Drunken Monkey Hypothesis’ – some serious evolutionary and molecular biology


This has to be a good read! Not just because it might be amusing but also because there is some serious evolutionary and molecular biology here. Our craving for alcohol seems to have a long, long evolutionary history, with a neat mutating gene, ADH4 (No! Not anti-diuretic hormone but alcohol dehydrogenase enzyme), which speeds up the digestion of alcohol, beginning in the mouth. Several primates are known to feast on fermented fruits and there is good evidence that this pursuit of alcohol has or had a significant calorific value for those animals.

From BBC, 23 February 2017



The evolutionary investigation done by Mathew Carrigan and his associates is so very interesting but of course way beyond what the IB might require. Nevertheless, if you are interested enough (Extended essay???) here is a link to the full text of Carrigan’s publication:  http://www.pnas.org/content/112/2/458.full. Early primate ancestors, about 50 million years ago, evidently possessed a gene to produce ADH in some form, and were able therefore to digest alcohol. Some 10 million years ago, primates began foraging on the ground and encountered fallen, fermenting fruit – an excellent source of sugar and thus calories. At about the same time the ADH4 gene underwent a significant, single mutation which enabled some primates to digest alcohol very much more efficiently and therefore be at a competitive and evolutionary advantage. In humans, this gene is one of a bunch of alcohol digesting genes on chromosome 4. The focus upon alcohol in different forms as a source of energy food, pre-dates the supposed time, maybe just 9,000 years ago, when humans apparently first began to enjoy alcohol as a drink and for its pleasurable effects of inebriation. Carrigan even argues that the pleasure ‘kick’ we modern humans get from alcohol can be explained by our ancient ancestors especially seeking out fermented fruits for their high energy value, and thus obtaining a cerebral ‘hit’ of satisfaction, even though they possibly did not obtain significant effects from inebriation.

I love this! it can go on and on and on ….!

What is the mutation? ADH is a zinc based enzyme. (See a molecular visualisation of it here: http://www.proteopedia.org/wiki/index.php/3cos.) The mutation is one of the most frequent sorts of mutation – a ‘snip’ or SNP, SINGLE NUCLEOTIDE POLYMORPHISM, which occurs when just one nucleotide and its base is changed, resulting in a the synthesis of a modified protein. Research has shown that in humans there are two variants of the ADH1 SNP, with a resultant protein carrying either the amino acid histidine or arginine – effectively two different alleles. The first of these alleles, with the amino acid histidine, is much more effective at the breakdown of ethanol. People with this allele are consequently more tolerant to alcohol. A wonderful piece of research in China has shown how the less effective allele, containing arginine, was selected out of a population about 10,000 years ago. This time coincides with the early domestication of rice in Eastern Asia. Supposedly early humans commonly consumed alcohol derived from the fermented rice. Those with the arginine-coding allele were less tolerant to alcohol and were therefore less likely to have reproductive success, so the allele became uncommon.  (http://bmcevolbiol.biomedcentral.com/articles/10.1186/1471-2148-10-15)