Wednesday, October 19, 2011

6 Medical Myths Even Your Doctor May Still Believe

Rituximab Clinical Trial Results

MAY BE REPOSTED

Chronic fatigue syndrome eased by cancer drug - health - 19 October 2011 - New Scientist >>

http://www.newscientist.com/article/dn21065-chronic-fatigue-syndrome-eased-by-cancer-drug.html

Techniques to Help with Physical Pain | Psychology Today

 
"I want to make it clear that I don't have a negative view of pain medication. I think it's misguided that so many people regard the taking of pain medication as a sign of weakness. We're told "no pain...no gain" or "push through the pain." I suspect that people who offer this type of advice have never suffered from chronic pain. Everyone has to find what's right for his or her body."
 
 
More words of wisdom from PWC Toni Bernhard
 
* * *
As Dr. Teicheira points out, we don't refer to a diabetic as an "insulin addict" so why do we criticize others who need prescription medication to function as "Vicodin addicts"?
 
I've tried all the self-help out there, and some days the only thing that makes a dent is Vicodin.  If it keeps me upright and working, it's necessary.

 

Tuesday, October 18, 2011

Dr. Peterson Talks

 
"he well remembered telling a well known researcher early on that some of his patients' TNF-a readings were as high as 50,000 and being told that was impossible because they would be dead."
 
"The Conspiracy Theory Tunnel - He believes it would be a huge mistake for the ME/CFS community to go down the conspiracy theory tunnel. Dr. Peterson has been involved in ME/CFS since Incline Village since the 1980s and he's very clear about all the problems ME/CFS has had getting recognition. Has an almost criminal lack of attention for ME/CFS been present? Yes. Do some researchers not believe the disease is real? For sure. Does bureaucratic inefficiency and inertia dog progress in ME/CFS? Absolutely. Has some cabal set out to undermine legitimate findings in the disorder? No way. He was emphatic that that was not true and that he felt there was no cheese down that tunnel for the ME/CFS community. The hyper-aggressive patients impugning researchers' integrity are, from his stance, only hurting the community and their own chances for help."

Monday, October 17, 2011

Medical Classification WHO ICD codes

There has of late been speculation that it would be bad for U.S. patients if CFS and M.E. were placed in the same category in the neurology chapter of ICD-10-CM, the "clinical manual" of ICD-10 that will be adopted for use in the United States.

But the fact of the matter is that in ICD-10, CFS already IS coded to G93.3, "PVFS and M.E." in the index, which is as authoritative as the tabular version. [PVFS stands for Post-Viral Fatigue Syndrome, and is not diagnosed very frequently any more - not at all in the U.S.]. It already IS coded in neurology.

110 nations use ICD-10 as-is, including the UK.  Australia has a clinical version that does not alter the codes for M.E. or CFS.  But Canada and Germany have clinical versions that place CFS in the tabular version of ICD-10, in G93.3 with M.E.  In fact, it was the Canadian clinical version, ICD-10-CA, which led to the highly regarded Canadian Consensus Criteria for ME/CFS  in 2003.

NOBODY EXCEPT THE UNITED STATES CODES CFS IN THE "R" CHAPTER.  If we coded CFS at R53.82, which was the plan of NCHS, we would have been the ONLY nation in the world to do so.

Furthermore, M.E. is not a known diagnosis in the U.S.  (WE know about it, but very few doctors do.)  There is no definition for it approved by CDC.  We can now point to the new definition that was published in the Journal of Internal Medicine, but that is more likely to enable researchers in the US and Canada to use M.E. if they want to, than to trickle down to U.S. clinicians.  Part of the problem is that when M.E. replaced atypical polio as a disease name in British commonwealth nations and Europe, in the U.S. the new name was epidemic neuromyesthenia, which has not (to my knowledge) been diagnosed in decades.

So if CFS gets coded as R53.82 in the U.S.'s ICD-10-CM, yes, M.E. will be less likely to confuse with CFS - but that would only be in the U.S., and in the U.S. we only get diagnosed with that revolting name CFS anyway.  At least we could get them scratching their heads and asking, "What is M.E.?" if both diseases were placed together where those of you outside the U.S. already have it. 

Given that U.S. doctors do not have a high opinion of CFS, keeping it under "R" in "vague signs and symptoms" would only reinforce their prejudice against it as a "garbage diagnosis" - something you diagnose when you run out of ideas.

Finally, there was an inadvertent error in an earlier Co-Cure message about getting CFS out of the "R" category.  The "R" category is not for psychiatric diagnoses. 

British psychiatrists use "fatigue syndrome," which is coded at F48.0 under neuroses at "neurasthenia.". Then when they write about it, they mix and match terms so it looks as if CFS is the same thing, and therefore it goes in F48.0.  That is a serious problem in the UK.  [I have to admit to being alarmed recently when a U.S. virologist connected CFS not to the history of post-polio syndrome, which is pretty well established, but to the arcane nineteenth century diagnosis of neurasthenia.  Please don't do that!]

We are not (I hope) in current danger of being coded under neuroses at F48.0, neurasthenia, in the U.S.  But the "R" diagnosis is sufficiently vague that it wouldn't be difficult to use it to claim CFS patients really have CSSD (Complex Somatic Symptom Disorder), the category British psychiatrist and CBT advocate Michael Sharpe is trying to shoehorn into DSM-5, the new version of the American Psychiatric Association's huge diagnostic tome.  So it does leave us vulnerable.

To those outside the US I would say, look to ICD-11.  That's what will affect you the most.  To those in the US (where we are finally getting around to adopting ICD-10-CM two decades after ICD-10 was written), what WE need is simply to get in step with the rest of the world now. 

Mary M. Schweitzer

CFSAC November 8-9, 2011

http://www.hhs.gov/advcomcfs/index.html



The next CFSAC meeting will be held on November 8, 2011 from 9 a.m. to 5 p.m. and November 9, 2011 from 9 a.m. to 4:30 p.m. at the Holiday Inn Capitol, Columbia Room, 550 C Street, S.W., Washington, D.C. 20024.  Hotel phone number:  202-479-4000.

The Federal Register Notice has not yet been issued, or an agenda.


The Minutes, Recommendations, Presentations, Meeting Materials, Testimonies and videocast of the Spring CFSAC Meeting held on May 10-11, 2011 are available at this URL:

http://www.hhs.gov/advcomcfs/meetings/index.html



Suzy Chapman
_____________________

me.agenda@virgin.net
http://dsm5watch.wordpress.com
http://meagenda.wordpress.com
http://www.facebook.com/MEagenda
http://twitter.com/MEagenda

Dr. Myhill on CoQ10

Note: Any supplement should be taken under the supervision of your
physician as interactions between foods, supplements and other
medications are all possible. Be careful about supplementing without
first testing to make sure there is actually a deficit. Dr. David Bell
has also written about mitochondrial dysfunction in ME and CFS
patients.

Dr. Sarah Myhill on Coenzyme Q10 in Chronic Fatigue Syndrome (ME/CFS)
ProHealth.com
by Sarah Myhill, MD


Dr. Sarah Myhill is a UK-based physician and clinical nutritionist
with a special interest in the treatment of fatigue and ME/CFS.
Pioneering research led by Dr. Myhill suggests that the cells' energy
generating mitochondria are dysfunctional in ME/CFS patients. The
phenomenon was measured directly by Acumen Lab in the UK, and the
report ("Chronic Fatigue Syndrome and Mitochondrial Dysfunction,"
http://www.ijcem.com/files/IJCEM812001.pdf) by Dr. Myhill, Dr. John
McLaren-Howard, and Dr. Norman Booth, was published in January 2009 by
the International Journal of Clinical and Experimental Medicine

_______________

Chronic fatigue syndrome is a symptom of mitochondrial failure,
resulting in poor production of ATP (adenosine triphosphate), which is
the currency of energy in the body.

To produce ATP, mitochondria need certain essential raw materials,
namely Coenzyme Q10 (CoQ10), D-ribose, L-carnitine, magnesium and
vitamin B-3.

In a normal healthy person, CoQ10 can be synthesized, but it requires
the amino acid tyrosine, at least eight vitamins, and several trace
elements. The vitamins include folic acid, vitamin C, B-12, B-6 and
B-5.

Synthesis of CoQ10 is inhibited by environmental toxins and chronic disease.

I am coming to the view that many of my CFS patients are metabolically
"dyslexic" - that is to say, even when all the raw materials are
available, they cannot make their own CoQ10 in sufficient amounts, and
therefore levels need to be measured and supplemented.

Indeed a recent study showed a close correlation between levels of
CoQ10 and severity of CFS. ("Coenzyme Q10 Deficiency in ME/CFS" by
Michael Maes, et al.
http://www.prohealth.com/library/showarticle.cfm?libid=15057)

Blood Levels of Coenzyme Q10

Certainly when I check blood levels, it is very common to find very
low levels of CoQ10. CoQ10 is the most important antioxidant in the
mitochondria, and since it is the rate at which mitochondria fail that
determines the normal ageing process, it may well be that CoQ10 is a
vital anti-ageing molecule!

I also see CoQ10 as an acquired metabolic dyslexia with age - as we
age we get less good at making certain key molecules, and CoQ10 is
one.

The normal range in blood given by Biolab Medical Unit
(www.biolab.co.uk) is 0.55 - 2.0 mmol/L (millimoles per liter). This
is equivalent to 0.637 - 2.3 ug/ml (micrograms per milliliter).
However, Coenzyme Q10 has been widely used in the treatment of heart
failure, which we now know is what happens in patients with severe
chronic fatigue syndrome.

There have been a great many studies done looking at Coenzyme Q10
levels in heart disease, and although the optimal dose of CoQ10 is not
known for every pathological situation, most researchers now agree
that blood levels of 2.5 ug/ml and preferably 3.5 ug/ml are required
to have a positive impact on severely diseased hearts.

Clearly not all patients I see with chronic fatigue syndrome have
severely diseased hearts, but my view is that we should be aiming for
a level above the Biolab Unit's 2.00 mmol/L.

How Much CoQ10 to Take

The question is, how much CoQ10 should be given to supplement levels?
Again, the dose of CoQ10 in order to achieve a response has been
worked out for cardiac patients and this varies from 200 mg to 600 mg
daily.

It is important that a hydro [water]-soluble form of Coenzyme Q10 be
used in order to ensure good absorption.

The absorption of CoQ10 can be improved if it is taken with a fatty or
oily meal. Or you could empty a capsule into a teaspoon of olive oil
before swallowing the lot.

(In the UK, it is possible for CoQ10 to be prescribed on National
Health Service Prescription. CoQ10 is not in the British National
Formulary, but it has not been blacklisted in capsule form, so can be
prescribed if your GP is willing to help.)

I am estimating that the following doses of CoQ10 will be required:

CoQ10 Blood levels 1.5 - 2.0 umol/l
100 mg CoQ10

CoQ10 Blood levels 1.0 - 1.5 umol/l
200 mg CoQ10 (split the dose: 100 mg twice a day)

CoQ10 Blood levels 0.5 - 1.0 umol/l
300 mg CoQ10 (split the dose: 100 mg 3 times a day)

CoQ10 Blood levels less than 0.5 umol/l
400 mg CoQ10 (split the dose: 200 mg am, 100 mg lunch, 100 mg evening)

Once a therapeutic effect has been achieved, then it should be
possible to reduce the dose to a lower maintenance dose, but a blood
test may be required to re-check that levels are adequate.

CoQ10 can be expected to work best in conjunction with:

• Magnesium,

• D-ribose,

• Acetyl L-carnitine (also available through eating red meat,
especially mutton, lamb, beef and pork - but to get 2 grams you need
to eat about a pound of meat a day!)

• And NAD (the conenzyme nicotinamide adenine dinucleotide). Levels
can be measured, but most people need 500 mg of NAD daily.

It may take up to 30 days to get blood levels up to a good level and
therefore start to see clinical response. Most studies of use of CoQ10
in heart disease assess patients at three months. I would also expect
to see improvements in heart related symptoms such as chest pain,
dysrhythmias, exercise tolerance, shortness of breath and mitral valve
disease.

There are virtually no side effects.

- Sarah Myhill, MD


[For more information on CoQ10 see "Coenzyme Q10 - The Energy Maker,"
by Karen Lee Richards.]

__

* This article is reproduced with kind permission from Dr. Sarah
Myhill's educational website (DrMyhill.co.uk)® Sarah Myhill Limited,
Registered in England and Wales: Reg. No. 4545198.

Living with ME/CFS

http://www.bmj.com/content/342/bmj.d3836.extract

BMJ 2011; 342:d3836 doi: 10.1136/bmj.d3836 (Published 22 June 2011)
Cite this as: BMJ 2011; 342:d3836

Commentary: Living with CFS/ME
Ollie Cornes

During my career I have co-written several books on computer software,
worked as a software engineer, and set up and sold two small
technology businesses. But in April 1999 I developed tonsillitis with
its usual malaise and fatigue. I naturally assumed I would be back to
health fairly quickly, but, although the tonsillitis cleared, the
malaise and low energy levels persisted. I felt like I was running on
fumes. I had no idea why. Then my health deteriorated further.

Months passed, then a year, and now 12 years. I have occasional
periods when I'm bed bound, and I am often house bound. I'm always
exhausted. I often move around at home like a frail, unstable, elderly
man—at the age of 38. It's certainly made worse by my not knowing what
is causing it.

My general practitioner, and many books, suggested the illness was in
some way psychosomatic ("yuppie flu," not a proper illness). I knew in
myself this wasn't true, but there was a nagging doubt. Maybe they're
right? Am I making this up? Am I really sick?

To ensure the illness was not psychological, I worked extensively with
a psychotherapist. Rather than finding evidence of emotional issues that could cause my symptoms, the therapy suggested the opposite—that, given how sick I am, I have surprisingly good mental health. It delivered no improvement in my health. In fact the only things I have
found that help are to get lots of sleep; to eat a simple diet of
fish, vegetables, and pulses; and to almost entirely avoid meat and
junk food.

Imagine having the flu, being severely jetlagged, and having not slept
for two days but without the sinus and lung congestion—that's the
closest I've found to a description of what this illness is like, but
it understates it. Sickness has become the new normal for me—my "I'm fine, thanks" is probably the same as your "I feel like death, I need to go back to bed."

On a scale of 1-10, my energy levels typically range from three to
five. Since becoming ill I lack mental clarity; I mix up words, and I
have memory problems and trouble focusing. I have an enormous need for
sleep, which never refreshes. There is an overwhelming, permanent, and
intense malaise. Pushing my limits—for example, with aerobic
exercise—provokes a severe worsening.

But I'm actually one of the lucky ones; many are far sicker than me
and largely invisible. Doctors will usually see patients with chronic
fatigue syndrome/myalgic encephalomyelitis (CFS/ME) only on a "good"
day. Nancy Klimas treats both HIV/AIDS and CFS/ME patients at the
University of Miami. In 2009 she told the New York Times, "I split my
clinical time between the two illnesses, and I can tell you if I had
to choose between the two illnesses . . . I would rather have HIV."1

The Canadian consensus case definition criteria for CFS/ME clearly
distinguish it from the UK's broad, wastebasket CFS diagnosis. The
Canadian definition requires the classic symptom of CFS/ME: delayed,
post-exertional malaise and fatigue. Even Peter White, who led the
largest UK CFS study to date, said recently: "The PACE trial paper
refers to chronic fatigue syndrome (CFS) which is operationally
defined; it does not purport to be studying CFS/ME." I believe CFS/ME
is a specific, identifiable disease subset of the UK CFS definition.

Harvey Alter, of the National Institutes of Health, recently said,
"I'm absolutely convinced that when you define this disease by proper
criteria, this is a very serious and significant medical disease, and
not a psychological disease. It has the characteristics of a viral
disease."2

I'm not aware of any treatments offered by the NHS to patients like
me, only illness management (pacing, cognitive behavioural therapy,
and so forth). My view is that because the UK has used such a loose
illness definition we have ended up in this appalling situation where
the term CFS is used to group together people with severe depression
(or other emotional difficulty) with a group of patients who to the
untrained eye look pretty much the same but who have what seems to be
a distinct physical illness, particularly characterised by
post-exertional malaise. I have enormous sympathy with general
practitioners faced with patients who say, "I'm tired all the time. I
just can't get out of bed." How do they tell the difference? I'd like
to see the UK adopt the Canadian definition to encourage research and
new clinical approaches with what we may find is a treatable viral or
immune dysfunction condition.

Notes
Cite this as: BMJ 2011;342:d3836

Competing interests: The author has completed the ICJME unified
disclosure form at www.icmje.org/coi_disclosure.pdf (available on
request from the corresponding author) and declares no support from
any organisation for the submitted work; no financial relationships
with any organisation that might have an interest in the submitted
work in the previous three years; and no other relationships or
activities that could appear to have influenced the submitted work.

Provenance and peer review: Commissioned; not externally peer reviewed.

References
1.Readers ask: a virus linked to chronic fatigue syndrome. New York
Times 2009 Oct 15.
http://consults.blogs.nytimes.com/2009/10/15/readers-ask-a-virus-linked-to-chronic-fatigue-syndrome/.
2.Alter HJ. Blood products advisory committee meeting transcript, 14
December 2010. www.investinme.org/InfoCentre%20Topics%20Dr%20Harvey%20Alter%20BPACM.htm.

Symptom Questionnaire

ME is such a complex disease; it can very difficult indeed , especially with
brain fog and cognitive dysfunction, separating out and listing  the many
symptoms that someone might have. Based upon the Canadian Criteria and our
own long  experience, we have constructed a simple  tool, which we hope
will greatly help people with ME to identify and easily list their
symptoms.

A comprehensive ME symptom list is presented, on the left. If the person
ticks any symptoms that apply to them , the  ME Symptom Tool will generate
an individualized symptom list, on the right.

If the person has any extra symptoms, not listed, they can easily add them
to  their list,before printing.

We have tried to make the tool as easy to use and as "ME - friendly " as
possible. This is only a first version; we would greatly appreciate any
feedback, comments or suggestions for  future  development.

The ME Symptom Tool can be found here :

http://www.stonebird.co.uk/mesymptomquestionnaire.html

--
Greg Crowhurst
www.stonebird.co.uk
(The Lived Experience of Severe ME)

Immunological Abnormalities in CFS

http://www.translational-medicine.com/content/9/1/81
fulltext- http://www.translational-medicine.com/content/pdf/1479-5876-9-81.pdf

Immunological abnormalities as potential biomarkers in Chronic Fatigue
Syndrome/ Myalgic Encephalomyelitis
Ekua W Brenu , Mieke L van Driel , Don R Staines , Kevin J Ashton ,
Sandra B Ramos , James Keane , Nancy G Klimas  and Sonya M
Marshall-Gradisnik
Journal of Translational Medicine 2011, 9:81doi:10.1186/1479-5876-9-81


Published: 28 May 2011

Abstract (provisional)

Background
Chronic Fatigue Syndrome/Myalgic Encephalomyelitis (CFS/ME) is
characterized by severe prolonged fatigue, and decreases in cognition
and other physiological functions, resulting in severe loss of quality
of life, difficult clinical management and high costs to the health
care system. To date there is no proven pathomechanism to
satisfactorily explain this disorder. Studies have identified
abnormalities in immune function but these data are inconsistent. We
investigated the profile of markers of immune function (including
novel markers) in CFS/ME patients.

Methods
We included 95 CFS/ME patients and 50 healthy controls. All
participants were assessed on natural killer (NK) and CD8+T cell
cytotoxic activities, Th1 and Th2 cytokine profile of CD4+T cells,
expression of vasoactive intestinal peptide receptor 2 (VPACR2),
levels of NK phenotypes (CD56bright and CD56dim) and regulatory T
cells expressing FoxP3 transcription factor.

Results
Compared to healthy individuals, CFS/ME patients displayed significant
increases in IL-10, IFN-gamma, TNF-alpha, CD4+CD25+ T cells, FoxP3 and
VPACR2 expression. Cytotoxic activity of NK and CD8+T cells and NK
phenotypes, in particular the CD56bright NK cells were significantly
decreased in CFS/ME patients. Additionally granzyme A and granzyme K
expression were reduced while expression levels of perforin were
significantly increased in the CFS/ME population relative to the
control population. These data suggest significant dysregulation of
the immune system in CFS/ME patients.

Conclusions
Our study found immunological abnormalities which may serve as
biomarkers in CFS/ME patients with potential for an application as a
diagnostic tool.

CoQ10 for CFS

A Note of Caution: Always consult with a physician before taking any
kind of supplement or medication. Not only can chemical compounds
cause reactions when taken alone, some side effects may occur in
combination with other chemical compounds including dietary
supplements. Pregnenolone is an over the counter hormone pill
considered a Dietary Supplement. It is thought to be a building block
for all other steroid hormones. The cells in the central nervous
system and adrenal gland produce pregnenolone. Generally there is a
significantly higher concentration of the hormone in the tissue of the
central nervous system than in the bloodstream. Production decreases
with age.

Pregnenolone supplements are synthetically made using substances found
in soybeans and wild yam. They can typically be purchased in capsule
form at health food stores and pharmacies. Like any chemical compound
whether "natural" supplement or synthetic supplement or drug, some
people may experience side effects including over-stimulation and
insomnia - areas where patients already have issues.  Anger, anxiety
and irritability have also been reported when higher amounts were
taken. Headaches might also occur with higher doses. Because
pregnenolone can convert into androgens, there is a possibility that
acne might occur. Scalp hair loss can also occur if the hormone is
used daily for a prolonged amount of time. Pregnenolone has also been
known to cause irregular heart rhythms, even with low doses.


Treating CFS, fibromyalgia with statins, coenzyme Q10 and pregnenolone
Published on May 26, 2011 by Jacob Teitelbaum, MD in Complementary Medicine

An Important Cautionary Note

I usually prefer to have broader research and more direct clinical and
personal experience exploring new treatment theories before I start
reporting on them (which would take 1-2 years). I have chosen instead
to put the theory out there to invite discussion. Bringing many expert
perspectives to bear will help it get tempered closer to the truth
more quickly. Much of what I discuss below is new, controversial and
hypothetical, and should be discussed with your holistic practitioner
or CFS specialist before attempting a trial of the statin
prescriptions.

Background

Many infections have been implicated in CFS, including the recent
reporting of XMRV. As part of their reproductive cycle, many viruses
require cholesterol-related molecules for many different functions,
including making their protective coat. As part of your body's
defensive functioning, your cells make an important family of immune
molecules called interferon, which seems to work in part by decreasing
the cholesterol production pathway and starving the virus.

Interferon levels (there are 27 different types) can be both high or
low in CFS. In CFS patients, interferon alpha tends to be low while
interferon beta is elevated. Interestingly, interferon injections can
trigger symptoms that feel like CFS. Paradoxically, in a small subset
of CFS patients interferon treatment helped (though not a lot).3-4

So what to do? You might be able to "eat your cake, and have it too"
by starving the virus while giving your body the natural support it
needs. This new research opens possible ways to suppress the many
viral infections in CFS, even retroviruses such as XMRV!

Found - A Key Missing Piece of the CFS Puzzle!

Although the energy crisis and associated hypothalamic dysfunction,
along with direct gland failure (e.g., low thyroid adrenal exhaustion)
explained most of the abnormalities we see in CFS and fibromyalgia,
there have been a few missing pieces over the years that were not
explained by these - which frankly left us puzzled. Here are a couple
items I've scratched my head over in CFS:

Very low cholesterol levels are often seen in CFS (sometimes high
levels are seen, but these are usually due to low thyroid function).
Dramatically low levels of a hormone called pregnenolone (made from
cholesterol, pregnenolone is the critical building block for steroid
hormones such as estrogen and testosterone).

This new study now explains why cholesterol and pregnenolone are
sometimes very low in CFS. Viral infections cause your body to make
interferon, which suppresses the mevalonic acid pathway that makes
cholesterol and pregnenolone.

This is likely another key reason - along with the hypothalamic
dysfunction, gland dysfunction and receptor resistance - for the
widespread hormonal disorders we see in CFS/FMS.

This finding is significant in that it not only suggests that low
cholesterol or pregnenolone in CFS may be caused by a viral infection,
it also suggests new possible treatments!

Key Points

This work uncovers a potential novel cause of CFS involving the
process your body uses to make cholesterol.  Here are the key points
to this:

The production of cholesterol, coenzyme Q10 (CoQ10, a key energy
metabolite), and other key hormones relies on your body's mevalonate
pathway. The new research suggests that viral infections "hijack" this
pathway to make their protective outer coats. In response, your body
makes interferon, which suppresses the mevalonate pathway, which in
turn suppresses the virus.
Acute infections respond well to this, as the interferon production is
helpful short term.  But long term, this can lead to starving your
body of CoQ10 and key hormones.  This appears to be part of what
happens in CFS.
Cholesterol blockers mildly block the same pathway and can actually
have a mild antiviral effect at low dose (and a strong effect at high
dose). These medications are used long term to treat high cholesterol.
But this may starve the body of CoQ10 and pregnenolone and can,
therefore, flare CFS/FMS. So I recommend against statins unless you
also give the body the CoQ10 and pregnenolone it is being starved of
at the same time.

Implications for Diagnosis

The presence of a low or low-normal pregnenolone level in someone not
taking statins suggests your body is making elevated levels of
interferon to fight a chronic viral infection, which also uggests a
high risk of inadequate hormone production and CoQ10 deficiency. Low
cholesterol levels may suggest the same thing.

Implication for Treatments

Have the pregnenolone and cholesterol blood tests performed. If either
is low or low normal, add CoQ10 and pregnenolone supplementation to
your diet.  Also add an Omega 3 fish oil to help give your cell walls
what they need while your body is blocking cholesterol production.

I also suspect the low pregnenolone is a marker for a viral infection.
Though it does not identify which infection, it does offer a
potentially powerful new way to stop the virus from growing. It might
not kill them, but it will make it hard for them to reproduce.

So here is an overall treatment regimen to consider - especially if
your CFS began with flu-like symptoms and has not improved adequately
with other treatments:

Take zinc 25 mg a day for 3 months, then 15 mg daily from then on, as
chronic infections will routinely cause zinc deficiency and immune
dysfunction.
For 4-6 weeks, also take the pregnenolone, CoQ10 and fish oil as
described above. Continue these for at least 3 months after taking the
medication described below. These by themselves may leave you feeling
a lot better at 6 weeks.
Here is the more experimental part that you will need to discuss with
your physician Your physician may consider adding a statin medication.
Take 20 mg a day for 2-4 weeks (to make sure it does not cause side
effects - it usually will not, but if it does, stop it), then 40 mg a
day for 3-4 weeks. If you feel OK on the medication, they can raise
the dose to 80 mg a day. Continue for 3-4 months more and check or
recheck your lab numbers.  If this is not helping after 4-5 months,
stop taking the statin - statins can cause liver and muscle
inflammation. This is unusual, but it is why the testing is important.

Which Viruses Have Been Shown to Be Suppressed by Statins?

Many different families of viruses, suggesting a broad antiviral
effect. These include:

Epstein Barr Virus (inhibits its triggering lymphoma)6
West Nile Virus7 - An RNA Virus
Rotavirus - In this FDA "test tube" study, the authors noted an
approximately 99% drop in some viral tests, and a bunch of deformed
inactive viruses8
Polio9
Hepatitis C - but effects were mixed10-12
HIV 1 (a cousin to the AIDS and XMRV viruses)13
RSV - Respiratory syncytial virus14
And perhaps even the flu virus15

Does This Mean I Need to Avoid Cholesterol in Food?

No. The studies I've seen suggest that the branch of the chemical
pathway that needs to be blocked for the antiviral effects occur
before the cholesterol step, and adding cholesterol did not impact the
statins antiviral activity. In fact, adding an egg or two a day (a
good cholesterol source along with other nutrients) may be helpful to
protect your cell membrane production.

Still to Be Answered

A lot. For example, with this theory if cholesterol levels are high,
pregnenolone should not be low. But in real life, we often see a
mismatch. So there are other pathways and issues going on here, and
this is reflected in the studies referenced below. In addition, there
are many members of the interferon family, and some are low while
others are high in CFS. Also, dozens of other immune chemicals may be
altered in CFS - though interferon may be a key "conductor of the
cytokine orchestra," and the theory I am discussing today is meant to
be an oversimplification. In addition, normal pregnenolone and
cholesterol do not mean there is no virus or that the treatment above
won't help. But low levels are suggestive of a viral issue.

But we do know CoQ10 helps. We know pregnenolone is often low (and is
very important). And we know that statins show antiviral effects in
many studies. So we have a really good start!

http://www.psychologytoday.com/blog/complementary-medicine/201105/exciting-new-discovery-in-treating-cfs-fibromyalgia?page=2

Chronic Fatigue Syndrome: A Salute To 10 Kinds of Heroes By Jody Smith HERWrite

Chronic Fatigue Syndrome: A Salute To 10 Kinds of Heroes

By Jody Smith HERWriter
April 26, 2011 - 8:49am

I don't think many people with Chronic Fatigue Syndrome see themselves
as heroes. Or, maybe they do but they don't expect anyone else to see
them in that light.

The limitations we face are so enormous that it can take everything
we've got to accomplish very little at times. It goes against our
grain, but we have to lower the bar for even small every day
activities.

But the people with CFS who accomplish things, and those whose
accomplishment is to just manage to keep breathing ... those who
overcome their bonds, and those who must learn to rest within them are
all heroes. Trying to move a rock that is too big, with energy that is
too small and very often with next to no help from ... well, from
anyone.

I have referred to our community in the past as a CFS Ghetto. But we
are also a clan. Here's to the heroes of Clan CFS. My hat is off to
every one of you.

1. To the heroes who manage to get up and go to work, then collapse
when they get back home.
They use up all their precious teaspoons of energy to earn a living.
Because they can work, people don't see them as ill. There's nothing
left of them by the time the workday is over but there's no other way
to pay the bills. And these are the lucky ones, who live a half-life.

2. To the heroes who stay home and raise their kids, from their beds
and couches.
If they are lucky they have pensions or they have healthy spouses who
shoulder the financial load. But their energy tank is always on E for
empty as they give their tiny all to care for their families.

3. To the heroes who write about CFS in blogs, articles and websites.
This takes a lot of energy. And it requires the mental clarity that is
so precious and rare in CFS. To protect this mental clarity, the rest
of their time is spent regenerating, working up just a little more of
that ability to get the word out that we exist.

4. To the heroes who must live cocooned away from the world.
Many people with CFS can't work, can't write, maybe can't read ...
can't function as normal people think of functioning.
Their accomplishments might be making breakfast and maybe getting
dressed. If they're lucky they can sit or recline near a window, their
only connection to the rest of the world.

5. To the heroes who petition for pensions.
People who are this sick should be on a disability pension. Many of us
aren't. We can't prove we're sick or we are too sick to make the
petitions and appeals. That minority who can speak up and make headway
in this arena are performing a service for all of us.

6. To the heroes who don't.
Getting by on next to no money when you are too sick to work or are
without a pension is a horrifying experience. It is however an
experience that is the daily reality for far too many of us. Much
harder than being able to work. Many end up homeless.

7.To the heroes who can't get out of bed. Can't hold their heads up.
Can't speak.
This is a special and unique kind of hell. This creates a kind of
isolation that's like being the living dead.

8. To the heroes who have been sick now for decades, heading into old age.
Many of us can look back on ten, twenty, thirty years of illness. The
hope for a better future dies hard when you're sixty and haven't been
well since early adulthood.

9. To the heroes who got sick so young they've never had a job, never
had a driver's license, never fallen in love.
These hurt my heart the most, I think. The old can treasure memories,
as they reflect back on healthier times. The young ones haven't had
the chance to form these memories. The future is uncertain at best.

10. To the doctors, scientists and researchers and journalists who are
determined to help us.
Chronic Fatigue Syndrome is not a popular disease. We don't have huge
sums of money or support for research. We don't make the evening news,
we don't have celebrity spokespersons or fund-raisers. The people who
want to find answers for us are few, but they are precious to us. They
are our lifeline. Many thanks.

http://www.empowher.com/chronic-fatigue-syndrome/content/chronic-fatigue-syndrome-salute-10-kinds-heroes?page=0,0

Results of Blood Working Group Study

http://www.research1st.com/2011/10/14/xmrv-updates/

The CFIDS Association of America hosted a webinar on Oct. 14, 2011 to
provide information about the Phase III results of the multicenter
study of XMRV known as the Blood XMRV Scientific Research Working
Group (SRWG) study.

Title:
Results of the Blood XMRV Scientific Research Working Group Study

Speakers:
Graham Simmons, PhD of Blood Systems Research Institute
Michael Busch, MD, PhD of Blood Systems Research Institute
Steven Kleinman, BSc, MD of University of British Columbia

Link to slides: http://www.cfids.org/xmrv/srwg-webinar-oct2011.pdf
Link to webinar recording:
http://www.youtube.com/watch?v=ayUUIT85KZQ&feature=channel_video_title


From the webinar:
Answers to 10 Common Criticisms of the SRWG study
by Graham Simmons, PhD

1. All of the controls were not screened by all of the labs.

Response: Controls were screened by at least five labs: WPI, National
Cancer Insitute/NCI-Ruscetti, Food and Drug Administration/FDA-Lo,
Centers for Disease Control & Prevention (CDC) and NCI/Drug Resistance
Program (DRP).

2. Control peripheral blood mononuclear cells (PBMCs) were not
screened prior to blinding, so could not have been ruled as negative.

Response: Three out of the 15 did have their PBMCs extensively
screened prior to blinding, yet two of these were still called
"positive" in various assays by the WPI and NCI/Ruscetti in the study.

3. No cryopreservative was used for the storage of the PBMCs, which
would prevent the WPI's assay from working. No Trizol was used.

Response: Due to the short-term nature of the study it was not felt
that preservatives were required for PBMC cryopreservation. The
Lo/Alter study detected sequences in PBMCs stored for 15 years in the
absence of preservatives. Trizol is for the extraction of nucleic acid
and laboratories were given the option of choosing their own
extraction methods

4. The length of time allotted for the serology and culture assays was
massively reduced, so that the WPI or NCI/Ruscetti assays were not
performed as desired.

Response: All the laboratories were allowed as much time as required
to perform their desired assays. The culture and serological assays
were performed by WPI and NCI/Ruscetti to their own specifications.

5. The WPI was not given the opportunity to complete virus culture assays.

Response: The WPI encountered mycoplasma contamination of their target
cell population, and used the plasma samples without results. This was
very unfortunate. There were no further stocks left to perform repeat
cultures with. It was deemed by both the WPI and the working group
that performing the studies on freeze/thawed material would be
invalid.

6. Samples and collection tubes were handled in the same laboratory as
22Rv1 cells used to spike the analytical controls.

Response: As stated in the paper, 22Rv1 cells were handled in a
separate facility to where all other activities were performed. The
fact that only one laboratory detected PCR and virus culture in
clinical samples supports the fact that 22Rv1 contamination did not
occur at the central laboratory.

7. Patients were on additional therapies that would produce false negatives.

Response: Lo/Alter patients were not on any additional treatments. It
is unclear what additional treatments patients were on at the time of
Lombardi et al. There is no published evidence that additional
treatments would have positive or negative effects.

8. FDA/Lo used the wrong assay from Lo et al. and instead used the one
that could not detect positives.

Response: Lo et al. used their own criteria to decide on which
assay(s) to use, but it is clear that both primer sets in their paper
are equally capable of amplifying diverse polytropic murine leukemia
viruses (MLVs), so it is not obvious that one would be better that the
other at detecting "positives."

9. The NCI did no PCR and could not use their clinically validated
serology and culture assays.

Response: NCI felt that they were not sufficiently experienced at PCR
to participate in the study. They did perform their serology and
culture assays – just as performed in Lombardi et al.

10. All the SRWG labs optimized their assays to VP62. VP62 does not
exist in nature and Lombardi et al. is now known to have discovered
HGRVs. Does your study include HGRVs? Or how do HGRVs relate to XMRV?

Response: As demonstrated in an earlier slide, although this study was
initiated after Lombardi et al. as a study of XMRV, as soon as Lo et
al. was published the mission of the study was broadened to include
all MLV-like viruses. Thus, almost all of the assays were designed to
perform against MLVs in general and were optimized and tested as such.
As our study has demonstrated there is no such thing as an
independently validated clinically positive sample against which to
test. Currently there is no such thing as human gammaretroviruses
(HGRV). No published virus has been isolated, cloned or sequenced from
a human.

Ottawa meeting recap

http://www.scribd.com/doc/66923259/Science-2011-Cohen-1810

The Waning Conflict Over XMRV And Chronic Fatigue Syndrome

OTTAWA, CANADA—Less than a day after a new study dealt what many
consider a lethal blow to the controversial theory that a newly
detected virus, XMRV, is linked to chronic fatigue syndrome (CFS),
proponents and skeptics of the theory squared off in a meeting here.

In one corner was Judy Mikovits, research director at the Whittemore
Peterson Institute for Neuro-Immune Disease (WPI) in Reno, Nevada, and
the main champion of the idea that XMRV and its relatives play a role
inCFS. Her opponent, an erstwhile supporter,was heavyweight
retrovirologist John Coffin of the Tufts University Sackler School of
Graduate Biomedical Sciences in Boston. When Mikovits and Coffin took
the stage at the meeting, which was organized by IACFS/ME (an
international association devoted to the disease)and attracted 460
researchers and patients, they sat on opposite sides of the lectern.
During their introductions, Coffin clasped his hands in front of his
mouth, looking like a man in prayer who wished this would all stop.
Neither addressed the other by name, and they avoided eye contact.

The controversy began shortly after Mikovits and colleagues published
a paper (http://scim.ag/mikovits) 8 October 2009 in Science that made
the startling link between XMRV, a mouse retrovirus, and CFS (23
September, p. 1694). But the finding, heralded by many patients as the
long-sought cause of their baffling disease, soon met a barrage of
criticism as lab after lab failed to replicate it.

The new study published by Science (http://scim.ag/xmrv-cfs) on 22
September and presented at the conference for the first time
convincingly showed that not one of nine labs, including WPI, could
reliably find XMRV or its close relatives known as murine leukemia
viruses (MLVs) in people who previously had tested positive for them.

Both Mikovits and Coffin were among the co-authors of the paper by the
so-called Blood Working Group. At the same time, Science also ran a
partial retraction (http://scim.ag/R-H-S) of the October 2009 paper
after one of WPI's collaborators discovered that a contaminant—as many
critics had asserted—explained the XMRV DNA it found in some patient
samples.

In Ottawa, Mikovits came out swinging. But she didn't make the case
for XMRV, which stands for xenotropic murine leukemiavirus–related
virus. Instead, she offered new evidence that people with CFS (known
as myalgic encephalomyelitis in some countries) had a virus "highly
related" to XMRV.

Unlike the original study that appeared in Science that showed entire
sequences of XMRV and infection of fresh cells, Mikovits revealed only
partial viral sequences that she said were from the XMRV and MLV
family known as gammaretroviruses. She said her team, which includes
Francis Ruscetti of the U.S. National Cancer Institute in Frederick,
Maryland, also had preliminary data that suggest these
gammaretroviruses may travel through the air. "That's pretty scary,"
she said.

Coffin began by stressing that he initially thought the XMRV-CFS theory
"was a wonderful hypothesis." But it rested on three legs of a stool.
After removing blood from CFS patients, Mikovits and co-workers had
used the polymerase chain reaction to pluck out DNA from the virus and
sequence it, found antibodies to XMRV, and shown that the isolated
virus could infect cells in lab experiments. All the legs have now
been kicked out for both XMRV and MLVs, he said. "To claim that
there's more than one XMRV, you're going to have to show a virus that
has a sequence that's different from XMRV," he said.

Mikovits's presentation underwhelmed several of the scientists
attending. "Without the full sequence, it's hard to judge," said
Graham Simmons, who presented the data for the Blood Working Group.
Simmons, who works at the Blood Systems Research Institute in San
Francisco, California, also said he was "dubious" about her claims
that the virus can be aerosolized. Virologist Konstance Knox of the
Wisconsin Viral Research Group in Milwaukee said Mikovits was "just
reaching." Knox, who once consulted for WPI and had a falling-out with
the institute, added that "this is obfuscating what the community finds
to be obvious." Jonas Blomberg, a retrovirologist at the University of
Uppsala in Sweden who like Knox has failed to find XMRV in his own
studies of CFS patients, said it's "hard to handle" Mikovits's
morphing theories. "It's like the argument follows the availability of
the data," Blomberg says.

Two other presentations offered some support for gammaretroviruses in
CFS patients, but both detected just antibodies and not the virus
itself. One study, led by Kenny De Meirleir of Vrije Universiteit in

Brussels, had WPI run its assays. When asked whether the new findings
invalidated his data, De Meirleir said, "I'm not going to say yes or
no." The other report came from Maureen Hanson, a plant geneticist at
Cornell University, who collaborated with CFS clinicians. "Even though
the XMRV sequences may be wrong, it's still certainly possible that
there's a virus in these patients that we need to identify," she said.

Cort Johnson, a CFS advocate, says many patients have held fast to
XMRV for good reason. "It was as if the medical gods, after years of
neglect, had bent down and offered up an apology in the form of a
simple answer that came gift-wrapped with hundreds of eager
researchers."

Nancy Klimas, a CFS clinician at the University of Miami in Florida,
stressed that the Blood Working Group had analyzed samples from just
15 people who had tested positive for gammaretroviruses in earlier
reports. "I would be much more confident putting these putative
retroviruses to rest if I had a larger, more powerful study," Klimas
said. Simmons agrees that a larger study would have more power, but he
says the 15-person study is enough "to make conclusions about the
assays being totally unreliable." Results of a larger study of 150 CFS
patients are expected early next year.

Mikovits said she hopes to have full sequences of her new viruses "in
a couple of weeks."

–JON COHEN

XMRV doesn't exist ... but it causes prostate cancer

While one cadre of scientists is loudly proclaiming that XMRV cannot possibly cause CFS because it's only a lab contaminant, another is proving that it does exist, and does cause prostate cancer.  How much of this debate is really about sexism rather than science?
 

http://bit.ly/mZJDTo

The Prostate

Original Article

XMRV accelerates cellular proliferation,
transformational activity, and invasiveness
of prostate cancer cells by downregulating
p27Kip1

Jui Pandhare-Dash1,2, Chinmay K. Mantri1,2, Yuanying
Gong2, Zhenbang Chen2, Chandravanu Dash1,2,*

Article first published online: 19 SEP 2011

DOI: 10.1002/pros.21491

Copyright © 2011 Wiley-Liss, Inc.

Keywords: XMRV;p27Kip1;CDK;miR221/222;MMP


Abstract

BACKGROUND

Xenotropic murine leukemia virus-related retrovirus
(XMRV) is a recently discovered gammaretrovirus that
was originally detected in prostate tumors.

However, a causal relationship between XMRV and
prostate cancer remains controversial due to conflicting
reports on its etiologic occurrence.

Even though gammaretroviruses are known to induce
cancer in animals, a mechanism for XMRV-induced
carcinogenesis remains unknown.

Several mechanisms including insertional mutagenesis,
proinflammatory effects, oncogenic viral proteins,
immune suppression, and altered epithelial/stromal
interactions have been proposed for a role of XMRV in
prostate cancer.

However, biochemical data supporting any of these
mechanisms are lacking. Therefore, our aim was to
evaluate a potential role of XMRV in prostate
carcinogenesis.

METHODS

Growth kinetics of prostate cancer cells are conducted
by MTT assay. In vitro transformation and invasion was
carried out by soft agar colony formation, and Matrigel
cell invasion assay, respectively.

p27Kip1 expression was determined by Western blot and
MMP activation was evaluated by gelatin-zymography.

Up-regulation of miR221 and miR222 expression was
examined by real-time PCR.

RESULTS

We demonstrate that XMRV infection can accelerate
cellular proliferation, enhance transformation, and
increase invasiveness of slow growing prostate cancer
cells.

The molecular basis of these viral induced activities is
mediated by the downregulation of cyclin/cyclin
dependent kinase inhibitor p27Kip1.

Downstream analyses illustrated that XMRV infection
upregulates miR221 and miR222 expression that target
p27Kip1 mRNA.

CONCLUSIONS

We propose that downregulation of p27Kip1 by XMRV
infection facilitates transition of G1 to S, thereby
accelerates growth of prostate cancer cells.

Our findings implicate that if XMRV is present in humans,
then under appropriate cellular microenvironment it may
serve as a cofactor to promote cancer progression in
the prostate.






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