The simplest method for dieting is to eat less and take more exercise. Specifically, to eat less fat and exercise for longer-than-normal periods so that stored fat (triglycerides) reserves are depleted or used up. The reasoning behind this is simple: more energy is used than is stored.

A question that is rarely tackled is why weight loss should be necessary in more than a handful of serious medical cases. Why do we want or need to lose weight in the first place?

Social and cultural factors form the basis for one set of reasons. Eating three times or more a day, eating food prepared by a global, profitable and well-structured industry, means whatever we might want is available at any time of the day or night. It is therefore easy to eat too much.

But what about at a genetic level? Why do some people seem to have the ability to turn food into reserves of energy seemingly easily, and others make muscle? Why is my hunger for beef burgers being fried not in step with the number of miles I have cycled in the previous 24 hours?

A simplistic answer is evolution. Recent research has provided evidence that the inter-breeding between human species several tens of thousands of years ago, led to a distinctive lipid catabolism in modern European populations [1]. The hypothesis is that in Europe, there was a selection pressure that resulted in human populations who stored fat easily surviving, and those who did not, perishing. Further, this selection pressure did not occur in Africa or in the Orient.

This hypothesis was informed by evidence published in the last decade, that shows that between 1% and 4% of the genome of European humans originates from Neanderthal individuals [2-4]. Importantly, a portion of this fraction is dedicated to lipid catabolism, and is one that contemporary African and Oriental humans do not possess. None of these genes are present in chimpanzees.

It has been suggested that the presence of Neanderthal genes is why lipid catabolism is so different between current human populations. It is also why a significant number of Oriental individuals appear to lay down muscle rather than fat, when they over-eat.

Kharmeeva et al. [1] describe the conclusion that the lipid catabolism of contemporary Europeans was the result of positively-selected gene flow from Neanderthals as appealing, stopping short of giving it cast-iron approval. They state that their observations are also consistent with other hypotheses, based on the number of variants of these genes that left Africa when human populations began a global spread.

Whatever the precise reason, the evidence that shows a genetic distinction in lipid catabolism between current human populations, is not in doubt. What might be of interest to an amateur evolutionary biologist, is what the future might hold for human populations, especially if the results of climate change are as catastrophic as some commentators suggest. Will the ability to grow muscle easily be selected for or against? Similarly, will the ability to lay down fat be an advantage or not?

For the moment, I want to find my bike and burn off a few calories.


[1] E. E. Khrameeva, K. Bozek, L. He, Z. Yan, X. Jiang, Y. Wei, K. Tang, M. S. Gelfand, K. Prufer, J. Kelso, S. Paabo, P. Giavalisco, M. Lachmann, P. Khaitovich, Nature Comm., 2014, 5, 3584. DOI: 10.1038/ncomms4584

[2] R. E. Green, J. Krause, A. W. Briggs, T. Maricic, U. Stenzel, M. Kircher, N. Patterson, H. Li, W. Zhai, M. H. Y. Fritz, N. F. Hansen, E. Y. Durand, A. S. Malaspinas, J. D. Jensen, T. Marques-Bonet, C. Alkan, K. Prüfer, M. Meyer, H. A. Burbano, J. M. Good, R. Schultz, A. Aximu-Petri, A. Butthof, B. Höber, B. Höffner, M. Siegemund, A. Weihmann, C. Nusbaum, E. S. Lander, C. Russ, N. Novod, J. Affourtit, M. Egholm, C. Verna, P. Rudan, D. Brajkovic, Ž. Kucan, I. Gušic, V. B. Doronichev, L. V. Golovanova, C. Lalueza-Fox, M. de la Rasilla, J. Fortea, A. Rosas, R. W. Schmitz, P. L. F. Johnson, E. E. Eichler, D. Falush, E. Birney, J. C. Mullikin, M. Slatkin, R. Nielsen, J. Kelso, M. Lachmann, D. Reich, S. Pääbo, Science, 2010, 328, 710–722 .

[3] P. D. Evans, N. Mekel-Bobrov, E. J. Vallender, R. R. Hudson, B. T. Lahn, Proc. Natl. Acad. Sci. USA , 2006, 103, 18178–18183.

[4] J. D. Wall, M. F. Hammer, Curr. Opin. Genet. Dev. , 2006, 16, 606–610.