Brotherhood of the Genes

It is certainly no understatement to say that one of the greatest expansion's in evolution's conceptual horizon has been the gene's-eye view, first formally articulated by G.C. Williams, and later amplified and extended by Richard Dawkins. Briefly, evolution from this vantage point is all about the differential survival of certain alleles over their competitors at a particular locus - what matters to evolution is genes, not the individuals that they make. Individuals are thus relegated to 'survival machines' (in Dawkins' famous phrase); far from being central to the selection process of evolution, they are mere servants, protectors of their potentially immortal creators.

It's easy to imbibe this sort of talk (once you've gotten over the shock of it), but it's quite another thing to actually start to thing of evolutionary adaptations in this way. It's still tempting to think of the whale's strong propeller tail as being for the benefit of the whale, but a gene-centred view renders this outlook false. A whale's strong tail is for the benefit of the whale's genes, not for the transient, and ultimately doomed, body they bring about.

Usually, such a correction borders on pedantic, since what is good for the whale is also good for the whale's genes (as in the above case). But it is nonetheless important to bear the distinction in mind, because there are some fascinating situations in which the interests of the body and its genes diverge. As we've stated already, in these cases, we should expect the genes to 'win' - adaptations, whether organs or behaviour, are for their benefit after all. Bodies don't even get a vote.

A typically enthralling and brilliant example is William Hamilton's theory of 'kin selection'. The theory, like so many in evolution, is so ingenious so as to appear almost banal. Yet it is anything but this. Recall that evolution can be anthropomorphised as genes struggling selfishly to replicate themselves. Now, with this in mind, how would the bodies that they created act? Well, in order to facilitate the genes' survival and replication, bodies might often appear to us as self-interested. In most cases, it simply wouldn't make evolutionary sense to program ones own 'survival machine' to work for the exclusive benefit of another survival machine holding rival genes. So I'll bet that, however well-intentioned you are, you don't think about world hunger as often as you do your own. And I'd bet you'd object to the idea of me summarily removing your heart to replace another man's ailing one. So would I, but did you ever stop to consider why?

However, selfish genes don't always translate into selfish bodies. Far from it, and this is where Hamilton's theory enters. When an animal behaves "selfishly" its behaviour is obviously controlled by its brain, the development of which was organised by its genes. But the particular genes in the animal's brain aren't directly replicated, of course - they are a dead-end lineage. The brain isn't passed on to ones offspring! Rather, they are working in the service of copies of themselves sitting in the animal's gonads. With this in mind, I'll let the brilliant Steven Pinker continue the narrative for a while:

But here is an important twist. The genes in an animal's gonads are not the only extant copies of the brain-building genes; they are merely the most convenient ones for the brain-building gene to help replicate. Any copy capable of replicating, anywhere in the world, is a legitimate target, if it can be identified and if steps can be taken to help it replicate. A gene that worked to replicate copies of itself inside some other animal's gonads could do as well as a gene that worked to replicate copies of itself inside its own animal's gonads. As far as the gene is concerned, a copy is a copy;
which animal houses it is irrelevant.

But how on earth could a gene identify copies of itself in another body? Clearly, it can't peer directly into the nuclei of a helpless colleague's cells and do a DNA analysis. What is required is a sort of 'rule of thumb' - a much more visible proxy marker that signals, with at least a reasonable degree of accuracy, that the animal shares some of your genes. The solution, as suggested by the theory's name of course, is to identify ones kin.

A brother shares approximately 50% of your genes by identical descent. So do parents and children. Zooming out gradually, a grandparent shares around 25% of your genes, as does a grandchild and an aunt or uncle, and a cousin shares roughly 12.5%, and so on. So when would it favour your genes (not you, remember) to try to get you to perform a costly action for the benefit of a relative? Obviously that depends on how close the relative is. The closer the relative, the more genes of yours he or she shares, and consequently the greater the benefit, to your genes, from any altruistic act targeted towards his or her body. Or, to approach from the opposite direction, animals should be predisposed to make greater sacrifices to closer relatives. This last insight was pithily summarised by biologist J.B.S. Haldane's remark that although he wouldn't sacrifice himself for his brother, he would gladly do so for either two brothers or eight cousins!

So kin selection fundamentally explains why we sacrifice our money, time and countless other resources for our children, and conversely why we love our parents, why calls to 'focus on the family' are often seen as virtuous, and why farmlands and trades are traditionally kept in the family instead of simply selling them off to the highest bidder. Of course, there are many fine-tunings to the basic theory as I've outlined it above. For instance, the emotion to assist and care for family (i.e. love) is tweaked according to who is likely to live the longer (hence parents give more to their children than they give back)... but such ingenious tinkering is another tale.

Kin selection also has a darker side, and it is this footnote that I wish to explore. I believe that it helps solve the riddle of apnoeas in newborns.

As the word suggests, an apnoea is a period where breathing ceases. (Neonatal apnoeas are not to be confused with the topical "sleep apnoeas" which share the respiratory arrest component, but little else.) Apnoea in the newborn period is a nightmare for parents, doctors and nurses. As the apnoea progresses, the child starts turning blue and the heart, starved of oxygen like the rest of the body, slows down. Sometimes the child starts breathing again spontaneously. Sometimes, as in an intensive care unit, it is noticed by a doctor, a nurse or a machine (in increasing order of likelihood) and the child is resuscitated. And sometimes, the child never recovers its respiration, and dies.

What could cause such a ruinous state of affairs? Well, the first distinctly odd thing about it is that it can be caused by almost any serious condition. So as not to feel so powerless, doctors are trained in some of the more likely causes, but even this list can't be rattled off quickly enough if you're late for an appointment. Forgive the medical jargon, but it is worth having look at how long one list of common causes is (in no particular order): hypoglycaemia, meningitis, septicaemia, asphyxia, pneumonia, hyaline membrane disease, anaemia, cardiac failure, patent ductus arteriosis, hypocalcaemia, hyponatraemia, convulsions, intraventricular haemorrhage, hypothermia, hyperthermia, maternal sedation, airways obstruction. If you've had any medical training, it may not escape your notice that that just about covers all the likely serious conditions a neonate could ever dream of having. This is odd fact number one.

Odd fact number two is that apnoeas are overwhelmingly likely to occur in premature babies. In fact, prematurity alone is probably enough to cause an apnoea. In 'term' (i.e. 9 month gestation) babies, one of the causes above is often found. But in premature babies, you usually search in vain.

The diversity of causes, and the targeting of premature babies, is often explained away by referring in a nebulous way to the supposed "immaturity of the respiratory system". Supposedly, the parts of the brain that regulate breathing are so delicate that even the slightest perturbation seems to cause the system to crash. And presumably, on this view, the respiratory centre is so underdeveloped in very preterm infants that their unexplained cases of apnoea are simply caused by a disturbance that is too mild to detect.

At first glance, this hypothesis seems to fit. It explains why prematurity is such a risk factor, as well as why adults (let alone older children) don't develop apnoeas in response to the same stresses. However, the explanation strikes me as deficient in at least one very important regard, namely that it comes very close to side-stepping the question totally. Even if it were possible to prove "prematurity" of the respiratory centre at all (which it isn't, at least yet), the answer stops abruptly short of answering the obvious follow-up question: why on earth would the respiratory centre be immature?

When you think about it, the "prematurity" answer starts to disintegrate before your eyes. For instance, to pick on another vital organ, the heart has had just as much time to develop as the respiratory centre, yet it is functional enough. In health a newborn's heart may comfortably pump a staggering 40 000 litres of blood around its little body per day. Even the lungs themselves are adequately-enough developed for the neonate's needs after only 34 weeks of gestation (average gestation is about 40 weeks). And the part of the brain that controls the cardiovascular system is apparently quite hardy and "mature". Yet we are asked to believe that the neighbouring respiratory centre simply packs up with the slightest nudge. Why? Basically the nub of the issue is this: if you were designing the body, wouldn't you want the vital respiratory centre online as early as possible? If survival is key, why not ensure that the last system to call it quits is the respiratory system? The child should surely struggle on despite any malady that afflicts it. It should valiantly struggle to breathe no matter what the odds. Shouldn't it?

Ah, but we viewing the scene from the vantage point of an actor that plays no part in this play. We have forgotten the doctrine of the selfish gene - bodies don't matter, except in so far as they ensure the replication of genes, remember? What does this paradox look like to a gene?

If you will pardon a quick diversion, let us approach the question with the help of an analogous case – that of a runt in a litter of pigs. Its prospects for survival are roughly proportional to its size. A pig only slightly smaller than the rest of the litter should struggle on and fight for maternal investment (food and time) as much as the rest of the litter, if not more so. Failure to do so would be silly, evolutionarily speaking, since the consequence for the pig, and the genes it carries, would otherwise be terminal. But what if the runt were very small, so that its chances of survival were extremely remote? Now we must remember kin selection and a gene-centred view. Such a runt would still take as much maternal investment as the rest of the litter, but the odds of this investment going to waste (if the runt dies) are now very high. Like human parental love, perhaps it can benefit its genes most by an act of altruism directed at kin who are likely to share some of its own genes. Indeed, it can, but in this case the sacrifice is the ultimate one: death. As shocking as it may seem, it is simply a matter of logic that there must be a point where the runt's chances of survival are so slim that it would be in its own genes' interests (via its siblings) if parental investment were cut off totally and spread around its brothers and sisters instead. Dawkins put it well in The Selfish Gene:

We might suppose intuitively that the runt himself should go on struggling to the last, but the theory does not necessarily predict this... That is to say, a gene that gives the instruction 'Body, if you are very much smaller than your litter-mates, give up the struggle and die' could be successful in the gene pool, because it has a 50 per cent chance of being in the body of each brother and sister saved, and its chances of surviving in the body of the runt are very small anyway. There should be a point of no return in the career of a runt. Before he reaches it he should go on struggling. As soon as he reaches it he should give up and preferably let himself be eaten by his
litter-mates or his parents.

Does this sound a little familiar? To me it does. Well, not the part about being eaten by ones litter-mates! Rather, about there being a point at which the best thing a very sickly animal can do for its genes is paradoxically to sacrifice itself, thus lowering the burden on those of its genes that find themselves in the bodies of kin. Of course, we don't have litters, but we do share 50 per cent of our genes with our parents and siblings. And to me, the neonatal apnoea phenomenon chimes all too well with this evolutionary 'runt' explanation. Apnoeas in newborns afflict exactly those babies who are most likely to die anyway - the very sick and the very young. There is no other obvious link between the massively diverse group of conditions that can cause it. Even the manner of the respiratory centre's demise is odd. No one is arguing the the respiratory centre is too immature to control respiration - all these children breathe fine at first, often for days. It's just that when things start to go very badly, that part of the brain throws in the towel. It's almost as if it starts working, takes a look around, assesses the situation, and makes a literally life or death decision. And we have already noted the absence of a cogent alternative explanation. So, could it be...?

Of course, such an explanation is still vulnerable to many of the criticisms levelled at 'adaptionism', which in its caricatured form is the belief that every aspect of an animal has some evolutionary advantage. For instance, it may be that the brain's respiratory centre is temporarily rendered vulnerable as an unavoidable consequence of some even more important goal - say, immune system development. However, for the moment at least, no such explanation is forthcoming. And there is at least one reason to doubt such a hypothesis in general: not many things are more important to develop than the brain's respiratory centre!

Finally, it is worth reiterating Hume's often forgotten principle that you can't derive an 'ought' from an 'is'. Evolution describes the world as it is, in all its amoral indifference to us. But we are in a position to temporarily overthrow nature's will. It may be 'natural' for very sickly children to effectively attempt suicide, but that doesn't remotely imply that we should put up with it. With modern medicine, we are throwing nature's slow calculations out of kilter. We can now save many of those who would otherwise have died, and in the process we are rendering evolution's equations obsolete. A very sickly child is no longer necessarily confined to the coffin - a simple course of antibiotics is often enough. Even the 'urge' towards apnoeas can often be attenuated by a simple dose of... caffeine. Caffeine? Yes, indeed - that's apparently all it takes to undo the work of millennia[1].


[1] Which is further circumstantial evidence, of course, that the apnoea response is 'designed', rather than unavoidable.