Feeling ill is good for you
OK, so you’re a bear. With a sore head. You feel like a human with a hangover. You really don’t feel like a day’s foraging, so it’s back to the cave and rest: exactly what your bear-frame needs to fight an infection, food poisoning, or whatever you are suffering from. You may be named Booboo and you may not be smarter than the average, but you didn’t need to be; your body has just stopped working normally and made it blindingly obvious what the next course of action, or more accurately inaction, is.
Now, your smarter friend Yogi feels just great. He notices some funny noises coming from his gut, remembers that Booboo wasn’t feeling too good and puts two and two together. He thinks that maybe he is coming down with something, but it’s getting on for winter and it’s time to lay down fat stores. So taking everything into account he works out that he might as well go on foraging and go back to the cave whan his gut gets a lot worse.
But Yogi doesn’t make it back to the cave. The virus starts turning his guts to mush way before then. He starts bleeding inside and doesn’t notice. He collapses just as the night starts to freeze. He dies before dawn.
Yogi had a good brain, which took a carefully calculated risk. Booboo had a body with an early warning system that processed the same information and came to a very different conclusion.
The take-home message? Feeling bad can be good for you. The individuals who feel bad when they start to become ill will be at a selective advantage to those who do not. It seems likely, therefore, that there is a physiological mechanism for an illness early-warning system, and that the warning is strong enough to over-ride any opposing messages from the thinking brain. As with Yogi, the brain might be smart, but the body has to be smarter.
What makes you feel ill?
I would guess that most of us, if we thought about it at all, think that the disease makes us feel ill. And it may well be, in many cases: the toxins produced, or the organs not working properly can directly affect the body. But with some fast-developing illnesses, notably viruses, if that was all you were relying on, large numbers of cells would be turning to mush before your body went into rest-and-defend mode.
But if the body had an active ‘feeling bad’ mechanism waiting to kick in as soon as a disease was detected, you could get your retaliation in first. Feeling bad would be your body’s way of telling you to divert energy away from activity and towards your immune/repair systems. It is a symptom of disease, but one produced ‘intentionally’ by the body rather than the disease itself.
If this system did exist, you would expect ‘feeling bad’ to be a common symptom to many unrelated illnesses, which is of course the case, although it is often neglected as an actual symptom as it is so common and therefore not diagnostic.
To be effective, though, this early-warning part of the body’s defences would have to be strong enough to overcome the Yogi in you: the smarter-than-average brain telling you to ignore it. It is no good it being just a feeling therefore; the body has to make the brain an offer it can’t refuse. The ‘feeling bad’ reaction has to be actually debilitating, to undermine the body’s natural desire for activity, so that the brain feels that it has no choice but to comply and rest.
But there is a conflict here, as with just about all body-control mechanisms, between the ‘brain’ (strictly ‘higher’ brain) that is signalling go on, and ‘body’ (including ‘lower’ brain) that is signalling stop. If this system gets out of balance, you’ve got problems.
What makes you go on feeling ill?
Assuming you accept the existence of a system as described so far, there are two main ways it could go wrong: not feeling bad when you are ill, and, conversely, feeling bad when you are not.
The first malfunction is potentially a killer. As in the Yogi example, there would be huge selective pressure against it. I’m sure medical experts will have examples of this however.
It is the second malfunction that is of most interest to ME theory, as it fits the symptoms of ME very well. But would it react like the symptoms of ME, which get worse following a number of trigger factors?
There would definitely be a selective advantage in it doing so. While most sensible bears go and rest when they feel ill, there will be a minority of Yogis who think they know better than their bodies and push themselves to go on after just a few more blackberries. In those cases the signal needs to be stronger. So if the body detects increased activity, or a greater or more prolonged response to stress, it seems likely that it would increase the ‘feeling bad’ reaction until the desired result was achieved, ie bear goes back to cave and rests.
There is a subtler point about this reaction that could be predicted: that it would be delayed. An immediate debilitating response would be just that: debilitating. It would not allow the bear to find a place of safety. It would be better, then, if the body could somehow keep a ‘tally’ of the amount of activity and stress it is undergoing while it keeps going for a bit longer and finds a good place to rest up. When it subsequently detects that it has got to saftey and is resting and relaxed, that would be the time for the ‘feeling bad’ reaction to kick in properly. And the more keeping-going it has tallied up, the stronger and longer the stay-put reaction should be.
So far, so nothing special. Bear recovers, feels better one day, goes off doing what bears do. But what if something went wrong with the signalling, so it didn’t turn off? Say, for example, the bear had a second illness, maybe a gut infection, on top of the first. And the body’s defence mechanism became either damaged or confused, so that the ‘feeling bad’ mechanism didn’t turn off properly.
In that case, more activity and stress would turn it back up again. But just as with the ‘tally’ system where the body adds up the recent activity and reacts proportionately, the reaction would just get stronger and stronger each time. Eventually there would be a cycle which will be very familiar to ME sufferers: Activity leads to feeling bad which leads to resting. Feeling better, but not totally well, leads to more activity, which leads to feeling bad, and maybe worse than before, which leads to a longer rest…and so on. However long the period of rest, the body never feels completely better, so eventually there has to be another episode of activity which leads to feeling bad again. Meanwhile the body keeps totalling up all the accumulated activity and increases the strength of the ‘feeling bad’ reaction, and the cycle is locked in. So now you are suffering from a progressive disease..
So now you are suffering from…what?
‘Feeling ill’ doesn’t sound that specific, even though it is accurate.
‘Long-term feeling ill’ would cover many other long-term illnesses.
‘Long-term feeling ill without a detectable long-term disease-causing agent’ …is getting a bit unwieldy, and is open to having holes picked in it for exceptions.
There seem to be three options on the table: ME, Fibromyalgia and Chronic Fatigue Syndrome*. The first two are more neutral, but much can be made of the differences between them. Myalgic Encephalomyelitis/pathy just means pain in the muscles and something wrong with the brain/brainstem, although currently the presence of ‘fatigue’ is also important despite being out of the name. Fibromyalgia means pain in the muscles and connective tissues.
Some medics seems to specialise in one or the other, and use various scoring systems to distinguish them. Woe betide any sufferer that fails to do so in their presence, though: I have actually been kicked out of an ME clinic by saying that I had pain and weakness, but not what I would call fatigue. I was deemed to have fibromyalgia and to be in the wrong place.
Sufferers, though, know that the condition varies from day to day, manifesting sometimes as pain in the muscles (more like fibro), and sometimes as overall grogginess/weakness (more like ME). As has been said many times, there is a spectrum between the two, although that doesn’t help the naming of the beast. I will propose a solution later on, but first need to rule out the third name, Chronic Fatigue Syndrome.
*Just found another one on the page title of Phoenix Rising: NeuroEndocrineImmune Condition. For me that is both clumsy and non-descriptive of what the condition does to us. I suppose it wants to rule out ‘mental health’ problems (in the insurance exclusion sense), but I don’t think that will happen until a mechanism is proven.
So what’s wrong with calling it Chronic Fatigue?
We all know what Fatigue is, don’t we? And how we detect that we are ‘fatigued’: muscle pains, ‘heaviness’ or weakness in the muscles, grogginess or dizziness. Then there is the need for sleep, another category of Fatigue.
Fatigue, mainly of the first kind, is almost invariably cited as being a symptom of ME, with those signals that tell us that we are fatigued being sub-symptoms. But there is no reason why those sub-symptoms (FEELING tired), necessarily tell us that we are suffering from the same condition as produced by a lot of activity (BEING tired). The word ‘fatigue’, as currently used by most in the ME field conflates these two meanings: the symptom of ‘feeling tired’ with the diagnosis of ‘being tired’.
But what if, as my ‘feeling-ill-reaction’ theory proposes, those ‘feeling tired’ symptoms were produced by an entirely different process than ordinary fatigue, or ‘being tired’? What if, as an adaptive defence reaction to illness, the body was trying to convince itself that it had real fatigue, by producing fake symptoms of fatigue? How fake those symptoms are, how deep the deception goes, need not concern us here; the take-home point is that it is entirely possible for the body to produce symptoms of fatigue when it is suffering from an illness, but is not actually fatigued. And that it would be a selective advantage for it to do so.
Now, even if this illness-fatigue is biochemically indistinguishable from the activity-generated fatigue, the ultimate cause is very different. To distinguish the two I therefore propose a new term, quasi-fatigue, which could be abbreviated QF (although there is probably another confusable QF I haven’t thought of). There would also have to be a corresponding term for ‘being tired’, which could be Activity-generated Fatigue, or AF.
That there is a physiological difference is suggested by the difference in behaviour between the two. AF is direct, immediate (although of course the effects can last some time), and usually easily reversible through rest. QF behaves like an inflammatory condition: delayed onset, long-lasting, and much harder to recover from.
The difference between the two would probably only be of academic interest unless there was a disease where the mechanism malfunctioned: in the case of QF, that the symptoms were permanently switched on, or kept recurring, in the absence of an obvious triggering illness. Of course, there is such a disease/s: ME/Fibromyalgia.
I therefore propose a new term for our illness: Quasi-Fatigue Syndrome. This has various advantages:
- it describes the condition.
- it opens and emphasises the possibility that the ‘fatigue’ might not be produced in the usual activity-related way, and may behave differently.
- it doesn’t confine the symptoms to a particular area, like ME or Fibro.
- it is non-judgemental and does not confuse a symptom with a pre-judged diagnosis, like Chronic Fatigue Syndrome.
- it does not imply that the experienced fatigue-symptoms are biochemically or physiologically different to those produced by activity, but just have a different causal agent.
- it is neutral regarding a ‘psychological’ theory/component of the symptoms. However I will discuss the probability or otherwise of a higher-brain malfunction cause below.
- it is neutral regarding a ‘virus’ theory of the symptoms.
Whether or not you like my ‘feeling-bad’ theory of this illness, the term QFS, Quasi-Fatigue Syndrome, opens the possibility of it being a contender without ruling out either of the current opposing paradigms or being too proscriptive about the symptoms.
Further implications of the theory
The hypothesis is constructed a priori, deduced from logic and a little experience of the illness rather than collected empirical evidence. Nonetheless I think it would be instructive to look at the implications of the theory to see where it might lead, and if evolutionary theory can solve any other of the puzzles surrounding the illness.
Although it is perfectly possible that a virus might have caused the initial fault in the body’s defence mechanism, and may even be perpetuating the condition, it is not necessary for the theory which relies on a malfunction of normal physiology without specifying a cause.
A psychological explanation is also unnecessary for this theory to work. Although it is perfectly possible for the ‘mind’, ie higher brain, to affect the body’s defence reactions, it seems more likely that, as with many defence system-related diseases such as cancer and auto-immune conditions, physiological mechanisms will provide sufficient explanation for this.
Many mammals and birds observed in captivity will exhibit a similar behavioural response to disease. It seems likely, then, that they are also experiencing quasi-fatigue. This implies that it is a basic attribute of higher vertebrates and controlled in a part of the body or brain that is common to all. This would tend to rule out psychiatric treatments that concentrate on higher brain function: the ‘think-yourself-better’ type of treatment.
An evolutionary approach can also provide an explanation of the results obtained by many Alternative Medicine treatments for QFS.
As many QFS sufferers will get better without any form of treatment, how do we know that those undergoing alternative treatments would not have got better anyway? The answer lies in the percentages of successful cures or improvements quoted by the practitioners, which always seems impressive. Sometimes it is 100% of those who complete the full course of treatment.
Most of the alternatives, however, do require considerable commitment, dedication, and persistence to get through to the end. A common end-of-treatment comment is that the treatment was hard, but it was worth the effort. This would include any graded exercise or cognitive behaviour therapies which may or may not be deemed ‘alternative’.
Now take a random group of QFS sufferers. There will be a spectrum of severity and, importantly, a spectrum of improvement. Many, if not most, will eventually get better anyway without any treatment. Now make them do something that requires effort: it might involve concentrated thought, or repeated actvity of some kind. For visualisation lets call it hill-climbing. Everyone is set a certain amount of hill to climb in a certain time. Some won’t make it and drop out. Maybe the treatment is a flexible one, and a smaller amount of hill is then set. Everyone eventually finds their own level of hill that they can climb.
But there is a spectrum of improvement. Some will be getting better anyway; some worse. Those improving will be set gradually higher levels of hill, and will succeed if the treatment is sensitive to them. So it appears that the more they do the treatment, the better they get. These are the ones who will end up on the testimonial pages of the websites, praising the treatment for curing them.
But what of the ones who are getting worse? They are far more likely to drop out before the end of the treatment, either because they are too ill to do even the minimum effort required, or because it doesn’t seem as though it is working. Some may bottom out and improve, in which case they will join the succeeder group. But most will just drop out. They will not appear among the testimonials, and, in terms of the practitioner, can’t expect to succeed with the treatment as they haven’t made the effort.
So apparent alternative cures can be explained purely by natural selection: those who are getting better will be ‘cured’; those who are getting worse will be ‘culled’ – from the statistics at least.
Anyone doing a study of alternative treatments of QFS needs to be aware of this by the way. Assuming a suitable placebo treatment can be devised, both treated and control groups would need to be carefully monitored for progress. Anyone dropping out of the treatment group for whatever reason should be deemed to be at the ‘worse’ end of the spectrum, and the ‘worst’ sufferer in the contol group needs to be eliminated from the study at the same time. I’d be interested to know if any studies have actualy done this, for example recent CBT/GET studies in the UK.
Searching for a cure
Given the possibility of this theory, it does have implications for research efforts: notably, the physiological basis of the QF-reaction. I realise that there is much research around the immune system relating to this illness, but do we really know, in a healthy individual, what makes us feel ill?
There is a possible explanation for the illness widely known as ME as an evolutionary adaptation of the body’s defence system that has malfunctioned.
I propose that ‘feeling ill’ is not entirely a direct effect or a by-product of disease, but is to some extent part of the body’s defence system, and actively produced by the body. This ‘feeling ill’ reaction to disease makes the sufferer go and rest. There is an adaptive advantage to this as the body’s energies can be diverted away from activity and towards fighting the illness. This reaction can be seen in a wide range of animals, which implies that it is controlled at a level within the brain that many animals have in common.
This can be interpreted as ‘fatigue’, because it is advantageous to the individual for it to mimic normal, or activity-generated fatigue. However there is no a priori reason for ‘feeling tired’ always to have the same physiology as ‘being tired’. At present the word ‘fatigue’ conflates the two meanings. To distinguish it from activity-generated fatigue (AF), I propose naming the feeling-ill reaction ‘quasi-fatigue’ (QF).
The quasi-fatigue reaction increases in intensity following increased activity of or stress on the body. There can be a struggle between the individual’s natural drive to activity and the body’s need for rest during illness. Resting is the more advantageous behaviour during illness, so there is an adaptive advantage for the reaction to increase in strength until resting is achieved.
If, when the illness is over, the ‘feeling bad’ reaction is not switched off, it will therefore continue to increase in intensity in response to restored levels of activity and a normal range of stress. This will lead to a cycle of activity, quasi-fatigue, rest, improvement, activity, more quasi-fatigue
The theory is consistent with many familiar aspects of the illness which have puzzled many sufferers and practitioners.
Because the illness can manifest in a variety of symptoms, because we don’t know the mechanism, and because the word ‘fatigue’ conflates ‘feeling tired’ with ‘being tired’, I propose a new term for the illness: Quasi-fatigue Syndrome or QFS.
I realise that here I am entering a much fought-over and bloody (literally according to some) academic battlefield of single-minded individuals and vested interests. I come to it in a deliberately naïve way in the hope that my arguments will be discussed on their merits, rather than after deciding which side I am on.