Friday, May 20, 2011

Patrick Kennedy's new frontier: Healing the brain -

Today, says Kennedy, the race is to inner space, the goal to create a detailed map of the brain in 10 years, with advances toward curing "every kind of brain disease."
 "If you have diabetes and have a chemical imbalance so you need more insulin, you don't get any questions about it. But if you need a neurotransmitter -- more serotonin, or dopamine -- then (people) look at that as something askew, as if the brain isn't part of the body," says Kennedy, his voice rising. "I mean, we're in modern times and people are still treating this illness, mental illness, as if it's back in the Dark Ages."

New HIV Drug Approved By FDA


The most common side effects with Edurant included depression, trouble sleeping, headache and rash.



Thursday, May 19, 2011

Urgent Message from Pat Fero


You may be receiving this e mail twice. (My address book is a mess and 
I have not updated my contact my apology...but please read 

You may not be involved with anyone who has neuroimmune disease, but 
please read on.

In THE LAST 10 years, public health agencies have spent about $3.64 
per patient per year for research on chronic fatigue syndrome (CFS), 
much of which is on psychological factors of fatigue and on coping 
mechanisms.  CFS is not about being tired. It is a disease that 
affects every organ system and people have head to toe symptoms. In 
fact, patients die from early onset diseases of the elderly. We need 
biological research. We are 3 generations into this illness. In 2011, 
we see grandparents, their sons or daughters, and their children sick 
with CFS and other related neuroimmune diseases. People are dying and 
yet few doctors know how to help patients.

The Whittemore Peterson Institute (WPI), located on the Reno medical 
school campus at Nevada State University recognizes the debilitating 
effects of neuroimmune disease on the entire family. WPI recognizes 
the large number of young adults and kids who are suffering from such 
awful symptoms that they cannot live on their own, attend school and/
or work to support themselves.

If the words don't do it for you, take a look at this video:

On May 10, I read Ben's testimony to the Chronic Fatigue Syndrome 
Advisory Committee in Washington, DC. This Rochester, NY TV report 

Please vote.



Round 2 of Chase Community Giving has begun!

The Whittemore Peterson Institute (WPI) is 1 out of 100 charities that 
won a $25,000.00 grant during the first round of Chase Community 
Giving. Now, WPI is competing for a $500,000.00 grant, and you can help!

IF YOU ARE ON FACEBOOK, please cast your vote, and ask your Facebook 
friends to vote. Vote for WPI by following the instructions below 
beginning today. The contest ends next week Wednesday, May 25th, 9 pm 

IF you are not on Facebook, please forward this message to your 
friends who may be Facebook users.


STEP-BY-STEP Instructions:

1. From your Facebook page, go to Chase Community Giving:
2. "Like" Chase Community Giving by clicking on the "Like" button.
3. Now search for Whittemore Peterson Institute for Neuro-Immune 
4. Cast your vote for WPI by clicking the "Vote Now!" button.
5. Please remember our neuro-immune disease community and share in the 
Love and Giving by voting for other organizations who speak to your 
heart -- you can vote for up to 5 organizations per Facebook account.

The Whittemore Peterson Institute for Neuro-Immune Disease (WPI) was 
created to answer a critical need for discovery and medical treatments 
for those with serious illnesses that impact the body and the brain. 
These often debilitating and life-long diseases, including M.E., CFS, 
fibromyalgia, post Lyme disease, GWI and autism, have too few medical 
solutions. WPI continues to make significant strides through the work 
of our innovative research program. Translating novel research into 
effective patient treatments for millions around the world will begin 
with the opening of our 10,000 sq. ft. medical facility. Here we can 
engage in revealing clinical trials and provide onsite care to those 
who are unable to afford care. We require funding for initial expenses 
and to establish a patient fund. WPI's commitment to discovery has 
already inspired much hope worldwide. Now it is time to put hope into 
action by offering meaningful patient care to these underserved 

‘Friendly fire’ may be at the root of Parkinson-like diseases

 a small protein produced by our bodies in response to infections, called interferon-gamma, can directly lead to the loss of cells in the brain

Win Half a Million for WPI's research

Please Help MILLIONS with Neuro Immune Diseases with 2 clicks.Voting is open to anyone on Facebook. You can vote by going to Click "like" then locate the Whittemore Peterson Institute by clicking on this link and Simply VOTE. Your vote will help them possibly WIN $500.000.00 for Research. "Please share this" with others and Thx♥

Wednesday, May 18, 2011

Whittemore Peterson Institute a national winner

For Immediate Release Wednesday ,May 18,2011 Whittemore Peterson Institute a national winner;

by Whittemore Peterson Institute on Wednesday, May 18, 2011 at 12:25pm

 FOR IMMEDIATE RELEASE Wednesday, May 18, 2011   

Whittemore Peterson Institute a national winner; Receives $25,000 grant from Chase Community Giving Campaign -WPI finishes in top five in round one; may receive up to $500,000 - Reno, Nev.

 – The Whittemore Peterson Institute (WPI) has advanced to round two in the Chase Community Giving campaign for an opportunity to receive a donation of $500,000 to support its research and medical programs.  This innovative charitable campaign lets Facebook fans of Chase Community Giving vote to help determine which nonprofit organization will receive the top donation of $500,000.  All charities that have progressed to round two have the chance to submit an original "big idea" that demonstrates how they would use the donation to further their mission.

The charity receiving the most votes between May 19 and May 25, 2011, will receive the donation.  "Additional funding is critical to one of the missions of the WPI which is to provide patient care to those who suffer from neuro-immune diseases," said Annette Whittemore, president and CEO of WPI. "Winning this money through the Chase Community Giving campaign will help to support the opening of our new medical practice at the institute and allow us to set up a special fund for patients who would otherwise be unable to pay for their medical care.  With literally thousands of nonprofits competing for these grants, we are so gratified to be selected to move on to the second round."  

WPI was recently announced as one of only 100 winners of $25,000 in round one of the competition. As a top vote-getter, WPI has the opportunity to be voted as the top charitable organization and win $500,000. WPI's "big idea" includes supporting the opening of its 10,000 square foot medical facility.   In addition to patient care, the institute hopes to begin clinical trials of new therapies within the first year of its opening. "We are delighted that Chase will make a contribution to these worthy causes," said Kimberly Davis, president of the JPMorgan Chase Foundation.  "We continue to be inspired by the number of outstanding charities that choose to participate in the Chase program and the millions of fans who visit the Facebook page and vote for them."   Beginning Thursday, May 19, the public can log on to Chase Community Giving on Facebook at or visit the following link,, to cast their vote.

For more information on WPI, please visit 

WPI is currently sponsoring neuro-immune disease awareness month in order to bring knowledge to these seriously debilitating diseases. In honor of awareness month, WPI will host a "Walk N Roll" on Saturday, May 28, starting at the Whittemore Peterson Institute on the campus of the University of Nevada, Reno. Proceeds from the half to one mile walk will support continued research and medical support for individuals affected by neuro-immune disease.

 The cost is $20 per person and children under the age of 12 are free. People interested in participating can visit   About Whittemore Peterson InstituteWhittemore Peterson Institute is the nation's first comprehensive translational medical research facility dedicated to neuro-immune disease research, treatment, education and outreach.    ### 

PACE and The Lancet

To whom it may concern,

The recently published results of the UK PACE Trial on 'CFS/ME' in The
Lancet[1] have received widespread professional and patient condemnation
of a high volume and nature rarely directed at a (so-called)
peer-reviewed scientific paper. Such condemnation follows upon similar
widespread concerns repeatedly voiced from the trial's questionable

The scientific criticisms centre around the highly controversial patient
selection criteria, the deeply flawed methodology used and the untenable
conclusions extrapolated by the study's authors on 'pacing', cognitive
therapies and graded exercise: particularly when applied to World Health
Organisation defined Myalgic Encephalomyelitis patients[2][3].

In my view and that of many others, supportive comment on PACE presented
by the UK Science Media Centre and The Lancet has been overwhelmingly
unbalanced and unrepresentative and has therefore rightly been the
subject of much criticism[4]. Much of the pro-PACE comment has also
attempted to misleadingly portray CBT/GET treatment for 'CFS/ME'
patients as comparative to adjunctive secondary use of such therapies
for other physically ill patients. The true nature of CBT/GET as applied
to 'CFS/ME' patients in PACE is however quite different as, unlike
standard CBT, without undertaking appropriate physical examination it
controversially assumes patients exaggerate their primary illness and
that muscles are simply de-conditioned. This questionable form of
combined CBT/GET is then applied as a substitute for biomedical
treatment of primary illness: all done in the face of a large body of
contra-indicating scientific evidence

The third broad area of condemnation of the PACE Trial is concerned with
bias, conflicts of interest and the alleged misuse of millions of pounds
of UK taxpayer's money. PACE trial architects and principal
investigators have demonstrable connections with the transnational
permanent health insurance industry that stands to gain substantial sums
of money if ME is misrepresented and mistreated as little more than a
somatoform disorder. The same can be said, in the medium term at least,
for the Department of Work and Pensions (DWP) - which is one of the
major UK public agencies funding PACE along with the Department of
Health and the Medical Research Council.

Whilst limiting biomedical support, treatment and research may
ultimately be a financial win win situation for permanent health
insurers, the same cannot be said of the UK state. If questionable or
exaggerated claims for psychosocial treatments, as alleged in the
state-funded PACE trial, lead to mistreatment and inadequate welfare
support for ME patients, as evidence shows that they undoubtedly
will[6], then patients' health will worsen in the long-run and amount to
an even greater burden upon NHS and welfare provision per patient.
for example, with PACE in mind, the 2006 report of the Parliamentarians'
Inquiry 'Group on the Scientific Research into ME (GSRME)' issued a
stern warning:

"There have been numerous cases where advisors to the DWP have also had
consultancy roles in medical insurance companies. Particularly the
Company UNUM Provident. Given the vested interest private medical
insurance companies have in ensuring CFS/ME remain classified as a
psychosocial illness there is blatant conflict of interest here. The
Group find this to be an area for serious concern and recommends a full
investigation of this possibility by the appropriate standards body. It
may even be that assessment by a medical expert in a field of high
controversy requires a different methodology of benefit assessment."[7]

Under such circumstances it is alarming to note that The Lancet has
chosen to publish less than one quarter of the correspondence it has
received that is critical of PACE[8][9]. Moreover, they chose to
unfairly limit it in length so as to make it extremely difficult to
adequately set out complex evidence. The Lancet's on-line article in
response to complaints about the PACE Trial entitled 'Patients' power
and PACE'[10] is, in my opinion, little more than an exercise in
pro-PACE spin. It states: "Once every few years, we publish a paper that
elicits an outpouring of consternation and condemnation from individuals
or groups outside our usual reach. The latest topic to have caused such
a reaction is chronic fatigue syndrome (CFS), and — more specifically —
Peter White and colleagues' randomised PACE trial published on March 5,
this year." The Lancet then makes the following assertion:

"But one cannot help but wonder whether the sheer anger and coordination
of the response to this trial has been born not only from the
frustration many feel about a disabling condition, but also from an
active campaign to discredit the research." [10]

This is a highly misleading, assertion that is not worthy of a
prestigious peer-reviewed journal and should be withdrawn. From the
outset, The Lancet appears to give the impression that it is only
patients who have complained when the truth is that PACE has received
widespread international condemnation from leading ME specialists and
other medical and science professionals.
Indeed, a formal, erudite and
comprehensive complaint was made to The Lancet about PACE and related
issues by Professor Malcolm Hooper that The Lancet editor, Richard
Horton, and his staff have spectacularly failed to satisfactorily
answer[11]. Moreover, to dismiss the concerned efforts of exhausted,
poorly resourced and struggling patients as a coordinated "active
campaign to discredit the research"[10] in the medico-political context
of the state and insurance-industry backed PACE trial[12] is not only
disgraceful, it is the intellectual equivalent of pretending that a
minnow is guilty of assailing a great White shark.

Adding more aspersion to apparent ignorance, The Lancet then goes on to
assert: "White and colleagues have been accused of having 'formed their
opinion about the intended outcome' before the [PACE] trial began. This
view is unjustified and unfair... The evidence might even suggest that
it is the critics of the PACE trial who have formed their opinions
first, ignoring the findings of this rigorously conducted work." [10]

It is my opinion that the authors of this Lancet response article have
not only failed to address erudite criticisms of PACE put to them[11],
but demonstrate little evidence of having actually read them. In my
view, in disregard of "rigorously conducted" PACE-critique, it is the
editor and staff of The Lancet "who have formed their opinions
first"[10]. Such behaviour makes The Lancet little more than a de-facto
platform for establishment policy-led junk-science[13] that has
abandoned the best-interests of vulnerable patients and the high
standards of genuine scientific peer-review. Richard Horton and his
colleagues should be ashamed.

Anglia ME Action.
May 2011.

'PACE and the end of The Lancet's claim to impartiality' is available
online as a pdf at:


[1] Comparison of adaptive pacing therapy, cognitive behaviour therapy,
graded exercise therapy, and specialist medical care for chronic fatigue
syndrome (PACE): a randomised trial; PD White et al; published online,
The Lancet, February 18, 2011 DOI:10.1016/S0140-6736(11)60096-2.

[2] 'Myalgic Encephalomyelitis / Post Viral Fatigue Syndrome (ME/PVFS)'
is categorised by the WHO as a physical neurological disorder in section
G93.3 of the tenth revision of the International Classification of
Diseases (ICD-10-G93.3). Idiopathic 'Fatigue Syndrome (FS)' is
categorised by the WHO as a psychiatric disorder in ICD-10-F48.0. The
WHO have made it abundantly clear that the two illnesses are entirely
separate and not to be conflated yet, from the outset, The PACE Trial
and its architects have apparently disregarded such taxonomical rigour.

[3] Such concerns have been eruditely set out in: 'REPORT: COMPLAINT TO
ARTICLES PUBLISHED BY THE LANCET. Comparison of adaptive pacing therapy,
cognitive behaviour therapy, graded exercise therapy, and specialist
medical care for chronic fatigue syndrome (PACE): a randomised trial. PD
White et al, published online February 18, 2011.
DOI:10.1016/S0140-6736(11)60096-2, and Chronic fatigue Syndrome: where
to PACE from here? G Bleijenberg and H Knoop, published online February
18, 2011 DOI:10.1016/S0140-6736(11)60172-4' Submitted by Malcolm Hooper,
Emeritus Professor of Medicinal Chemistry (with grateful acknowledgement
to members of the ME/CFS community), March 2011. At:

[4] See for example: 'The Media and ME', Margaret Williams, 16th April
2011. At:
of adaptive pacing therapy, cognitive behaviour therapy, graded exercise
therapy, and specialist medical care for chronic fatigue syndrome
(PACE): a randomised trial. PD White et al, published online February
18, 2011. DOI:10.1016/S0140-6736(11)60096-2, and Chronic fatigue
Syndrome: where to PACE from here? G Bleijenberg and H Knoop, published
online February 18, 2011 DOI:10.1016/S0140-6736(11)60172-4' Submitted by
Malcolm Hooper, Emeritus Professor of Medicinal Chemistry (with grateful
acknowledgement to members of the ME/CFS community), March 2011. At:

[5] As Professor Komaroff rightly stated back in 2006: "...there are now
over 4,000 published studies that show underlying biomedical
abnormalities in patients with this illness. It's not an illness that
people can simply imagine that they have and it's not a psychological
illness. In my view, that debate, which has waged for 20 years, should
now be over." Professor Anthony Komaroff, Harvard Medical School:
Speaking at the USA Government CDC (Centers for Disease Control and
Prevention) press conference on 3 November 2006:

[6] See for example: 'The involvement of the PACE Trial Principal
Investigators and the Director of the Clinical Trials Unit with the
Department for Work and Pensions', Margaret Williams, 31st March 2011. At:

[7] See page 30 of the 2006 report of the Parliamentarians' Inquiry
'Group on the Scientific Research into ME (GSRME)' at:

[8] The article entitled 'PACE is dead, long live PACE?' sent by Anglia
ME Action to The Lancet on 28 April 2011 was not even acknowledged let
alone published by them. This document is available online at the AMEA

[9] Necessarily brief letters critical of PACE published on The Lancet
website are at:

[10] Patients' power and PACE, The Lancet, Early Online Publication, 17
May 2011 doi:10.1016/S0140-6736(11)60696-X

of adaptive pacing therapy, cognitive behaviour therapy, graded exercise
therapy, and specialist medical care for chronic fatigue syndrome
(PACE): a randomised trial. PD White et al, published online February
18, 2011. DOI:10.1016/S0140-6736(11)60096-2, and Chronic fatigue
Syndrome: where to PACE from here? G Bleijenberg and H Knoop, published
online February 18, 2011 DOI:10.1016/S0140-6736(11)60172-4' Submitted by
Malcolm Hooper, Emeritus Professor of Medicinal Chemistry (with grateful
acknowledgement to members of the ME/CFS community), March 2011. At:

[12] See for example: CORPORATE COLLUSION? Professor Malcolm Hooper,
Eileen Marshall, Margaret Williams. September 2007. At:

[13] See for example: Professor Bruce Charlton – Zombie Science – a
sinister consequence of evaluating scientific theories purely on the
basis of enlightened self-interest, Medical Hypotheses (2008) 71
327-329, DOI: 10.1016/j.mehy.2008.05.018:

And see: 'PACE is dead, long live PACE?' Anglia ME Action, 28 April
2011. At:


Tuesday, May 17, 2011

NeuroImmune Disease fact sheet

Highlights of Peterson's Calgary Speech April 29



Highlights of Dr. Daniel Peterson's presentation to medical practitioners:
April 29, 2011, Calgary

By Anne-Marie Woynillowicz Kemp, B.A., Dip.T., M. Ed.

Dr. Peterson began his presentation by describing ME/CFS as a complex
scientific journey in research.  Viral infections, endotoxemia,
altered intestinal microflora, GI muscosal barrier dysfunction,
cytokines and inflammation including  low NK cell function, increased
activation markers, oxidative stress, and mitochondrial dysfunction
are  a few of the possible markers found in patients with ME.  There
are no diagnostic tests available, however, there are definitive
bio-markers for ME.
  Finding a diagnostic test is critical for the
validity of the condition and to stimulate more treatment research.


Currently there is much exciting research being published including
the Schutzer et al. study that compared cerebrospinal fluid proteomes
to differentiate ME and Post Treatment Lyme Syndrome
(PTLS).  Patient
sets were 43 ME subjects that met the Fukuda Criteria, 25 subjects who
met the CDC  criteria for Lyme disease and had completed a minimum of
three weeks of IV antibiotic therapy at least four months earlier, and
11 healthy controls.  Using mass spectroscopy and liquid
chromatography, the research team generated a comprehensive list of 30
000 peptides in the sample pooled from the subjects in each disease
group. The results were as follows:

-738 proteins were found only in the ME subjects
-692 proteins were only found in PTLS samples
-724 proteins were only found in the normal controls.

Conclusions drawn from this study are that there are distinct sets of
proteins that can distinguish ME patients from PTLS patients and
normal controls.  PTLS patients also have a distinct profile. Proteins
relevant to specific neurological functions were lower in ME patients
indicating that the brain is not functioning properly and proteins
specific to immune function were markedly elevated.

Another study presented was the LEUKOTROPIC (living in white blood
al., March 2011.  The goal of this study was identification of chronic
active herpes virus infections in individuals in order to prevent the
misdiagnosis of "ME/CFS" and thereby justify new intervention
strategies, such as antiviral therapy.  All subjects met the CDC
criteria for ME and had systemic signs and symptoms of an active,
ongoing infection. They also met the Canadian Consensus Criteria
(CCC), Carruthers et al., 2003, which Dr. Peterson stated should be
referred to as the "World Definition" for ME.

Below are the results of patients positive for the following:

HHV-6 (human herpes virus 6)             54/194    27.8%
HCMV  (human cytomegalovirus)        71/249     28.5%
EBV (Epstein Barr virus)                         79/153     51.6%

An association has been found between several critical human molecules
such as the thyroid peroxidase protein and leukotropic human herpes
viruses.  This suggests a mechanism for the commonly reported finding
of increased prevalence of autoantibodies in people with ME and
strengthens evidence that autoimmunity can be triggered by infection.
Furthermore, there is speculation that the immunosuppressive potential
of HHV-6 may synergistically enhance the reactivation and replication
of both CMV and EBV.  Dr. Peterson added that beta herpes viruses are


HHV-6 antibodies in individuals with psychiatric disorders were
discussed, Yolken and Dickerson, March 2011.  This research showed
that individuals with established schizophrenia had elevated levels of
antibodies to HHV-6, which suggests schizophrenia can be treated with

CMX001-CIDOFOVIR PIM CONJUGATE is an antiviral drug in phase 3 trials.
By linking a lipid to the phosphonate group of cidofovir, a drug has
been formed which is able to cross the intestinal wall and penetrate
target cells before being cleaved to free the antiviral, cidofovir.
Improved potency has been demonstrated in preclinical studies.  In
cell culture assays, CMX001 is significantly more active than
cidofovir against double-stranded DNA viruses including:

-orthopox viruses (variola, monkepox, vaccinia, cowpox and ectromelia)
-herpes viruses (CMV, herpes simplex virus (HSV)-1,and 2, HHV6,-8,
varicella zoster virus(VZV), Epstein Barr virus (EBV)
-multiple adenoviruses.

Dr. Peterson suggested that CMX001 is an almost perfect drug as it
only needs to be administered orally 2 times a week.  This makes it
much more accessible than the current intravenous options for the
human herpes viruses.


Apoptosis is a natural process of self-destruction (programmed cell
death) in certain cells that is determined by the genes and can be
initiated by a stimulus or by removal of a repressor agent.  In March,
2011, Chronix Biomedical filed a provisional US patent application
jointly with Hemispherx Biopharma, Inc on a blood test for ME.
Chronix is developing disease-specific biomarkers based on DNA
fragments that are released into the bloodstream by damaged and
apoptotic cells.

The Chronix Biomedical blood test for ME is limited to investigational
use because it has not been evaluated by any regulatory agents yet. It
is expected that this test will be 100% accurate and that it will be


XMRV is proving to be highly controversial and is providing much
healthy debate and research.  Xenotropic viruses originate in mice but
can only infect cells from another species.  Most retroviruses,
especially members of the gamma retrovirus genus, can induce tumors as
a consequence of integrating their viral genome into the host cell
chromosome and activating proto-oncogenes (a normal gene that has the
potential to become an oncogene).

To date, there have been at least 21 studies of XMRV research in ME.
Two studies, Lombardi et al, October 2009 and Lo et al, September
2010, have supported XMRV in ME.  Nineteen studies have not found a
link to XMRV.  These include Erlwein et al., January 2011, Groom et
al., February 2010, Hong et al., September 2010, Heinrich et al.,
October 2010.

There are suggestions that some test kits were contaminated.


Currently there are two large studies for ME. The first is at Columbia
University, headed by Dr. Ian Lipkin.  Dr. Lipkin is internationally
recognized for his work with SARS.  He is responsible for discovering
SARS and is credited with saving millions of lives, especially in

The ME world is truly fortunate that Dr. Lipkin has agreed to do two
studies on ME.  Through viral assays for known and unknown pathogens,
Dr. Lipkin will be looking for all human viral pathogens.  As well,
there is a study of 240 post SARS patients from Toronto, Canada.
These patients are being tracked and approximately 6 to 8% developed
identical symptoms to ME.

Dr. Peterson is involved with the second large study which is being
conducted at Bond University, Gold Coast, Australia.  This research
study is looking at Natural Killer (NK) cell phenotype and functional
study.  Currently, the team is applying for permission to do spinal
fluid tap for a viral assay on ME to determine the cause of NK cell
At this time, Dr. Peterson recommends measuring of NK function for diagnosis of ME as it is the most reliable marker for ME.


Significant strides are being made in research due to registries and
biobanking.   Nosology is the branch of medicine dealing with the
classification of diseases, which traditionally was built using signs
and symptoms.  Now, nosology can be based on gene expression and is
improved with clinical markers, lab markers and biotech markers.
Because all disease could be redefined from a molecular perspective,
patient outcomes will improve.

Translational medicine allows researchers and clinicians to work
together.  Future direction of the translational model will ensure
there is large scale clinical data gathering through multiple
international sites involving patient and provider.  It will allow
biospecimen collection with connection to a clinical database with RNA
expression, DNA sequencing as well as other molecular testing.  There
will be focus on chronic and syndromic diseases such as ME.

The future looks promising.


Schutzer SE, Angel TE, Liu T, Schepmoes AA, Clauss TR, et al. (2011)
Distinct Cerebrospinal Fluid Proteomes Differentiate Post-Treatment
Lyme Disease from Chronic Fatigue Syndrome. PLoS ONE 6(2): e17287.

Knox K et al. Systemic Leukotropic Herpesvirus Infections and
Autoantibodies in Patients with Myalgic Encephalomyelitis-Chronic
Fatigue Syndrome. 7th International Conference on HHV-6 and 7. March
1, 2011. Reston, VA.

Yolken R, Dickerson F  Elevated Levels of HHV-6 Anitbodies in
Individuals with Psychiatric Disorders. 7th International Conference
on HHV-6 &7. March 2011. Reston, VA.

Shin, Clifford H. Absence of XMRV and other MLV-related viruses in
CFS. J. Virol.
Doi:10.1128/JVI.00693-11. Published online ahead of print on 4 May 2011.

Moldofsky H & Patcai J.  Chronic widespread musculoskeletal pain,
fatigue, depression and disordered sleep in chronic post-SARS
syndrome; a case-controlled study. BMC Neurol. March 24 2011;11:37.


Is Living With Illness Choosing to Give In?

Vote for more research funds!

You get 5 votes, so you can vote for both CAA and WPI.  That still leaves you 3 votes to trade with friends, you'll vote for their pet project if they vote for yours.  Post this to all your groups, Facebook, the pages of Facebook friends who have zillions of friends.....
The second round of the Chase Community Giving contest is to start on
May 19, 2011 and go through May 26. Both the CFIDS Association and the
Whittemore Peterson Institute won $25,000 in Round 1. In Round 2 they
both again are eligible for even more money. Each voter gets 5 votes
which can only be used once per charity, leaving 4 extra votes. If
these votes are not used then they are wasted and so potentially is
this great opportunity to score hundreds of thousands of dollars for
much needed CFS research. Please vote for the CFIDS Assoc. and the WPI
with your votes. Thank you.

CFIDS Assoc. contest page-

WPI contest page-

•Round 2: Chase will donate to the 25 Charities receiving the most
votes in Round 2 in the following amounts:
◦$500,000 to the Charity receiving the most votes (rank 1);
◦$400,000 to the runner-up Charity (rank 2);
◦$300,000 to the next runner–up Charity (rank 3);
◦$200,000 to the next two runner-up Charities (ranks 4-5);
◦$100,000 to the next five runner-up Charities (ranks 6-10);
◦$40,000 to the next five runner-up Charities (ranks 11-15); and
◦$20,000 to the next ten runner-up Charities (ranks 16-25).

Round 2: From May 19, 2011 to May 25, 2011, users can vote for any of
the Round 2 Charities through the Chase Community Giving application
on the Facebook platform. On or about May 26, 2011, the votes will be
tallied and the 25 eligible Charities receiving the most votes will be
considered the winners of Round 2 and will share in $2,500,000 in
donations from Chase.


Research: Research Grants Program

The first program funded by the Association was its research grant
program. Since 1987 the Association has provided nearly $5.33 million
in direct support of CFS research studies, has hosted scientific
symposia and has cosponsored meetings to identify promising areas of

The CFIDS Association of America issues funding announcements as part
of its research grants program. Its most recent Request for
Applications was issued on April 6, 2011. This Request for
Applications (RFA) solicited research proposals that will advance
objective diagnosis and effective treatment of CFS. Letters of intent
are due June 3, 2011 at 5:00 pm (EDT). For more information about this
funding opportunity, please visit

The current purpose of the CFIDS Association's research program is to
accelerate progress toward accurate diagnosis and effective treatment
of CFS by directly supporting research studies, facilitating
collaboration among investigators and pursuing increased investment in
CFS research by public, private and commercial institutions.

2008-2010 Awarded Research Grants


During the 2008-2010 funding cycle, six CFS research projects totaling
$647,940 in support were awarded, as described below.

PI Name: Gordon Broderick, PhD
Institution:  University of Alberta
Title:  Molecular patterns of persistent immune activation in a
post-infectious adolescent cohort

Objective: To use network analysis of gene expression and endocrine
measures to identify biomarkers that describe the events from
infectious mononucleosis (IM) to post-infection CFS.
Method: Construct immune and endocrine profiles for 12 post-IM
subjects and 12 matched controls.  Examine blood from acute IM, 6, 12
and 24 months by gene expression and correlating with blood cell
subsets and endocrine measures.
Why This Study is Important:
Epstein-Barr Virus causes IM that can trigger (possibly cause) CFS.
By studying the immune and endocrine response in people from the time
of IM to development of CFS, we can identify early disease and disease
progression biomarkers.
Studying subjects over time allows identification of the series of
events that precede disease and perturbed pathways.
These markers are important for early detection, objective diagnosis,
targets for intervention.
About Dr. Broderick: Young, new investigator to CFS. Associate
Professor in the Department of Medicine since 2007. Intrigued,
engaged, innovative. Recently voted Small Group Teacher of the Year by
the Medical Students' Association at University of Alberta.
Collaborators: Renee Taylor (University of Illinois-Chicago); Ben Katz
(University of Illinois-Chicago); Sol Efroni (National Center for
Biotechnology Information and Weizmann Institute)


PI Name:  Kathleen  Light, PhD
Institution:  University of Utah Health Sciences Center
Title:  Novel ion channel-based biomarkers in CFS

Objective: 30 to 70% of CFS patients have chronic muscle and joint
pain. Acid-sensing and ion channel receptors affect pain sensation and
in CFS, this receptor sensing system is overactive. The objective of
this study is to expand the findings of post-exercise increases in
acid-sensing and ion channel receptors on blood cells.
Method: 30 CFS (60-70% likely to have chronic widespread pain) and 30
pain-free healthy controls.  Blood drawn before and after physical
exertion for 25 minutes on Airdyne bicycle. Measure cardiovascular
function and assess cytokines, acid-sensing, ion-channel and SNS
receptors on blood.
Why This Study is Important:
Receptors important for the sensation of pain and fatigue are found on
blood cells.
By expanding NIH-funded pilot study, investigators will identify blood
biomarkers of post-exercise pain and fatigue.
Combination of blood markers will identify CFS subtypes that will help
guide and improve treatment.
Will guide research on ways to alleviate symptoms by studying markers
in CFS subjects on certain medications and physical exercise programs.
About Dr. Light: Recipient of an NIH R21 to study neuroimmune
mechanisms in CFS in 2006; this grant will extend her preliminary
data. Very well published on the topic of pain conditions, but new to
Collaborators: Alan Light, PhD (University of Utah) and Lucinda
Bateman, MD (CFS expert in private practice)


PI Name: Marvin Medow, MD
Institution: New York Medical College
Title: Splanchnic vasoconstriction is impaired by microbiomic nitric
oxide production reducing cerebral blood flow in CFS

Objective: To determine if postural hemodynamic changes cause
neurocognitive deficits as a result of impaired cerebral blood flow
and modulation of nitric oxide (NO) and reactive oxygen species (ROS).
Methods: 15 CFS/POTS, 15 CFS, 15 matched controls from same cohort as
those patients studied by Dr. Shungu. Extensive cardiovascular
measurements during tilt. Plethysmography, transcranial Doppler,
real-time cutaneous readings of nitrous oxide bioavailability and ROS.
Why This Study is Important:
Provides the measurements necessary to determine if chronic
inflammation and oxidative stress help explain increased brain
Identify autonomic nervous system (ANS) subtypes of CFS.
Provides objective evidence of sympathetic nervous system
activation/excitation in CFS.
Findings could implicate the "root" of the problem since investigators
have noted patients develop POTS after infection.
About Dr. Medow: Established physiologist and associate director of
the Center for Hypotension at New York Medical College.
Collaborators: Benjamin Natelson, MD; Julian Stewart, MD, PhD (New
York Medical College); Dikoma Shungu, PhD (Weil Cornell Medical
College); Bud Mishra, PhD (New York University)


PI Name: Bud Mishra, PhD
Institution:  New York University School of Medicine
Title:  Translate science to a cure for CFIDS

Objective:  To seek an etiologic explanation for CFS symptoms by
designing a system that combines published literature with
experimental data.
Methods:  Construct a database of full text articles, existing
databases (e.g., KEGG) and develop a statistical method to capture
meaningful relationships that allows the construction of models that
describe aspects of CFS.
Why This Study is Important:
Unbiased approach to explain CFS (compared by reviewers to creating a
"Google for CFS").
Build an invaluable knowledgebase of CFS.
Provide mechanistic explanations for CFS only possible by integrating
existing and experimental data.
Provide a suite of tools that will allow investigators to query all
aspects of the CFS system, all of which will be available to other
investigators as open access tools.
Computer hardware and software required to conduct this study would
cost millions of dollars.
Exciting discovery potential
About Dr. Mishra: Established mathematician who has published
extensively and holds many patents. 28 graduate students,
collaborations with IBM, Google and biomedical industry.
Collaborators:  29th graduate student; Dikoma Shungu, PhD (Weil
Cornell Medical College); Julian Stewart, MD, PhD (New York Medical


PI Name: Sanjay Shukla, PhD
Institution:  Marshfield Clinic Research Foundation
Title:  Metagenomics approach to study chronic fatigue syndrome patients

Objective: Determine if there is an altered ratio of gut commensal and
pathogenic bacteria in CFS and if exercise increases microbe
translocation to cause post-exertion symptoms.
Method: 6 CFS and 6 household controls. Exercise challenge with stool
and blood samples taken before and after exercise. Catalogue bacteria
in stool; examine blood for inflammatory markers.
Why This Study is Important:
Metagenomics involves sampling the genome sequences of a community of
organisms inhabiting a common environment (in this case the intestinal
Could explain increase gut disturbance and post-exertional relapse
common in CFS;
Could provide evidence for metabolic disturbance;
Could provide evidence for chronic inflammation and immune dysfunction; and,
Could suggest intervention strategies.
About Dr. Shukla: Established microbiologist. Introduced to CFS in
2000.  Novel and powerful approach, strong team.
Collaborators: Dane Cook, PhD (University of Wisconsin); Dan Frank,
PhD (Colorado University); Steve Yale, PhD (Marshfield Clinical
Research Foundation)


PI Name: Dikoma Shungu, PhD
Institution:  Weill Medical College of Cornell University
Title:  MR neuroimaging assessment of cerebral metabolic substrates
and regional blood flow in CFS

Objective: Use magnetic resonance spectroscopy (MRS, an advanced MRI
method) to measure specific brain chemicals. The investigators build
upon preliminary evidence showing elevated lactate in CFS patients.
Examine chemicals in blood and brain that are indicators of oxidative
stress and mitochondrial dysfunction.
Method: Compare the brain profiles between 20 CFS, 20 MDD and 20
healthy controls. Examine blood samples for markers of oxidative
stress. CFS subjects will come from Drs. Medow and Natelson.
Why This Study is Important:
Increased brain lactate indicates abnormal metabolism in CFS.
By expanding study to additional disease control groups, can determine
whether elevated lactate is specific to CFS.
Provides objective evidence of metabolic problem in CFS that could be
used for disability.
Findings could implicate the "root" of the problem causing CFS.
About Dr. Shungu: Established researcher in neuroimaging and
neurometabolism. Relatively new to CFS research, although is a past
Association grantee. Dr. Shungu's earlier study was recently published
in NMR Medicine.
Collaborators: Sanjay Mathew, MD (Columbia University); Benjamin
Natelson, MD; Marvin Medow, MD; Julian Stewart, MD, PhD (New York
Medical College); Bud Mishra, PhD (New York University)


All research projects funded received the highest evaluation scores
for scientific and strategic merit as assessed by two independent
panels. All investigators have agreed to conditions of award
identified by the reviewers, one of which was to collaborate as the
first funded CFS network of investigators. All awardees must fully
comply with the Association's Policies Governing the Award of Research
Grants, including rigorous reporting requirements, for funding to
continue in a timely manner.

Additional Required Meetings for All Investigators:

First Investigators Meeting, January 18-20, 2009

Investigators receive background information on CFS and objective
classification of subjects and controls. Establish consistent study
entry criteria, per the hypothesis being studied
Investigators present respective studies to gain input from other
investigators and selected invited reviewers.
Link all investigators and establish active collaborations.
Ensure full understanding of reporting and other compliance
requirements for timely grant distributions.
Solidify project timelines and milestones.
Interim Investigators Meeting, September 13-16, 2009

Funded investigators present mid-term data to Association staff and
other funded investigators with generous question and answer periods
to optimize remaining stages of study.
Invited subject matter experts deliver presentations to expand context
of studies.
Strengthen ongoing collaborations
Ensure appropriate compliance with reporting and other policy requirements.
Facilitate site visits (if warranted).
2008 Research Papers by Dr. Suzanne Vernon, the Association's
Scientific Director


Smith AK, Dimulescu I, Falkenberg VR, Narasimhan S, Heim C, Vernon SD,
Rajeevan MS.  Genetic evaluation of the serotonergic system in chronic
fatigue syndrome. PNE. 2008 Feb;33(2):188-97.
Fuite J, Vernon SD, Broderick G.  Neuroendocrine and immune network
re-modeling in chronic fatigue syndrome: An exploratory analysis.
Genomics. 2008 Sep 30. [Epub ahead of print].
Bolshin C, Aspler AL, Vernon SD, Broderick G. Evidence of inflammatory
immune signaling in chronic fatigue syndrome. Behavioral Brain
Function 2008 Sep 26;4:44.
Ben-Zvi A, Vernon SD, Broderick G. Model-based therapeutic correction
of hypothalamic pituitary adrenal axis dysfunction. PLoS Computational
Biology, in press.
Sorensen B, Jones JF, Vernon SD, Rajeevan M. Transcriptional control
of complement activation in an exercise model of chronic fatigue
syndrome. Molecular Medicine, in press.


Hickie I, Davenport T, Vernon SD, Nisenbaum R, Reeves WC, Lloyd A and
the International Chronic Fatigue Syndrome Study Group.  The construct
validity of chronic fatigue syndrome is supported by a multi-national,
cross-cultural study.  Under consideration with BMJ.
Presson A, Sobel E, Papp J, Whistler T, Rajeevan MS, Reeves WC, Vernon
SD, Horvath S.  A systems genetic analysis implicates FOXN1 in chronic
fatigue syndrome. BMC Systems Biology, under consideration.
Nater UM, Whistler T, Lonergan W, Mletzko T, Vernon SD, Heim C.
Impact of acute psychosocial stress on peripheral blood gene
expression pathways in healthy men. Submitted to
Whistler T, Fletcher MA, Lonergan W, Zeng XR, Lin JM, LaPerriere
A,Vernon SD Klimas NG.  Natural killer cell function is depressed in
Gulf War Illness. BMC Medical Genomics,

The Shell Game

"It should be remembered that an efficacious treatment paradigm may turn out to be completely different from what has evolved for HIV. It may be possible to take antiretrovirals for a time to knock it back, clean out reservoirs, in conjunction with other things that are conducive to proviral latency."
* * *
This was my experience (though not with ARVs).  I got sicker and sicker until finally I got some effective sleeping pills.  After a few months of sleeping 8-10 hours a night instead of 0-2, I started to run a fever, which didn't go away.  A nurse friend's response to my concerned e-mail began "Congratulations, you have a functioning immune system again!"
Getting adequate, good quality sleep allowed my resurrected immune system to get the upper hand over the virus again.  Cured?  No -- a couple years later, after the clinical trial of the magic pills was over, I had a C-Reactive Protein test that was 10x what it should be ... and joked with the doctor if it was that bad when I felt so good, I'd love to know what it had been when I was thinking death was the next step. 
Now that I'm sleeping 5-6 hours most nights (which is about what I was getting while I was still employed), my immune system does seem to be keeping the virus down to a dull roar.  Not clearing it away entirely, but the CRP tests are not as sky-high as they were.
And this fits in with what my first specialist recommended: fix the sleep problem and let the body begin to heal itself.  Then you can see what remains to be fixed pharmacologically.  Things which were a daily problem are now down to an occasional annoyance, reduced in both frequency and severity.  I certainly wouldn't consider myself "cured", nor even capable of returning to work, but when I compare 2011 to 2001, I can definitely see a big difference in my abilities.  In 2001, I was horizontal almost all day.  Now I'm vertical much of the time.  In 2001, a 15 minute doctor visit 4 blocks from home had repercussions for nearly a week.  Last week, I spent a couple hours at the Capitol (a mile from home) for activism, and although I had to lie down when I got home, I felt decent the next day and back to normal-for-me after 48 hours.
As Dr. Jamie says, sometimes it just takes a little help to knock the virus back.

Toward a cure for retroviruses


"It's known that if you're lucky enough to have this mutation, the delta32 CCR5, from both your parents -- something we call homozygous, technically -- you are resistant to getting infected by most forms of HIV."

"number 61 turned out to have the delta32 CCR5 mutation that would make the cells being put back into the body of the Berlin patient resistant to virtually any kind of HIV we know of."

"If you vaccinate someone, say, against the measles or polio and test them for antibodies a year or five years later, he or she will be positive for antibodies. But as you start getting on in time from that initial vaccination -- and it's why we give boosters against certain diseases -- the antibody levels fall off. And that's what's happening to this patient.

"It has been about two and a half years since the patient has been off of all of his antiviral drugs and had the transplant, and he still has absolutely no detectable virus, either active virus or latent virus.

"I predict that, in a couple of years, his HIV antibody test will be negative."His antibody levels -- we call them titers -- are declining just the way you'd expect them to if you'd given someone a vaccination against HIV and then looked at the levels of antibodies. They'd be very strong in the beginning, but would weaken if they are not re-exposed to the virus.

"We believe this person has no HIV in his body and therefore there is nothing to re-expose him, so the concentration of HIV antibodies in his blood is decreasing. I predict that, in a couple of years, his HIV antibody test will be negative."

"This could never, ever have been done in the United States first. It could be done in Europe because they have a socialized medicine system. No one asked the question who's paying for this."


Chronic Illness and Divorce


Living with a chronic illness like rheumatoid arthritis can take a toll on your emotions and on your relationships, and can lead to intimacy difficulties and even divorce. "Divorce is certainly a potential consequence of having a chronic disease like rheumatoid arthritis," says Kristin Flynn Peters, PhD, a clinical health psychologist and clinical assistant professor at the School of Health Professions at the University of Missouri in Columbia. In fact, the divorce rate among people with rheumatoid arthritis (RA) has been reported to be as much as 70 percent higher than that in the general population.

Surveys also show that many people with rheumatoid arthritis who are divorced do not remarry, Flynn Peters says.

* * *

You're not alone.  If your spouse can't cope with your illness, it's a reflection on him, not you.  Marriages involving chronic illness, where it's the wife who's sick, are far more likely to break up -- 90% of them by some estimates -- because, to quote my own ex, "I didn't get married to have to cook and clean".




Skip the Sugar: 6 Healthy Alternatives to Flavored Milks

Also good if you're lactose intolerant

Xenotropic Murine Leukemia Virus - Distinct Inflammatory Signature

Xenotropic Murine Leukemia Virus-related Virus-associated
Chronic Fatigue Syndrome Reveals a Distinct Inflammatory Signature

The recent identification of xenotropic murine leukemia virus-related virus (XMRV) in the blood of patients with chronic fatigue syndrome (CFS) establishes that a retrovirus may play a role in the pathology in this disease. Knowledge of the immune response might lead to a better understanding of the role XMRV plays in this syndrome. Our objective was to investigate the cytokine and chemokine response in XMRV-associated CFS. The purpose of this study was to evaluate differences in cytokine and chemokine profiles between XMRV-infected CFS patients and healthy control subjects. This study clearly demonstrates XMRV-infected CFS patients display an inflammatory cytokine and chemokine signature that distinguishes them from healthy control subjects. The availability of complete viral genome sequences from many symptomatic and asymptomatic individuals may lead to a greater understanding as to why some individuals manifest symptoms of neuroimmune disease while oth ers do not.
Vincent C Lombardi, Judy A Mikovits et al, in vivo 25: 307-314 (2011)
Related Links:
Presence Of Murine Leukemia Virus Found In Chronic Fatigue Syndrome Patients
FDA Press Release
Detection of MLV-related virus gene sequences in blood of patients with chronic fatigue syndrome and healthy blood donors (FULL TEXT)
Shyh-Ching Lo, Harvey J. Alter et al PNAS
Detection of an Infectious Retrovirus, XMRV, in Blood Cells of Patients with Chronic Fatigue Syndrome

Judy A. Mikovits et al, 10.1126/science.1179052, Science Express

How To Smash The Flawed ME/CFS PACE Trial Results

 How To Smash The Flawed ME/CFS PACE Trial Results

Professor Simon Wessely, psychiatrist:
"What the patient doesn't know won't hurt."
UNUM Insurance, Chief Medical Officer's Report 2007

This document is a discussion of the outcome of the PACE trials which coincide with a shake-up of the UK state benefit systems. The latter involves a move towards a 'comply or be sanctioned' culture. Strategies for differentiating yourself from the PACE trial patients and for holding on to state benefits are discussed. Key to success is having the strong financial support from ME/CFS charities to fund individual biomedical testing for patients. The flaws and weaknesses of the biopsychosocial model and the increasingly nebulous definitions that identify CFS patients as having only 'subjective fatigue', psychological in origin, can be exposed with thorough biomedical testing. Start lobbying your charities to pay for it now or face being characterised as having a Functional Somatic Syndrome and your resources cut off indefinitely. How PACE was allowed to come to fruition in this manner is a travesty. Patients have fought for over 50 years to get proper reco gnition for their illness, and several thousand research papers elucidating many of the biomedical factors behind their symptoms have been published. So why were they not taken seriously, and who failed to fight their corner?  Could it be the ME/CFS charities who insisted that patients did not need any more than a set of standard blood tests (in line with Wessely School dogma); who seem content to broaden the definition of ME/CFS to include patients with no evidence of inflammation of the brain or spinal cord? The same charities who did not give their wholehearted support to the Canadian Criteria; which, while not perfect, at least recognised the neurological and other biomedical factors central to ME/CFS. And even now, what are the charities really doing about the mess that is the PACE trial publication?  Very little seems to be the answer, and for that reason patients must now look to themselves, and each other to limit the damage. One Click Note: With the useless publication today of letters to The Lancet regarding the PACE Trial, now would seem an appropriate juncture to republish this stellar article. In this life, tangible results equal action.
Lara, Health Advocate
Related Links:
The PACE Report - The MRC/PACE Trial Scandal
Jane Bryant, The One Click Group

Mastro Case re SSR 99-2p

Although this case upholds the denial of Ms. Mastro's benefits, it gives some guidelines for how SSR 99-2p should be applied.  In other words, make sure your doctor gets some objective evidence -- in my case, it was a C-Reactive Protein test, which will show infection or inflammation -- good for demonstrating that you have a virus for which there is no test yet!

SSR 99-2p, 64 Fed. Reg. at 23381. The ruling instructs that, before rejecting a claim based on CFS, the ALJ must first consider the medical evidence and evaluate the condition as any other unlisted impairment. Therefore, the CFS claim is analyzed under the same five step framework applied to every social security disability claim. See 20 C.F.R. S 416.920.


The five step analysis begins with the question of whether the claimant engaged in substantial gainful employment. 20 C.F.R. S 404.1520(b). If not, the analysis continues to determine whether, based upon the medical evidence, the claimant has a severe impairment. 20 C.F.R. S 404.1520(c). If the claimed impairment is sufficiently severe, the third step considers whether the claimant has an impairment that equals or exceeds in severity one or more of the impairments listed in Appendix I of the regulations. 20 C.F.R. S 404.1520(d); 20 C.F.R. Part 404, subpart P, App.I. If so the claimant is disabled. If not, the next inquiry considers if the impairment prevents the claimant from returning to past work. 20 C.F.R. S 404.1520(e); 20 C.F.R. S 404.1545(a). If the answer is in the affirmative, the final consideration looks to whether the impairment precludes the claimant from performing other work. 20 C.F.R. S 404.1520(f).

...  the Commissioner recognizes that "no specific etiology or pathology has yet been established for CFS." SSR 99-2p, 64 Fed. Reg. at 23381. Still, the Commissioner's directive in SSR 99-2p explicitly requires a CFS disability claim to be accompanied by medical signs or laboratory findings. SSR 99-2p, 64 Fed. Reg. at 23381. Recognized examples of medical signs, clinically documented over a period of at least 6 consecutive months, that will establish the existence of a medically determinable impairment include: palpably swollen or tender lymph nodes on physical examination; nonexudative pharyngitis; persistent, reproducible muscle tenderness on repeated examinations or any other medical signs that are consistent with medically accepted clinical practice and are consistent with the other evidence in the case record. SSR 99-2p, 64 Fed. Reg. at 23382.



Monday, May 16, 2011

Living Within My Envelope

New featured success story on the Lapp-Campbell website:

"Living Within My Envelope"
One person's formula for reducing symptoms and bringing stability to life.

Explaining the new website, Dr. Lapp said, "What you'll find here is the
combination of the Stepwise Approach I developed many years ago with Dr. Paul
Cheney and the tools taught in Dr. Campbell's classes. This is the same
integrated approach I now use with my patients. We have found that with
encouragement, lifestyle changes, and targeted medications, more than 80% of
people we treat can improve significantly."

Bruce Campbell, Ph.D., Executive Director
CFIDS & Fibromyalgia Self-Help Program
* * *
This is the most important thing any CFS patient needs to learn -- stay within what Dr. Jason calls your Energy Envelope.  Read Ellen Goudsmit's research on Pacing.
At one point, I was so sick that even three times a day to the kitchen was too much.  When I started to keep bottled water, nutrition shakes and snacks next to the bed, and reduced my energy usage to one trip per day to the kitchen, I was finally staying within my envelope and, while not improving by leaps and bounds, at least was not going further downhill every day.
By paying attention to your body and not using more energy than your body is able to make, you'll feel better.

Sunday, May 15, 2011

Why Vaccinate?

If you didn't have to spend your childhood like this: can thank vaccines for pretty much eradicating Polio. Same for smallpox and measles.

Read more: The 6 Most Misguided Causes Ever Made Famous by Celebrities |

Don't Listen to Jenny McCarthy

"autism by its nature will manifest in infancy, between 18 months and three or four years, and that's also when babies are receiving their vaccinations, which is probably why people assume the correlation. Now, we still don't know what's causing the current rise in autism, but as of now there is no link"