Effects of Brain Evolution on Human Nutrition and Metabolism

Department of Anthropology, Northwestern University, Evanston, IL 60208, USA.
Annual Review of Nutrition (Impact Factor: 8.36). 02/2007; 27(1):311-27. DOI: 10.1146/annurev.nutr.27.061406.093659
Source: PubMed


The evolution of large human brain size has had important implications for the nutritional biology of our species. Large brains are energetically expensive, and humans expend a larger proportion of their energy budget on brain metabolism than other primates. The high costs of large human brains are supported, in part, by our energy- and nutrient-rich diets. Among primates, relative brain size is positively correlated with dietary quality, and humans fall at the positive end of this relationship. Consistent with an adaptation to a high-quality diet, humans have relatively small gastrointestinal tracts. In addition, humans are relatively "undermuscled" and "over fat" compared with other primates, features that help to offset the high energy demands of our brains. Paleontological evidence indicates that rapid brain evolution occurred with the emergence of Homo erectus 1.8 million years ago and was associated with important changes in diet, body size, and foraging behavior.

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Available from: William R. Leonard, Dec 28, 2013
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    • "cardiovascular disease [ 97 ] , respiratory disease [ 98 ] , cancer [ 99 ] and stroke [ 100 ] . However , it is not clear if this association is due to the inherently higher bilirubin levels or whether more bilirubin is degraded due to the disease [ 92 ] . Modern human populations derive more of their dietary energy from meat than the great apes ( Leonard , Snodgrass et al . 2007 ) . Improved diet quality due to cooking and consumption of animal protein and fat has been proposed as one among other factors allowing the increased brain size in humans [ 101 , 102 ] . Our results indicate that expression of UGT1A1 is higher in mice fed a raw plant diet than in mice fed either a meat or cooked - plant diet ( Fig 3 ) "
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    ABSTRACT: Although human biomedical and physiological information is readily available, such information for great apes is limited. We analyzed clinical chemical biomarkers in serum samples from 277 wild- and captive-born great apes and from 312 healthy human volunteers as well as from 20 rhesus macaques. For each individual, we determined a maximum of 33 markers of heart, liver, kidney, thyroid and pancreas function, hemoglobin and lipid metabolism and one marker of inflammation. We identified biomarkers that show differences between humans and the great apes in their average level or activity. Using the rhesus macaques as an outgroup, we identified human-specific differences in the levels of bilirubin, cholinesterase and lactate dehydrogenase, and bonobo-specific differences in the level of apolipoprotein A-I. For the remaining twenty-nine biomarkers there was no evidence for lineage-specific differences. In fact, we find that many biomarkers show differences between individuals of the same species in different environments. Of the four lineage-specific biomarkers, only bilirubin showed no differences between wild- and captive-born great apes. We show that the major factor explaining the human-specific difference in bilirubin levels may be genetic. There are human-specific changes in the sequence of the promoter and the protein-coding sequence of uridine diphosphoglucuronosyltransferase 1 (UGT1A1), the enzyme that transforms bilirubin and toxic plant compounds into water-soluble, excretable metabolites. Experimental evidence that UGT1A1 is down-regulated in the human liver suggests that changes in the promoter may be responsible for the human-specific increase in bilirubin. We speculate that since cooking reduces toxic plant compounds, consumption of cooked foods, which is specific to humans, may have resulted in relaxed constraint on UGT1A1 which has in turn led to higher serum levels of bilirubin in humans.
    PLoS ONE 08/2015; 10(8):e0134548. DOI:10.1371/journal.pone.0134548 · 3.23 Impact Factor
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    • "In humans, the colon represents only 20 % of the total volume of the digestive tract, whereas in apes it is about 50 % (Milton 1999, 2003). The sizeable colons of most large-bodied primates permit fermentation of low-quality plant fibres, allowing for extraction of energy in the form of volatile fatty acids (Leonard et al. 2007). Thus, humans, having small colons, are relatively poor in utilising uncooked plant fibre. "
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    ABSTRACT: We discuss the relations of processed foods, especially cooked foods, in the human diet to digestive tract form and function. The modern consumption of over 70 % of foods and beverages in highly refined form favours the diet-related classification of humans as cucinivores, rather than omnivores. Archaeological evidence indicates that humans have consumed cooked food for at least 300–400,000 years, and divergence in genes associated with human subpopulations that utilise different foods has been shown to occur over periods of 10–30,000 years. One such divergence is the greater presence of adult lactase persistence in communities that have consumed dairy products, over periods of about 8,000 years, compared to communities not consuming dairy products. We postulate that 300–400,000 years, or 10,000–14,000 generations, is sufficient time for food processing to have influenced the form and function of the human digestive tract. It is difficult to determine how long humans have prepared foods in other ways, such as pounding, grinding, drying or fermenting, but this appears to be for at least 20,000 years, which has been sufficient time to influence gene expression for digestive enzymes. Cooking and food processing expands the range of food that can be eaten, extends food availability into lean times and enhances digestibility. Cooking also detoxifies food to some extent, destroys infective agents, decreases eating time and slightly increases the efficiency of assimilation of energy substrates. On the other hand, cooking can destroy some nutrients and produce toxic products. The human digestive system is suited to a processed food diet because of its smaller volume, notably smaller colonic volume, relative to the intestines of other species, and because of differences from other primates in dentition and facial muscles that result in lower bite strength. There is no known group of humans which does not consume cooked foods, and the modern diet is dominated by processed foods. We conclude that humans are well adapted as consumers of processed, including cooked, foods.
    Journal of Comparative Physiology B 06/2015; DOI:10.1007/s00360-015-0919-3 · 2.62 Impact Factor
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    • "Nevertheless, it is the energy consumed by human muscles during locomotion which is almost twice as low compared with, for instance, in chimpanzees (332 versus 564 kcal/day) [22] providing enough energy for brain development and function. The consequence is that humans' brains are three times bigger than the brains of chimpanzees, and brain metabolism accounts for 25% of the basal metabolic rate in humans and only 7 to 8% in other primate species [26]. Overall, there seems to be sufficient scientific support to suggest that the increase of human brain size and metabolism has been possible because of a change of locomotion, higher central fat depot storage [27], and (although not addressed in this review) a change of food intake (see review [24]). "
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    ABSTRACT: In recent years, it has become clear that chronic systemic low-grade inflammation is at the root of many, if not all, typically Western diseases associated with the metabolic syndrome. While much focus has been given to sedentary lifestyle as a cause of chronic inflammation, it is less often appreciated that chronic inflammation may also promote a sedentary lifestyle, which in turn causes chronic inflammation. Given that even minor increases in chronic inflammation reduce brain volume in otherwise healthy individuals, the bidirectional relationship between inflammation and sedentary behaviour may explain why humans have lost brain volume in the last 30,000 years and also intelligence in the last 30 years. We review evidence that lack of physical activity induces chronic low-grade inflammation and, consequently, an energy conflict between the selfish immune system and the selfish brain. Although the notion that increased physical activity would improve health in the modern world is widespread, here we provide a novel perspective on this truism by providing evidence that recovery of normal human behaviour, such as spontaneous physical activity, would calm proinflammatory activity, thereby allocating more energy to the brain and other organs, and by doing so would improve human health.
    Behavioural neurology 05/2015; 2015:1-11. DOI:10.1155/2015/569869 · 1.45 Impact Factor
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