I just can't agree with your objections to the introduction. The writing looks to me like the standard ways of describing disease severity, what we know about disease physiology and drawing on respected authorities like WHO. I can't see saying that the ICD-10, even on a little known disease like ours, isn't evidence based. I don't think this intro should draw more ire than the intros that band on about ME/CFS being "unexplained", subtext psychosomatic. And I think it would be better to focus on the results.
The reason the problems in the introduction are worth discussing is that it is in a paper on research supported by OMF. Scientists funded by OMF and with plenty of experience in ME/CFS should be getting the introduction right by now. This introduction is a long way from 'right', and so many of the introductions we see from OMF funded scientists are poor.
I don't think making a comparison with introductions that 'bang on about ME/CFS' being psychosomatic is setting the bar at the right level. Yes, of course the introduction in this paper is better than one that suggests that ME/CFS is psychosomatic. It doesn't mean that it can't be more accurate and more persuasive. The ME/CFS community is not funding the psychosomatic proponents, it is contributing to the funding of Bergquist and his team.
It seems, wabi-sabi, that you feel that you are not qualified to evaluate what these scientists have written. I think you are capable of evaluating at least some of what they have written if you take the time to give some attention to it.
If you keep reading the critiques of research here, I think you will come to realise that any scientist can get something wrong, and many of the ME/CFS researchers held in high esteem by many in the ME/CFS community get many things wrong. And that motivated people with ME/CFS who take the time to read these papers can make worthwhile observations.
They may seem silly to you (and hey, maybe they are), but people in healthcare take them seriously. If we are going to be understood, we need to speak the language they understand. Papers are meant to start off with the seriousness of the illness to grab the reader's attention. Typically you do that either with numbers of affected or severity of illness. It's a legit tactic for the authors to use. It really, really doesn't make us look hysterical.
How many 'people in healthcare' have you tried to tell 'ME/CFS is worse than cancer and stroke'? I disagree with 'it really, really doesn't make us seem hysterical'.
There are many ways to give an impression of severity that would work better. I gave an example of one that would not give a knee-jerk impression of over-claiming among readers familiar with the awfulness of significant cancers and stroke.
We routinely see ME/CFS papers on biochemistry devote too many paragraphs to trying to justify ME/CFS as a problem worthy of consideration. Working too hard to convince readers that the disease is worthy of attention can actually give the opposite impression, as the introduction in this paper does. Papers on diseases like multiple sclerosis don't usually feel the need to say that it is coded by the WHO as a disease of the nervous system.
However, I can't focus on the results since I don't have the expertise to evaluate them properly. But I am glad the authors are doing this research, even if it is awfully preliminary. I feel like there's some biting the hand that feeds us going on here.
You seem to feel that you have the expertise to dismiss what I am saying and suggest that I am biting the hand that feeds us though. I'm assuming that you, like the authors, understand how fundamentally hormone levels change at different stages of the menstrual cycle, and with hormonal contraceptive use and between females with regular menstrual cycles and without. It only requires a very basic understanding of statistics to understand how even quite minor differences in the life stage and contraceptive use of the participants in the small samples could result in different hormone ratios between the groups.
If you want to compare people with ME/CFS to pets, dependent on their owners to feed them, let us then extend the metaphor. What should those pets do if what they are fed, instead of something sustaining, is as nutritious as sawdust? The pet can appreciate the intent of its owner to care, be deeply grateful even, but, at some point if it is to survive, it becomes necessary to note that things need to be better. There's no biting going on here, just a pointing out that this paper doesn't help and a request for things to be better.
The authors acknowledge all of the menstrual cycle and birth control and menopause stuff you bring up, so they do understand that it is an issue and are not accidentally ignoring it.
It's great that the authors acknowledge the issues, but they have still made claims as if these problems do not make their findings probably worthless and at best highly questionable. Here are the abstract's conclusions.
abstract said:
Despite no significant differences in absolute steroid levels, network analysis revealed profound disruptions in steroid-steroid relationships in ME/CFS compared to controls, suggesting disrupted steroid homeostasis.
Collectively the results suggest dysregulation of HPA axis function and progestogen pathways, as demonstrated by altered partial correlations, centrality profiles, and steroid ratios.
These findings illustrate the importance of hormone network dynamics in ME/CFS pathophysiology and underscores the need for more research into steroid metabolism.
See how definitive those statements are? But, different percentages of people on hormonal contraceptive and different percentages of people at different points in their menstrual cycle will have an enormous impact on ratios of hormones found. These factors have such a big impact that it means that it is not reasonable to draw any conclusions from this data. Especially when the conclusions have a lot to do with progesterone.
This paper muddies the waters, contributing to misinformation rather than moving the field of ME/CFS forward. It's impossible to know what, if anything, is a finding with any relevance to ME/CFS.
Great that the authors do understand that the problem is an issue and that they aren't accidentally ignoring it. But, that means that, when it comes to them making the conclusions in their abstract, they have deliberately ignored the problem. And that is arguably worse.
"Research on cortisol, one of the most studied steroid hormones and potential biomarkers in ME/CFS, generally supports the presentation of mild hypocortisolism inpatients [37] which is in contrast with the current findings.
Research on cortisol does not support the presentation of 'mild hypocortisolism'. I think it's probably accurate to suggest that mean cortisol levels are often found to be slightly lower in ME/CFS than in the control groups, but the means are still almost always found to be within normal ranges, and there is range of cortisol levels among the patient cohort. A slightly reduced cortisol level is to be expected in people not doing vigorous physical activity.
It's just not correct to claim that mild hypocortisolism (i.e. cortisol slightly below normal ranges) is a characteristic of ME/CFS - the literature does not support it. It's particularly disappointing, because I directed Chris Armstrong to our thread discussing the problem with the claims around cortisol in ME/CFS a while back.
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