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Review
. 2017 May 2:10:1178646917704661.
doi: 10.1177/1178646917704661. eCollection 2017.

Meat and Nicotinamide: A Causal Role in Human Evolution, History, and Demographics

Adrian C Williams  1 , Lisa J Hill  2
Affiliations
Review

Meat and Nicotinamide: A Causal Role in Human Evolution, History, and Demographics

Adrian C Williams et al. Int J Tryptophan Res. .

Abstract

Hunting for meat was a critical step in all animal and human evolution. A key brain-trophic element in meat is vitamin B3 / nicotinamide. The supply of meat and nicotinamide steadily increased from the Cambrian origin of animal predators ratcheting ever larger brains. This culminated in the 3-million-year evolution of Homo sapiens and our overall demographic success. We view human evolution, recent history, and agricultural and demographic transitions in the light of meat and nicotinamide intake. A biochemical and immunological switch is highlighted that affects fertility in the 'de novo' tryptophan-to-kynurenine-nicotinamide 'immune tolerance' pathway. Longevity relates to nicotinamide adenine dinucleotide consumer pathways. High meat intake correlates with moderate fertility, high intelligence, good health, and longevity with consequent population stability, whereas low meat/high cereal intake (short of starvation) correlates with high fertility, disease, and population booms and busts. Too high a meat intake and fertility falls below replacement levels. Reducing variances in meat consumption might help stabilise population growth and improve human capital.

Keywords: Malthus; Meat; NAD(H); evolution; fertility; immunological tolerance; longevity; nicotinamide; vitamin B3.

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Conflict of interest statement

DECLARATION OF CONFLICTING INTERESTS: The author(s) declared no potential conflicts of interest with respect to the research, authorship, and/or publication of this article.

Figures

Figure 1
Figure 1
Evolution seen as the acquisition of NAD. Mitochondrial usage and rising O2 levels followed by animals hunting for NAD followed by even bigger human brains. NAD indicates nicotinamide adenine dinucleotide.
Figure 2
Figure 2
Our early evolution in a nutshell. Steadily increasing nicotinamide powered biological and cultural evolution.
Figure 3
Figure 3
Our later evolution in the light of oscillations in the nicotinamide supply. Variances provoked population booms and some busts with friction over meat resources between populations and between social classes.
Figure 4
Figure 4
Omnivores and domesticated diets. Domestication of animals and plants but also of ourselves, our microbiome, and the microbiomes of our domesticates whether of ruminant cattle or the mycorrhiza of legumes.
Figure 5
Figure 5
Steady rise of meat/nicotinamide in surviving hominids until the Neanderthals. Homo sapiens survived, but only just, and then we subjected ourselves to large meat variances with demographic consequences.
Figure 6
Figure 6
Pellagra has an extra-ordinary wide phenotype. Many mimic modern diseases of ageing. Premature ageing may have been traded off against greater fecundity when the diet is poor. NAD disruption may be a final common pathway of ageing diseases whether from dietary under- or over-dosage or high NAD consumption from stressors. NAD indicates nicotinamide adenine dinucleotide.
Figure 7
Figure 7
Life expectancy plotted against meat consumption 1820–1960. Overall life expectancy increased and positively trended with increased meat consumption (r = 0.685; P = .067).
Figure 8
Figure 8
Life expectancy plotted against meat consumption now is significant (r = 0.641; P < .001).
Figure 9
Figure 9
Death and fertility rates plotted against meat consumption. Overall death rates and infant mortality fell and correlated strongly with increased meat consumption (for fertility rate vs meat r = −0.815; P < .001; for death rate vs meat r = −0.864; P < .001).
Figure 10
Figure 10
Fertility and meat across the contemporary world (P < .01).
Figure 11
Figure 11
Literacy rates plotted against meat consumption in the United Kingdom 1850–1900 (r = −0.988; P < 0.001).
Figure 12
Figure 12
Literacy rates plotted against meat consumption in the contemporary world across nations (r = 0.531; P < .001).
Figure 13
Figure 13
Increased height correlates strongly with higher meat intake in the past (r = 1; P < .001).
Figure 14
Figure 14
Increased height correlates strongly with higher meat intake currently (r = 0.635; P < .001).
Figure 15
Figure 15
Recent percentage population growth rates correlate with average rise in meat and nicotinamide intake (P < .01).
Figure 16
Figure 16
Decreased meat availability from climate change or over-hunting may have pushed the agriculture revolution, but a bigger pull may have come from increased fecundity.
Figure 17
Figure 17
Meat intake was not the same in every European country. This may explain the relative success of England during this long period up to the industrial revolution.
Figure 18
Figure 18
Low nicotinamide in diet biases the ‘de novo’ pathway towards catabolising tryptophan to nicotinamide. This increases tolerance of the foetus but risks illness and deaths from dysbioses and pathogens.
Figure 19
Figure 19
High nicotinamide could influence fertility rates by various compounding mechanisms.
Figure 20
Figure 20
A summary of the demographic effects of nicotinamide dose on fecundity Moderation works.
Figure 21
Figure 21
Classic Malthusian trap and deadlock on low-nicotinamide diet. Malthusian escape on a moderate nicotinamide diet. Affluence trap on a high-nicotinamide diet – rise of fertility clinics and necessary immigration.
See this image and copyright information in PMC

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