Having not seen any change in the M.E. conversation since my previous post about M.E. in bears three years ago, I thought I’d finally have another try. However, one thing did give me encouragement: the recent discovery that there could be a biochemical link between M.E. and hibernation. That chimes with my ‘bear’ theory pretty well, although it was pure coincidence I chose a bear for the example!
So rather than asking “How did M.E. evolve?”, which nobody seems to get, I’ll ask another question which may spark a few people: “What is the function of M.E.?”
If you think that infectious disease symptoms are an accidental by-product of the disease, you won’t even get the question. But, as most medical folk will tell you, symptoms are produced by the body’s response to the disease, not the disease itself. And many, if not most of them, are signs of the body fighting back against the disease. I heard an analogy in a medical lecture years ago, quoted from a doctor who was a pilot in the First World War. A flight across the front lines at night showed a snaking curve of fire, explosion and light. But on either side was absolute darkness. That darkness hid hundreds of thousands of occupying troops, where the war, on one side anyway, had been lost. The only evidence of war was the line where the battle still raged.
It is the same with infectious disease. Where you can see symptoms, the war against the disease is still being fought. Symptoms are the evidence of the body fighting back, and are also in many cases themselves part of the fight-back. Many symptoms themselves have quite specific functions, and have evolved to be part of our immune response.
And yet, many symptoms are also ignored by doctors, mainly because the ‘interesting’ symptoms are the diagnostic ones: the various spots, rashes and lumps found in medical textbooks. Yet often under ‘additional symptoms’ for many infections you will find listed again and again ‘flu-like symptoms’. And that is as far as it goes.
Nobody that I have yet found thinks to wonder why ‘flu-like symptoms’ are so common to so many different conditions. Because they are so common, it seems that they are being commonly ignored. And yet, surely, these flu-like symptoms are likely to have a disease-fighting function, just like many others? And because they are so common, must it not be a very important function, which fights infections in general?
So there is your paradigm shift, before you can see why I’m asking about the function of M.E.: symptoms are not accidental by-products of disease. They are, instead, functions of the body that have evolved quite specifically to fight the disease that produces them.
The Function of ‘Flu-like Symptoms’
Let’s get rid of one symptom to start with: a high temperature. I think most medics would agree that this has some disease-fighting function, even if not all are agreed as to what it is. To be as vague as possible, we can probably agree that a high temperature produces an environment in which the body’s immune system can fight infection more easily.
But it is the other ‘Flu-like Symptoms’ that concern us, as they are pretty universally agreed to be at the core of M.E.: aches & pains (no, I don’t know the difference either), feeling “woozy”, and being more than usually sensitive to various stimuli. When all these come together, they can be interpreted by the body as ‘fatigue’, but as we don’t seem to have any evidence that genuine fatigue (the natural effect of exertion) is an actual symptom, I would call these symptoms together “quasi-fatigue”.
Quasi-fatigue has, I hypothesise, the same function as genuine fatigue: to signal to the body that it is time to rest. This is an obviously advantageous reaction to an infection: the body does not want muscle and brain using up scarce resources that need to be diverted to the immune system.
So my first hypothesis is this, and it would underpin the relatively new science of neuro-immunology:
The symptoms I have lumped together as “quasi-fatigue” are an evolutionary adaptation of the immune system with the function of signalling to the body that it should rest while it is fighting an infection.
There is one other part of quasi-fatigue that I haven’t dealt with here. Not only does it occur in response to infection, I suggest that it also responds itself to extra activity or stress: the very things it is trying to prevent. In other words, if the body ignores the quasi-fatigue signals and indulges in activity and/or stress, the body responds by amplifying the signal.
I have no evidence that this response actually does occur in infectious diseases, but it is a diagnostic feature of M.E., whose symptoms are identical to the quasi-fatigue outlined above. Whether it does or not, I think that if readers have got this far, they will see where this is heading – to my second hypothesis,.:
The condition known as M.E. is caused by the continuous switching-on of the quasi-fatigue response to infection.
So the ‘function of M.E.’ in the title follows on from the two hypotheses. M.E. can be seen as part of the immune system, evolved to signal the body to rest during infections, that has become permanently switched on. It is a dysfunction rather than a function, but the symptoms themselves certainly do have a function in a healthy body.
Two things arise from this. Firstly it seems to me to be a good way to explain M.E. to the wider public. As far as I know, there is no current comparable theory of what M.E. is, in terms of what specifically has gone wrong with the body.
Secondly, an overview like this could help direct research. For example we need to know as much as possible about the mechanism of healthy ‘flu-like symptoms’ before we can begin to work out how their switch became stuck in the On position.