Friday, June 4, 2010

Post-Exertional Relapse

 
Great description by Anonymous Patient

Wednesday, June 2, 2010

What is stopping ME/CFS from getting research funding?

What is stopping ME/CFS from getting research funding? Obviously there is an
entrenched belief system that a) this is not a real disorder and b) if
it is a real disorder it's impossible or at least very difficult to
study. But there is another factor as well and it's gender….most people
with ME/CFS are female and, rather disconcertingly, the same is true
for many of its allied disorders such as fibromyalgia, IBS, FM, TMJ,
interstitial cytisus, etc. - none of which are getting much funding.

Given that people are power and that about 50 million women  in the US are tired of getting shoddy treatment  and little research the CFIDS Association and several other 'women's disease' organizations joined together to create the Overlapping Conditions Alliance - an Alliance that will advocate for equal funding and equal treatment for women with these mysterious disorders.

It's an exciting endeavor - no one's tried this before - and it could reap big rewards. Check out the "Campaign to End Chronic Pain in Women' from  the 'Bringing the Heat' blog.

http://blog.aboutmecfs.org/?p=1581

A Practical Guide to Severe ME

 
*Stonebird : *
*the Lived Experience of Severe ME*

Just published :

A Practical Guide to Supporting  Someone with Severe ME :

http://www.stonebird.co.uk/A%20Practical%20Guide.pdf

and

Care Sheets :

http://www.stonebird.co.uk/Care%20Sheets.pdf


Greg

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

Health and Safety Concerns of CFLs

> More and more Canadians are replacing regular incandescent light bulbs
> with
> more energy-efficient products, such as compact fluorescent lamps (CFLs).
> While CFLs are being promoted because they are energy-efficient, their use
> has also raised health concerns.
>
> The It's Your Health article on The Safety of Compact Fluorescent Lamps
> has
> been updated with new information and is now available at:
>
> http://www.hc-sc.gc.ca/hl-vs/iyh-vsv/prod/cfl-afc-eng.php
>
> Thank you for your interest in It's Your Health!
 

How to explain it to people when you can't do it all

 

Sunday, May 30, 2010

Impaired Cardiovascular Response to Standing in CFS

[This is probably not the easiest discussion section to fully understand, especially without the tables, graphs, etc. but hopefully many can get the gist of it or some of it.  Check out the extract at least.  It says at the end, "funding was provided by the Medical Research Council, ME Research UK, Irish ME Trust, John Richardson Research Group and CFS ⁄ME Northern Clinical Network", but the (UK) ME Association is also funding important research by Dr. Newton in this area. Tom]


Extract:

" We would therefore
suggest that there are a group of patients with CFS who have
an underlying cardiac abnormality and it is only on performing
appropriate examination that these high-risk patients will
be identified
, and understanding of the physiological mechanisms
that lead to the abnormality explored. It is unclear
what the long-term impact of the cardiac abnormalities will
have for those with CFS. However, our findings of reduced
survival in those with the fatigue-associated chronic disease
and primary biliary cirrhosis [31] and studies confirming a
comparable fatigue phenotype between primary biliary cirrhosis
and CFS [32] would point to an (as yet) unidentified
risk for those with CFS, and our findings of cardiac dysfunction
in a proportion of patients may suggest the group at
increased risk."

31 Jones DEJ, Bhala N, Burt JA, Goldblatt J, Newton JL. Four year follow
up of fatigue in a geographically defined primary biliary cirrhosis
patient cohort. Gut 2006;55:536–41.

32 Jones DEJ, Gray JC, Newton JL. Perceived fatigue is comparable
between difference disease groups. QJM 2009;102:617–24.

-----------------


Discussion

We have demonstrated that the skeletal muscle bioenergetic
abnormality recently described in patients with CFS [1] associates
with a similar cardiac bioenergetic abnormality. This
impairment is associated with an increase in cardiac contractility
on standing (i.e. the heart has to work harder for the same
degree of physiological stress), the severity of which associates
with symptoms on standing in those with CFS.


Our study provides a significant way to defining a bioenergetic
phenotype in those with CFS, which appears to be systemic
and associates with the symptoms on standing frequently
described by those with CFS. The finding of varying degrees of
muscle abnormality may account for the contradictory results
in the previous CFS muscle literature [25–29] and underlines
the need for a whole organ systematic approach to studies in
CFS. Clearly, from this data, the cardiac status of the CFS population
recruited for a given study will matter. If our CFS
patients are considered as a single group, then oxidative muscle
metabolism is not significantly impaired compared with controls,
as we had previously reported [1], and this would not
change by recruiting greater numbers: division by cardiac status,
however, suggests the presence of subgroups within the
population, one of which has impaired oxidative muscle metabolism.
Within the observation that the maximal oxidative function
is impaired, it is not possible to determine from these MRS
experiments whether this is due to primary mitochondrial
defects or alterations in muscle blood flow. Given the relationship
between autonomic parameters and cardiac metabolism,
the latter may well be true: further large studies are required to
confirm the true prevalence of this bioenergetic phenotype in
CFS with subsequent interventional studies to explore this relationship.
We had previously reported abnormalities in proton efflux in
the CFS group as a whole [1] while end-exercise and minimum
pH were not significantly different. Stratification by cardiac
energetics helps us to explore this further and suggest that the
impaired cardiac energetic group are weaker and less able to
access anaerobic pathways, therefore producing less acid during
exercise and having smaller proton effluxes post-exercise.


Considering the high prevalence of orthostatic symptoms in
CFS [2], it was no surprise to find strong correlations between
cardiac bioenergetics and cardiovascular responses to standing.
The relationship between cardiac contractility on standing and
symptoms was an important finding as it suggests that symptoms
in those with CFS are potentially modifiable by treatment
of the underlying cardiac abnormality. These abnormalities
were CFS-specific, as there were no such correlations in the control
population.


At this stage, we have not proven causation, and it is difficult
to determine whether the impaired cardiac bioenergetics in
CFS ⁄ME represent 'cause' or 'effect'. Two mechanisms are possible.
First, those with CFS have an intrinsic cardiac abnormality
[30] that leads to impaired functional cardiac impairment,
subsequent hypotension and reduced organ perfusion, all of
which manifests as the characteristic symptoms of CFS. Alternatively,
afterload abnormalities involving impaired vascular
response to orthostatic pooling may lead to a secondary cardiac
dysfunction. Our findings of a relationship between total
peripheral resistance and cardiac bioenergetics would support
this alternative hypothesis, but further work is needed to elucidate
each of these mechanisms completely.


When we considered cardiac energy metabolism in the
whole CFS patient group, this appeared to be mixed, with
many individuals falling in the normal range with some individuals
showing impairment. This suggests that within the
symptom complex of CFS, there is a group of patients in
whom an actual cardiac abnormality is present (defined by
the presence of PCr ⁄ATP ratio < 1.6 [17]). The heterogeneity
of patients included in CFS studies is well recognized, however,
despite the usage of specific diagnostic criteria for inclusion,
and we could not symptomatically differentiate between
the normal and impaired cardiac energetic group. This underlines
how important it is to correctly characterize patients
with CFS and to study the underlying physiological parameter
rather than the symptom complex. We would therefore
suggest that there are a group of patients with CFS who have
an underlying cardiac abnormality and it is only on performing
appropriate examination that these high-risk patients will
be identified, and understanding of the physiological mechanisms
that lead to the abnormality explored. It is unclear
what the long-term impact of the cardiac abnormalities will
have for those with CFS. However, our findings of reduced
survival in those with the fatigue-associated chronic disease
and primary biliary cirrhosis [31] and studies confirming a
comparable fatigue phenotype between primary biliary cirrhosis
and CFS [32] would point to an (as yet) unidentified
risk for those with CFS, and our findings of cardiac dysfunction
in a proportion of patients may suggest the group at
increased risk.


This study has examined the tolerability and diagnostic
potential of assessment protocols that examine haemodynamic
responses to immediate and prolonged standing in CFS and,
for the first time, examines the relationship between measures
of cardiovascular function, cardiac energetics at rest and muscle
energetics under exercise in CFS patients. HUT is one of the
assessment modalities of choice in the evaluation of those with
unexplained syncope, and is recommended in national and
international guidelines [33–35]. In contrast, the UK NICE CFS
guidelines [36] actively discourage the assessment by HUT.
This is surprising considering the apparent pathophysiological
overlap between neurally mediated hypotension and CFS
[37,38,39]. Our study confirms a comparatively high diagnostic
rate in CFS particularly in those with a history of syncope. We
would recommend therefore that referral for cardiovascular
testing, including HUT testing, is encouraged in those where
symptoms on standing are predominant, and particularly
where there is a history of syncope or presyncope. Importantly,
our positivity rate in our control group was similar to previous
controls [40].


This study has some limitations. The study group could
clearly be considered to be self-selected, and as a result biased,
as they were recruited via the local patient support group.
However, all participants had been seen within a local CFS service
within 2 years and been diagnosed with the formal Fukuda
criteria. A further limitation is that this study cannot establish a
direction of causality for the associations seen in cardiac metabolism,
skeletal muscle metabolism and autonomic function. The
findings are, however, consistent with a model in which a cardiovascular
impairment might lead to impaired oxidative function,
perhaps through impaired venous run-off post-exercise.
Our future work will involve assessing groups of newly diagnosed
CFS patients to determine their cardiac and muscle phenotypes
and following them through time. In addition, largescale
bioenergetic phenotyping of cohorts of patients with CFS
are required with a view to understanding those biomarkers
that are unique to CFS, which will subsequently allow the
development of investigative treatment algorithms specific to
this disease.


Sources of funding
Funding was provided by the Medical Research Council, ME
Research UK, Irish ME Trust, John Richardson Research Group
and CFS ⁄ME Northern Clinical Network.

Author contributions
None of the funders contributed to the design, performance or
interpretation of the results of this study.



---------------
'Impaired cardiovascular response to standing in Chronic Fatigue Syndrome'
Hollingsworth KG, Jones DE, Taylor R, Blamire AM, Newton JL.
Eur J Clin Invest. 2010 May 20. [Epub ahead of print]

Institute of Cellular Medicine, Newcastle University, Newcastle upon Tyne, UK.

http://www.ncbi.nlm.nih.gov/pubmed/20497461


[TK: I've spaced this out a little]

Abstract

Background:
Impaired skeletal muscle metabolism is recognized in chronic fatigue syndrome (CFS).

This study examined the relationship between skeletal and cardiac muscle function and symptoms on standing in CFS using magnetic resonance spectroscopy (MRS) and impedance cardiography.


Materials and methods:
Phosphocreatine (PCr)/adenosine triphosphate (ATP) ratio by cardiac MRS, PCr/ADP and proton efflux by muscle MRS were performed in 12 CFS (Fukuda) and 8 controls.

Head up tilt (HUT) and cardiac contractility (left ventricular work index, LVWI) (n = 64 CFS and matched controls) were found.

Fatigue impact was accessed by Fatigue Impact Scale and orthostatic symptoms by Orthostatic Grading Scale (OGS).


Results:
Cardiac PCr/ATP correlated with measures of muscle bioenergetic function (half-time PCr recovery [kappa = -0.71, P = 0.005] and half-time ADP recovery [kappa = -0.60, P = 0.02]) suggesting that the muscle and cardiac bioenergetic function correlate in CFS.

Four of 12 (33.3%) CFS patients had PCr/ATP values consistent with significant cardiac impairment.

Those with impaired cardiac energy metabolism had significantly reduced maximal and initial proton efflux rates (P < 0.05).

Cardiac PCr/ATP ratio correlated with myocardial contractility (LVWI) in response to standing (P = 0.03).

On HUT, LVWI on standing was significantly higher in CFS (P = 0.05) with symptoms on standing (OGS) occurring in 61/64 (95%) (vs. 25/64 [39%] controls; P < 0.0001).

OGS scores were significantly higher in those with abnormal LVWI responses to standing (P = 0.04), with the LVWI on standing correlating with OGS scores (r(2) = 0.1; P = 0.03). HUT was positive in 19 (32%).


Conclusions:
Skeletal muscle and cardiac bioenergetic abnormalities associate in CFS.

Cardiac bioenergetic metabolism associates with increase in cardiac contractility on standing.

Haemodynamic assessment in CFS is well tolerated and safe with a high diagnostic yield comparable with unexplained syncope.

PMID: 20497461 [PubMed - as supplied by publisher]