Why some of us digest milk well and some do not
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Lactose intolerant people lack the enzyme lactase that breaks down lactose into two simpler sugars
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HIGH PREVALENCE: Pastoralist populations, have a high Lactase persistence than the others.
A NEWBORN infant drinks nothing but mother's milk. Upon weaning (in about 3 years), the ability to digest the lactose in the milk gradually weakens. Milk drinking moves from the breast to a bottle to a beaker to a burden.
Indeed, there are two classes of people in the world — one comprising those who can down up to a litre of milk in a day quite comfortably, and the other of those who cannot. The latter is lactose-intolerant or LI.
Gene shut off
The undigested lactose leads to stomach-ache, gas formation and even diarrhoea.
These are LI because they have shut off, early in life, the gene that produces the enzyme called lactase, which breaks down lactose into two simpler sugars, glucose and galactose.
Lactose intolerance is what geneticists call an autosomal recessive trait. Autosomal because the gene for lactase is not located in the gender-determining chromosomes X (female) or Y (male), but in the chromosome 2.
Mutation's role
Each of us inherits a pair (alleles) of the gene — one from each parent. Any mutation in the lactase gene can lead to the malfunctioning enzyme. If both alleles are normal and unmutated, the child gets two copies of the good gene and there is no problem.
If he inherits one good and one faulty gene, he may still have no problem since at least one good gene is expressed and can dominate. But if each parent carries one mutant and the child, in a one-in-four chance, inherits two mutant alleles, he becomes LI.
Interestingly, LI or its opposite, lactase persistence (LP), is not evenly distributed across the populations of the world. People from North and Central Europe are largely LP and handle milk quite comfortably even in their seventies and eighties.
They have the dominant Mendelian trait for the enzyme lactase. In contrast, people from some parts of Africa and Middle East show a more complex distribution. Close to 90 per cent of the Bantu people of Southern Africa are LI, while their neighbouring Tutsis and Fulanis are over 80 per cent LP. What about we Indians?
A multi-centre study in 1981 by Dr. R.K. Tandon and co-workers suggested that people from South India (Thiruvananthapuram and Puduchery were the towns studied) were 66 per cent LI, while those from New Delhi were more tolerant (LI 27 per cent).
A more recent study in 2004 by Dr. S.V. Rane and others suggests that as many as 50 per cent of Indians tested are LI.
We seem to fall somewhere between the Europeans and the West Asians in our ability to digest milk. There is also a hint that South Indians do not handle milk as well as Northerners.
Why does such a spread of LI/LP occur across the world, particularly since we all came out of a common set of ancestors out of Africa, and over 99.5 per cent of our genes are identical?
A tentative answer to this puzzle is emerging, based both on our genetic and cultural history.
One hint came when a group of European geneticists suggested a few years ago that they had found a noticeable difference between dairying communities and non-pastoralists. Pastoralist populations, by and large, have a high LP prevalence than the others.
Chicken-egg question
This distinction of LP distribution raises the chicken-egg question of culture and gene selection. One could argue that LP positive persons preferred other LPs as mates, founded families and enriched the LP in their descendants.
This enrichment gave them selective advantage when dairying was invented over 8000 years ago. But one would have to ask what special advantage LP-ness had before milk as an adult food got introduced.
After all, LP offers only milk digesting ability and nothing else. It is Mendelian, a single gene, single effect.
Alternative hypothesis
The alternative hypothesis, called the culture-historical model, argues that LP was driven from very rare cases of pre-adaptation to higher prevalence and frequencies in communities only after dairying was practised.
There was no pre-selection, dairying produced the pairing of LP couples and their offspring, which grew into large pastoral communities.
How does one test which model is correct? A group of geneticists led by Leena Peltonen of UCLA came out with a useful marker in the DNA chain close to where the lactase gene is located.
Called the T allele of the C/T variant, it is strongly associated with LP in Europeans. The question one can thus ask is: did the T allele already segregate with the lactase gene in Neolithic Europeans even before dairying started?
Anthropologists from Mainz, Germany, led by J. Burger, working with the London geneticist M.G. Thomas analysed a large number of human DNA samples obtained from Neolithic sites from Germany, Poland and Hungary and looked for the T allele near the lactase gene.
They did not find this association (Proceedings of the National Academy of Sciences, March 6, 2007).
This means that no pre-adaptation of LP into communities occurred before domestication of milk cattle. Instead, dairying drove people to choose mates with LP, found families and enable the community to use milk as an important adult food.
D. BALASUBRAMANIAN
dbala@lvpei.org
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