How Many Friends Does One Person Need? (11 page)

The problem for us humans is the sheer size of our
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brains. On the basis of the pattern we find in the rest of the mammals, we humans ought to have a gestation of twenty-one months. Yet as we all know, it is actually just nine months. The reason is very simple. Several million years before our ancestors decided it might be a good idea to have such big brains, they thought it was an even better idea to walk upright. This led to the evolution of our very distinctive bowl-shaped pelvis, quite different from the rather elongated pelvis of all the other monkeys and apes. This bowl-shaped pelvis provided a much better base on which to balance the trunk and head, especially once that big bulging brain came along. The modern human pelvis has been with us for the better part of the last two million years, ever since the first members of our genus,
Homo erectus
, developed their striding walk and the capacity to migrate over long distances.

The problem is that, as invariably happens in evolution, it is impossible to get a perfect engineering design. One of the sacrifices we have had to put up with to get the benefits of long-distance striding has been a weak lower back. Evolutionary processes could, of course, have solved the problem by making the lower backbones out of cast iron, or perhaps bone ones of massive proportions, but that would have added measurably to the weight we have to carry around, and would have made our lower back much less flexible. That flexible spine is a trait of enormous value to our walking pattern – and of major significance to cricketers who fancy themselves as fast bowlers – and so, by definition, to our many ancestors who made their way in the world by spearing wild animals for meat. What we have is a classic Heath Robinson
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evolutionary compromise – a consequence of trying to get the best of two worlds that have conflicting interests. The painful result is a lower back that is still prone to ‘go’.

Then, when their descendants decided to increase the size of their brains dramatically several million years later, they hit a bit of a problem: the bowl-shaped pelvis had dramatically narrowed the birth canal. Since it is the size of baby’s brain that is the limiting factor, the result was... well, an eye-watering problem.

At this point, the options were rather limited. Of course, we could have backtracked rapidly and given up this stupid idea of having bigger brains – who needs brains anyway, for heaven’s sake? But that would have meant staying put in our evolutionary niche. Since, thanks to climate change, the world was altering dramatically around this time, staying put would have meant becoming ecologically more embattled, just like the other great apes whose terminal decline towards extinction was already well in motion by then. To survive, we had to change and adapt to new ecological niches. Big brains were the key to that, and without them those kinds of changes wouldn’t have been possible. So something dramatic was called for.

The inspired solution our ancestors eventually came up with was to reduce dramatically the length of time for which the mother carries the baby before birth... from the twenty-one months we ought to have, to the nine we finally settled for. But this came at a cost: giving birth to a baby whose brain is only half-developed means a very vulnerable baby. Whereas monkey and ape babies are active and busy within a few hours or at most days of birth, human babies take a full year – the missing twelve months – to reach that stage.
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Compared to monkey and ape babies, human babies are on the very edge of survival even when they are full-term. This is why they really do struggle when they are born prematurely. Research in the last decade or so has found that premature babies suffer disproportionately high frequencies of developmental difficulties, including poorer academic performance and more physical problems later in life. This is not, of course, to say that every single one of them does, but rather that the risks are just much greater.

So it is that for the first year of life, normal human babies are basically just lumps of flesh and bone that need an awful lot of TLC. And since TLC is hard work for parents, babies had better have winning ways and lots of baby-appeal. And that raises a whole new host of problems. One of these is the fact that, from the mother’s point of view, it pays to have your man on side. But if the baby is not his, that can create – shall we say – difficulties. At this point, you have two choices: you can make sure the baby really looks just like dad, warts and all, or you can make it look like no dads. The first is fine so long as dad always really is dad. But if dad – shall we say with even greater delicacy – isn’t always dad, maybe the second is the better option. And that, it seems, is what humans have done. Human babies by and large look much more like each other than adults do. So much so, in fact, that all babies have blue eyes to begin with, and only change into brown or green later. It helps keep dad guessing.

But anxious not to leave anything to chance, we back this up with a bit of psychology. Next time you are around a newborn baby – probably best not yours – listen to what people say about it. A study by Martin Daly and Sandra
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Wilson of McMaster University in Canada found that both the mother and her parents make great efforts to emphasise how much the baby looks like dad as soon as he comes into the room. ‘Hasn’t he got your eyes/nose/forehead/chin...’ And this wasn’t just a Canadian or European thing: similar results were reported from another study in Mexico. Now, excuse me... but nothing on baby’s face looks anything like any of its progenitors’ equivalent bits. It’s not meant to. Still, it does provide a lot of scope for leverage to persuade dad that he had better get his sleeves rolled up. Just as well, probably.

I’ll confess straight away that I am fascinated with sex. Never in the course of biological evolution has anything more complicated ever evolved. And I don’t just mean the complications of the relationships that emerge from it. I mean biologically. I’ll bet you think that sex is just about X and Y chromosomes. At least, that’s what you were probably taught in school biology lessons. And, up to a point, it’s true: we are bog-standard mammals, and our sex is determined by the chance event of whether we inherited an X or a Y chromosome from our father to pair up with the X provided by mum. XX gives a girl, XY a boy. Simple, isn’t it? Well, yes, up to a point. But in fact, it’s a bit more complicated, even in humans. Your sex chromosomes are only part of the story. You may have an XY pair, but you need not have turned out to be a boy.

In fact, you only get to be male if a whole series of things fall into place at the right time – otherwise you will be female, whatever your sex chromosomes. One of these
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key events is known as the ‘race to be male’. The foetus lays down a particular type of fat cell early on, and it requires a specific density of these to switch an XY-chro-mosome foetus over from its default female body form to a male one. The right density of fat cells triggers the release of testosterone that switches the foetus’s brain over into a male brain, and this sets in motion the conversion of all the other bits that matter.

In fact, even chromosomal sex can get pretty confusing. Accidents of genetics can result in any number of possible combinations – X0 (one X chromosome and nothing else), XXY, XXYY, XXXYY, XYY (the so-called ‘super male’). The only one you can’t have is Y0 (no X chromosome): the Y chromosome is tiny and only a very small segment of its DNA has any function, and that is associated with the business of changing the default female form into the male one. But if you don’t have the female bit to start with... curtains, I’m afraid. However, that said, most of this bewildering array of chromosome types are associated with fairly serious disabilities and abnormalities, so their product is often distressing. Fortunately, most of them are rare.

But things begin to look even odder when you look beyond us mammals. Birds, butterflies and amphibians do it the other way around. In birds, it is the XY sex that lays eggs and the XX sex that has gaudy plumage, sings songs and rushes around defending its territory. To avoid confusion, the bird people usually refer to these as W and Z chromosomes, rather than X and Y, but that doesn’t hide the fact that they are the mirror image of us mammals. What this tells us is that it’s an accident of history which way things turned out: there is no ‘natural’ way of
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doing sex.

And it gets worse. In turtles and crocodiles, your sex depends on the temperature of the nest in which you were incubated as an egg. In crocodiles, warm temperatures produce males, cooler ones females, but in turtles, it’s the reverse. Famously in bees, females have two sets of chromosomes, but males have only one (because they arise from unfertilised eggs). In many of the small coral reef fish like wrasses, it depends on social circumstance. Everyone begins life as a female, but if there is no male, the dominant female in any community undergoes a rapid metamorphosis and miraculously turns into a male before your very eyes. When she – or should it be he? – dies, the cycle starts again and the current dominant female changes sex and becomes the breeding male. I guess that gives a new meaning to the phrase ‘change of life’.

But of all the bizarre and weird ways in which species produce two sexes, perhaps the first prize goes to the humble bonellia worm, a ten-centimetre-long member of an obscure worm family found in the Mediterranean sea. All bonellia begin life as tiny flake-like larvae, floating free. Those that happen to get attached to rocks or other substrates turn into females; those that get eaten by a female before finding somewhere to attach migrate down into the female’s uterus and turn into males. They then spend the rest of their lives in the safe confines of the female’s interior – which they may share with up to twenty other males.

Sex is fascinating – I rest my case.
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The medical profession has a great deal to answer for. For millennia, it has held us in the palm of its hand because of our desperation to avoid the inevitable consequences of our biology – disease, disability and death. As medical science has become more sophisticated, it has seemed able to perform miracles. But one of the problems is that, more often than not, those miracles pander to our short-term desires rather than to what is best for us in the long run. We are desperate for short-term cures that solve a problem now, but we ignore the fact that doing so may create bigger problems for us in the future.

It seems that we never learn. During the 1950s, DDT and penicillin seemed to be the wonder drugs of the century: we could cure anything from malaria to infections that had previously killed hundreds of thousands of children and adults every year. So we liberally sprinkled DDT over tropical habitats, and dosed ourselves and our animals on penicillin. But natural selection, the engine of evolution, soon undermined all this good work. Within just a few decades, we had successfully, if unintentionally, bred DDT-resistant mosquitoes, penicillin-resistant bacteria, MRSA and a string of other horrors that have made
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our original problems seem like kids’ play. The moral is that it isn’t always sensible to try to interfere with evolution – especially when, like most members of the medical and pharmaceutical professions, you don’t really understand the principles of Darwin’s theory of evolution by natural selection.

If you have the impression that we are being progressively swamped by new and more troublesome diseases, it’s now official: we are. An analysis of 335 major new disease outbreaks that have occurred since 1940 has shown that the frequency of new diseases has increased steadily with time. The number of new diseases that have hit us each decade has increased three- to four-fold in the last half-century alone. Among the more familiar ones are the likes of MRSA and the various new strains of ‘superbug’ that are resistant to antibiotics, SARS, HIV, and drug-resistant strains of malaria. Given that malaria was already one of the great killers – it afflicts 515 million new people each year, and kills between one and two million of them, mostly children – the prospect of worse to come is not appealing.

Around fifty-five per cent of these new diseases are bacterial in origin, with many fewer than had previously been expected being due to viruses or prions (the most familiar of which is ‘mad cow’ disease). Many are associated with the appearance of drug-resistant forms of old diseases rather than something entirely new... a stark and terrifying reminder of the speed with which micro-organ-isms can evolve when challenged – and of the fact that
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we have been hoist upon our own petard through the over-liberal, and invariably careless, use of antibiotics and other drugs.

It seems that sixty per cent of these new disease outbreaks are caused by zoonotic pathogens – pathogens that we have caught from animals – and seventy per cent of those have come from wildlife. The notorious Ebola, HIV, SARS and the Nipah virus (a pathogen from fruitbats which appeared in Malaysian pig farms in 1999 and resulted in 105 human deaths) are all cases of pathogens that jumped the species barrier from their natural animal hosts to humans.

This is not entirely new, of course. Many of our more familiar diseases – often ones that, in the past, have caused very high mortality rates – had their origins thousands of years ago in domestic animals that our ancestors decided to have living with them or were brought into our houses by rodents of one kind or another. Chickenpox, cowpox (and its close relative smallpox), measles, rabies, Lassa fever and haemorrhagic fever all have their origins in pre-history, thanks to our having had too close an association with their respective animal hosts.

The tropics have been notorious breeding grounds for most of these historic diseases, and it has long been recognised that the tropics are among the least healthy places to live – unless one happens to descend from a racial group that has evolved some kind of immunity over time. Examples of the latter include the well-known case of sickle cell anaemia among west African Bantu peoples. Sickle cell is a recessive allele that confers significant resistance to the malaria parasite, but when a recessive allele is inherited from both parents, the result is an excruciat-
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ingly painful condition whose sufferers rarely make it beyond their teens.