arewenearlythereyet
Senior Member (Voting Rights)
Pretty much then leads you back to the role of cytokines. It's interesting that the CNS turns off inflamation once the message is received. This happens also for some pain receptors. A bit like the brain says...yep got the message dealing with it.Just reporting back on @Mij's article. The Maes one.
I'm not interested in what they have to say about ME right now. I'm interested in what they say about bodily responses to acute infection - whether there's evidence for a coordinated "sickness behaviour" response.
The review of what happens during actue infection is quite helpful. In contrast to the sickness behaviour idea, most of the studies they reference show that the various "behaviours" that accompany infection are NOT mediated by the brain. The mechanisms are mostly peripheral (e.g., cytokines interfere with mitochondrial activity, which leads to fatigue). Some changes involve the CNS - for example the systematic increasing in body temp seen in fever involves the hypothalamus. And the changes in heart rate and blood pressure involve the CNS signalling to the autonomic nervous system. Neither fever nor cardiovascular changes are "behaviours" strictly speaking, but I suppose they may contribute to the general shitty exhausted feeling that inclines you to want to rest.
So much for the centrally coordinated adaptive behavioural modification system. Not much support there.
The paper also reviews the ways in which the CNS might be involved in the whole bodily response to infection. A surprise to me was that the role of the CNS is largely in switching off the inflammation, not heightening it. They explain that peripheral inflammation can activate microglia and astrocytes in the brain via various routes (some cytokines, like TNFa, can cross the blood brain barrier efficiently; others operate more indirectly via the peripheral nervous system). In respnse, the brain up-regulates the production of glucocorticoids, which has an anti-inflammatory effect, and also initiates the release of catecholamines and acetylcholine, which also inhibit the production of proinflammatory cytokines (e.g. IL1, IL6 and TNFa), and also of T helper cells.
My conclusion:
- Low-level brain structures coordinate some body-wide responses to infection (fever, heart rate changes). But most of the changes leading to "sickness behaviour" occur outside the central nervous system. They are things like cytokines interfering with mitochondrial function.
- Sickness behaviour is not a useful concept. Its adds little, and is open to misinterpretation and abuse. A much clearer way to talk about behaviour changes that occur during an acute infection is simply to call them "behaviour changes that occur during an acute infection".
- As for its relation to MECFS, I don't think that matters, if the concept itself is stupid.
As with most psychological theories, they tend to fall apart when you start talking at the molecular level.