There is a surging interest in perspectives of evolution to shed light on solutions for health—not at all discounted by this year’s Charles Darwin’s 200th birth anniversary. Many health-care professionals have even called for a return to a more primitive pattern of diet, environment and exercise that first made our ancient genome thrive (1-8).
Cordain et al (3) and others (1;4) make nothing short of an understatement in suggesting that contemporary chronic diseases and health issues are partially, if not largely, due to an evolutionary “clashing” (3;4) with new patterns introduced in our modern world.
Attempts of Cordain et al (3), however, of pointing out nutritional alterations since the agricultural revolution to reveal “evolutionary discordance” between Western diet and one in line with “genetically determined biology” can be considered far reaching.
An example is Cordain et al’s case that refined sugar consumption increased since 500 BC and high-fructose corn syrup since the 1970s may have caused discordance (3). Lacking evidence directly associated with hominin diets, it is left unknown how simple sugars may have actually shaped evolution of hominins.
The data, however, on ape diets suggests a fruitarian ancestry governed by plants (1). Although the sugars of these fruits are evidenced to have been accompanied by diverse dietary fiber sources (5), nutritional variations may have occurred not unlike refined sugars and large amounts of fructose. It is also unclear why fructose, heavily associated with diabetes (9-11), should be prevalent in the main foods of a hominin ancestral diet.
Science must ultimately make up perceptions on factual matter regarding nutrition and medicine where historical and archeological evidence fall short and can only present clues.
Double-blind, randomized cross-over designed trials on each discordance—cereals, refined sugars, refined vegetable oils, alcohol, salt, fatty domestic meats, etc.—and how differing amounts affect health must be researched for proper nutritional determinations.
For example, two interventions over a year’s time could be performed in which one group could be given wild-caught salmon and deer meat and the placebo group would receive farmed salmon and deer meat. Blood lipids and abdominal fat stores can be measured throughout the year.
Because of possible interplay from each discordance that should not be discounted, double-blind randomized cross-over trials should also include versions of whole, supposed Paleolithic diets.
Each study performed, in turn, may also offer revelations into evolutionary past. And perhaps, to make things more interesting, the studies should also be performed on bonobos and chimpanzees.
1. Boaz N. Evolving Health: The Origins of Illness and How the Modern World is Making us Sick. New York: John Wiley & Sons, 2009.
2. Cordain L. The Paleo Diet. Hoboken, New Jersey: John Wiley & Sons, 2002.
3. Cordain L, Eaton SB, Sebastian A et al. Origins and evolution of the Western diet: health implications for the 21st century. Am J Clin Nutr 2005;81:341-54.
4. Gibson G. It Takes a Genome: How a Clash Between Our Genes and Modern Life is Making us Sick. Sydney, Australia: FT Press, 2009.
5. Leach JD. Evolutionary perspective on dietary intake of fibre and colorectal cancer. Eur J Clin Nutr 2007;61:140-2.
6. Marean CW, Bar-Matthews M, Bernatchez J et al. Early human use of marine resources and pigment in South Africa during the Middle Pleistocene. Nature 2007;449:905-8.
7. Nesse RM, Williams GC. Why We Get Sick: The New Science of Darwinian Medicine. New York: Vintage, 1996.
8. Wrangham R. Catching Fire: How Cooking Made Us Human. New York: Basic Books, 2009.
9. Sartorelli DS, Franco LJ, Gimeno SG, Ferreira SR, Cardoso MA. Dietary fructose, fruits, fruit juices and glucose tolerance status in Japanese-Brazilians. Nutr Metab Cardiovasc Dis 2009;19:77-83.
10. Ouyang X, Cirillo P, Sautin Y et al. Fructose consumption as a risk factor for non-alcoholic fatty liver disease. J Hepatol 2008;48:993-9.
11. Basciano H, Federico L, Adeli K. Fructose, insulin resistance, and metabolic dyslipidemia. Nutr Metab (Lond) 2005;2:5.