Childhood predictors of self reported chronic fatigue syndrome/myalgic encephalomyelitis in adults: national birth cohort study
BMJ 2004; 329 doi: https://doi.org/10.1136/bmj.38258.507928.55 (Published 21 October 2004) Cite this as: BMJ 2004;329:941All rapid responses
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Several studies have found a strong association between CFS/ME/GWS/FMS and coagulation issues -- often with inherited coagulation defects [1,2,3,4]. Typically exercise triggers both coagulation and fibrinolysis in a balanced relationship. With a coagulation defect, fibrinolysis is impeded and the child would become fatigue faster than a normal child.
A child displaying a seditary nature may simply be exhibiting a symptom of a coagulation problem in some.
A study of UK children with CFS/ME should be done looking for coagulation issues. I would strongly urge that Dr Graham Hughes, at the Rayne Institute, St Thomas' Hospital, London, should be approached to do this study. He is extremely familar with antiphospholipid syndrome which often display the same cognitive issues as seen with CFIDS/ME.
1: Garrison RL, Breeding PC. A metabolic basis for fibromyalgia and its related disorders: the possible role of resistance to thyroid hormone.
Med Hypotheses. 2003 Aug;61(2):182-9.
2: Hannan KL, Berg DE, Baumzweiger W, Harrison HH, Berg LH, Ramirez R, Nichols D.
Activation of the coagulation system in Gulf War Illness: a potential pathophysiologic link with chronic fatigue syndrome. A laboratory approach to diagnosis.
Blood Coagul Fibrinolysis. 2000 Oct;11(7):673-8.
3: Berg D, Berg LH, Couvaras J, Harrison H. Chronic fatigue syndrome and/or fibromyalgia as a variation of antiphospholipid antibody syndrome: an explanatory model and approach to laboratory diagnosis.
Blood Coagul Fibrinolysis. 1999 Oct;10(7):435-8.
4: Wysenbeek AJ, Leibovici L, Amit M, Weinberger A.
Disease patterns of patients with systemic lupus erythematosus as shown by application of factor analysis.
J Rheumatol. 1992 Jul;19(7):1096-9.
Competing interests:
None declared
Competing interests: No competing interests
In the article, The Authors report results from a cohort study
exploring risk factors that may have a role for development of CFS/ME. The
study appears to have problems with the unit of analysis. They initially
state that family related factors, operating in the genetics or in the
environment have been suggested to influence disease development. In the
analysis however, they mainly test the association between maternal health
and the risk of self-reported disease. The results of an interview with
both parents at 10 years age are reported almost parenthetic in the
discussion section. The maternal risks are used to test risks reported
earlier in other studies, which does not fully explain the omission of
reports from both parents, interviewed at 10 years age, from the results
section. The weakness of the study what regards the theoretical
assumptions, in particular the behavioural factors, is also revealed in
the way the Authors use p-values and significance testing as a selection
procedure for inclusion of variables in the multiple logistic regression.
There is no explanation of how the maternal health links to the
development of disease by children and why the father’s health is not
associated with later onset of the disease in adolescent or adult off-
spring. The initial statement that family is an appropriate unit of
analysis is not executed in the statistical analysis.
The use of p-values means that Authors transit from the initially
stated, theoretical hypothesis testing to numerical methods as base for
inclusion or exclusion of risk factors in their regression models.
Bivariate associations are not of interest when performing a multivariable
regression. Methods such as forward or backward selection has been widely
criticised by statisticians not only theoretical grounds but also due to
computational problems, in particular flowed standard error of the mean
affecting confidence intervals etc. There is also a problem with external
validity when applying results from selected models to other populations
of relevance for further hypothesis testing (Mantel, 1970; Sun et al,
1996; Sribney link, Derksen and Keselman, 1992, etc.).
The ground for my critique here is mainly the discrete use of various
variables in the analysis, solely on the ground that they were earlier
suggested as explanatory, without any real behavioural theory as a base
for inclusion or exclusion. In addition, in the regression models the
Authors include measurements made by various time points during the
subjects life, which pose problems with statistical independence, probably
associated mutually sine behavioural factors often are affecting the life
of an individual during long periods of time and not occasionally (problem
of repeated measurements). They do not report interaction testing or
effect modifications, which mean that the lack of statistical independence
may bias their final results.
Confidence intervals in diagnostics and performance assessment
Another reflection is also here in place, as in the behavioural
scales the Authors use 1 SD above or under the sample mean as indicative
of illness, disorders or problems. This means that in many cases the
values above or under this cut-off not significantly will differ from the
mean at 95%CI. In the previous issue of the BMJ, the Keogh B et al discuss
measurement of outcomes (cardiothoracic surgery) from a professional
perspective. In order to secure that no “innocent” individual surgeon will
be accused for poor performance, the profession agreed to use 99.99%CI,
that is 4SD, for analysis of aggregated three years values per surgeon.
This threshold means that “an outlier is likely to be real – there is less
than 1 in 10 000 chance that the society would assert that any particular
surgeon with average case mix did not meet its standard”. The reason to
use 99.99%CI for safety purposes in cardiac surgery is to take into
account the variation due to heterogeneity of individual patients.
Obviously, another view on safety is applied by paediatricians and
psychiatrists relying of self-report of patients and relatives that also
constitute an important source of information in operational diagnostics.
There is an obvious discrepancy between thresholds scales used for
diagnostic purposes and those used in the context of performance
assessment. What does it say on how the medical profession views the
safety of patients? A diagnosis of psychiatric or behavioural disorder may
“kill” a person but not the same quick way as surgery. The mortality due
to false diagnosis occurs slowly, over long periods of time in opposite to
surgery and the patients demonstrate probably more heterogeneity what
regards behaviour as compared to biological variation. The limits of
99.99%CI “become very wide at lower volumes during shorter period of time
than three years, opening the way to accusations of professional
protectionism for surgeons with lower volumes.” – Who protects patients
from diagnosis labelling and unnecessary interventions?
Reference
Keogh B, Spiegelhalter, Bailey A, Roxburgh J, Magee P, Hilton C. The
legacy of Bristol: public disclosure of individual surgeons’ results. BMJ
2004;329:450-4.
Sun GW, Shook TL, Kay GL. Inappropriate use of bivariable analysis to
screen risk factors for use in multivariable analysis. J Clin Epidemiol
1996;49(8):907-16.
Sribney B. What are some of the problems with stepwise regression?
http://www.stata.com/support/faqs/stat/stepwise.html, accessed 7/24/98.
Derksen S, Keselman HJ. Backward, forward and stepwise automated
subset selection algorithms: frequency of obtaining authentic and noise
variables. Br J Math Stat Psychol 1992;45:265-82.
Mantel, N. Why stepdown procedures in variable selection? N
Technometrics 1970;623-5.
Competing interests:
None declared
Competing interests: No competing interests
This report refers to “children who were sedentary at 10 years” and
that “sedentary children are at greater risk of later CFS/ME”. The
editorial by Peter White also refers to sedentary children. No explanation
is given of how these children were identified but the implication is
that they are children who were described by their parents as playing
little or no sport in their spare time. While we would expect some
relationship between a lack of spare-time sport and sedentary behaviour it
is unacceptable in a research report in a reputable journal to assume or
infer a close connection without good evidence. Children, especially those
in the higher socio-economic groups, may be expected to engage in other
activities such as ballet, cycling, scouts, guides, music, leisure
swimming etc or just playing with their friends, all of which should
discourage a “sedentary” label but are unlikely to be described as sport.
And might some parents count competitive chess as a (self-reported) sport?
As it happens, the Maternal Self-completion form used in the 1980
study did ask about such activities and also about watching TV. To
identify sedentary behaviour what is most relevant – playing sport or
watching TV? Perhaps the choice depends on which gave the “required”
result!
A more rational analysis of the data presented in this paper might
show that children who do engage in sport regularly, especially contact
sports such as football, are more likely to have or develop a robust and
versatile immune system to cope with the bumps, scratches and frequent
contact with Mother Earth. Has this angle been studied yet?
May I also suggest that a regrettable feature of much research into
CFS/ME and other illnesses is the search for only “bad” features at onset
on which blame for the condition can be placed – viruses, traumas, less-
than-perfect behaviour or attitudes, toxins, etc. Where an illness such as
CFS/ME is closely associated with the immune system (and appears to many
to be primarily a chronic malfunction of this system) surely we should be
looking at all events, especially uncommon ones (e.g. excitement,
exceptional exercise, the removal of anxiety or mental stress) which might
make demands on this system. If the system is damaged (by itself or some
other agent), would this be more likely to occur at a time when it is
required to concurrently cope with several (good and bad) unusual events?
The heterogeneous nature of the problem might be because each person has a
differing set of onset conditions resulting in a differing specific damage
and consequent symptoms. I am unaware of any research, including that of
the CHROME charity (Case History Research on ME) which I support, which
has actively looked for complex demands on the immune system at onset.
Competing interests:
None declared
Competing interests: No competing interests
A 47-year-long clinical experience with the aid of Biophysical
Semeiotics (See HONCode website 233736, www.semeioticabiofisica.it) allows
me to state that today the unknown biological base of chronic fatigue syndrome
(1), i.e., its conditio sine qua non, is an inherited (almost by mother,
like all other similar mitochondrial disorders) functional impairment of
mitochondria. It varies in its intensity, from individual to
individual, from tissue to tissue (particularly affected are skeletal
muscle and cerebral as well as peripheral nervous system), and from part
to part in the same tissue. I termed such a mitochondrial disorder, which
proved to be also the base of all other most serious and common human
diseases, as DM, ATS, Malignancies, a.s.o., Congenital Acidosic Enzyme-
Metabolic Histangiopathy (CAEMH) (2-5) (See above-cited website:
Biophysical-Semeiotic Constitutions). Interestingly, women get chronic
fatigue syndrome, also known as myalgic encephalomyelitis, more commonly
than men for the precise reasons, I just referred to. In addition,
clinical evidence suggests a genetic, mitochondrial in origin, influence
on the illness (1).
Indeed, my explanation accounts for the reason that
until now “research about its cause has been hampered by the absence of a
biological marker, the heterogeneous nature of the illness, and
difficulties in differentiating cause from effect” (1). As a consequence,
on the one hand, research on chronic fatigue syndrome must be performed,
from now on, only in subjects positive for CAEMH. On the other hand, we
can finally understand why infections, physical inactivity, obesity,
a.s.o, may all play a part, worsening mitochondrial activity and, thus,
hampering ATP production. Finally, the treatment of such a complex
disorder needs necessarily understanding of drugs (as Co Q10, Melatonin-
Adenosine, a.s.o.) that notoriously improve mitochondrial activity and
enhance Co Q10 cycle, as I demonstrated in former papers (5-12)
1) White PD. Musculoskeletal syndromes (including chronic fatigue
and Gulf war syndromes). What causes chronic fatigue syndrome? BMJ 2004;329:928-929 (23 October), doi:10.1136/bmj.329.7472.928
2) Stagnaro S., Istangiopatia Congenita Acidosica Enzimo-Metabolica
condizione necessaria non sufficiente della oncogenesi. XI Congr. Naz.
Soc. It. di Microangiologia e Microcircolaz. Abstracts, pg 38, 28
Settembre-1 Ottobre, Bellagio 1983
3) Stagnaro S., Istangiopatia Congenita Acidosica Enzimo-Metabolica. X
Congr. Naz. Soc. It. di Microangiologia e Microcircolazione. Atti, 61. 6-7
Novembre, Siena 1981
4) Stagnaro S., Istangiopatia Congenita Acidosica Enzimo-Metabolica. Una
Patologia Mitocondriale Ignorata. Gazz Med. It. – Arch. Sci. Med. 144, 423
(Infotrieve) 1985
5) Stagnaro Sergio, Stagnaro-Neri Marina. Introduzione alla Semeiotica
Biofisica. Il Terreno oncologico”. Travel Factory SRL., Roma, 2004.
http://www.travelfactory.it/semeiotica_biofisica.htm
6) Stagnaro S., Stagnaro-Neri M., La Melatonina nella Terapia del Terreno
Oncologico e del “Reale Rischio” Oncologico. Ediz. Travel Factory, Roma,
2004.
7) Stagnaro-Neri M., Stagnaro S., Acidi grassi W-3, scavengers dei
radicali liberi e attivatori del ciclo Q e della sintesi del Co Q10. Gazz.
Med. It. – Arch. Sc. Med. 151, 341 (Infotrieve)1992
8) Stagnaro-Neri M., Stagnaro S., Carenza di Co Q10 secondaria a terapia
ipolipidemmizante diagnosticata con la Percussione Ascoltata. Settimana
Italiana di Dietologia, 9-13 Aprile 1991, Merano. Atti, pg. 65. Epat. 37,
17, 1990
9) Stagnaro-Neri M., Stagnaro S., Sindrome clinica percusso-ascoltatoria
da carenza di Co Q10. Medic. Geriatr. XXIV, 239, 1993
10) Stagnaro-Neri M, Stagnaro S. C0Q10 in the prevention and treatment of
primary osteoporosis. Preliminary data. Clin Ter. 1995 Mar;146(3):215-9 [
MEDLINE]
11) Stagnaro-Neri M., Stagnaro S., Acidi grassi w-3, scavengers dei
radicali liberi e attivatori del ciclo Q e della sintesi del Co Q10. Gazz.
Med. It. – Arch. Sc. Med. 151, 341 (Infotrieve), 1992
12) Stagnaro-Neri M., Stagnaro S., Proprietà antiossidante degli acidi
grassi w-3. Gazz. Med. It. – Arch. Sc. Med. 151, 27
Competing interests:
None declared
Competing interests: No competing interests
What ever happened to rigorous peer-review?
Following the paper on 'self-reported' chronic fatigue syndrome
(Viner and Hotopf, BMJ, 2004, 329, 941), will we also be offered a study
on 'self-reported' schizophrenia, or 'self-reported' flu?
The adults who claimed to have developed CFS/ME apparently became ill
at a median age of 24 years (range 14 - 29). Yet CFS is far more common in
the mid-late thirties and forties. I'd add a reference here but have
learnt that facts are not valued when it comes to this illness. (If
gossip, sorry, self-report, is enough for the editor and leader writer,
then it'll do for me).
If I had reviewed this paper, I would have asked the authors to check
if those affected had raised antibodies to EBV. Only 48 were ill at the
time of the study. Someone could have phoned them. Arranged a blood test
if there was uncertainty.
The bottom line is that we're being asked to accept that a complete
lack of exercise at ten predisposes people to develop an illness which
presents as an infection, feels like an infection and is accompanied in
many cases by signs of immune activation, up to thirty years or more
later. All on the basis of the finding that there was a statistical link
connecting a tiny minority who were highly inactive at ten and the
occurence of a self-reported, undefined, illness between 14 and 29.
Kelly Holmes has said that she suffered from CFS a few years ago. I
wonder how inactive she was as a child and why her very active lifestyle
since did not protect her?
Competing interests:
Psychologist with a special interest in myalgic encephalomyelitis and chronic fatigue syndrome, and in covert editorial policies directed at psychologising illness.
Competing interests: No competing interests
Editor,
I welcome the publication of this paper which must be one of the
largest longitudinal papers involving "CFS/ME" ever published. Given the
paucity of properly designed biomedical studies in the field, sufferers
(and their families) often have to put up with all sorts of speculation
with regard to the illness and the data showing no significant link
between maternal psychopathology, parental illness, childhood or
adolescent psychological distress, academic ability, atopy, birth order,
birth weight, and obesity, in the aetiology of lifetime self reported and
physician diagnosed CFS/ME, may help in this regard.
Given that 42% of those in the lifetime CFS/ME group played sport
"often" in their spare time (at age 10) and another 42% played sport
"sometimes", caution should be taken before inferring that advising
children to exercise more is going to make much difference to the
incidence of CFS/ME, especially given the figures which show that more
(52%) of the lifetime CFS/ME group played >2 hours/week of sport at
school at 10 years (compared to 44% of the others).
Speaking anecdotally, I doubt advising me to exercise more at age 10
would have made much difference to me becoming ill with ME later in life.
When I was 10 (2 years after the cohort in this study), I played numerous
sports in and out of school and won the 400m in athletics for my age group
in junior schools for my local region (Leinster, Ireland) without any
specific training, so my underlying fitness was obviously fine. In the
months preceding the onset of the illness at age 16, I was even more
active, playing or training for a sport virtually every day. In my case,
the illness appeared to be triggered by exercising when I had some sort of
viral illness. So, again, any advice to me at age 16 to exercise more is
unlikely to have made much difference in preventing the onset of the
illness.
Even if it is definitively proven in the future that inactivity has
contributed to the onset of the illness in a subgroup of patients, when
someone has the illness, there is an unusual response to exercise; thus
any studies which found that exercise helped certain symptoms and fatigue
levels in people who don't have ME need to viewed with caution by those
involved in the care of people with ME. I have learned this to my cost as
I have gone from being mildly affected to being severely affected
following attempts to exercise more. My experience is not unusual given
the findings from other patients. For example in one study submitted to
the Chief Medical Officer's report on "CFS/ME", 1,214 of 2,338 patients
had tried graded exercise. Of these 417 found it to be helpful, 197
reported no change and 610 (50%) indicated that it made their condition
worse. This was the highest negative rating of any of the pharmacological,
non-pharmacological and alternate approaches of management covered in the
questionnaire, and may help explain the high drop out rates noted in some
of other studies in the area.
Progress in research has been hampered, it appears, both by a lack of
interest from many researchers who could provide useful insights, and a
lack of available funding for biomedical research from relevant bodies.
Hopefully there will now be a recognition that questionnaires alone are
not going to provide all the answers in this illness, which is currently
so frustrating for both medics and patients because of the dearth of
knowledge about the biological processes involved.
Competing interests:
Severely affected patient with ME
Competing interests: No competing interests
Well, I have to say it makes a change. ME is not being blamed on the
usual convenient cop-outs such as growing pains, menopause, and old age.
It is not even being blamed on malingering, hysteria, hypochondria or
depression any more! Finally we know the answer! As children we were all
lazy lay-abouts!
It is just unfortunate that the results of the questionnaire upon
which Viner and Hotopf came to this conclusion, does not align with
reality. Whoever filled in those questionnaires, few can have been
genuine ME sufferers. Case histories make it clear that most who suffer
this disease led very active lives prior to the onset. Now thanks to the
illness, a large percentage are confined to their homes, beds, wheel
chairs or crutches.
I would like to make one more observation. A couple of decades ago,
those who were struck down with this disease were described as young
upwardly mobile executives and ME was demeaningly referred to as Yuppie
Flu. Then there was a U-turn. Professor Simon Wessely (psychiatrist)
stated that those who suffered ME (which he calls the chronic fatigue
syndrome) came from the poorly educated, lower-socio economic classes.
They were mainly female, subject to suggestibility and they imagined
themselves to be ill presumably due to lack of intelligence.
But now there seems to have been another U-turn! According to Viner
et al, those most affected are still women, but from a “high social
class in childhood”. Could the good doctors please make up their minds?
Competing interests:
None declared
Competing interests: No competing interests
If Viner and Hotopf have stumbled onto something significant here and
not just an anomaly of how exercise is defined, (children are able to
exercise more do not go on to develop CFS or ME) , a likely explanation
could be found with a genetic variation such as the ACE gene. A variation
in this gene (which can affect endurance) has been shown to be prevalent
in Gulf War Veterans who go on to developed CFS or Idiopathic Chronic
Fatigue (ICF).
This could mean that some people with CFS and ME are genetically
unable to cope with large amounts of exercise (endurance) and could do
badly if forced to do so.
The children reported by Viner and Hotopf as "sedentary" could have
been acting in a way that this protective of their future health or could
have been exercising at the very limits of their endurance. An
exhortation to exercise further or a claim that increasing exercise is a
protective factor could be detrimental to the health of this subgroup.
The July 2004 issue of the Journal "Nerve and Muscle" reported the
work of Professor Vladutiu of the Robert Guthrie Biochemical Genetics
Laboratory at the Women and Children's Hospital of Buffalo which
specialise in the laboratory diagnosis of metabolic muscle diseases.
Prof. Vladutui looked at Gulf War veterans who met the criteria for CFS or
who had ICF.
Earlier research had shown that persons with an insertion variant
(added genetic material) of the ACE gene had higher endurance. Are these
the people described by Viner and Hotopf as being able to exercise more
and not go on to develop CFS or ME?
Vladutiu theorized that veterans with CFS would have a lower
prevalence of the insertion variant (called II) with a correspondingly
higher prevalence of the deletion variant (no added genetic material -
called DD), which rendered them especially susceptible to a variety of
environmental triggers that can bring on the muscle pain and reduced
physical abilities characteristic of CFS/ICF. The DD variation is
believed to have a potentially negative impact on muscle function
Veterans with the DD genotype were 8 times more like to develop CFS
or ICF than veterans with the protective II type.
It is not know how many non-veteran people with CFS and ME have the
DD genotype but it shows that research is needed to determine what genetic
factors are at play here. In Prof. Vladutiu's research the DD genotype was
less common in the non-Vet CFS group. However, we need to compare
populations of people who can exercise and people with CFS to determine
what differences are at play here.
Is the ACE type II variation (demonstrated by greater endurance)
protective of CFS and ME?
In the meantime it would be irresponsible to claim that exercise is
protective for CFS and ME or to put further "spin" on this research just
because it appears to support the work of a particular lobby.
A questionnaire of members of a charity for people with ME and CFS
reported that Graded Exercise Therapy was responsible for making their
condition worse or no change in the majority of respondents. This fits
with the description of "post exertional malaise" by people with ME which
is a hallmark of the illness.
http://www3.interscience.wiley.com/cgi-
bin/abstract/108565410/ABSTRACT
Competing interests:
person with M.E.
Competing interests: No competing interests
Editor,
Unless there's been a development that I don't know about, a child's
body doesn't know whether it is exercising in an activity organised in
school or outside school. Thus, before coming to any conclusion about
whether activity levels are in any way related to "the aetiology of
lifetime self-reported and physician-diagnosed CFS/ME", it would be useful
to try to combine the figures regarding activity levels in and out of
school, to get some sort of daily or weekly activity total.
If one looks at one piece of the data, the statistics regarding
activity levels in school, the lifetime CFS/ME group were more active
(although the figures didn't quite reach statistical significance); but if
one looks at another piece of the data, regarding activity levels outside
school, the lifetime CFS/ME group were less active. The authors could
have tried to combine these two sets of data, experimenting with different
weightings, to see whether the combined figures showed any trends; they
could also have reminded readers that any dichotomy between activity
levels in and out of school is probably meaningless in terms of a person's
physiology. Even giving a breakdown of what percentage of the group (16%
of the total lifetime CFS/ME group) who appeared to be sedentary at home,
played >2 hours of sport at school could have given the reader an idea
of whether these children were truly more inactive, or whether it was just
a quirk of a subset of the data. If, for example, most or all of these
children did pay sport for >2 hours a week at school, they could hardly
have been described as sedentary.
The more one breaks data down, the greater the chance that any individual
comparison will be statistically significant (using the threshold of
p<.05 for any individual comparison).
Following on from this, one is left wondering, if the result had been
the opposite, and it could have been said (by simply using one piece of
the data) that being sedentary decreased the risk of developing CFS/ME,
whether this would have been highlighted as much in the press release (1)?
Ideally actometers or pedometers could be used to give a true picture
of activity levels of individual children as the data available is clearly
insufficient to come to any firm conclusions. However, given that the
results on this particular aspect of the longitudinal study would unlikely
make much difference to public policy nor to people with "CFS/ME" once
they develop the illness, this contributor feels money could be better
spent in other areas of "CFS/ME", such as trying to understand the
underlying pathophysiology of the condition.
Given that a body as important for basic medical research as the
Medical Research Council (MRC) has never, it appears, awarded a research
grant for projects into "CFS/ME" headed by researchers other than
psychologists or psychiatrists, it is difficult to see how people can
expect researchers to ever understand the biological processes involved.
Do people really think we would have the understanding of the illnesses
and diseases today, especially those that were psychologised or put down
to lifestyle factors in the past (such as Multiple Sclerosis, Epilepsy,
Diabetes, AIDS, Gastric Ulcers, etc), if the only research projects
supported by grant-making bodies were done by psychologists and
psychiatrists?
Until this approach changes, despite the findings of this paper, I
expect speculation regarding "CFS/ME" will continue and those children who
are 10 now, who develop the condition in the future, may have just as
difficult a life with the condition as those that are affected currently,
who were 10 in 1980.
Tom Kindlon
(1) http://www.newswise.com/articles/view/507442/
Competing interests:
Severely affected patient with ME
Competing interests: No competing interests
Children’s ME/CFS, APS and nutritional deficiences
Ken Lassesen writes that several studies have found a strong
association between CFS/ME/GWS/FMS and inherited coagulation defects,
which would explain fatigue on exercise.
He recommends that Dr Graham Hughes undertakes a study at the Rayne Institute, St
Thomas' Hospital, London, because of his familarity with the
antiphospholipid syndrome (APS). Patients with APS which often display the
same cognitive issues, he writes, as seen with CFIDS/ME.
I would hope that any future studies will also include mineral,
vitamin and essential fatty acid analyses. Thermal myothermograms show
impaired muscle contractions when magnesium is deficient in children’s and
adults’ sweat and red blood cells. Common zinc and copper deficiencies
impair brain and nerve function and cause immune system disorders. Such
essential nutrient deficiencies are easily treatable with monitored
nutritional supplementation.
ellengrant@onetel.com
Competing interests:
None declared
Competing interests: No competing interests