A study on the effects of milk consumption on growth hormone (GH) and insulin-like growth factor 1 (IGF-1) in children suggests that milk drinking may cause increases in pituitary growth hormone levels of prepubertal girls and boys.

The article, published in Nutrition Journal[1] measured the effects of drinking three 8-ounce tetrapak “boxes” (710 ml) of conventional U.S. UHT-pasteurized vitamin D fortified whole milk daily for one month (the producer of the milk accepts milk only from dairies that do not use bovine somatotropin). A class of Mongolian children (who rarely consume milk) were compared with American children: the Mongolian children experienced rapid linear growth (the equivalent of 12 cm/year) compared to an average height velocity of 5-6 cm/year in U.S. children age 10-11 years. It is suggested that this was not the effects of correcting undernutrition, but that milk intake may raise GH levels. This is a novel finding, and the authors suggest that "nutrients or bioactive factors in milk may stimulate endogenous GH production," that is, secretion of hormones from the pituitary gland may be increased by drinking milk.

Apart from stimulating abnormal growth in prepubertal children, what could be the long-term side-effects of an increase in the pituitary growth hormone in those with otherwise normal growth hormone levels? Another study [2] notes how GH/IGF-1 provides an anti-apoptotic environment (a situation where programmed cell death is delayed) that may favour survival of genetically damaged cells.

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The ability to digest starch may have given our human ancestors an evolutionary advantage in certain circumstances, according to an article by George Perry et al. in Nature Genetics.[1] The enzyme amylase, secreted by salivary glands (and also by the pancreas), helps to hydrolyse or break down starch in the diet when mixed with water. The gene that produces the enzyme in saliva, called AMY1, is on chromosome 1, other authors have theorised that the salivary amylase gene evolved from the pancreatic amylase gene via an upstream retrovirus insertion.[2]

Perry's team took salivary and DNA samples from people of Datog, Hadza, Mbuti, Biaka, Japanese, Yakut and European-American populations and analysed their typical dietary protein and starch intake. The results indicate that geographically distinct groups of humans tend to have variable levels of the AMY1 gene according to the level of starch in their diets: Those whose diets consist of higher protein levels tended to have on average fewer copies of the gene, and vice versa. More copies of the gene leads to a higher level of salivary amylase. Fruit-eating chimpanzees however have few copies of the gene. The authors suggest that: "This behavioral variation raises the possibility that different selective pressures have acted on amylase", i.e. it could be evidence for genetic adaptation to the availability of starch in the environment.

Another study in the American Journal of Human Genetics[3] published just a month prior to Perry's article suggests that the gene for lactase persistence (LP, the ability to digest the lactose sugar in milk after childhood) came about through evolution of two groups geographically and chronologically distinct, and that "there is a still-ongoing process of convergent evolution" of the LP alleles in humans".

It appears that we are still evolving according to what we eat, but can our genes keep up with the pressures inflicted on us by modern western diets?

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