Another stunning piece of from Crawley. Kids who are ill and unable to do much sometimes put on weight.
The factors behind obesity are complex, so it is never a good idea to try to reduce it to a simple so-called "common sense" etiology like "kids who are ill and unable to do much sometimes put on weight".
Well, d'oh! By stopping here, and not devoting any ink as to why activity levels might be reduced, the paper cleverly skirts around the wider medical context.
An the idea that lack of exercise might cause obesity makes little sense, because the amount of kilocalories burnt through exercise is minimal. The average human consumes around 2,000 kilocalories per day in food and drink.
If you were to go for a jog for 15 minutes every day, the amount of kilocalories that would burn is only 200. So that is going to make little difference to your net total kilocalorie intake. By comparison, the amount of kilocalories in a jam donut is 250. Thus food intake is far, far more influential than exercise on your net kilocalories.
But in any case, food intake is only part of the equation that leads to obesity.
The article seems explicitly set up to not raise reader awareness of a broader ME picture, thus luring them into connecting the two dots - obesity and ME/CFS - that it does provide.
You are confusing advocacy and media articles raising of public awareness with the publication of scientific study. It is not really purpose of a study to raise the reader's awareness of the broader ME picture.
Take
Dr Chia's seminal study finding enteroviruses in the stomach tissues of 82% of ME/CFS patients. Where in that paper does Dr Chia raise the reader's awareness of the broader ME picture?
Given the complex physiopathology of ME/CFS, one can cherry-pick to cross-correlate two phenomena.
There are many diseases that are statistically more prevalent in ME/CFS patients, including the following: irritable bowel syndrome, interstitial cystitis and overactive bladder (irritable bladder), chronic pelvic pain syndrome, endometriosis, Raynaud’s disease, atopy (predisposition to allergies), multiple chemical sensitivity, temporomandibular joint disorder, myofascial pain syndrome, attention deficit hyperactivity disorder, depression, generalized anxiety disorder, eating disorders, Hashimoto’s thyroiditis, prolapsed mitral valve, Sjögren's syndrome (sicca syndrome), postural orthostatic tachycardia syndrome (POTS), and neurally mediated hypotension.
The above statistical comorbidities were found be studies like Esther Crawley's. Are you saying that all these studies just cherry-picked data in order to make it look like there was a statistical association?
That doesn't however mean any causation exists. And even if there is causation, statistics leaves its direction unspecified.
Every scientist knows that correlation does not necessarily imply causation, so you not saying anything new here. And of course, we know that you cannot deduce from the statistics of association whether there is causality, let alone the direction of causality.
But this problem also applies to viral ME/CFS studies or metabolic studies: when an association is found between a viral infection and ME/CFS, such as the association between enterovirus and ME/CFS, this does not prove that the virus causes ME/CFS. Likewise, an association found between metabolic abnormalities and ME/CFS does not prove those metabolic abnormalities cause ME/CFS, nor vice versa.
So the points of criticism you make apply just as much to the viral ME/CFS studies.
I've had another look at this paper, and what upsets me is its subtle strategic ambiguity; possible agenda-science at its most insidious masquerading as an honest exploratory research article.
That's just far too much conspiracy theory and paranoia for me.
The Canadian consensus criteria, under the neuroendocrine manifestations section, says that ME/CFS may involve a "marked weight change," meaning either weight gain or weight loss. Does that mean the CCC are also in on this "possible agenda-science at its most insidious".
Ironically, I was 15 stone pre-illness, but am now a trim 10 1/2 after 18 years of illness, largely because weight drops off me whenever things get bad. Where's my study Esther?
If you read the first paragraph of Esther's paper, you will find your answer:
Little research has been conducted investigating the relationship between chronic fatigue syndrome/myalgic encephalomyelitis (CFS/ME) and obesity, especially in adolescents. The few cross-sectional studies which have been conducted have provided conflicting findings,1–4 while a large longitudinal study found no association between obesity at 10 years and self-reported CFS diagnosis by the age of 30 years.5
So different studies have shown different results. And as I mentioned, the CCC says ME/CFS may involve marked weight loss or marked weight gain.
It is possible that the particular virus which triggered the ME/CFS may be one factor that determines whether there is weight loss, weight gain, or neither.
But an individual's own metabolism and endocrinological state likely also play a role. I said earlier that as my ME/CFS-triggering virus spread to 30+ people, some of them, like me, developed central obesity (weight gain on the abdomen). But others with the same virus remained lean.
. Its sad that Crawley cant understand some basic life fact that patients who are housebound and cant exercise or play sports due to thier disability, could be more likely to end up with weight issues.
