Chronic Fatigue Syndrome Linked to Three Genes

[Guest guest]

I wonder what genes these are?

Chronic Fatigue Syndrome Linked to Three Genes

http://www.medpagetoday.com/Neurology/GeneralNeurology/dh/3130

[Please visit the original website to view the whole article. - Mod.]

By , MedPage Today Staff Writer

Reviewed by Jasmer, MD; Assistant Professor of Medicine,

University of California, San Francisco

April 20, 2006

Also covered by: Forbes, LA Times, MSNBC, Washington Post

MedPage Today Action Points

* Explain to interested patients that this research effort has

begun to clarify the biological basis of chromic fatigue syndrome.

* Note that the studies link the syndrome with variations in genes

that code for parts of the body's stress response mechanism.

* Caution that the studies are still preliminary and will need to

be replicated.

Review

ATLANTA, April 20 - Chronic fatigue syndrome (CFS) has been linked to

five mutations in three genes that are related to the body's ability

to handle stress.

" For the first time ever, we have documented that people with CFS have

(variations in) certain genes that are related to those parts of brain

activity that mediate the stress response, " said Reeves, M.D.,

director of CFS research at the CDC here.

Also, people with the syndrome have differences in genetic activity

levels that affect the way they respond to stress accumulated over a

lifetime, Dr. Reeves said in a media telebriefing to announce 14

research papers arising from a CDC study in Wichita, Kan.

The findings could lead to better diagnostic tools for the syndrome,

which is often regarded as ill-defined, and to better treatments,

including both cognitive and behavioral therapies and new drugs, Dr.

Reeves said.

....

The flurry of research papers arose from a longitudinal

population-based study in Wichita, from 1997 to 2000. That study found

70 people classified as having CFS, and in 2002 and 2003, they were

invited to take part in exhaustive two-day clinical and genetic

evaluations.

The researchers also included 55 matched controls for the 58 CFS

patients who agreed to take part, as well as 59 people with fatigue

symptoms who did not meet the full CFS criteria (dubbed ISF). Also,

they included 55 people with either ISF or CFS and concurrent

melancholic depression.

The data gathered from the 227 participants, at a cost of about $2

million, included a full clinical evaluation, electrophysiologic

measurements of sleep physiology, cognitive function, autonomic

nervous system function, and detailed blood work that included DNA and

gene activity analysis, Dr. Reeves said.

....

It turned out that all four groups zeroed in on five single nucleotide

polymorphisms (SNPs) in three genes - those coding for the

glucocorticoid receptor, for serotonin, and for tryptophan hydroxylase

- which, she said, " are very important in the function of the HPA,

which is the body's stress response system. "

The effect of the variations, Dr. Reeves said, appears to be that

people with them are less able to cope with stress.

One of the research groups, he said, identified three distinct

fatigued groups - those with extreme fatigue, those with symptoms such

as heart-rate variability and cortisol disturbances, and a group that

was primarily menopausal women.

" The genes that Dr. Vernon mentioned distinguished the three fatigue

groups from those that were not fatigued and two of those genes

distinguished between the fatigue groups, " Dr. Reeves said.

....

Dr. Reeves said the Wichita effort is being followed by a larger study

in Georgia, which will attempt to replicate and expand on the results.

= -- = -- = --

http://www.futuremedicine.com/toc/pgs/7/3

Table of Contents (Abstracts are available, full-text requires a

subscription)

Pharmacogenomics

Apr 2006, Volume 7, Number 3

Perspective

A public health approach to pharmacogenomics and gene-based diagnostic tests

L , Muin J Khoury

Pharmacogenomics, Apr 2006, Vol. 7, No. 3, Pages 331-337.

Collaborative Study: chronic fatigue syndrome – Editorial

The postgenomic era and complex disease

J A Witkowski

Pharmacogenomics, Apr 2006, Vol. 7, No. 3, Pages 341-343.

Collaborative Study: chronic fatigue syndrome – Introduction to the study

The challenge of integrating disparate high-content data:

epidemiological, clinical and laboratory data collected during an

in-hospital study of chronic fatigue syndrome

Suzanne D Vernon, C Reeves

Pharmacogenomics, Apr 2006, Vol. 7, No. 3, Pages 345-354.

Collaborative Study: chronic fatigue syndrome – Research Report

An empirical delineation of the heterogeneity of chronic unexplained

fatigue in women

Uté Vollmer-Conna, Aslakson, D White

Pharmacogenomics, Apr 2006, Vol. 7, No. 3, Pages 355-364.

The validity of an empirical delineation of heterogeneity in chronic

unexplained fatigue

Aslakson, Uté Vollmer-Conna, D White

Pharmacogenomics, Apr 2006, Vol. 7, No. 3, Pages 365-373.

Gene expression profile of empirically delineated classes of

unexplained chronic fatigue

Liran Carmel, Sol Efroni, D White, Aslakson, Ute

Vollmer-Conna, Mangalathu S Rajeevan

Pharmacogenomics, Apr 2006, Vol. 7, No. 3, Pages 375-386.

Polymorphisms in genes regulating the HPA axis associated with

empirically delineated classes of unexplained chronic fatigue

K , D White, Aslakson, Ute Vollmer-Conna,

Mangalathu S Rajeevan

Pharmacogenomics, Apr 2006, Vol. 7, No. 3, Pages 387-394.

Gene expression correlates of unexplained fatigue

Toni Whistler, , R Cameron Craddock, Gordon Broderick,

Klimas, R Unger

Pharmacogenomics, Apr 2006, Vol. 7, No. 3, Pages 395-405.

Identifying illness parameters in fatiguing syndromes using classical

projection methods

Gordon Broderick, R Cameron Craddock, Toni Whistler, ,

Klimas, R Unger

Pharmacogenomics, Apr 2006, Vol. 7, No. 3, Pages 407-419.

Exploration of statistical dependence between illness parameters using

the entropy correlation coefficient

R Cameron Craddock, , Gordon Broderick, Toni Whistler,

Klimas, R Unger

Pharmacogenomics, Apr 2006, Vol. 7, No. 3, Pages 421-428.

Gene expression profile exploration of a large dataset on chronic

fatigue syndrome

Hong Fang, Qian Xie, Roumiana Boneva, Fostel, Perkins, Weida

Tong

Pharmacogenomics, Apr 2006, Vol. 7, No. 3, Pages 429-440.

Exploration of the gene expression correlates of chronic unexplained

fatigue using factor analysis

Fostel, Roumiana Boneva, Lloyd

Pharmacogenomics, Apr 2006, Vol. 7, No. 3, Pages 441-454.

Linear data mining the Wichita clinical matrix suggests sleep and

allostatic load involvement in chronic fatigue syndrome

M Gurbaxani, F , N Goertzel, M Maloney

Pharmacogenomics, Apr 2006, Vol. 7, No. 3, Pages 455-465.

Chronic fatigue syndrome and high allostatic load

M Maloney, M Gurbaxani, F , Lucio de Souza

Coelho, Cassio Pennachin, N Goertzel

Pharmacogenomics, Apr 2006, Vol. 7, No. 3, Pages 467-473.

Combinations of single nucleotide polymorphisms in neuroendocrine

effector and receptor genes predict chronic fatigue syndrome

N Goertzel, Cassio Pennachin, Lucio de Souza Coelho,

Gurbaxani, M Maloney, F

Pharmacogenomics, Apr 2006, Vol. 7, No. 3, Pages 475-483.

Allostatic load is associated with symptoms in chronic fatigue syndrome

patients

N Goertzel, Cassio Pennachin, Lucio de Souza Coelho,

M Maloney, F , Gurbaxani

Pharmacogenomics, Apr 2006, Vol. 7, No. 3, Pages 485-494.

Improved prediction of treatment response using microarrays and

existing biological knowledge

Simon M Lin, Jyothi Devakumar, Warren A Kibbe

Pharmacogenomics, Apr 2006, Vol. 7, No. 3, Pages 495-501.

Collaborative Study: chronic fatigue syndrome – Review

Interpreter of maladies: redescription mining applied to biomedical

data analysis

Waltman, Pearlman, Bud Mishra

Pharmacogenomics, Apr 2006, Vol. 7, No. 3, Pages 503-509.

Statistical challenges with gene expression studies

Shoemaker

Pharmacogenomics, Apr 2006, Vol. 7, No. 3, Pages 511-519.

Collaborative Study: chronic fatigue syndrome – Perspective

Clinical methodology and its implications for the study of therapeutic

interventions for chronic fatigue syndrome: a commentary

Mark A Demitrack

Pharmacogenomics, Apr 2006, Vol. 7, No. 3, Pages 521-528.

[Guest guest]

Excellent evaluation of the matter! These are the same concerns that came

to my mind, too. (Although I don't think I could have written it so

eloquently). Besides this aspect, one thing that set off an alarm in my mind

was all

the media outlets in which this story ran. Forbes, Washington Post, Med-which

ever. Whenever one sees a medical article in that many and those particular

outlets at the same time, there is usually a PR firm with an industry

friendly slant, somewhere in the equation. The message: Anything - but an

origin

that could be indicative of liability - is the cause of illness.

Sharon

In a message dated 4/21/2006 6:51:51 PM Pacific Standard Time,

quackadillian@... writes:

I think that plasma cortisol levels (i.e. stress) and genetics clearly

do have a role in the etiology of CFS. But environmental (fungal, for

example) toxins clearly do too, and I don't see anything in this story

that indicates that steps were taken to rule that factor out.

Perhaps thats the hidden side of this story. Otherwise, its another

case of 'blame the victim' where the implications of doing so mean

that a major environmental cause of illness could easily go

unaddressed for another decade or two, with an ugly potential that

millions of people (those who have proven to be 'genetically

succeptible' and their offspring/relatives) become marginalized in the

future due to inability to get insurance or employment. (

Important bit of context here:

Its my and many others opinion that genetic testing is - for reasons

of adverse selection - incompatible with private insurance in many

ways -

Insurers are already complaining about " asymmetrical information " and

pushing for laws that will give them access to all stored health

information that has genetic implications, with few protections. The

GOP-controlled Congress and Senate is itching to do so as well.

This will give rise to massive genetic discrimination in employment

and elsewhere.

[Guest guest]

I think that plasma cortisol levels (i.e. stress) and genetics clearly

do have a role in the etiology of CFS. But environmental (fungal, for

example) toxins clearly do too, and I don't see anything in this story

that indicates that steps were taken to rule that factor out.

Perhaps thats the hidden side of this story. Otherwise, its another

case of 'blame the victim' where the implications of doing so mean

that a major environmental cause of illness could easily go

unaddressed for another decade or two, with an ugly potential that

millions of people (those who have proven to be 'genetically

succeptible' and their offspring/relatives) become marginalized in the

future due to inability to get insurance or employment. (

Important bit of context here:

Its my and many others opinion that genetic testing is - for reasons

of adverse selection - incompatible with private insurance in many

ways -

Insurers are already complaining about " asymmetrical information " and

pushing for laws that will give them access to all stored health

information that has genetic implications, with few protections. The

GOP-controlled Congress and Senate is itching to do so as well.

This will give rise to massive genetic discrimination in employment

and elsewhere.

[Guest guest]

<quackadillian@...> wrote:

>

> I think that plasma cortisol levels (i.e. stress) and genetics

clearly do have a role in the etiology of CFS. But environmental

(fungal, for example) toxins clearly do too, and I don't see

anything in this story that indicates that steps were taken to rule

that factor out.

>

Perhaps thats the hidden side of this story. Otherwise, its another

case of 'blame the victim' where the implications of doing so mean

that a major environmental cause of illness could easily go

unaddressed for another decade or two, with an ugly potential that

millions of people (those who have proven to be 'genetically

succeptible' and their offspring/relatives) become marginalized in

the future due to inability to get insurance or employment. <

Yes. you are right, that is the hidden side of this story.

Despite my requests, no steps were taken to rule out fungal toxins.

You might consider reading the chapter in Mold Warriors that

addresses this:

" Mold at Ground Zero for CFS " .

-

[Guest guest]

On Sat, 22 Apr 2006 04:09:54 +0000, you wrote:

> I think that plasma cortisol levels (i.e. stress) and genetics

>clearly do have a role in the etiology of CFS.

> But environmental

>(fungal, for example) toxins clearly do too, and I don't see

>anything in this story that indicates that steps were taken to rule

>that factor out.

It's called bait and switch.

>>

> Perhaps thats the hidden side of this story. Otherwise, its another

>case of 'blame the victim' where the implications of doing so mean

>that a major environmental cause of illness could easily go

>unaddressed for another decade or two,

That is the plan.

[Guest guest]

Christ wrote:

> It's called bait and switch.

> > Perhaps thats the hidden side of this story. Otherwise, its

another case of 'blame the victim' where the implications of doing

so mean that a major environmental cause of illness could easily go

unaddressed for another decade or two,<<

> That is the plan.

>

To be fair, it should be noted that oblivious mold sufferers have

fought mold survivors trying to warn them about mold illness even

harder than oblivious doctors fought to stay oblivious of mold

illness.

In '98 I told Rick that my experience was an objective

confirmation of his paper: " Trichothecene Mycotoxicosis may be

indistinguishable from CFS " .

I was surprised when he had no interest in pursuing the matter.

But then he explained that he had approached various groups and had

been stomped on by sick people and CFS groups just as hard as from

medical professionals and he did not intend to waste any more effort

trying to help people who had literally thrown his incredibly

accurate information in the trash.

I told Rick that it wouldn't be so easy to dismiss my experience as

a CFS prototype and ampligen program participant who proved the

concept by literally walking out of a death sentence from doctors

and recovering to the point of mountain climbing through a strategy

of extreme mycotoxin avoidance.

As I told Rick, I thought that it would be virtually impossible for

anyone seriously interested in finding something that helps to be

disinterested, but the reality has been that people tell me that if

I recovered, my experience does not apply. If I say that I have

information about mold and the very origins of CFS as an Incline

Village CFS " original " then I'm an arrogant name dropper.

And if I say Dr Shoemaker has examined my genetics and concerted

strategy of avoidance, and found my story to be worthy of inclusion

in Mold Warriors, why then I'm a narcissistic self-glorifier with

delusions of grandeur for nothing other than the happenstance of

being selected as an example in Dr Shoemakers book.

When all the doctors and researchers rejected my story, I really

thought that they must have some incredibly criminal intent for

their inexplicable behavior. But the even MORE fierce rejection and

opposition from mold sufferers themselves has forced me to reach a

different conclusion.

Rick told me what I was in for, and he was exactly right! (again)

-

[Guest guest]

PLEASE could someone send me a copy of this paper:

" Trichothecene Mycotoxicosis may be indistinguishable from CFS "

And/or does anyone have contact information for the author?

Or any other resources on the effects of trichothecenes or other

stachybotrys toxins, or testing for them, or detecting trichothecenes

in homes - that they might be willing to send me.

(attachments are fine)

This is exactly the point I have been trying to make to somebody

important in my life right now.

Just because a space does not have much 'visible mold' at one point in

time, does NOT mean that it does not have mycotoxins, esp. when there

has been serious stachy in the building.

What about trichothecenes in house dust?

[Guest guest]

Murtaugh wrote:

>

> ,

That is unfortuate that sufferers/patients are fighting each other

and researchers. We have even seen it on this board.....people

fighting each other over what is true. The reality is, the scope of

this disease so immense that one person's symptoms could be totally

different from the next.

>

So true!

The scope and variability of this illness is so complex that dealing

with it requires an individualized strategy tailored to your own

personal requirements.

People not only have different symptoms from each other, they also

have different symptoms and levels of reactivity in themselves over

time- which dictates the need for the PIR so that people can

communicate a bit more effectively on " where they are in the illness " .

But it's counterproductive to say " we are all completely different

and you cannot project your experience upon others " when the fact is

that in some fundamental ways - we are very much the same.

We all have an extraordinary reactivity to mold.

We have to learn how to deal with it as best we can.

Staying away from mold is better than not.

If someone is steadily " losing it " due to exposure beyond their

tolerance - and all accessible therapies have failed to stop the

decline - a more concerted effort at avoidance is literally all they

have left to try.

When one is dealing with an exposure level that results in inexorable

decline, taking measures sooner gives people a better chance at

survival than waiting until they hit PIR 6.

I feel pretty safe in saying that this applies to everyone who is a

mold responder.

-

[Guest guest]

On Sat, 22 Apr 2006 20:49:58 +0000, you wrote:

> To be fair, it should be noted that oblivious mold sufferers have

>fought mold survivors trying to warn them about mold illness even

>harder than oblivious doctors fought to stay oblivious of mold

>illness.

>

I hear what your saying, an individual Dr has even more of a

disadvantage in that they believe the institutions they get their

information from are generally on the up and up.

But they are the institutions, without them their is no institution,

so you have to ask yourself are they not responsible for this

conspiracy to hide the truth about mold illness at least partially.

To hide the truth from the American people

From those who suffer so horribly

From those that will suffer

From those that stand to loose property

From those property and business owners that are the defendants in

law suites

From the insurers that have to bare the burden of the cost of

inadequate and unnecessary medical treatment

From the government that has to support these people that become so

disabled, UNESASARY DISABLED!

Clearly institutions with billions of dollars at their disposal can do

more than write the papers that do so much damage to us.

One of the most fundamental things you do in science when someone

makes a claim is you try to reproduce it. Clearly they haven't done

this or they would know that it is in fact reproducible.

If someone doesn't voice their complaints how are Dr's going to know

how to fix it?

If I don't object to the fraud going on how are Dr's going to know?

If they knew do you think they would stand for it?

If they can't rely on these institutions how can they do their jobs?

These institutions are nothing but tobacco lawyers for everyone

ironically but big tobacco.

Didn't you know tobacco companies kill and maim people?

Chemical, pesticide, depleted uranium and breast implant

manufactures never do this and their's no such thing as Toxic MOLD!