"
I argue that a monocausal claim cannot be correctly asserted..." Good, so we're all agreed. And who is making such a claim? No one. Great. So let's move on and go and have a nice cup of tea.
Oh, wait... what's this all about... "
I argue that a monocausal claim cannot be correctly asserted, either on the basis of the single case of an unexpected, although positive, result or on the basis of the empirical research that has followed up on that result." Sure, a monoclausal claim can't be made based on a single (unexpected) positive case, but neither a monocausal case has been made and nor has there been just a single (unexpected) positive case. As for the empirical research that has followed the initial chance observations, it's a fascinating and promising work in progress, upon which the researchers have not made any monocausal claims.
I don't have a major problem with Copeland's conclusion: "
In sum, when an unexpected finding occurs in clinical practice or medical research, the value of following up on that finding is to be found not in the projected value of a singular causal relationship inferred from the finding but rather in the process of research that follows."
But I find the rest of the abstract confusing, bizarre, illogical, and waste of time. Is the author really trying to convince the public, media and scientific communities not to speculate?
To suggest that all speculation is harmful seems like rather an authoritarian and controlling thing to say. What is a hypothesis if it's not speculation? And hypotheses are a fundamental part of the scientific process. Copeland implies that there are unwelcome and deleterious "
risks involved in drawing a theoretical hypothesis from an unexpected observation". But how would science have progressed if unexpected leads had never been followed and hypothesis were never formed on the basis of observations?
The focus of Copeland's criticisms seems to be allegations in relation to "
researchers' speculations that their research results indicate a causal mechanism for CFS". But speculation as to a 'casual' mechanism is not the same as speculation as to a 'monocausal' mechanism. The author has carefully avoided directly accusing the researchers themselves of making monocausal claims, but has (neglectfully or carefully) conflated issues and used phrasing which makes it appear that the researchers have made monocausaul claims.
As for speculation relating to casual mechanisms, why on earth would researchers not speculate about the reasons a certain treatment might be working? What are they supposed to do? Switch off their brains and abandon all scientific curiosity?
She says: "
I argue that a monocausal claim cannot be correctly asserted, either on the basis of the single case of an unexpected, although positive, result or on the basis of the empirical research that has followed up on that result." But who is arguing that there is a single cause for all ME/CFS patients? No one. (Apart from the biopsychosocial school.) So, what's the author talking about? Is she conflating issues? If Copeland is claiming that the Norwegian researchers have speculated that there is a single cause for ME/CFS then she is wrong; they haven't, and this paper is based on a false premise. But if she's muddling and conflating issues and she is not making such a claim, then what's the whole paper about, exactly?
To be fair, I've only read the abstract, but the argument in the abstract is childlike and illogical. My understanding of it is that Copeland doesn't want the scope of CFS research to be widened and to follow new research leads because it will result in a break-out of scientific and public curiosity, and a resulting narrowing or restricting of the field, especially treatment choices?
Eh?
How does that work? This abstract would have been OK as an A'level student blog, but to have it published in a scientific journal makes a mockery of scientific journals.
