Mutants

OUR SPECIES HAS, SINCE 1758, borne the flattering, if not always accurate, name Homo sapiens – thinking Man. At least that is what the Swedish naturalist Carl Linnaeus called us in the tenth edition of his Systema naturae, the work which tax-onomists even now accept as the first authoritative source of the names which they have given the world’s creatures. It was nearly otherwise. In Linnaeus’ text, directly adjacent to the word ‘sapiens‘ is another designation, an apparent synonym for ourselves, yet one that is somehow never explained: ‘H. diurnus’ – Man of the day. It is a name that seems to have had particular resonance for Linnaeus. His notebooks show that he toyed with sapiens vs. diurnus for much of his life, and it is only in the tenth edition that the latter is firmly relegated to second place. On the face of it, Linnaeus’ belief that diurnality captured something special about our species is puzzling. Although we are undoubtedly daylight-loving creatures, so too are many others. It is only when one pages through the staggered typography and compressed Latin of Linnaeus’ text that one finds the explanation for his diurnal dreams. Linnaeus, godfather to humanity, believed that we were not alone.

Long before palaeontologists unearthed from Serengeti dongas the bones of our extinct Hominid cousins, Linnaeus believed that the remoter parts of the world were peopled by other species of humans. He was not thinking about the humans who lived in Asia, Africa or the New World; they clearly belonged to the same species as himself. He was thinking of something altogether more exotic: a species of human that was bowed and shrunken in form, that had short curly hair rather like an African’s, only fair, that had skin as white as chalk and slanted golden eyes. With eyesight as poor by day as it was acute by night, they were crepuscular, cavern-dwelling creatures who emerged at dusk to raid the farms of their more intelligent cousins. They were ancient; perhaps they had even ruled the earth before Man, but now they were on the retreat. This species, Linnaeus said, was ‘a child of darkness which turns day into night and night into day and appears to be our closest relative’. True, he had never seen one, but had not Pliny and Ptolemy written of the Leucaethopes? And had they not been seen more recently, not least by his own students, in Ethiopia, Java, the Ternate Islands and Mount Ophir of Malacca? The reports seemed vivid and precise: in Ceylon they were called Chacrelats; in Amboina, Kakurlakos – from the Dutch for ‘cockroach’; and everywhere they were despised. This was enough for Linnaeus, and true to his classifier’s instinct, he gave them a name: Homo troglodytes – cave-dwelling Man. And next to that he wrote ‘H. nocturnus’ – Man of the night.

What was Linnaeus thinking of? As the founder of modern biological classification, his name is second only to that of Darwin in the naturalist’s pantheon. But no one reads Systema naturae any more, much less his many other works, and we forget that his mind was as much the mind of a medieval mystic as of an Enlightenment savant. Linnaeus was frankly credulous. He believed that swallows hibernate at the bottom of lakes; that if the back of a puppy were rubbed with acquavit it would grow up dwarfed; and that Lapland was the home of a creature called the Furia infernalis, the Fury of Hell, that flew through the air without the aid of wings and fell upon men and cattle, fatally running them through.

This last was clearly fantastic even to Linnaeus’ contemporaries. Not so Homo troglodytes. By the 1750s it was well known that Africa at least contained creatures similar to man; Edward Tyson, after all, had dissected his ‘pygmy’ or chimpanzee more than fifty years previously. Another such creature, half man-half ape – the matter was all very obscure – was thought to live in the Malay Archipelago. The Dutch naturalist Jacob Bontius had illustrated just such an ‘ourang-outang’ in his Historia naturalis indiae orientalis (1658). Bontius’s ourang is a fairly human, if hairy, female wearing nothing but an alluring expression; a century later Linnaeus borrowed this woodcut and relabelled it Homo troglodytes. Bontius himself had little to say about his ourang (though he rightly questioned the Malay belief that it was the progeny of Javanese women and the local apes), so Linnaeus grafted onto its image the ancient tradition that spoke of a remote and secretive race of unnaturally white, golden-eyed and profoundly photophobic people. It is these characteristics that yield the identity of the remainder of the melange that is Homo troglodytes. Shorn of its body hair and cavernicolous habitat, it is clear that Linnaeus’ Man of the night is just an ordinary human albino.

GENEVIÈVE

Linnaeus was not the only eighteenth-century naturalist with an interest in albinos. His French rival Buffon was another, but unlike Linnaeus, Buffon actually met one. In his Histoire naturelle, he writes of an encounter with a girl named Geneviève. She was eighteen years old, a native of Dominica, the daughter of slaves transported there from the Gold Coast, and now the servant of a wealthy Parisienne. Buffon examined her minutely. She was 151 centimetres (four feet eleven inches) tall, with slanted grey eyes slightly tinted orange towards the lens, and skin the colour of chalk. Yet her facial features, he said, were absolutely those of a négresse noire, a black African woman. True, her ears were stuck unusually high on her head, yet even so they were quite different from those of the Blafards, the albinos of the Darien Peninsula, whose ears were said to be both small and translucent. Buffon measured her limbs, her head, her feet, her hair; he devotes a paragraph to her breasts, notes that she was a virgin, and then, with interest, that she could blush.

What made Geneviève white? Buffon was certain that Linnaeus’ Homo troglodytes was just an ape. As for the Blafards, Kakurlakos and Chacrelats, these were merely descriptions of anomalously depigmented people living amid an otherwise dark-skinned population. One in ten children born in the Caribbean islands, he was told, was an albino. Geneviève’s parents were black, as were her siblings; whatever the cause of her whiteness it could not be contagious or even racial. Though he failed to solve the problem of albinism, when compared to the fantasies of Linnaeus, Buffon left it immeasurably clearer. He also commissioned a lithograph of Geneviève, which shows her standing amid tropical fruit, quite naked and snow-white, as if in a photographic negative, smiling gently, perhaps at the absurdity of scientists.

THE PALETTE

We are a polychrome species. Yet the palette of human colour has only two pigments on it. One, eumelanin, is responsible for the darker shades in our skin, hair and eyes, the browns and the blacks; the other, phaeomelanin, for the fairer shades, the blonds and reds. As a painter mixes three primary colours to get all others, so too the various shades of our skins are given by the mix of these pigments.

Blacks have lots of eumelanin; redheads have lots of phaeomelanin; blonds have little of either. Albinos have no skin pigments at all. The pigments themselves are made in cells called melanocytes that are found within the top layers of the skin, the epidermis. These melanocytes package pigments into sub-cellular structures called melanosomes which they then transfer to the skin cells immediately above them, giving them colour. Mutations in several genes cause albinism. The most common disables one of the enzymes that melanocytes use to make pigment. In such cases even the eyes are devoid of pigment, and their redness comes from the retina’s blood vessels. The absence of pigment makes albinos sensitive to light and they often squint – hence the photophobia and slanted eyes of the Kakurlakos and Blafards. But some albinos have at least some pigment in their eyes, and in these cases the defect lies in a protein that is called, somewhat enigmatically, ‘P’, used in the packaging and transport of melanosomes. Geneviève’s eyes were grey, not red, and it is almost certain that both copies of her P gene were defective. We can even guess what the mutation was. The most common cause of albinism in Africa is homozygosity for a 2.7 kilobase-pair deletion in the P gene. The same mutation is found in the Caribbean and among blacks in the United States as well, carried there by the slave trade.

There are no tribes, races or nations of albinos anywhere in the world; however, Pliny’s Leucaethopes are not entirely without foundation. About 1 in 36,000 Europeans is born albino, and 1 in 10,000 Africans. But the number jumps to 1 in 4500 among the Zulu and 1 in 1100 among the Ibo of Nigeria, and in very local populations the frequency can become even higher. In 1871, en route to his encounter with the Aka pygmies, George Schweinfurth came across some.

That albinism can be so common is a bit surprising. African albinos have, by any account, a hard time of it. Not only do they often suffer social discrimination and have difficulty finding marriage partners, but for want of pigment they cannot work for any length of time outdoors, and they are also prone to melanomas, a particularly destructive variety of skin cancer. These selective disadvantages should act to keep albino genes, and hence albinos, rare. Some geneticists have suggested that one reason for the high frequency (1 in 200) of albinism among the Hopi Indians of Arizona is that albino men, excused from working in the fields, stay at home and therefore dally among the women. But the evidence for this seems to rest on the charms of one old Hopi gentleman who was reputed to have fathered more than a dozen illicit children.

PIEBALDS

Those children would have fascinated Buffon. In his search for an explanation for albinism, grasping at a theory of inheritance that did not yet exist, he was keen to know what the offspring of a union between an albino and someone with normal pigmentation would be. He thought they might be piebald. In the Histoire naturelle he gives another lithograph. This one is of a girl, perhaps four years of age, standing amid a clutter of exotic artefacts: a parasol, axes, a blanket and a feathered headdress. A small parrot, a household pet, perches upon her hand suspended in mid-air. The girl has a two-tone body: a mosaic of black and white.

Buffon never met the child, knew little about her origins, and described her entirely from a picture. Painted in Columbia by an unknown artist around 1740, the portrait was dispatched to Europe on a Spanish vessel which was promptly seized by the West Indies squadron of the Royal Navy. Now a trophy of war, the picture was taken to Carolina where it was copied at least twice. One of these copies, or perhaps the original, was sent to London, but this ship was plundered as well – it was the French navy’s turn – and the painting was placed in the hands of the Burgomaster of Dunkirk, a M. Taverne, who sent it to Buffon. And so the War of the Spanish Succession brought Marie Sabina, the piebald child, to the eyes of Europe’s greatest naturalist.

Buffon was enchanted. His copy of the portrait, which is now lost, bore the following inscription:

In a letter that he sent with the portrait Taverne wrote: ‘In spite of the legend, I think that the child is the issue of a union between a white and a négresse, and that it was to preserve the honour of both the mother and the Society [of Jesus] whose slave she was, that it states that both the parents were black.’ Buffon replied that although he initially thought that Taverne’s explanation might be true, upon reflection he doubted that it could be. There were thousands, millions, of people of mixed black and white blood, and they all appeared to be uniform brown in colour. Perhaps, he continued, the child was the progeny of a black and an albino – one of those anomalous Blafards. And that is all we know about Marie Sabina, bar a brief mention by the Jesuit geographer and ethnographer José Gumilla, who in his Orinoco illustrado, y defendido, historia natural y geographica de este gran rio (Madrid, 1745) records that he encountered her as an infant in a plantation hospital, told her mother (who was recuperating) to beware that others did not cast an evil eye upon her daughter, and concluded that the child’s peculiar appearance could almost certainly be blamed on the dog, a household pet, which had the misfortune to be spotted as well.

Buffon’s hypothesis – that piebald children were the progeny of albinos and blacks – ran for nearly two hundred years. It was certainly a more reasonable theory than Gumilla’s spotted dog, yet its longevity remains surprising, since in that time at least four other piebald children emerged from the Caribbean onto the pages of learned journals, and not one had an albino parent. Besides Marie Sabina, there were John Richardson Primrose Bobey (b.1774, Jamaica), Magdeleine (b.1783, St Lucia), George Alexander Gratton (b.1808, St Vincent), and Lisbey (b.1905, Honduras). Each child was celebrated in its day. Portraits of Marie Sabina now hang in Williamsburg, Virginia, and at the Hunterian Museum in London; Magdeleine has a statue at Harvard University; and in Marlow, Surrey, George Gratton has a grave with the epitaph ‘Know that there lies beneath this humble stone/a child of colour haply not thine own.’

The most recent of these Caribbean piebalds, Lisbey, featured in an article written by the British geneticist Karl Pearson in 1913. Like Buffon, Pearson thought that piebalding had something to do with albinism. He does not suggest that the child’s mother had an affair with an albino – a photograph of the family shows a lace-clad matriarch of seemingly imperturbable moral rectitude. Instead he questions Lisbey’s ancestry, postulating the existence of an albino forebear. Pearson’s hypothesis was a bit more complex than this, for he also proposed that an albino ancestor will only cause piebalding when one of the parents is particularly dark – and Lisbey’s father was, in Pearson’s words, ‘a coal black negro’. It is a convoluted explanation and one that is difficult to understand from a modern point of view. We now know that piebalding has nothing to do with albinism but is instead caused by dominant mutations in an altogether different set of genes, and that these mutations can occur in people of any colour – not to mention horses, cats, and a strain of mouse called ‘splotch’. They are no less fascinating to us than Marie Sabina was to Buffon. Among other things, they tell us about the strange origin of the cells that colour our skins.

Melanocytes spend their lives in the skin, but they are immigrants there. Where most of the skin is ectoderm, melanocytes are the products of a tissue called the neural crest. At about day 28 after conception, neural crest cells flow out of the newly formed dorsal nerve cord and pour themselves around the foetal head to make the face. But some neural crest cells travel much further than this. As a river fans out over its delta, streams of neural crest cells course down from the escarpment of the dorsal nerve cord and penetrate to the embryo’s farthest reaches. In one part of the body they form nerves, in another muscles, yet elsewhere they invade developing glands. And some become melanocytes which, early in foetal life, invade the lower layers of the skin where they settle down to produce pigments. Neural crest cells make our faces, and they also lend them colour.

Molecular devices are required to make a naive neural crest cell form a melanocyte rather than some other kind of cell, and also to guide the melanocytes to their final destinations. Mutations in at least five distinct genes cause piebaldism, and each of them disables one or more of these devices, so causing patches of skin that are devoid of melanocytes and therefore perfectly white. Some piebalds have only a white forelock, some have bodies covered in patches, and some have eyes of different colour. Yet others have more serious disorders. A few piebald infants have a debilitating intestinal condition known as ‘megacolon’ – a lower intestine that is swollen with massive constipation caused by the absence of gut nerves that drive defecation. These nerves too have their origin in the neural crest. Piebald children are also prone to deafness, for it seems that melanocytes serve some critical function in the inner ear.

DINKA VS. DUTCHMAN

Guinea pigs, dogs, cats and cattle may have been bred for variety of colour, but only humans come naturally in so many different shades. What gives us our skin colours? It is a curious thing, but for all that geneticists have learned about the causes of abnormal pigmentation, they have yet to give an account of the genes responsible for the difference in skin colour between, say, a Dinka and a Dutchman.

Why is this? In part it is due to the sheer difficulty of the problem. Geneticists agree that more than one gene makes the difference between naturally dark and fair skin (were it only one gene, we would know it by now), but beyond that the guesses range between two and six, interacting in complex combinations to give any particular shade of pink, tan, brown or black. This makes things difficult. When many genes, each of which has many variants, combine to affect some property of the human body, the molecular identification of those genes becomes a challenging exercise in applied statistics. When the property in question is a disease – heart disease or non-insulin-dependent diabetes – geneticists have embraced the challenge with a will. They have been more cautious about studying skin colour.

This is understandable. Ever since Linnaeus divided the world’s people into four races – Asiaticus, Americanus, Europaeus, Afer – skin colour has been misused as a convenient mark of other human attributes. Linnaeus distinguished his four races not only by the colour of their skins but also their temperaments: Asiaticus was ‘stern, haughty, avaricious and ruled by opinions’; Americanus ‘tenacious, contented, choleric and ruled by habit’; Afer, seemingly devoid of any redeeming virtue, was ‘cunning, slow, phlegmatic, careless and ruled by caprice’. What of his own race? Europaeus, Linnaeus thought, was ‘lively, light, inventive, and ruled by custom’. This was the beginning of an intellectual tradition that, via the writings of Arthur, Comte de Gobineau, the nineteenth-century theorist of Aryan supremacy, culminated in the most systematic chromatocracy that the world has ever known: apartheid South Africa.

For nearly half a century the architects of the South African laager held the world at bay and devoted much of that nation’s abundant resources towards the hopeless task of dividing the racial seas. In the endless negotiations as to who could or could not sit on park benches marked net blankes (whites only) every policeman, magistrate, employer, practically every citizen, became an expert on racial identity. South African law was always deliberately vague as to what made someone blank, swart or a kleurling (‘coloured’ – in apartheid’s parlance, someone of mixed African and European descent). In part it was just who you knew, where you came from, what people thought you were. But mixed in with these social criteria was an elaborate array of pseudo-scientific tests that would, their proponents declared, infallibly betray African ancestry in someone trying to ‘pass for white’. Some placed their faith in the ‘pencil test’ – predicated on the notion that a pencil stuck in someone’s hair would only remain there if the subject was at least part black. Others held that the colour of the skin beneath the fingernails was critical, or else spoke of knowledgeably of eyelids and the Mongolian Spot. Yet others appealed to the colour of the genitals (‘the scrotum test’). In the segregation of schools, hospitals, jobs, indeed every aspect of public life in South Africa between 1948 and 1990, the destiny of a child could turn on the precise shade of almost any of his or her body parts.

In 1973 a forty-year-old Cape Town housewife named Rita Hoefling, who had until then enjoyed the privilege and security that came with being a white South African, began to turn black. She had been diagnosed with Cushing’s disease, a disorder caused by hyperactive adrenal glands. The glands were removed and for a while all seemed well, until she noticed that her skin was becoming rather dark. It wasn’t just a matter of a tan, but rather a deep bronze, that altered her whole appearance – indeed, made her look like a kleurling.

The first humiliations were small ones, the stuff of ‘petty’ apartheid. Thrown off a ‘whites only’ bus by a zealous conductor, she was forced to carry a card that explained and excused her dark skin. But in apartheid South Africa any citizen could be a self-appointed Race Commissioner, and it was not long before Rita felt compelled to move to another area – only to have her new neighbours issue a petition of protest as well. All this in Cape Town, even then South Africa’s most cosmopolitan and racially tolerant city. The strain eventually told on her family. When her father died, Rita was not allowed to attend his funeral: ‘I do not want,’ said her mother, ‘to be embarrassed by your black body at Daddy’s grave.’

Driven from the white community, Rita Hoefling was befriended and sustained by blacks. They welcomed her into their homes in the segregated townships, and kept her sane. She became fluent in Xhosa. And then, one day in 1978, Rita spontaneously turned white again. She attempted to return to her old life, but by then her husband – a former Royal Navy officer – and her children had left her. For the last ten years of her life she lived on charity and a small pension and moved between grimy bedsits in Cape Town’s slums. It was in such a bedsit that in 1988, aged fifty-five, she died of bronchial pneumonia.

Rita Hoefling had a disorder called ‘Nelson’s syndrome’ which occurs in about a third of patients who have adrenodectomies. One of the critical tasks that the adrenal gland does (rather like the thyroid) is keep the pituitary gland in check. In the absence of her adrenals, Rita’s pituitary began to grow, became tumorous, and produced a surplus of pituitary hormone that caused her skin to darken.

Charlie Byrne, the Irish Giant, also had a pituitary tumor. It may seem surprising that a tumor in a single organ can manifest itself in such different ways, but the pituitary is a remarkably versatile organ. Not so much a hormonal factory as an industrial park, each of the half-dozen-odd hormones that it secretes is the product of a group of specialist cells. This means that tumors that start in different pituitary cell types can have very different consequences. Most pituitary tumors start in cells devoted to producing growth hormone and so cause either gigantism or acromegaly. More rarely the tumor starts in cells devoted to the production of a group of hormones called melanotropins.

Like growth hormone, melanotropins circulate throughout the body; however, where growth hormone affects nearly all of the body’s cells, melanotropins tend to be more discriminating. Among the cells they affect most spectacularly are the melanocytes. When the hormone binds to its receptor on the melanocyte, the cell begins to produce eumelanin, the pigment that gives us the dark shades in our skin, hair and eyes. Just as too much pituitary growth hormone causes the over-multiplication of flesh and bone, an excess of melanotropin causes our skin to bronze – at least it does in fair-skinned people. But melanotropins do not simply turn eumelanin production on. Children who have no melanotropins are not blonds, but redheads. And they are fat.

They are fat because one of the melanotropins, a molecule called a-melanocyte-stimulating hormone (?-MSH), does more than its name suggests. On melanocytes it binds to, and activates, a molecule called melanocyte-stimulating hormone receptor-1 or MC1R. In the brain, however, it binds to another receptor called MC4R that is encoded by a different gene. The brain receptor controls appetite. When ?-MSH activates MC4R a neuronal signal tells us to stop eating. Children who lack α-MSH are obese because they simply do not know when to say to say ‘when’.

Yet not all redheads are fat. Indeed, casual recollection suggests that rather few are. Why is this? The answer appears to be that most redheads do not owe their fiery locks and translucent skins to a lack of any hormone but to unusual receptors. When MC1R is active, melanocytes make eumelanin – brown and black pigments; inactive, they make phaeomelanin – red pigments. Red-haired Celts have receptors that are more or less permanently inactive – something they share with red setters, red foxes, and red-haired Highland cattle.

Note the weasel-word – ‘unusual’. Throughout this book, I have used the language of clinical genetics. I have spoken of ‘mutations’ that ‘disable’ proteins or else render them ‘defective’. But there are so many redheads around that it seems a bit harsh to speak of their genes in this invidious fashion. And yet the question niggles: are redheads mutants?

Whether a given genetic sequence is a mutation rather than a polymorphism hinges on two issues: its global frequency and its usefulness – mutations being rare and harmful, polymorphisms being generally neither. As far as frequency goes, redheads may be common in northern Europe (6 per cent in Aberdeen), but globally they are rare. Worse, a count of heads overestimates the frequency of the ‘redhead gene’. This is because each redhead is unusual in his or her own way. MC1R comes in at least thirty different versions, and many of them are found in Ireland. Six, but perhaps as many as ten, of these human MC1R versions, in a multiplicity of combinations, cause red hair – be it auburn, deep red, orange or strawberry blond. Africans, by contrast, all have just one kind of MC1R.

Globally, any single red hair version of the MC1R gene is so vanishingly rare that we must, it seems, call it a mutation rather than a polymorphism. But perhaps an argument can be made for utility? Some have speculated that northeners need lighter skins in order to garner sunlight for the manufacture of vitamin D, without which they would suffer rickets, a bone deformity. Darwin thought that the variety of human colour was due to sexual selection – generations upon generations of perfectly arbitrary choice for beautiful mates. This is a pleasing but difficult-to-prove hypothesis – at least if we discount Henri Toulouse-Lautrec’s belief that redheads give off an especially erotic odour.

On the other hand, it is easy to make a case against the usefulness of red hair. The uniformity of MC1R in Africa tells us that dark skin is needed in the tropics – there is no doubt that it protects against skin cancer. Removed from soft northern light, redheads are easily ravaged by the sun. Their MC1R genes give them delicate complexions that refuse to tan but only burn. Many Australian children are descended from Scottish and Irish immigrants, and Australian law ensures that they all wear hats and long sleeves in their schoolyards. None of these arguments is conclusive. But the evidence tends to suggest that, delightful though it may be to look at, red hair is not good for anything at all. MC1R in northern Europeans may simply be a gene that is decaying because it is no longer needed, rather as eyes decay in blind cave-fish.

THE STORY OF PETRUS GONSALVUS AND SHWE-MAON

Pale, and proud of it, nineteenth-century European anthropologists typically ordered humanity by skin colour. Perhaps unsurprisingly, scholars from elsewhere have often seen matters differently. Upon returning from a European tour, the Chinese savant Zhang Deyi (1847–1919) informed his compatriots that many Frenchwomen had long beards and moustaches. Eschewing the skin-colour geographies of their European counterparts, Chinese anthropologists made maps showing which of the world’s people were or were not hairy. They were fascinated by the Ainu, a relatively hirsute northern Japanese people whom they depicted as a race of dwarfish ape-men. The Ainu are, of course, nothing of the sort. True, Ainu men take a traditional pride in the length of their locks and beards (neither of which they trim), yet they have no more body hair than most Europeans. But then, learned Qing commentators also compared European visitors to macaques, a pleasant tradition that persists in Singapore, where foreigners are still called angmo or angmogao, Hokkein for ‘red-haired ape’.

It is perhaps not quite fair to single out the Chinese for their preoccupation with hair (it was, after all, almost certainly a white South African who invented the ‘pencil test’). And Europeans may be hairy, but this has never made them especially sympathetic to people who are hairier yet. Several genetic disorders called hypertrichoses cause infants to develop lush growths of hair on their noses, foreheads, cheeks and ears, limbs and torsos – parts that are, in most babies, only modestly clad. Grown up they have been the wild men, Waldmenschen and femmes sauvages of early travellers; the hommes primitifs and Homo hirsutus of taxonomists, and the dog-bear-lion-ape-people of fairground hucksters.

In the collection of the Capodimonte Museum in Naples there is a painting by Agostino Carracci, elder of the Bolognese artist brothers. Two figures frame the scene: a humorous dwarf and a bearded man of middle age whose teeth are bared in a grimace. Their attention is fixed upon a third figure, young, handsomely proportioned and serene, who sits between them. He is, it seems, a wild man, a man of the woods. Apart from a rude cloak he is naked, and his face is covered in hair – not just a beard, but locks that grow high on his cheeks and low on his forehead. The background foliage is lush, and a parrot, two monkeys and two dogs complete the bucolic scene. The whole thing could be an allegory of Nature were it not for the title, Arrigo Peloso, Pietro Matto e Amon Nano – Hairy Harry, Mad Peter and Tiny Amon – which tells us that it is really the inventory of a zoo.

The painting, commissioned by Cardinal Odoardo Farnese, was completed in 1599. It was only a trifle compared to the magnificent interiors of the Palazzo Farnese in Rome that the Carraccis had already done for him. Attached to this palace, which now houses the French Embassy, were a botanical garden and a small menagerie, almost certainly the source of the animals depicted in Agostino’s painting. The wild man, a gift from the Cardinal’s kinsman Ranucci Farnese, lived there as well. His cloak hints at his status and identity. It is a tamarco, the robe of the Guanches, who once inhabited Tenerife in the Canary Islands but who had been briskly subjugated and largely exterminated by the Spanish a hundred years before.

Arrigo Gonsalvus, to give the wild man his full name, was not himself a Guanche. He was, however, the son of one, and a rather unusual one at that. In 1556 Petrus Gonsalvus arrived at the court of Henri II of France, brought there possibly as a slave from Tenerife. He could not have been more than twelve, but already a thick pelt of facial hair obscured his features. He seems to have been treated kindly there and was even given some education. In 1559, after the King’s death, Gonsalvus appears at the court of Margaret, Duchess of Parma, despot of the Spanish Netherlands, where he married a young and rather pretty Dutchwoman who bore him at least four children of whom three were exceptionally hairy as well, among them Arrigo.

Margaret of Parma returned to Italy in 1582, the hairy family trailing in her wake. They were wonders, marvels of nature, and the Hapsburgs and Farneses could not get enough of them. Frederick II, Archduke of Tyrol, commissioned a set of individual portraits for his Wunderkammer at Schloss Ambras near Innsbruck where they may still be seen, part of his collection of natural curiosities. A group portrait of the family by Georg Hoefnagel appears in the illuminated Bestiary of Rudolf II, Emperor of Austria and Frederick’s nephew, the only humans to do so. Perhaps the loveliest of the many portraits that depict this remarkable family is by the Bolognese painter Lavinia Fontana. It is of Arrigo’s younger sister, Tognina, and shows the little hairy girl dressed in silvery brocades, smiling sweetly as she holds a document recounting her history aloft, and looking much like a preternaturally intelligent, if amiable, cat.

It may be thought that these portraits exaggerate the family’s hairiness, but this is certainly not so. The travels of the family Gonsalvus in northern Italy were noted by that assiduous encyclopaedist of nature Ulisse Aldrovandi, by then Professor of Natural History at the Papal University of Bologna. In his Monstrorum historia, he records meeting the family, describes them with care, and includes four woodcut portraits of them. Some scholars have suggested that Mad Peter, who stares so fixedly at the hairy man in Agostino Carracci’s painting, is a portrait of Aldrovandi himself. In support of this charming conceit, it is certainly true that the bearded figure resembles Aldrovandi, and artist and naturalist had known each other since their student days. But in 1599 Aldrovandi would have been in his seventies, whereas Mad Peter is clearly in his vigorous prime.

Aldrovandi refers to Petrus Gonsalvus as the ‘man of the woods’ from the Canaries, and evidently believes that there were others like the Gonsalvus family there, a race of hairy people. There were not, of course. Petrus Gonsalvus was merely a man who happened to have been born with a mutation that caused a layer of hair to grow over parts of his face and body where in most people it does not. Nothing is known about the ultimate fate of Petrus, his wife, or his son. We do know that Petrus’ daughter Tognina eventually married and bore several children who were as hairy as she.

Petrus Gonsalvus and his family were not the only hirsute people to have attracted royal curiosity. In 1826 John Crawfurd, British diplomat and naturalist, visited the Burmese capital of Ava to the north of Mandalay. On the throne was Bagydaw, scion of the Konbaungs, a family noted chiefly for the savagery of its dynastic struggles. (One of Bagydaw’s predecessors had celebrated his succession to the throne of Ava in 1782 by slaughtering his brothers, their families, and some hundreds of his subjects – most of whom he immolated on a single gigantic pyre.) The Kongbaungs were also expansionist, a policy that attracted the ire of the dominant regional power, the British government in India. After the First Anglo–Burmese war, a humiliating peace was imposed upon the Burmese. The treaty was carried to Ava by Crawfurd, who found in Bagydaw’s court a scene of medieval splendour complete with white elephants and human albinos. He also found Shwe-Maong.

‘We had heard much,’ wrote Crawfurd,

Shwe-Maong was a Lao, a hills-man who as a five-year-old had been sent as tribute to Bagydaw’s court by a local chieftain. Slightly built with mild brown eyes, he lived precariously, weaving baskets and playing the buffoon; as a boy he had been taught to imitate the monkeys that lived in the teak forests of the Burmese hinterland. When Shwe-Maong was in his early twenties, Bagydaw gave him a court beauty in marriage by whom he fathered four children, one of whom, a ‘stout and very fine’ girl named Maphoon, was also hairy. Born with hairy ears, by the time she was six months old the rest of her body was covered in fine grey down. When Crawfurd saw her she was two or three years old and her face was no longer visible. Thirty years after Crawfurd’s account Maphoon appears again in the record of another diplomatic mission to Ava sent to deal with the ever-fractious Kongbaungs. By then she was a mature woman who looked much like her father, long since dead. Silky hair flowed over her face, leaving only her eyes and lips exposed; her neck, breasts and arms were covered with a fine down, and she also had her father’s gentle manners. She had married – Bagydaw’s successor, perhaps out of intellectual curiosity, had offered a reward to any man who would have her – and was the mother of two boys, both of whom were hairy as well. One of them later married, and a photograph that dates from perhaps 1875 shows three generations of the family – Maphoon, her son, and his daughter – all identically hairy.

In 1885 the British finally conquered Upper Burma in the Third Anglo–Burmese War, and the palace at Ava was destroyed. Maphoon and her family fled into the forests where, some weeks later, they were found by an Italian army officer who persuaded them to travel to Europe. And it is there, in the summer of 1886, that we last hear of Shwe-Maong’s family, exhibiting themselves at the Egyptian Hall in Piccadilly and in Paris at the Folies Bergère.

THE TOPOGRAPHY OF HAIR

We are born with about five million hair follicles, and that is all we will ever have. The hair follicles are arranged in rows, adjacent follicles intercalated between each other in strict order. How does this regularity come about? If hair follicles were simply scattered randomly upon our scalps, each of us would have at least a few gaps in the thatch. The problem of how follicles come to be arranged with such precision is deep and difficult. It is the problem of how to make a regular pattern out of nothing.

The difficulty lies in the word ‘regular’. It is fairly easy to imagine how an organism can make unique parts – five different fingers, for example. It is merely a matter of having preprogrammed cells respond to a single gradient in the concentration of some molecule. Our fingers are, indeed, specified in just this way. But what if, instead of a hand with five unique fingers, one wished to make a hand with only two alternating finger-types, say, ring fingers and index fingers? A strange variety of hand that looked something like this: ring-index-ring-index-ring? No such hand has ever existed. But this, in essence, is the problem that our skins present. Out of bland embryonic uniformity the skin must somehow order itself into a lattice of regularly spaced hair follicles separated by bits of skin. Clearly, some subtle device is needed.

The exact form of that device is still quite obscure, but the logic of its workings is not. What is needed is a way of making hair follicles, but of not making them everywhere. A foetus begins to develop the first of its follicles around three months after conception. Five million hair follicles do not appear all at once: instead, they début on our brows, then spread like a rash, first to the rest of the head and face, then down the neck, throat and torso, across the hips and shoulders, and finally down arms and legs.

I like the simile of a rash, for it suggests the spread of some infectious change in the skin cells, a change that expands outwards from a small beginning. This change transforms the cells of the skin from a quiescent state to one capable of producing follicles. It probably happens cell by cell. Perhaps it begins with just one cell somewhere on the forehead which induces the same change in its neighbours, which then transform their neighbours, and so on and so on. No one knows what the nature of the change is, but it is possible to make some guesses.

Each hair follicle is a chimera, a hybrid, of two different tissues. So is skin itself. The skin that we see, that we touch, and that weathers the elements, is the epidermis, a stratified layer of cells that originate in the outermost germ layer of the embryo, the ectoderm. Underneath the epidermis is another, thicker, layer, the dermis, which comes from the mesoderm. Dermis and epidermis are intimate collaborators in the making of a hair follicle. Their relationship is of the nature of talkers holding a conversation, a molecular dialogue of signal and counter-signal.

There is a simple, if slightly eccentric, experiment that shows this. In 1999, trading on a shared devotion to each other and to science, a married pair of scientists used each other as guinea pigs. They excised a piece of dermis from his scalp and then transplanted it to the hairless region underneath her arm. It may seem surprising that she didn’t reject (in the immunological sense) her spouse’s tissue, but it appears that hair follicles are somehow protected from immune-system surveillance. In the event, shortly after the wound healed she started growing long scalp hairs in the area that had received the transplant. The experiment showed that the dermis has a voice, one that tells the epidermis: ‘make follicles here’. Indeed, the change that spreads like a rash across the foetus as it develops hair follicles is the dermal cells acquiring that voice in succession – a volubility that spreads to dermal cells everywhere bar those in the fingertips, palms, soles, lips and genitals, which for some reason remain silent.

If, in the conversation of the skin, the dermis’s instructions are the opening gambit, it is one to which the epidermis has immediate right of reply. As dermal cells spring to life, urging the epidermis to make follicles, it must, with regularity and firmness, reply ‘no’. Were it not to do so, the foetus’s skin would become a single giant hair follicle, or perhaps a tumorous mass of malformed follicles and hairs. The way in which the epidermis counters the dermis is what gives hair follicles their precise spacing. Each newly formed hair follicle issues instructions that prevent the epidermal cells around it from also becoming hair follicles. Not only does each newly formed follicle prevent surrounding cells from hearing the dermis’s insistent demands, it probably shuts them off at source.

The words in this conversation seem to be signalling molecules of the sort that we have come across before. Bone morphogenetic proteins are good candidates for the epidermal inhibitor. Bird feathers are distantly homologous to mammal hair, and if a bead soaked with BMP is placed on a chicken embryo’s skin, the infected patch will not form feathers. If the same experiment is done with fibroblast growth factor, extra (albeit weirdly distorted) feathers will form – perhaps it is the original follicle-inducing signal. These molecules are thought to work in the same way in our hair follicles. But the signals around the developing follicle are so various, abundant and dynamic that it is difficult to know what they all do. We do know that mice engineered with defective hair-follicle signals are often bald.

GRASSLESS FIELDS

The one thing that many of us would dearly like to know about hair is why we lose it. Just how many men suffer from ‘androgenetic alopecia’ or ‘male pattern balding’ is a matter of definition, but claims that it can be detected in 20 per cent of American men in their twenties, 50 per cent of thirty-to-fifty-year-olds, and 80 per cent of seventy-to-eighty-year-olds seem about right. Balding is truly a white man’s burden: Africans, East Asians and Amerindians (Native Americans) all have lifetime probabilities of balding lower than 25 per cent. Medically innocuous, it is a dispiriting disorder. When Ovid wrote in Ars amatoria: ‘A field without grass is an eyesore/so is a tree without leaves/so is a head without hair,’ he spoke for legions. For at least a century Americans have shown a marked aversion to electing bald men to their nation’s highest office. Excluding Gerald Ford (1974–77), who was bald but not elected, the last bald president was Dwight D. Eisenhower (1953–61). Europeans have been more sympathetic to the bare-headed politico (Churchill, Papandreou, Simitis, Giscard d’Estaing, Mitterrand, Chirac, Craxi, Mussolini), but even they lagged behind the Soviets, who inexplicably installed, if not exactly elected, bald and hirsute leaders in strict alternation: Lenin (bald), Stalin (hairy), Khrushchev (bald), Brezhnev (hairy), Andropov (bald), Chernenko (hairy), Gorbachev (bald) – a tradition that has been maintained in the Russian Republic with Yeltsin (hairy) and Putin (comb-over).

What causes balding? Samuel Johnson’s views on the matter – ‘The cause of baldness in man is dryness of the brain, and its shrinking from the skull’ – may be safely discounted, as can the theory, popular around 1900, that it was due to the wearing of hats. But dermatologists are hard pressed to offer more convincing explanations. Baldness obviously runs in families, but claims that it is due to a single recessive mutation or else ‘inherited from the mother’s side’ (recessive X-linked) are wrong. Male pattern balding is caused by several genes, none of which has been yet identified. Whatever they are, they must affect the life-cycle of the hair follicle.

Hair follicles have the peculiar habit of periodically destroying and then reconstructing themselves. Most of the time they simply produce hair. A single scalp follicle can work on lengthening a hair for anywhere between two and eight years; the longer it does so, the longer the hair becomes. Mouse follicles work on a given hair for only two weeks, which explains why their fur is so short. When the follicle comes to the end of its growth period it begins to retreat within the skin and die, and the hair falls out. Halfway down the follicle, however, there is a bulge of epidermal cells – ‘stem cells’ – that have two remarkable properties: they are immortal, and they can become all the other types of epidermal cells of which the follicle is made. They are the stuff from which the follicle rebuilds itself.

But not in bald men. Instead of rejuvenating into a fully productive follicle, all that is produced is a pale and feeble imitation of the real thing; a follicular epigone capable only of making tiny hairs. Why this happens remains a mystery. One fact is, however, known: to go bald you need testosterone, and plenty of it. In the passage of Historia animalium in which Aristotle tells us that eunuchs are tall, he also says that they do not go bald, an observation confirmed in 1913 by a study of the last of the Ottoman eunuchs. The first rigorous demonstration that testosterone, rather than any other testicular hormone such as estrogen, is the culprit came from a 1942 study by the American physician James Hamilton. Some of the fifty-four eunuchs he studied were born without testes; some had been castrated as boys out of medical necessity (inguinal hernias, for example). Hamilton does not reveal where he found the rest of his experimental subjects, but one of his later papers suggests that they were mentally retarded men who had been castrated as boys in Kansas mental institutions, a legacy of eugenic programmes that ran in the United States until the 1960s (and even later elsewhere). Consistent with Aristotle’s claim, none of the men who had been castrated before their late teens developed any sort of baldness, not even the relatively high foreheads that nearly all mature men have. This wasn’t because they all happened to come from families with good hair – several had balding male relatives. Proof that the eunuchs’ boyish hairlines were due to their lack of testosterone came when Hamilton gave them male hormone supplements and some of them began to lose their hair. When he stopped the treatment, it promptly grew back.

The need for balding men to have their testicles is the likely origin of the idea that prematurely bald men are unusually virile. It is a claim that has the ring of wistful propaganda about it. (Even Julius Caesar, it is said, rejoiced in the title ‘the bald adulterer’.) To be sure, there is a sad irony in the fact that the very hormone that gives men their beards in puberty denudes their scalps a few years later, but there is no evidence that prematurely bald men either have more testosterone than their hairier contemporaries or father more children. On the other hand, it is probably a lack of testosterone that prevents women from going bald. Women who acquire, for whatever reason, abnormally high levels of testosterone not only grow beards but tend to go bald as their baldness genes, hitherto silent, manifest themselves.

Is there any hope for the bald? Contrary to the folklore of depilation, shaving does not make hair grow faster, thicker, or darker – so there’s no point removing what little you have left except on aesthetic grounds. More usefully, at least one of the baldness therapies currently marketed, said to be quite effective, is an inhibitor of dihydroxytestosterone (DHT), the more potent version of testosterone. If this doesn’t appeal (and only a few users suffer impotence as a side-effect), then other therapies may soon be available. The resting hair follicles of a young mouse can be made to produce hair if dosed with a virus expressing high levels of sonic hedgehog. The surplus sonic probably forces the proliferation of the stem cells in the bulge of the hair follicle; if it could do the same for the crippled follicles on bald scalps, then a cure for baldness would surely be at hand. But maybe the hair follicles of bald scalps cannot be rejuvenated; if so, it will be necessary to make new ones. This may well be possible. Mice that have been engineered to overproduce a special form of the protein ?-catenin make entirely new hair follicles at an age when normal mice don’t. Unfortunately, both sonic hedgehog and ?-catenin are extremely potent molecules. Excess amounts of either tend to produce hair-follicle tumors – the product of all those extra stem cells. It may be easy to spur skin to make new hair; rather harder to tame it.

BENEATH THE NAKED APE

Four centuries and two continents apart, Petrus Gonsalvus and Shwe-Maong are startlingly alike. Were Petrus to discard his richly sombre robes with their scarlet facings and knot a lungyi about his waist, the two men could be brothers. Nineteenth-century scientists such as Carl von Siebold and Alexander Brandt were, however, more impressed by the resemblance of the hairy men to orangutans. Influenced by the new Darwinismus they suggested that hairiness was atavistic. This may seem like a version, albeit dressed up in scientific terminology, of the ancient equation between hairiness and bestiality. But the scientists were careful to note that though their subjects may have looked like apes, they were in fact quite human.

One can still, occasionally, come across claims that surplus-hair mutations reveal the fur beneath the naked ape. But there is reason to think that the atavism hypothesis is wrong – at least as applied to these two families. Both the hairy Burmese and Canary Islanders are described as having exceptionally fine, silken hair. This does not really resemble the robust pelt that covers adult apes – nor even human scalp or pubic hair. And hairy as great apes are, they are less so than the hairiest humans. Petrus and Shwe-Maong had noses, cheeks and ears that were covered in hair – exactly where great apes have rather little.

Where, then, does the surplus hair come from? One possible source is the foetus. Around five months after conception every human foetus grows a dense coat of hair. This ‘lanugo’ hair is fine, silky, less than a centimetre long, and enigmatically fleeting. Just weeks after it has grown it is shed again. Were it not for the occasional child born with lingering remnants of lanugo (often on the ears), we would hardly know that it was ever there. It seems likely that the mutation that afflicted the hairy families caused this lanugo to be retained. Instead of switching over to the normal pattern of juvenile, and then adult, hair production, their hair follicles were arrested in foetal mode.

And not just their hair follicles. In his description of Shwe-Maong, John Crawfurd notes that the hairy Burmese man had only nine teeth: four incisors and one canine in the upper jaw, four incisors in the lower, and no molars in either. Shwe-Maong’s daughter, Maphoon, had even fewer. Careful inquiries showed that they had not lost their missing teeth: they had never grown them. It was as if their teeth and hair had simply come to a halt somewhere around the sixth month of foetal development even as the rest of their bodies marched on.

Darwin himself knew of the Burmese hairy family. In The descent of man and selection in relation to sex (1859) he cites the bribe needed to secure Maphoon a husband as proof that hairiness in women is universally unattractive. Nowhere, however, does he suggest that hairiness is an atavism. He is, instead, interested in the connection between hair and teeth. A Mr Wedderburn had told him of a ‘Hindoo’ family in the Scinde – modern-day Pakistan – in which ten men from four generations were almost entirely toothless, but, far from being hairy, were rather bald – and had been so from birth. The bald, toothless Hindoos also lacked sweat glands; unable to perspire, they wilted in Hyderabad’s heat.

Hair, teeth, sweat glands and (though Darwin does not mention them) breasts, organs seemingly so various in their purpose and plan, are intimately connected. They are all places where skin has swollen or cavitated to make something new. The simple tube that is a hair follicle, the robust anvil of dentine and enamel that is a tooth, and the bulging burden of ducts that is a breast, are all variations on a constructional theme. A genetic disorder – there are more than a hundred – that affects one of these organs will often affect another.

These organs do not merely share an origin in skin; they are also made in much the same way. Even as hair follicles are forming throughout the foetal epidermis, other epidermal cells are clumping and cavitating to form teeth or mammary glands. Like the hair follicle, each of these skin organs is a chimera: part ectoderm, part mesoderm.

The kinship between all these organs can be seen in the molecular signals that make them. The ‘Hindoos’ still live near Hyderabad, where, confusingly, they are known as ‘Bhudas’ but are in fact Muslim. By 1934, six generations of Bhudas had spread across eight families. Now there are many more. Their distinctive appearance means that they recognise each other as relations, but the name of their mutant forebear seems to be forgotten. Just as Darwin’s correspondent said, they have neither sweat glands nor teeth (except for the occasional molar), but they do have at least a little scalp hair. They carry a mutation in a gene that encodes a protein called ectodysplasin, named for the disorder its absence causes: Ectodermal dysplasia. A mutation in the same gene may also explain the Mexican hairless dog. Alias El perro pelon or the Xoloitzcuintle, the dog is said to have been bred by Aztecs in the fourteenth century, possibly for meat but more likely as a kind of bed-warmer. It, too, is bald, toothless and has dry and crinkly skin for want of sebaceous glands.

An even deeper organ-kinship is evident in an odd variety of aquarium fish. Since at least the start of the Tokugawa Shogunate in the early seventeenth century, Japanese fanciers have bred the Medaka, Oryzias latipes, a small fish that normally lives in rice-paddies. A sort of poor man’s Koi, they can be bought from the night-stalls in Japanese cities where, among the varieties for sale – albino, spotted, long-fin – there are mutants that have no scales. The Medaka’s nudity, like the Bhudas’, is caused by a mutation that disables ectodysplasin signalling.

The use of a single molecule in the making of human teeth, hair follicles and sweat glands is a legacy of the evolutionary history that these organs share. This history is evidently also shared – at various removes – with the feathers of birds and the scales of fish and reptiles. All these organs have evolved from some simple skin organ possessed by some ancient, long-extinct ancestor of the vertebrates. No one knows exactly what this organ was. The best guess is that it resembled the tooth-like scales that give shark skin its roughness.

The right signal can even bring about the unexpected resurrection of organs long buried by evolution. Birds don’t have teeth, but their dinosaur ancestors certainly did. If a piece of ectoderm from a foetal chicken’s beak is grafted onto a piece of mesoderm from a foetal mouse’s mandible, and both are placed in the eye-orbit of a young mouse, the chicken tissue, which has not seen a tooth for sixty million years, suddenly begins to make them: hen’s teeth, shaped something like tiny molars, complete with dentine and enamel. This implies that the molecular signals used by Tyrannosaurus rex to make its mighty fangs are the same that a mouse uses to make its miniature molars. Signals that chickens just seem to have lost.

Perhaps it is also the retrieval of an ancient signalling system, partly buried by evolution, that causes some people to have extra nipples or even breasts. Humans and great apes have only two nipples but most mammals have many more. Sometimes extra nipples are little more than a small dark bump somewhere on the abdomen; at other times they are fully developed breasts. They are common: between 2 and 10 per cent of the population have at least one. In Europeans extra nipples or breasts are usually found somewhere below the normal ones, often in a line running directly down the abdomen. Japanese women, curiously, seem to get them above the normal breasts, often in the armpits.

These patterns of extra nipples may recollect an ancient ‘milk line’ – a row of ten pairs of teats that ran from the armpits to the thighs in some ancestral mammal. Armpit breasts are found in the lemur, Gaelopithecus volans, and the record number of nipples found on a single person seems to be nine (five on one side, four on the other). Wherever they are, extra breasts often work like normal ones, swelling and even lactating during pregnancy, and there are even accounts of women suckling children from supernumerary thigh-breasts. Extra nipples and breasts run in families, though the mutation (or mutations) that causes them has not been identified. However, a group of London researchers are attempting to determine the mutation behind a strain of mice that have eight nipples instead of the usual six. They have already dubbed the gene Scaramanga – for the villain of the James Bond film The Man with the Golden Gun who had, as a mark of his depravity, a supernumerary nipple on his upper left chest.

ARTEMIS EPHESIA

Breasts bring us back to Linnaeus. In 1761, made famous by Systema naturae, Linnaeus published one of his lesser-known works, a synopsis of the Swedish animals called Fauna svecica. The name was revolutionary: it was the first time that the word ‘fauna’ – from the Roman name for Pan-the-God – had been used to describe a work of this sort; a direct counterpart to the ‘floras’ that were already proliferating. As a frontispiece to this work Linnaeus chose a curious emblem, a representation of the Greek goddess Artemis, or Diana, of Ephesus. We don’t know why he picked this particular emblem, but there are several possibilities.

Artemis Ephesia was, in the inexplicably duplicitous way of Greek deities, goddess of both nature and cities. In her original incarnation as the object of a cult that flourished in Asia Minor from around the sixth century BC, her image was hung on city walls to protect them from evil, while being surrounded by icons of the country: garlands of vines and climbing animals such as lions, snakes, birds and harpies. Retrieved from the ruins of Ephesus, the eighteenth century made her into a symbol of wild-ness and of reason. The Jacobins even dedicated a Temple of Reason to her that once stood in Strasbourg, but is now gone. Perhaps this is why Linnaeus placed her at the front of his Fauna – as a symbol of the mastery of Reason over Nature, albeit a Swedish nature, in which, far from her Mediterranean home, Artemis stands among browsing reindeer.

But perhaps she had another, more direct, meaning for Linnaeus as well. What is most striking about his Artemis are not the animals that surround her, but her four prominent breasts. In this she is a direct echo of the statues of her in antiquity, all of which are laden with a varying number of thoracic and abdominal protuberances. In the Renaissance these bumps were invariably interpreted as a case of extreme polymastia, but more sceptical modern scholars say they are more likely to have simply been strings of dates, bulls’ testicles, or perhaps just part of the cuirass in which the goddess was clad. Be that as it may, Linnaeus’ Artemis obviously has four fine breasts, and it seems quite possible that they are a direct allusion to one of his finest inventions, the Mammalia. For Linnaeus made the presence of mammary glands one of the defining features of what we are: members of that great class of creatures that embraces simultaneously the pygmy shrew and the blue whale.

There is a third possible source of Linnaeus’ Artemis, one that brings us back to where we started – the way in which we differentiate ourselves from the rest of brute creation. When describing a species, Linnaeus did what taxonomists still do – he listed the things that distinguish it from all others. For all species, that is, but one: our own. When it came to Homo sapiens, instead of speaking of the number and kinds of teeth we have, the density of our hair, the distribution of our nipples, Linnaeus wrote only this: Nosce te ipsum. In a footnote he says that these are the words of Solon written in letters of gold upon the temple of Diana. Perhaps in choosing Artemis Ephesia as his icono-graphic symbol, Linnaeus is remembering and alluding to this account of the human species, the most concise possible: know thyself.

That is where Linnaeus’ discussion of Homo sapiens ends, but for a few strangely exigent epigrams in which he instructs us in the meaning of the new identity that he has given us. ‘Know thyself,’ he says, created by God; blessed with minds with which to worship Him; as the most perfect and wonderful of machines; as masters of the animals; as the lords of creation – all sentiments that today ring with the poignancy of certainties long since gone. Yet it is his parting shot that is most telling, and that could be taken as epigrammatic of much of what I have written here: