from cysteine down to sulfate, you were
able to boost your glutathione by taking large doses (2 grams per day)
of NAC, which I also dont recommend that you continue, because of
the
potential for raising cysteine too high and producing neurological
effects from that.

It seems to me that by trial and error you found ways of working with
your genetic makeup to partially compensate for this ongoing vicious
circle, but you didnt really correct the vicious circle. And what
you
did wouldnt work for all PWCs, because it depended on your
particular
combination of normal genes and SNPs. I also dont think its the
best
approach for you, either, for the reasons given above. But as time
went on, you have been moving to things that really will correct this
block, which are FolaPro and hydroxocobalamin (so long as there is
enough SAMe and glutathione to convert enough hydroxocobalamin to
methylcobalamin, and that seems to be the case, since you report
benefit from hydroxocobalamin).

What else can I suggest?

Honestly, Garrett, I think you are now going in the right direction and

that what have started doing recently is going to continue to bring you

improvement. You probably have some toxins to dispose of (since as you

point out, efforts at detoxing have been beneficial for you), and that
may take some time, but I think you are doing the right things with the

FolaPro and the hydroxocobalamin, though your FolaPro dosage (2 per
day) seems somewhat high. I dont know whether you will need
Intrinsi/B12/folate for the folinic acid, because it seems that you are

able to use regular folic acid alright, but you might add that as well,

because is could help with your folate metabolism. If you add it, I
would suggest lowering your FolaPro dosage so as to keep the total
folate per day at 800 milligrams. Some PWCs who have gone too high on
the folates have developed detox with high momentum, and that has been
unpleasant for them and has taken some time to slow down after stopping

the supplements. I do recommend that you take the HHC Complete
Vitamin, because it has several things designed to help lift the
methylation cylcle block, as well as supplying essential nutrients as a

foundation for the biochemistry of the body as a whole. I would also
encourage you to try the phosphatidylserine complex. This will help
repair your membranes, somewhat like the Propax with NT Factor will do.

It will also supply some choline to stimulate the BHMT pathway from
homocysteine to methionine. It should also help with your cellular
response to cortisol. Basically, Im suggesting that you take all
five
supplements in the current version of the simplified treatment approach

that Ive suggested. I think they will match your genetics well. I
think that the other supplements that you are taking that I have not
commented on are O.K. The charcoal is probably taking out some toxins.

Its important to take it separated in time from nutrients, so that
it
wont bind them and take them out, too.

If you want to incorporate some of Dr. Yaskos step 1 programs, in
addition, I think the ones directed toward helping to keep down
excitotoxicity and the ones directed toward supporting the adrenals and

the gut would be the most helpful for you. I mention the
excitotoxicity program because you find benefit from Klonopin, and it
acts in a similar way, but of course can produce dependency and
withdrawal in some people, so should be decreased carefully and with
the help of a doctor. Dr. Yaskos step 1 programs are discussed in
The Puzzle of Autism and on her discussion forum.

As you do this treatment, Garrett, I cannot overemphasize the
importance of being monitored by your doctor. As I think you know,
over the past several weeks, a few PWCs using this treatment approach
have developed some rather serious adverse effects, apparently because
of individual health issues they had in addition to the usual chronic
fatigue syndrome issues. If you experience anything that appears to be

beyond the common die-off and detox symptoms I described in my update
on the treatment approach dated July 18, 2007, I urge you to stop the
supplements and get checked out by your licensed physician right away.

I hope this analysis and these recommendations are helpful to you.
Please feel free to share them with your doctor or anyone else you
think would be interested.

New CFS Research Newsletter !
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This entry was posted on Monday, July 23rd, 2007 at 1:12 pm and is filed under Rich Van Konyenburg - Case Study, Treatments. You can follow any responses to this entry through the RSS 2.0 feed. You can leave a response, or trackback from your own site.