"Ancestral nutrition: An alternative approach" by Don Matesz, MA, MS from Ancestry on Vimeo.
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Due to time constraints, I was not able to go into details explaining how each of the items I pointed to as adaptations to a plant-based diet could prove maladaptive for a diet providing a major proportion of energy from meat or fat. I will expand on one example here and leave the others for others to think through.
Humans as well as other primates have uric acid levels higher than other mammals due to knock-out of the uricase-coding gene at least 15 million years ago. [1] This appears to have occurred as an adaptation to several environmental factors including 1) high dietary vitamin C (which lowers uric acid), 2) low sodium intake, and 3) low dietary fat combined with high fructose intake.
Elevated uric acid appears to have at least two adaptive functions in such a context: 1) It raises blood pressure in the face of very low sodium and very high potassium intake, and 2) it facilitates the conversion of fructose into fat for adipose storage when vitamin C intake declines (in autumn, when fruits contain more fructose and less vitamin C).
This human/primate feature has positive effects in the context of a diet low in sodium and dietary fat, but high in potassium and fructose.
However, it is potentially maladaptive when dietary sodium, fructose, or meat increase, and dietary potassium and vitamin C decrease.
Meat typically has a K:Na ratio of ~5:1 or lower, whereas fruits (the presumed main foods of the common ancestor of humans and chimps) have so little sodium, that the ratio is 100:1 or more. Therefore, simply switching from plant-based to meat-based, without any addition of granular salt, automatically results in a relatively high sodium intake, for an animal adapted to the reverse, a low sodium, high potassium diet.
In addition, meat provides purines, which feed into the production of uric acid. Elevated serum uric acid can produce overt gout, but before it does that, it can promote general inflammation [2], and elevated uric acid has been linked to chronic heart failure and increased cardiovascular risk [3, 4], metabolic syndrome [5], and elevated blood pressure [6, 7]. It also appears that uric acid increases the storage of body fat [1]:
Specifically, uric acid causes mitochondrial dysfunction with specific effects to increase fat accumulation by both increasing fat synthesis and by blocking fat oxidation (Sánchez Lozada LG et al, manuscript in preparation). Indeed, acutely raising serum uric acid with a uricase inhibitor in rats will result in fat accumulation in the liver within 24 hours, and this is not observed if the rise in uric acid is prevented. Other studies have suggested effects of uric acid on blood pressure, insulin resistance, and adipocyte activation (28, 29). Indeed, Cheung et al recently reported that mice that cannot produce uric acid (XOR knockout mice) have a central defect in adipogenesis and fail to get fat (30).
Vitamin C reduces uric acid concentrations [8]. Therefore, low intake of vegetables and fruits rich in vitamin C, combined with high intake of meat and fat, may promote abnormal elevated uric acid levels and all of the disorders above.
Fructose also feeds the production of uric acid, and vitamin C blocks the undesirable effects of fructose (which explains why eating fruits has a different metabolic effect than eating refined sugars) [9]. In the ancient environment, when our ancestors had diets low in fat but high in fruit, the pathway that converts fructose to fat when vitamin C concentrations are low was adaptive. In the fall, when wild fruits had an increase in fructose content and a decrease in vitamin C content, the liver converted a higher proportion of the fructose into fat to be stored as adipose, as a combination of insulation against colder weather and a supply of energy to draw on when food supplies declined through the winter. In the modern environment with a high ratio of fructose to vitamin C, the same system is maladaptive, resulting in increased uric acid levels, body fat accumulation, inflammation, and metabolic syndrome.
So, human uric acid metabolism remains adapted to a diet with a high ratio of potassium to sodium, and a high ratio of vitamin C to fructose. In the context of a high dietary ratio of animal protein and fat reducing vitamin C intake and the K:Na ratio and providing purines, this system will likely prove maladaptive for at least some individuals. The imbalance can manifest in variety of ways: inflammation effects, metabolic changes, hypertension, increased cardiovascular disease risk, increased fat storage, gout, etc..
This then provides one example where the effect of meat consumption depends on the quantity and dietary context, as well as individual variation in uric acid metabolism. The higher our ratio of meat and fat to vegetables and fruits, the lower our vitamin C intake and K:Na ratio, and the more purines we have feeding the production of uric acid. Higher intakes of vegetables and fruits rich in vitamin C and potassium will tend to counter the effects of the purines and sodium, which will delay the appearance of symptoms and reduce their severity.
If someone eats a diet containing a high proportion of animal protein but also includes a fairly large amount of vegetables and fruits, he or she may not see any adverse symptoms related to excess serum uric acid appear for a long period of time. The context (high intake of fruits and vegetables) modifies the effect of the high meat intake. Further, the body's ability to adapt to any stressor (e.g. excess serum uric acid) declines as exposure continues for a longer period of time. The adverse effects creep in slowly, at a rate as noticable as hair growth, or become more noticable after she or he reduces produce intake, or some other factor (e.g. stress) reduces the body's ability to deal with the excessive uric acid, or, simply, the body's ability to deal with the excess uric acid declines due to long exposure to the overload. As things change, the person naturally gravitates toward non-nutritive ingestive behaviors that tend to reduce the symptoms.
For example, she has a premenstrual headache. She doesn't immediately think, "Oh, this is due to the long accumulation of congesting effects of my diet." Instead, she takes a nap, or an aspirin, gets relief, and goes on her way. If another person notices a little extra inflammation in a chronic skin condition that naturally fluctuates anyway, he doesn't immediately think that his food caused this, instead he puts some soothing balm on it, or takes an anti-inflammatory, which reduces the discomfort enough that he loses interest in exploring it further. The use of non-nutritive ingestive behaviors is evolved and hence the natural approach to discomfort: We "take something for it" because our species evolved to use non-nutritive ingestion as an integral part of dietary adaptation. People start looking deeper only when the non-nutritive ingestive behaviors no longer control the discomfort adequately. So small things so gradually turn into large things that we often don't figure things out until they have gotten very persistent and distracting of our attention.
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