Gene-Food Responsiveness: Lactose tolerance/Adult lactose persistence

Gene-Food Responsiveness

A person may have a unique response to food based on their genes.

Food responsiveness genes that may be tested via SmartDNA or 23andme include lactose intolerance, salt sensitivity, caffeine metabolism, gluten, co-enzyme Q10, Omega 3 and Omega 6 fats and iron.  Your genetic predisposition for metabolising alcohol may also be determined.

Knowing your genetic profile in relation to food responsiveness allows for personalised food recommendations and/or suggests further areas of investigation.  In the first of a series of posts, I explore the evolution of lactose tolerance.

The evolution of lactose tolerance, or ‘Adult Lactose Persistence’.

Fresh milk in a glass jug on a blue napkin with a flower

The lactase enzyme is active in infants and generally decreases after weaning. In some people the gene which activates the lactase enzyme remains ‘switched on’ into adulthood, and they are said to be lactose tolerant, or have Adult Lactose Persistence (ALP). It is unlikely these individuals will experience significant gastrointestinal symptoms on consumption of moderate amounts of lactose containing dairy products.

In others, the gene down regulates after weaning and they are likely to become lactose intolerant as an infant or more likely from kindergarten/primary school onwards.

The gene-culture co-evolution of lactose persistence is fascinating. The ALP gene variant is found in approximately 35 percent of adults (worldwide), with a greater frequency found in northern Europe (89-96% in the UK and Scandinavia) and less (15-54%) in central and southern Europe. Greater ALP frequency is found in northern India than southern (63% v 23%), and in Africa, ALP predominates in areas with traditional pastoral populations (with 64% in certain areas of Sudan).  The ALP trait is considered rare in eastern Asia1.

The single nucleotide polymorphism (SNP) thought highly likely for ALP (where the DNA base is changed to thymine) 13910*T is not in the lactase (LCT) gene but in a neighbouring gene, MCM6.  This SNP does not correlate to the total distribution of ALP in Africa, with other variants including 14010*C found there.

Chicken or Egg?  Or in this case, did the SNP come before the Cow?

The dates estimated with the emergence of these SNPs are associated with the agricultural practice of dairying for milk production1, estimated between 8,000 – 11,000 years ago2.

Two hypothesis underpinning ALP are at opposite ends of the spectrum. One -the culture-historical hypothesis – proposes that lactose persistence developed as a result of increased dairy consumption and the other – the reverse cause hypothesis -suggests that dairying only took hold in populations where the frequency of the lactose persistence variation was significant enough to warrant adopting the practice. The later doesn’t appear to correspond however to organic residue which provides evidence of milk use in pottery found in archaeological digs in areas with a low frequency of ALP1.  This includes pottery vessels from the Stone Age (7,000 years ago) found in central Poland, which had distinctive perforations similar to what is still used today to separate whey when making cheese. When tested, the preserved residues of milk were found in these vessels2.

Did dairy consumption confer a selective nutritional advantage?

Milk is nutrient dense and a good source of calories. In those populations which experienced crop failure, famine or epidemic, milk would have provided an alternate food source (at least while there was sufficient food to feed the cow!). Genetic selection would have favoured those with the ALP variation in acrid regions, where milk provided a pathogen free source of hydration, which could have been drunk without adverse digestive symptoms or exacerbating dehydration1.  Herders also used the process of fermentation to make cheese and yoghurt, which decreases lactose to more tolerable levels2 for consumption by all, and in the case of hard cheeses, allows for storage.

The frequency and distribution of these SNP’s are amongst the highest for any human genes over the past 30,000 years1, and is ‘one of the strongest genetic signatures of natural selection yet reported in humans’ (Tishiff et al in 3).

Adult lactose persistence, Malaria and Rickets

As well as nutritional intake, the selective advantage for ALP in sub-Saharan Africans is reduced malaria mortality3. The pastoralist Fulani African ethnic group have a higher rate (60%) of ALP, and lower susceptibility to Plasmodium falciparum and malaria morbidity than neighbouring groups4. Abundant dairy consumption may confer a benefit by displacing p-aminobenzoic acid (PABA) and folate rich foods from the diet, which decreases P. falciparum replication3 and milk may also contain probiotics and immunomodulatory constituents which have an anti-malarial effect4.

The largest frequency of ALP is found in Northern Europe, near the Baltic and North Sea regions. Early farmers in this region took advantage of an ideal microclimate for growing cereal crops (mainly wheat and barley). The high latitude and large cereal intake favoured the development of rickets, a bone disease of childhood causing soft bones. Rickets may also flatten the pelvis in adult women which is thought to have increased maternal mortality during childbirth, prior to the development of modern surgical techniques. A predominate whole grain diet is high in fibre, which may encourage the elimination of  25-hydroxyvitaminD3. Whole grains may also be a poor source of calcium and contain phytates, which if incorrectly prepared, further impairs calcium absorption.  This coupled with reduced sunlight at high latitudes may have contributed to high mortality rates in these Neolithic populations. ALP favoured survival in these populations as calcium rich milk was protective against developing rickets. Selective skin depigmentation in these regions also conferred a benefit by increasing the de novo synthesis of vitamin D3 in the skin3.  ALP is also common however in Spain – a wonderfully sunny country, so more research is need to establish what role Vitamin D played in lactose persistence2

Are you curious and want to find out more about your individual gene – food responsiveness? Call me to arrange a consult.

Side note

Other factors may contribute to lactose malabsorption issues such as enzymatic processes which slow down as we get age, altered gut flora, and small intestinal bacteria overgrowth.

References

(1)             Gerbault, P.; Liebert, A.; Itan, Y.; Powel, A.; Currat, M.; Burger, J.; Swallow, D.; Thomas, M. Philos. Trans. R. Soc. 2011, 366, 863.

(2)             Curry, A. Nature 2013, 500, 20.

(3)             Cordain, L.; Hickey, M. S.; Kim, K. In In Biodiversity in agriculture: domestication, evolution and sustainability; Gepts, P.; Bettinger, R.; Brush, S. B.; Famula, T.; McGuire, P.; Qualset, C., Eds.; Cambridge University Press: Cambridge, UK.

(4)             Lokki, A.; Jarvela, I.; Israelsson, E.; Maiga, B.; Troye-Blomberg, M.; Dolo, A.; Dorumbo, O.; Meri, S.; Holmberg, V. Malar. J. 2011, 10.

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