Like a Virgin (8 page)

The Red Queen hypothesis assumes that only the healthiest (that is, parasite-free) creatures are able to reproduce. These healthy creatures pass on their DNA to produce a genetic range among
their young, which also have a better chance of avoiding parasite infestation. This evolutionary tactic does not strictly favour sex above no sex; rather, it favours diversity, however generated,
over no diversity. Even in animals that reproduce without sex, genes are shuffled to a certain degree, but in relative terms, sex does more to mix things up. Not being able to effect or incorporate
change into your genome is, in this view, a one-way ticket to extinction.

For this reason, it is surprising that there is little or no direct evidence showing that accumulating mutations or a reduced ability to adapt in the face of environmental pressures causes
increased extinction risk in animals that only reproduce without sex. In fact, asexual species do not just die out as the predictions say they should. Those that survive use a range of unusual
biological tactics to alleviate the negative genetic effects of their chosen approach to reproduction. These include being able to disperse their offspring to wide geographical distributions
(large, sometimes very diverse habitats) and dormant resting stages (periods with low activity, sexual and otherwise) – mechanisms of maintaining population equilibrium that help to increase
the chances of long-term survival for an animal with low genetic diversity. These tactics take the place of natural selection through sex, which weeds out the genes that are least adapted to the
environment.

Sex provides survival strategies, but it is by no means perfect. Among other things, sex does not allow the creation of a clone from a genetically super-successful parent, a parent that has the
ideal make-up for meeting a particularly harsh environment. This, however, is a problem that can be circumvented by approximating asexual reproduction, say, through
inbreeding.

What makes a baby healthy and bonny, that is, a ‘good’ baby? In 1938, the eminent biologist J. B. S. Haldane wrote
Heredity and Politics
, a book he described
as being ‘addressed to such as are unacquainted with the science of genetics, but who are attracted or disturbed by eugenic doctrines’. The doctrines he discussed are disturbing indeed.
Written at a time when, in many places, miscegenation was outlawed and apartheid was actively enforced, the book raised several controversial issues surrounding the genetics of human offspring.

Haldane asked whether inequality among men was fundamental and genetic, if the sterilization of genetic ‘defectives’ was appropriate or wrong, and what could be expected if mixed
race children were accepted (and more regularly born into the world). He looked at whether certain races and certain social classes might be endowed with innate superiority, or stand as a
‘pure’ race – a belief he attacked. He wrote that recent learning about human inheritance had ‘been used to support proposals for very drastic changes in the structure of
society’ – a clear reference to the treatment of Jews in contemporary Germany. He continued: ‘And the stringent measures which have been taken... are said to be based on
biological facts. I do not believe that our present knowledge of human heredity justifies such steps.’

After seventy-five years, the questions Haldane posed remain incendiary, and though our present knowledge of human heredity is growing exponentially each year, the sum total of
accumulated data that has anything to do with race is minimal.

In 2008, two members of Parliament called for a ban on marriages between first cousins in the UK. In large part, their reasoning was based on data suggesting that Pakistani families from the
West Midlands of England accounted for about thirty-three percent of the recessive genetic disorders in the region, but only around 4.1 percent of total live births, a dramatic statistic. The
disorders were recorded, in the language of medicine, as ‘recessive metabolic errors’. These are mistakes that only affect a child if that child inherits a copy of the
‘bad’, mutated, disorder-creating gene from both of his or her parents. And this is more likely to happen among parents who are closely related – who are consanguineous, that is,
‘share blood’.

For several reasons, however, the statistics that the politicians used were skewed. There were problems with the way the data were gathered, and other studies over the years have shown that the
risk of first cousins having a child with a recessive disease is quite low – no more than for the community overall. The issue wasn’t that first cousins were marrying, it was that
everyone in this particular community was slightly more likely than the general population to carry the mutant gene.

When epidemiologists want to investigate the chances that a certain group may be prone to recessive errors, they look at
genetic load
, the overall number of harmful mutations the average
person is carrying, rather than specific gene mutations. Unfortunately, genetic load is not always simple to translate into morbidity and mortality rates – the chance that a foetus will not
make it to full term, or that a child will have difficulty surviving into adulthood, let alone inheriting a genetic disorder. The medical statistics, for example, do not indicate that rare
recessive genes are more likely to cause miscarriage than other factors. Moreover, imagine that one of the shared grandparents of two married cousins carried a gene for albinism, which would give
each of the cousins’ offspring a fifty percent chance of being albino. That doesn’t necessarily mean that this grandparent carried any other recessive mutant gene,
or that the children will automatically be unhealthy or have any other disorder – the genetic load would be small, but the chance of being albino would be relatively high. Finally,
consanguineous marriages tend to be more prevalent among people with lower socio-economic status, which coincides, in and of itself, with higher rates of morbidity and mortality, as shown in Sir
Michael Marmot’s famous study of Whitehall bureaucrats. The politicians’ motion was based on an oversimplified view of heredity and epidemiology, to say the least.

Apart from the fact that the proposed law did not take into account all of this evidence, it would have turned a blind eye to risky reproductive behaviours that are currently accepted among many
other groups. It is not questioned, for instance, that women nearing menopause should be able to procure fertility treatments, even though it is understood that older mothers are more likely to
give birth to children with chromosomal abnormalities; nor that people with Huntington’s disease or other debilitating genetic disorders should retain the right to have children, despite an
established fifty percent risk of the condition being inherited. Should a consenting adult be penalized for choosing a partner who might increase the risk of a genetic anomaly in his or her
children? If so, would health services be required to screen potential reproductive partners, in the way that the charity Dor Yeshorim checks enrolled Orthodox Jewish families for a handful of
recessive disorders before an arranged marriage goes forward? The law would have taken the choice of looking for a recessive trait out of the hands of the people having the child and put it in the
hands of the government – a very drastic change in the structure of society. It would set a very disturbing precedent. Yet, the premise on which the law
was proposed is
quite basic: the premise that genetic variation is good and inbreeding is bad.

Inbreeding, of course, is what we normally call it when close relations mate. Between the closest of relations, we brand this
incest
, from the Latin for unchaste or impure. Genetically
speaking, this labelling could not be further from the truth, however, because inbreeding
limits
the genes available to create any offspring, and so maintains a relatively pure familial gene
pool; no truly foreign DNA is involved. As such, you could say that the ultimate form of inbreeding is making babies without a partner – that is, when reproduction does not involve sex at
all.

The incest taboo is universal, though what it means for a particular community depends on whom a group defines as being too close a relation for sexual relations. In many
Western cultures, there is an informal taboo around marriages between first cousins or between uncles and nieces. These proscriptions may be fostered partly by religious laws, economic imperatives,
or long-standing prejudices, including the socially taught belief that children who grow up together cannot (or should not) develop a sexual attraction to each other. Regardless, most Westerners
would not hesitate to say that consanguineous liaisons (those between ‘blood’ relations) are inherently
unhealthy
, triggering a range of physical and mental deformities –
such as the outsized ‘Hapsburg jaw’ you read about in school biology lessons, but also including infertility and early death. The conventional wisdom is so ingrained that, in recent
decades, some scientists have begun to argue that the impetus to avoid inbreeding is itself genetic – that there is a gene that discourages inbreeding and promotes a taboo against incest in
families that carry it.

In many cultures, however, consanguineous marriages, including between cousins, remain widespread. These marriages are most prevalent in Arab countries, with India, Japan,
Brazil, and Israel following them in the rate tables. The liaisons are more common among people with less education (as well as lower socio-economic status), perhaps because higher status groups
are more likely to have been influenced by Western beliefs about ‘inbreeding’.

Conventionally, consanguineous marriages are considered to carry social benefits, such as being able to aggregate family wealth and ensure better treatment of the bride, and thus increase
stability and security for the whole family. Many arranged marriages occur between ‘blood’ relations. But while those social benefits may hold sway in many families, there can also be
biological benefits to marrying within the family: marrying a close relative might save your lineage’s genes from extinction. In fact, there are cases in which inbreeding has actually
facilitated a population’s adaptation to an inhospitable environment and parasite threats.

Take, for example, the telling statistic that in many parts of Asia, the Middle East, and Africa, marriages between close biological relatives account for up to sixty percent of all unions.
These geographic areas share a long history of exposure to malaria. Indeed, the five hundred million to eight hundred million people who are married to a ‘blood’ relation mostly live in
the world’s malarial regions. There are simply more consanguineous marriages in places where there is more
Plasmodium falciparum
, the protozoan parasite that makes its way into humans
through the bite of the
Anopheles gambiae
mosquito and causes the most lethal form of malaria.

In 1949, Professor Haldane noted an apparent connection between malaria and a high prevalence of thalassaemia, an inherited blood disorder. Thalassaemia gets its name from the
Greek for ‘sea’ (
thalassa
) and ‘blood’ (
haema
), since one type of the disease is especially prevalent in regions circling the Mediterranean. The
condition causes the body to make fewer healthy red blood cells and less haemoglobin, the iron-rich protein in red blood cells that carries oxygen around the body. In people with thalassaemia, this
undersupply of red blood cells and haemoglobin leads to an undersupply of oxygen in the bloodstream. In its mild form, thalassaemia may cause tiredness, but when severe the spleen becomes enlarged,
and the person may suffer from liver, heart, and bone ailments. Haldane believed that, for some reason, malaria seemed to be ameliorated among patients with thalassaemia. Could it be that the
presence of malaria parasites in the environment had promoted the survival of the inherited genes that caused the disorder?

In humans today, the gene that causes the α+ type of thalassaemia is the single most common disorder caused by a mutation on a single gene, what is known as a monogenic disorder. Over five
hundred million people carry the gene, and they live primarily in regions where malaria is or was endemic (in the past, malaria was endemic around all of the Mediterranean, including much of
Southern Europe). As the Red Queen hypothesis would predict, when malaria emerged ten thousand years ago, humans adapted to the threat. In regions where malaria parasites were present, the
population has much higher rates of gene variants – and not just those for inheriting thalassaemia – that decrease the likelihood that you will die from malaria if you are infected.