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ME/CFS submission for MRC consultation
The consultation document can be downloaded here
The report arising from this consultation can be downloaded from
Dear Sir or Madam,
I am an ME/CFS sufferer, science graduate and medical science Masters student and would like to submit some comments on your draft research strategy on ME/CFS.
I thought that the draft was very thorough and of very high quality, so my comments are relatively small points which may or may not be of use to you. I will list them in the order in which the associated points were made in the draft. You may well have already taken some or all of the matters into account, of course, so please forgive my presumption..
Re initial summary points 10 and 11: there is a need to distinguish factors which trigger the development of the illness from factors which aggravate the condition after it has developed. Although some factors may be involved in both processes, others are probably only involved in one or the other. There is potential for substantial symptomatic relief via the identification and removal of aggravating factors, and this can probably be done relatively easily via the scrutiny and collation of clinical records.
Re point 48: because initial triggering factors may no longer be detectable after the illness has developed, there is a need to take biological samples and measurements at the earliest possible stage when patients present with ME/CFS-like symptoms. In my own case I believed that a trigger was organophosphate poisoning, but I did not have my plasma AChE tested until long after the exposure. The other problem with this test is that a baseline (pre-exposure) measurement is required in order to assess the significance of post-exposure measurements. Perhaps it would be possible for such measurement to be done on a routine basis in well people. (Also see comments on points 113 & 117)
Re point 63: there appears to be genetic susceptibility to Bell's Palsy (or possibly another illness with similar consequences, such as a herpes infection) in my family, so this may be a useful pointer, although I do not know of any relatives with ME/CFS. I developed this paralysis at the age of 5.
Point 76 refers to some seriously affected patients never fully recovering (my underlining). I am not seriously affected but have had the condition for 7 years, with very gradual deterioration, so do not expect to recover. Thus I do not believe that non-recovery necessarily correlates with severity. Also see my comment re point 155.
Point 106 appears to suggest that there is reduced motivation and responsiveness and appetite and weight loss in ME/CFS sufferers. In my view this is over-generalising. Many sufferers are very well-motivated (indeed many are high-fliers and workaholics) before the illness develops and, although a period of depression may be associated with these symptoms in the early stages, such symptoms are by no means universal in later stages. My depression (probably part-emotionally and part-physically-based) only lasted for about two years, including the first year in which physical ME/CFS symptoms were present, and has been absent for the past 6 years, during which time I have been very highly motivated and with a hearty appetite. Perhaps this apparently incorrect conclusion has arisen due to the inappropriate use of animal studies. One must bear in mind that humans have very different and additional motivational systems from other species, and I believe that the 'sickness behaviour syndrome' (SBS) referred to may relate to co-occurring depression rather than to ME/CFS. You cannot ask a non-human animal whether it is feeling depressed. Pursuance of such a red herring risks wasting resources, developing inappropriate treatments and delaying more productive research.
Point 108 advocates studying SBS further using 'chronic models'. I am strongly opposed to using animal models for the reasons given above as well as for ethical reasons.
Re points 112 & 113, from conclusions drawn from the precursors of, and progression of, my own illness I believe that there is a strong likelihood that a sustained over-release of cortisol (e.g. due to stress of some kind) may lead to a pathological negative-feedback process, perhaps via a reduction in cortisol receptors, culminating in a drastic and persistent reduction in cortisol release, which may be a primary factor in CFS/ME aetiology.
If interpretation of basal cortisol levels is problematic, is this partly due to not knowing what a patient's levels were before developing ME/CFS? If so, perhaps cortisol levels should be measured routinely (as recommended for AChE in my comment re point 48).
Re point 117: Biochemical tests for all patients presenting with possible early ME/CFS symptoms might help here (as recommended in my comment re point 48).
Re point 120: a district nurse told me that she had observed a generational alternation between rheumatoid arthritis and irritable bowel syndrome. It may be worth looking at such generational alternations in the case of ME/CFS. My IBS manifested itself before the ME/CFS, and IBS or similar bowel dysfunctions appear anecdotally to be relatively common in people with ME/CFS (from my correspondence with other sufferers). My father had RA.
Re point 123: I profoundly disagree with the idea of studying human diseases in animals on both scientific and ethical grounds. As stated in your draft, there is a huge mass of actual and potential information available on human sufferers. Causing further suffering is totally unjustifiable. See my first point re Annex 1.
Point 137 asks whether depression is integral to, or a response to, CFS/ME. It also needs to be considered whether depression can have a causal role (see my comment on points 112-3 re cortisol).
Re point 155: This suggests a correlation between severity and duration of illness. I am not convinced of this as it does not seem to apply in my case (also see my comment re point 76). Thus it is important to treat severity and duration as separate variables.
I was somewhat dismayed at the reference to 'competitiveness' in point 184. This is not a competition - it is about human welfare. Information in medical science should be shared at all stages, and collaboration should be maximal both nationally and internationally. In case 'the need to attract high-quality researchers' suggests that this must involve high monetary rewards and 'perks', I do not believe that the best researchers require a high income to motivate them. Financial inducements are more likely to attract those whose motivations are non-altruistic. Scientific discovery and advances in human well-being are their own rewards for the right people.
Re Annex 1, I agree strongly with the charity representative's statement submitted by Kate Saffin, Annette Hacket and Adele Wright about the need to use the vast body of information which already exists. This should be one of the first steps undertaken in the quest to solve the mysteries of CFS/ME. This is relevant to my comments on points 106, 108, 123 on animal experiments.
Re 'Gaps in research; defining the research agenda; there appears to be no agreed starting point' (also in Annex): the untapped resource which I refer to above would help to identify such a starting point. Although it is likely to be rife with artefact and subjectivity, the size of the resource may be large enough to iron out many such confounding factors.
Re 'Obstacles' (also in Annex): Physical and psychological causes appear to be treated here as discrete and separate. However, it may be difficult or impossible (or indeed counter-productive) to separate them; it may be that in combination they lead to the crossing of a threshold of some kind of stress (adrenocortical?). For example, psychological stress depresses the immune system, which can then allow opportunistic infections and perhaps anthropogenic toxins to further weaken physiological systems.
Another potential obstacle I would add is possible conflicts of interest in funding bodies. Companies which manufacture chemicals (including pharmaceuticals) may be reluctant to support research or publish findings which implicate their products as causative or exacerbating factors in the illness. They may also be over-eager to seek drug-based solutions, notwithstanding the fact that a substantial proportion (perhaps the majority) of sufferers have very low tolerance to pharmaceutical drugs (as has been my own experience), and may actually have their condition worsened by them (as I believe may be the case for myself).
Appendix: 'Finding the cause': May I suggest also looking at Candida, IBS and 'leaky gut' (see my comment on point 120). Re candida, we appear to have deliberately engineered, via both conventional breeding and genetic modification, strains of yeast which are highly resistant to destruction for the production of alcoholic drinks and bread. Could this indestructibility also persist within the body?
Also in Appendix:
'What it does to the body; area examples' refers to 'looking across systems
and traditional boundaries.' I agree with this approach totally,
for aetiology as well as pathology, as I have stated above.
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