As we approach the end of what in the United States has been termed the decade of the brain, and with a complete map of the human genome in sight, it may be time to try to re-evaluate what the vast increase in molecular knowledge of brain processes has achieved.
Certainly there has been no shortage of claims. The abnormal genes and their protein products associated with neurodegenerative diseases such as Huntington’s chorea have been identified. Genetic risk factors for Alzheimer’s disease are known, and the molecular processes which culminate in the devastating neuronal death and malfunction that are responsible for the disease are subject to intense investigation. However, for neither of these conditions has the new genetic knowledge brought—yet—any effective treatment or prevention. Of course it may come, although not, as many of the advocates of the new genetics once promised, as a result of genetic engineering, but rather because the increased biochemical understanding that follows from genetic information may help in constructing more precisely targeted drugs. Indeed, the best pointer to neuroprotection against Alzheimer’s disease has come from epidemiological evidence of the protective effect of hormone replacement therapy in older women rather than from molecular studies.
Summary points
Genes have been identified for several neurodegenerative diseases, but so far this has not led to effective treatment
The tendency to view the complexities of human behaviour as genetically determined has important consequences
One is the construction of new diseases—for example, disruptive children are diagnosed as having attention deficit hyperactivity disorder and are prescribed methyphenidate hydrochloride
Another is that social problems such as violence and alcoholism can be regarded as neurogenetically determined; solutions are then seen as lying in molecular research rather than in reshaping society
Genes for all reasons
But when we move beyond the terrain of relative diagnostic certainty represented by such traditional neurological disorders, things become much murkier. Gene markers, if not genes, associated with conditions such as schizophrenia or manic depression have been proclaimed, amid great ballyhoo, only to be quietly withdrawn as non-replicable. The trouble is that as each old claim disappears into the mists, newer and even more extravagent ones appear. Genes, it is said, are responsible for such diverse features of human conduct as sexual orientation; poor behaviour in school; alcoholism; drug addiction; violence; risk taking; criminal, antisocial, and impulsive behaviour; political anti-authoritarianism; religiosity; tendency to midlife divorce; and even compulsive shopping. Major funding programmes are under way, mainly in the United States but also in the United Kingdom and elsewhere in Europe, to identify such genes, presumably with a view to either screening for and aborting fetuses which show the potential for such undesirable characteristics or generating drugs which will alleviate the condition, turn gays into straights, or radicals into conservatives.
The universalistic claims made for selective serotonin reuptake inhibitors such as fluoxetine (Prozac) are by now very familiar; it is as if all too many of us have too little fluoxetine in the brain without regular recourse to the drug. Less well known is the case of methylphenidate hydrochloride (Ritalin), an amphetamine-like drug now apparently prescribed for anything up to 10% of all American children—mainly boys between the ages of 8 and 131—but coming soon to a general practice near you. Some 40 000 prescriptions for methylphenidate hydrochloride were being issued annually in the United Kingdom by the mid-1990s. Methylphenidate hydrochloride is supposed to treat a condition known as attention deficit hyperactivity disorder, characterised by a child being naughty at home and a poor learner and disruptive at school. Furthermore, this disorder in childhood is supposed to predict criminal and antisocial behaviour in adulthood.
Diagnostic neologism
The condition was almost unknown in the United Kingdom a decade ago, even though it is supposed to be genetically caused. This sudden emergence of a genetic disorder is puzzling. The result of mass mutations? Scarcely likely. Far more likely is that it is yet another example of diagnostic neologism, the invention of new diagnostic categories to feed into the ever burgeoning diagnostic and statistical manual, along with age associated memory impairment, dissociative identity disorder, and many more. All part of the medicalisation of daily life. Naughty and disruptive children have doubtless always existed. In the past their unruly behaviour might have been ascribed to poor parenting, poverty, impoverished schools, or unsympathetic teachers. Of course we might all have conceded that some children were simply wicked. Now we blame the victim instead; there is original sin in them there genes.
I’m not trying to argue that there may not be authentic cases of children with dysfunctional genes or a faulty neurotransmitter metabolism being included among the many given a diagnosis of attention deficit hyperactivity disorder. As the label is given primarily on the basis of reports about the child’s behaviour, we simply don’t know, whatever the loudly voiced claims of the drug’s advocates. Neither am I arguing that that the drug doesn’t “work,” although it is worrying that there are no long term follow up studies of its chronic use and that, according to government reports, it is being sold on American streets along with other less legal drugs. Methylphenidate hydrochloride does seem to have a calming effect, making it easier for the child to concentrate and thus providing a welcome respite for hardpressed teachers and parents. But methylphenidate hydrochloride doesn’t cure the problem, any more than aspirin cures toothache, and its mass use does raise serious questions about the behaviourally medicalised world into which we seem to be moving.
Neurogenetic determinism
The situation is even worse when we turn to the many other conditions now claimed to have genetic origins—a phenomenon I have called neurogenetic determinism.2 Take violence as an example. Violence is clearly a social problem, whether manifest as terrorist bombing of street markets, cruise missile attacks on pharmaceutical factories, genocide in Kosovo, drive-by shootings in Los Angeles, or the savagery with which certain football and cricket heroes beat up their partners. The neurogenetic argument is that these diverse activities are all manifestations of an underlying property of individuals—aggression. And aggression is widely assumed, seemingly almost entirely on the basis of a single study of eight people from three generations of a family in the Netherlands,3 to be associated with an abnormality in a gene coding for one of the monoamine oxidase enzymes. Gene knockout mice for this system have been bred that are also claimed to be aggressive, but as they are also visually impaired, cannot walk well, and don’t live long it is hard to see aggression as a primary result of the deletion.4
The problem is that complex social activities, whether in mice or humans, entail multiple interactions and processes, and to reduce them all to a unitary phenomenon—for example, aggression—is to oversimplify.5 Businessmen, and surgeons, are often praised for their aggressive approach. The same violent act may be socially desirable or condemned; a soldier shooting a suspected terrorist may receive a medal—or be charged with murder. Socially complex, interactive processes cannot be reduced to the properties of individual neurotransmitters or genes. Yet the temptation to seek genetic causes is very strong.
Consider the investment in research into the molecular biology of alcoholism and drug addiction—now major programmes in the United States, in Russia, and even in China. Far easier not to have to face explaining and resolving the social causes for the misery on the streets of Moscow or the Native American reservations in the United States. If it is all in the genes, governments can avoid the hard problems of social engineering in favour of funding research on molecular technology.
If not eugenics, then euphenics, as it has been termed, is clearly on the agenda as we approach the millennium. The prospects for medical intervention, and for the pharmacuetical industry, have never been brighter. In Aldous Huxley’s Brave New World one universal drug, soma, fixed it all. The next century’s neurogenetics and neuropharmacology will instead offer us personal somas, one for each of our many imperfections, and, with a bit of luck, we shall all behave in a socially desirable way ever after.
References
- 1.Breggin PR. Talking back to Ritalin. Monroe, ME: Common Courage Press; 1998. [Google Scholar]
- 2.Rose SPR. The rise of neurogenetic determinism. Nature. 1995;373:380–382. doi: 10.1038/373380a0. [DOI] [PubMed] [Google Scholar]
- 3.Brunner HJ, Nelen M, Breakfield XO, Ropers HH, van Oost BA. Abnormal behavior associated with a point mutation in the structural gene for monoamine oxidase A. Science. 1993;262:578–580. doi: 10.1126/science.8211186. [DOI] [PubMed] [Google Scholar]
- 4.Cases O, Seif I, Grimsby J, Gaspar P, Chen K, Pournin S, et al. Aggressive behavior and altered amounts of serotonin and norepinephrine in mice lacking MAOA. Science. 1995;268:1763–1766. doi: 10.1126/science.7792602. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 5.Rose SPR. Lifelines: biology, freedom, determinism. Harmondsworth: Allen Lane; 1997. [Google Scholar]