HEALTH / Second Opinion
Sunday 30 October 1994
Outside northern Europe the adult human small intestine lacks the enzyme essential for the digestion of lactose, the sugar in milk. As a result, when milk is drunk in any quantity the sugar passes unchanged into the lower bowel, where it becomes fermented, generating gas and leading to distension of the belly, flatulence and diarrhoea. Infants digest their mother's milk (or bottled milk) readily enough, but as early as the second year the amount of the essential enzyme in the intestines begins to decline and the ability to digest milk is lost completely by around the age of six.
The racial variation in persistence of intestinal enzymes has been known for many years, but the explanation for it has continued to puzzle geneticists.
The difference seems to be due to a mutation in the gene responsible for the enzyme lactase, but no one can be certain whether the earliest humans had the gene for persistent lactase or the gene for rapid loss of the enzyme.
The persistence gene is not confined to northern Europeans: it is found also in milk-drinking nomads in both Africa and Asia, and might have been present in early man before the major races separated. What has to be explained is the clear contrast between the peoples of the temperate zones, most of whom are able to be milk drinkers, and the peoples in the tropical and equatorial regions, most of whom cannot drink milk unless it has been fermented to remove the sugar.
In Darwinian theory, the explanation would be expected to be an environmental one: some difference in the climate or lifestyle would favour milk drinkers in one region and non-milk drinkers in the other. The latest theory, advanced in the specialist medical journal Gut by two doctors working in Italy, is that lactase deficiency is a protection against malaria. Malaria still kills a million or more people every year, most of them children. The parts of the world where lactase deficiency is predominant are those in which malaria is common, and in particular the most dangerous variety, falciparum malaria. Malaria is not a health problem in the deserts and highlands in which the nomads have a tradition of milk drinking and retain their lactase until late in life.
A child who becomes lactase-deficient will soon stop drinking milk because of the discomfort it causes, says the new theory. Milk is the richest source of the vitamin riboflavin, and children on a poor diet who give up milk will become mildly deficient in riboflavin. Malaria parasites multiply less well in red blood cells that lack riboflavin: so, children who do not drink milk may be less likely to die in infancy from falciparum malaria.
If, indeed, lack of intestinal lactase helps children in tropical Africa to survive, this will be yet another example of a genetic variation having an unsuspected plus side. A second lesson to be learnt is that for most of the world's children over the age of six, milk has only a small place in the diet.
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