Drug addiction

Treatment on a plate

Oct 16th 2008
From The Economist print edition

A dietary approach to treating addiction seems worth investigating

Alamy

PEOPLE are programmed for addiction. Their brains are designed so that actions vital for propagating their genes””such as eating and having sex””are highly rewarding. Those reward pathways can, however, be subverted by external chemicals (in other words, drugs) and by certain sorts of behaviour such as gambling.

In recent years, neuroscientists have begun to understand how these reward pathways work and, in particular, the role played by message-carrying molecules called neurotransmitters. These molecules, notably serotonin, dopamine and gamma-aminobutyric acid (GABA), hop between nerve cells, carrying signals as they go. Some drugs mimic their actions. Others enhance them. Either way, the body tends, as a result, to give up making them. At that point the person needs the drug as a substitute for the missing transmitter. In other words, he is an addict.

Unfortunately, this improved understanding of the biochemistry of addiction has yet to be translated into improvements in treatment. The latest figures from Britain’s National Treatment Agency suggest that only 11% of those who start treatment complete it and are drug-free after 12 weeks. A new approach that acknowledges the underlying biochemistry might improve this situation. And on October 11th and 12th delegates to a conference in London, organised by Food for the Brain, an educational foundation, heard accounts of such an approach. Its tools are not drugs but dietary changes. The theory is that providing food rich in the precursors of lost neurotransmitters will boost the levels of those chemicals, and thus reduce craving. At the moment, only preliminary trials have been carried out. But they look promising and if larger trials confirm them, a useful, new front in the war on addiction might open up.

Mind what you eat

Anxiety and sleeplessness are common withdrawal symptoms. They happen because many addictive drugs reduce the supply of a chemical called glutamine, a precursor to GABA. One of GABA’s roles is to promote relaxation. (The molecular receptors for GABA are the target of tranquillisers such as Valium.) But glutamine levels can be restored, and production of GABA boosted, by the consumption of an amino acid called N-acetylcysteine (NAC) that is found in nuts and seeds.

This is not just theory. A controlled study published last year in the American Journal of Psychiatry by Steven LaRowe, of the Medical University of South Carolina, and his colleagues, found that giving NAC to cocaine addicts reduced their desire to use the drug sufficiently for it to be recommended as a treatment. A different study found that NAC reduced the desire to gamble in more than 80% of those addicted to this pastime, compared with 28% of those who were given a placebo.

Serotonin is another neurotransmitter that is usually deficient in an addicted brain. This probably accounts for the depressive side of withdrawal symptoms (serotonin receptors in the brain are the target of antidepressant drugs such as Prozac). Serotonin is made from an amino acid called tryptophan, which is found in foods such as meat, brown rice, nuts, fish and milk. Philip Cowen, a psychiatrist at Oxford University, has found that reducing the amount of tryptophan in someone’s diet increases depressive symptoms and also that increasing it can induce a more optimistic outlook.

Another molecule that shows promise in treating addiction is DHA, a fatty acid belonging to the nutritionally fashionable class called omega-3. In this case it is believed to act not by affecting neurotransmitter levels but by changing the physical characteristics of nerve cells’ outer membranes, and thus the way they conduct nerve impulses.

A lack of DHA has been associated with all sorts of psychological problems””learning difficulties, excessive hostility and even suicide. It has also been associated with the relapse into addiction.

Here, though, the waters are muddy. Correlation is not causation, and no decent trials have yet been done to show whether DHA supplements do in fact reduce addiction. Indeed, the whole area is, as it were, under-trialled. As David Smith, another Oxford-based researcher and the chairman of the conference, pointed out, drug companies are not interested in carrying out such trials because the results, even if favourable, are unlikely to be patentable.

Governments do not seem interested at the moment, either; the welfare of addicts, rhetoric aside, is rarely a priority. Similar studies of the effect of diet on the behaviour of prisoners are, though, provoking interest. John Stein, yet another Oxford man, is currently conducting such a study in three British prisons. If a change of diet really can help addicts, it would be a shame not to find out. It might even save the public purse some money.