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 funeraclass="underline" ‘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?