By David Tuller, DrPH
Professor Ponting on the biopsychosocial approach
Chris Ponting, a geneticist at the University of Edinburgh, has long been a critic of biopsychosocial treatments for ME/CFS, Long Covid, and related illnesses. Professor Ponting is the lead investigator of the groundbreaking DecodeME study, which included more than 15,000 DNA samples from UK patients and identified several locations on the genome that are linked to ME/CFS.
Professor Ponting recently wrote a post for ME/CFS Research Review, a blog hosted by Simon McGrath, a longtime patient. In the post, called “On BPS & disease causation: George Davey Smith’s cautionary tale,” Professor Ponting once again takes on the biopsychosocial approach. It is a short but effective read.
Here’s an excerpt:
“A guide to the Biopsychosocial model recently put out by Long Covid Advocacy ultimately brought me to a 2005 book chapter, written by Professor George Davey Smith, entitled The biopsychosocial approach: a note of caution in Biopsychosocial Medicine: An Integrated Approach to Understanding Illness, edited by Peter White and published by Oxford University Press. The chapter is available from a University of Bristol website. I thought the divergence of opinion between Profs Davey Smith and Wessely was sufficiently interesting to write this short commentary.
“In the book chapter, Davey Smith asked the question “what is the evidence that psychosocial factors are direct aetiological factors in chronic diseases, acting through psychoneuroendocrinological (or other currently fashionable) mediating mechanisms?” Using examples of peptic ulcer and ischaemic heart disease, he ultimately concluded that “When interventional studies have been used to examine the efficacy of a psychosocial approach the results have been disappointing.”
“He quoted Susan Sontag’s 1978 book Illness as a metaphor: “Theories that diseases are caused by mental state and can be cured by willpower are always an index of how much is not understood about the physical basis of the disease.” He further commented that ‘Her reason for being sceptical of the BPS model was that she saw it as a way of putting blame for disease on the people with disease.’”
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New study on viral reactivation
It has long been known that infection with SARS-CoV-2 can lead to the reactivation of latent viruses. It remains unclear, however, whether such reactivations are related to the ongoing symptoms that characterize Long Covid—and if so, how. An article in Science discusses the issue in reference to a new study published by its major rival, Nature,
Here are some of the study’s key findings, per the article:
“EBV [Epstein-Barr virus] and CMV [cytomegalovirus, also a herpes virus] showed up frequently in the samples, albeit at different points in the course of COVID-19: EBV was often detected at hospitalization, whereas CMV detections spiked a few weeks later. Anelloviruses, a group of extremely widespread, seemingly harmless human viruses, were also common around the time of hospitalization and several weeks afterward. Reactivation of any of these viruses was associated with more severe COVID-19 in those early weeks, the data showed.
“The researchers also compared virus reactivation and longer term symptoms such as fatigue or brain fog. Unlike earlier studies, they didn’t detect a link between EBV and these signs of Long Covid. (The discrepancy could be because of differences in how viral presence is measured: Earlier studies often used antibody-based detection rather than gene transcripts, Melamed notes.) But the team did find an association between anellovirus reactivation and fatigue or other physical challenges.
“The study couldn’t determine whether anelloviruses help cause these Long Covid symptoms. But Melamed highlights another finding from the study: The presence of reactivated anellovirus in a sample was associated with higher activity in certain white blood cells. That suggests these viruses ‘may not be entirely passive bystanders, but are actually contributing to immune dysregulation,’ she says.”
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A blog comparing ME/CFS and HIV/AIDS
Sam Schofield, my friend Jane’s 20-year-old son, has severe ME. This year, he launched a Substack called “Confessions of an Unproductive Overachiever.” (I love the title.) Under the circumstances, it’s hard for him to write as much as he would like. I thought it was worth highlighting his most recent post, in which he compares ME/CFS and HIV/AIDS. (Disclosure: I am quoted.)
Here’s the opening:
“In 2009, Dr. Nancy Klimas, who spent her career treating both HIV and ME/CFS patients at the University of Miami, said that if she had to choose between the two diseases as they existed at that time, she would rather have HIV. Her HIV patients were doing well thanks to decades of investment. In contrast, many of her ME/CFS patients were terribly sick and unable to work or participate in life.
“Her answer is backed up by data. Komaroff et al. (1996) found that ME/CFS patients scored lower on functional status measures than patients with HIV, heart failure, multiple sclerosis, diabetes, and depression — using the same standardised instrument. In a peer-reviewed paper in Frontiers in Pediatrics, Friedman et al. (2019), said that ME/CFS had been ‘documented to be more severely disabling than HIV/AIDS.’
“Why compare these diseases? Because the comparison is the clearest available way to show — with evidence — that the failure to treat ME/CFS is a political and institutional choice…”
You can read the rest here.