2050 words

Diet is the main driver of our evolution. Without adequate energy, we wouldn’t be able to able to have a brain as large as we do that has the number of neurons we have due to how calorically expensive each neuron is (6 kcal per billion neurons). However, as I’m sure everyone can see, our current diets and environment has caused the current obesity crisis in the world. What is the cause of this? Our genomes are adapted for a paleolithic diet and not our modern environment with processed foodstuffs along with an overabundance of energy. With an overabundance of novel food items and situations due to our obesogenic environments, it is easier for a higher IQ person to stay thinner than it is for a lower IQ person. Tonight I will talk about the causes for this, how and what we evolved to eat and, of course, how to reverse this phenomenon.

“Gourmet Sapiens” arose around 1-1.5 mya with the advent of cooking by Homo erectus. Even before then, when we became bipedal our hands were freed which then allowed us to make tools. With these tools, we could mash and cut food which was a sort of pre-digestion outside the body (exactly what cooking is). Over time, our guts shrank (Aiello, 1997) and we became adapted for a certain diet (Eaton, 2006). Over time, we evolved to eat a certain way—that is, we had times of feast and famine. Due to this, eating three meals a day is abnormal from an evolutionary perspective (Mattson et al, 2014). This sets the stage for the acquisition of diseases of civilization along with the explosion of obesity rates.

When looking for the causes—and not symptoms—of the rise of obesity rates, the first thing we should do is look at our current environment. How is it constructed? What type of foodstuffs are in it? What kinds of foods get advertised to us and how does this have an effect on our psyche and what we eventually buy? All three of these questions are extremely important to think of when talking about why we are so obese as a society. First-world environments are obesogenic (Galgani and Ravussin, 2008) due to being evolutionarily novel. Our genomes are adapted to a paleolithic diet, and so the introduction of the neolithic diet and agriculture reduced our quality of life, with a marked decrease in the quality of skeletal remains discovered after the advent of agriculture. However, agriculture is obviously responsible for the population boom that allowed us to become the apes the took over the world, cause being the population boom that followed the agricultural revolution (Richards, 2002).

Evolutionary mismatches occur when the rate of cultural or technological change is far faster than the genome can change to adapt to the new pressure. These dietary mismatches occur when cultural and technological change which can vastly outstrip biological evolution. The two big events that occurred in human history that have vastly outstripped biological evolution are the agricultural and Industrial Revolution. Contrary to Ryan Faulk’s belief, East Asians are not ‘less sensitive to carbohydrates’ and he did not “solve Gary Taubes’ race problem” in regards to diabesity rates. The rate of cultural and technological change has had large deleterious effects on our quality of life, and our increasing obesity rates have a lot to do with it.

Cofnas (2016) showed that mice taken off of their ancestral diet lead to worse healthy outcomes. The results of Lamont et al (2016) show that we, as animals, are adapted for ancestral diets, not the diets of the environment we have currently made for ourselves. This is a big point to take home from this. All organisms are adapted/evolved for what occurred in the ancestral past, not any possible future events. Therefore, to be as healthy as possible, it stands to reason you should eat a diet that’s closer to the ones your ancestors ate, especially since it can reverse type II diabetes and reverse bad blood markers (Klonoff, 2009). Even a short-term switch to a paleo diet “improves BP and glucose tolerance, decreases insulin secretion, increases insulin sensitivity and improves lipid profiles without weight loss in healthy sedentary humans.” (Frassetto et al, 2009) Since we evolved for a past environment and not any possible future ones, then eating a diet that’s as close as possible to our paleolithic ancestors looks like a smart way to beat the evolutionary mismatch in terms of our new, current obesogenic environment.

In one extremely interesting study, O’dea (1984) took ten middle-aged Australian Aborigines with type 2 diabetes and had them return to their ancestral hunter-gatherer lifestyle. With seven weeks of an ancestral diet and exercise, the diabetes had almost completely reversed! Clearly, when the Aborigines were taken off of our Western diet and put back in their ancestral environment with their ancestral diet, their diabetes disappeared. If we went back to a more ancestral eating pattern, the same would happen with us. This one small study lends credence to my claim that we need to eat a diet that’s more ancestral to us for us to ameliorate diseases of civilization (Eaton, 2006).

Further, looking at obesity from an evolutionary perspective can and will help us understand the disease of obesity (Ofei, 2005) better. Speakman (2009) reviewed three different explanations of the current obesity epidemic and assessed their usefulness in explaining the epidemic. The thrifty gene hypothesis states that obesity is an adaptive trait, that people who carry so-called ‘thrifty genes’ would be at an adaptive advantage. And since we have an explosion of obesity today from the 70s to today, this must explain a large part of the variance, right? There is evidence pointing in this direction, however (Southam et al, 2009). The second cause that Speakman looks at is the adaptive viewpoint—that obesity may have never been advantageous in our history, but genes that ultimately predispose us to obesity become “selected as a by-product of selection on some other trait that is advantageous.” (Speakman, 2009) The third and final perspective he proposes is that it’s due to random genetic drift, called ‘drifty genes’, predisposing some—and not others—to obesity. Whatever the case may be, there is some truth to their being genetic factors involved in the acquisition of fat storage. Though drifty genes and the adaptive viewpoint on obesity make more sense than any thrifty gene hypothesis.

For there to be any changes in the rate of obesity in the world, we need to begin to change our obesogenic environments to environments that are more like our ancestral one in terms of what foods are available. Once we alter our obesogenic environment into one that is more ancestrally ‘normal’ (since we are adapted for our past environments and not any possible future ones) then and only then will we see a reduction in obesity around the world. We are surrounded and bombarded with ads since we are children, which then effects our choices later in life; children consume 45 percent more when exposed to advertising (Harris et al, 2009). Clearly, advertisements can have one eat more, and the whole environmental mismatch in regards to being surrounded by foodstuffs not ancestral to us causes the rate of obesity to rise.

Finally, one thing we need to look at is the n-3 to n-6 ratio of our diets. As I covered last month, the n-6/n-3 is directly related to cognitive ability (Lassek and Gaulin, 2011). Our obesogenic environments cause our n-3/n-6 levels to be thrown out of whack. Our hunter-gatherer ancestors had a 1:1 level of n-3 and n-6 (Kris-Etherton, 2000). However, today, our diets contain 14 to 25 times more n-6 than n-3!! Still wondering why we are getting stupider and fatter? Further,  Western-like diets (high in linolic acid; an n-6 fatty acid) induces a general fat mass enhancement, which is in line with the observation of increasing obesity in humans (Massiera et al, 2010). There is extreme relevance to the n-3/n-6 ratio on human health (Griffin, 2008), so to curb obesity and illness rates, we need to construct environments that promote a healthy n-3/n-6 ratio, as that will at least curb the intergenerational transmission of obesity. Lands (2015) has good advice: “A useful concept for preventive nutrition is to NIX the 6 while you EAT the 3.” Here is a good list to help balance n-6 to n-3 levels.

In sum, obesity rates are a direct product of obesogenic environments. These environments cause obesity since we are surrounded by evolutionary novel situations and food. The two events in human history that contribute to this is the agricultural and Industrial Revolution. We have paleolithic genomes in a modern-day world, which causes a mismatch between our genomes and environment. This mismatch can be ameliorated if we construct differing environments—ones that are less obesogenic with less advertisement of garbage food—and we should see rates of obesity begin to decline as our environment becomes more and more similar to our ancestral one (Genné-Bacon, 2014).

The study on mice showed that for them to be healthy they need to eat a diet that is ancestral to them. We humans are no different.The evidence from the study on Australian Aborigines and the positive things that occur after going on a paleo diet for humans—even for sedentary people—shows that for us to be as healthy as possible in these obesogenic environments that we’ve made for ourselves, we need to eat a diet that matches with our paleolithic genome. This is how we can begin to fight these diseases of civilization and heighten our quality of life.

Note: Diet and exercise only under Doctor’s supervision, of course

References

Aiello, L. C. (1997). Brains and guts in human evolution: The Expensive Tissue Hypothesis. Brazilian Journal of Genetics,20(1). doi:10.1590/s0100-84551997000100023

Cofnas, N. (2016). Methodological problems with the test of the Paleo diet by Lamont et al. (2016). Nutrition & Diabetes,6(6). doi:10.1038/nutd.2016.22

Eaton, S. B. (2006). The ancestral human diet: what was it and should it be a paradigm for contemporary nutrition? Proceedings of the Nutrition Society,65(01), 1-6. doi:10.1079/pns2005471

Frassetto, L. A., Schloetter, M., Mietus-Synder, M., Morris, R. C., & Sebastian, A. (2009). Metabolic and physiologic improvements from consuming a paleolithic, hunter-gatherer type diet. European Journal of Clinical Nutrition,63(8), 947-955. doi:10.1038/ejcn.2009.4

Galgani, J., & Ravussin, E. (2008). Energy metabolism, fuel selection and body weight regulation. International Journal of Obesity,32. doi:10.1038/ijo.2008.246

Genné-Bacon EA, Thinking evolutionarily about obesity. Yale J Biol Med 87: 99–112, 2014

Griffin, B. A. (2008). How relevant is the ratio of dietary n-6 to n-3 polyunsaturated fatty acids to cardiovascular disease risk? Evidence from the OPTILIP study. Current Opinion in Lipidology,19(1), 57-62. doi:10.1097/mol.0b013e3282f2e2a8

Harris, J. L., Bargh, J. A., & Brownell, K. D. (2009). Priming effects of television food advertising on eating behavior. Health Psychology,28(4), 404-413. doi:10.1037/a0014399

Klonoff, D. C. (2009). The Beneficial Effects of a Paleolithic Diet on Type 2 Diabetes and other Risk Factors for Cardiovascular Disease. Journal of Diabetes Science and Technology,3(6), 1229-1232. doi:10.1177/193229680900300601

Kris-Etherton PM, Taylor DS,  Yu-Poth S, et al. Polyunsaturated fatty acids in the food chain in the United States.  Am J Clin Nutr, 2000, vol. 71 suppl(pg. 179S-88S)

Lamont, B. J., Waters, M. F., & Andrikopoulos, S. (2016). A low-carbohydrate high-fat diet increases weight gain and does not improve glucose tolerance, insulin secretion or β-cell mass in NZO mice. Nutrition & Diabetes,6(2). doi:10.1038/nutd.2016.

Lands, B. (2015). Choosing foods to balance competing n-3 and n-6 HUFA and their actions. Ocl,23(1). doi:10.1051/ocl/2015017

Lassek, W. D., & Gaulin, S. J. (2011). Sex Differences in the Relationship of Dietary Fatty Acids to Cognitive Measures in American Children. Frontiers in Evolutionary Neuroscience,3. doi:10.3389/fnevo.2011.00005

Massiera, F., Barbry, P., Guesnet, P., Joly, A., Luquet, S., Moreilhon-Brest, C., . . . Ailhaud, G. (2010). A Western-like fat diet is sufficient to induce a gradual enhancement in fat mass over generations. The Journal of Lipid Research,51(8), 2352-2361. doi:10.1194/jlr.m006866

Mattson, M. P., Allison, D. B., Fontana, L., Harvie, M., Longo, V. D., Malaisse, W. J., . . . Panda, S. (2014). Meal frequency and timing in health and disease. Proceedings of the National Academy of Sciences,111(47), 16647-16653. doi:10.1073/pnas.1413965111

O’dea, K. (1984). Marked improvement in carbohydrate and lipid metabolism in diabetic Australian aborigines after temporary reversion to traditional lifestyle. Diabetes,33(6), 596-603. doi:10.2337/diabetes.33.6.596

Ofei F. Obesity- a preventable disease. Ghana Med J 2005;39: 98-101

Richards, M. P. (2002). A brief review of the archaeological evidence for Palaeolithic and Neolithic subsistence. European Journal of Clinical Nutrition,56(12), 1270-1278. doi:10.1038/sj.ejcn.1601646

Southam, L., Soranzo, N., Montgomery, S. B., Frayling, T. M., Mccarthy, M. I., Barroso, I., & Zeggini, E. (2009). Is the thrifty genotype hypothesis supported by evidence based on confirmed type 2 diabetes- and obesity-susceptibility variants? Diabetologia,52(9), 1846-1851. doi:10.1007/s00125-009-1419-3

Speakman, J. R. (2013). Evolutionary Perspectives on the Obesity Epidemic: Adaptive, Maladaptive, and Neutral Viewpoints. Annual Review of Nutrition,33(1), 289-317. doi:10.1146/annurev-nutr-071811-150711