By David Tuller, DrPH
October is a crowdfunding month at University of California, Berkeley. If you’d like to support my work, you can make a donation to the university (tax-deductible for US taxpayers) here.
In February, the journal Nature Communications published the US National Institutes of Health’s long-awaited paper, “Deep phenotyping of post-infectious myalgic encephalomyelitis/chronic fatigue syndrome.” The study included 17 ME/CFS patients, along with 21 healthy controls.
The paper immediately triggered howls of protest for a number of reasons, and in particular for the controversial claim at its core–that the profound fatigue reported by patients is the result of a novel and rather convoluted construct called “effort preference” that has never previously been used to assess this cohort of patients. As noted in the third sentence of the abstract, “one defining feature of PI-ME/CFS [post-infectious ME/CFS] was an alteration of effort preference, rather than physical or central fatigue.”
Members of the patient community have conducted extensive and robust analyses of the flaws of the “effort preference” construct. Jeannette Burmeister, a lawyer as well as a patient, posted a blockbuster four-part series about it on her blog, Thoughts About M.E. In an extensive thread, members of the Science for ME forum also whacked through the thicket of data shenanigans that led to the NIH’s problematic and unwarranted conclusion. The agency has since indicated that it is reviewing the study and its methodology. (I also wrote a post about the offensive decision to use the term “preference” in connection with these patients—akin to callng a serious disease “chronic fatigue syndrome.”)
Last month, The Sick Times published an essay by John Bolecek, a former pedestrian and bicycle transportation planner in Virginia disabled by Long Covid. We recently spoke about his piece, called “Five reasons why the NIH should retract the ‘effort preference’ claims in their intramural ME/CFS paper.”
Thank you for staying on top of the whole NIH “Effort Preference” thing, and for sharing this interview!
I remain convinced that the root cause of this strange conclusion is that the special interest who started messaging practicing physicians, policymakers including NIH, and the general public roughly 40 years ago to deny and trivialize ME/”CFS” managed to achieve regulatory capture of NIH (that is, plant its disinformation narrative that what it caused to be called “CFS” is “just fatigue” or “deconditioning” so thoroughly that the people at NIH tasked with solving this problem (including management’s choice of a very good scientist who is in the role of looking for “it’s all in your head” explanations of syndromes science can’t yet figure out, as PI for all work on ME/”CFS” and LC))…
that the researchers are, in the image of that summer camp skit of my childhood long long ago, looking for the lost coin here under the streetlamp of “psych” “learned behavior” “deconditioning”, instead of looking over there in the dark where the coin was actually lost (a novel physical mechanism which cannot possibly occur if what’s taught in med school is correct and complete).
Me? I’m just the retired computer designer who went looking for the human nervous system’s “decoupling capacitors” in the course of failing to solve a different complex chronic illness my family suddenly got 28 years ago, and found an application of those insights to many of the two dozen or so complex chronic illnesses over the years, but thought PEM PESE PENE was different…until seeing it from a different perspective a couple of years ago.
My heretical, blasphemous conjecture is that PEM PESE PENE starts with a ubiquitous molecule which gets from the environment (inhale, touch, from digestive tract) into the bloodstream, and which the body must “keep out from underfoot”; a first failure in which the body’s mechanism to “keep it out from underfoot” fails (which I propose is an autoimmune attack on a blood albumin circulating protein plus that ubiquitous molecule as hapten); the molecule subsequently is loose in the bloodstream; and a second failure in which that molecule lands on the pathway a muscle cell or neuron uses to bring some raw material for making energy into that cell, times all of those cells in the body, creating a different protein+hapten combination the immune system learns to destroy. My presumption that this is a tunnel, based in part on myoglobin or neuroglobin, which brings oxygen into the cell clearly contradicts (without evidence) the long standing science consensus that oxygen enters cells by diffusion which works really, really well. So the performance athlete who’s off by 10% has lost just 10% of those oxygen pathways into the relevant cells; the typical non-athlete person with ME (PEM PESE PENE) has lost maybe 80% of those oxygen pathways into relevant cells; and the bedbound unmoving patient in a dark silent room has lost 100% of them and must use anaerobic metabolism for the slightest use of energy beyond diffusion keeping the cell alive.
My point is not here that my conjecture is correct; it’s almost certainly wrong. It’s that NIH is researching a disinformation narrative from 40 years ago about what the nature of PEM PESE PENE must be, rather than looking for a physical mechanism which contradicts today’s science and medical consensus, but explains the patient experience.