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Our earliest ancestors ate their food raw — fruit, leaves, maybe some nuts. When they ventured down onto land, they added things like underground tubers, roots and berries.
It wasn't a very high-calorie diet, so to get the energy you needed, you had to eat a lot and have a big gut to digest it all. But having a big gut has its drawbacks.
"You can't have a large brain and big guts at the same time," explains Leslie Aiello, an anthropologist and director of the Wenner-Gren Foundation in New York City, which funds research on evolution. Digestion, she says, was the energy-hog of our primate ancestor's body. The brain was the poor stepsister who got the leftovers.
Until, that is, we discovered meat.
"What we think is that this dietary change around 2.3 million years ago was one of the major significant factors in the evolution of our own species," Aiello says.
Brain tissue is metabolically expensive, but there is no significant correlation between relative basal metabolic rate and relative brain size in humans and other encephalized mammals. The expensive-tissue hypothesis suggests that the metabolic require- ments of relatively large brains are offset by a corresponding reduction of the gut. The splanchnic organs (liver and gastrointestinal tract) are as metabolically expensive as brains, and the gut is the only one of the metabolically expensive organs in the human body that is markedly small in relation to body size. Gut size is highly correlated with diet, and relatively small guts are compatible only with high-quality, easy-to-digest food.
The often-cited relationship between diet and relative brain size is more properly viewed as a relationship between relative brain size and relative gut size, the latter being determined by dietary quality. No matter what is selecting for relatively large brains in humans and other primates, they cannot be achieved without a shift to a high-quality diet unless there is a rise in the metabolic rate. Therefore the incorporation of increasingly greater amounts of animal products into the diet was essential in the evolution of the large human brain.
One cause of vitamin B12 deficiency is inadequate oral intake. This can potentially occur in vegetarians, particularly those following the strictest vegan diets. Other people who are susceptible include chronic alcoholics and individuals attempting certain fad diets. Read more at Suite101: Vitamin B12 Deficiency: Effects of Inadequate Amounts of an Important Nutrient
Strict vegetarians and vegans are at greater risk than lacto-ovo vegetarians and nonvegetarians of developing vitamin B12 deficiency because natural food sources of vitamin B12 are limited to animal foods . Fortified breakfast cereals are one of the few sources of vitamin B12 from plants and can be used as a dietary source of vitamin B12 for strict vegetarians and vegans.
n many developed countries, up to 15% of the population have a partial deficiency of 5,10-methylene-tetrahydrofolate reductase, a key folate-metabolizing enzyme. This is due to a point mutation and is associated with an increase in neural tube defects and hyperhomocysteinaemia, which may lead to cardiovascular damage. In the USA folic acid fortification of enriched cereals at 1.4 mg per kg grain is done and other countries may also increase their daily folate requirements.
Originally posted by DevolutionEvolvd
reply to post by The Utopian Penguin
I suppose. But I would lean more toward the established thought that increasing B12 would increase energy and promote general health. Certainly that would have an effect on brain development.
[edit on 3-8-2010 by DevolutionEvolvd]
The human physiology of vitamin B12 is complex, and therefore is prone to mishaps leading to vitamin B12 deficiency. Unlike most nutrients, absorption of vitamin B12 actually begins in the mouth where small amounts of unbound crystalline B12 can be absorbed through the mucosa membrane.
Choline is a chemical precursor or "building block" needed to produce the neurotransmitter acetylcholine, and research suggests that memory, intelligence and mood are mediated at least in part by acetylcholine metabolism in the brain