Diabetes – a two-edged sword?

Diabetes was the only specific disease to which Bernard committed his research: all his other work – such as on poisons, on fermentation and on the chemical balance of the body (le milieu intérieur) were phenomena which he targeted in order to understand the normal functioning of the body: in his eyes the essential first step towards understanding its malfunction. The reason for his focus on diabetes is not clear from any of his writings. He probably saw it as a prime example of ‘spontaneous physiological dysfunction’.

And so it has remained for 150 years.

Part genetically determined, part environmental, we still do not really know why it occurs, nor exactly how the inherited and environmental factors inter-relate. In particular, we do not understand why diabetes prevalence in the population varies from one percent (eg Alaskan Eskimos) to forty percent (eg Pima Indians and Nauruans). What does this enormous variation tell us? Neither nutritional levels nor the degree of obesity entirely explain it – even though increasing prevalence of obesity is the most important cause of the current almost epidemic explosion of diabetes across the world.

Exactly 50 years ago, the geneticist JV Neel suggested that the gene(s) responsible for diabetes carried a survival advantage under conditions of famine – that those without ‘diabetic’ genes were more likely to die from starvation – that those with the genes had the advantage of storing calories.  (see ‘thrifty genotype hypothesis’ entry in Wikipedia). In evolutionary terms, Neel’s hypothesis proposes that one or more genes promote selective survival of that sub-section of the community and thus contribute to the survival of the community as a whole.

In my own research 40 years ago, I showed that animals from more arid, food-spare regions (eg deserts) were more likely to become diabetic in captivity. I also found that when fasted, they were able to ‘economise’ by reducing their metabolic rate. Therefore they maintained their weight when challenged by fasting – and were also more resistant to high environmental temperatures. In addition, running low blood sugar  levels causes infertility (at least in rats and rabbits!): accordingly, any biological system which allows the blood sugar to run at rather higher levels should help to maintain the fertility level of that species.

Some years later, I was not surprised when my field studies showed that more than 30 percent of Australian aboriginals – originally nomadic hunter-gatherers in the heart of Australia but now living in urbanized society – had diabetes. Was it their diabetic gene(s) that had allowed them to (selectively) survive millenia of relative food scarcity? Do ‘diabetic genes’ indeed confer a survival advantage  – under the right conditions?  Natural selection was only proposed by Charles Darwin during the latter part of Bernard’s life, but Neel’s theory slots neatly into the concept of ‘survival of the fittest’. Notwithstanding a whole host of parallel theories on the fundamental nature of diabetes, it is an interesting concept worth preserving until something more conclusive comes along.



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