Abstract
The intent of this theoretical exposition is to explain the evolutionary antecedents of human encephalization and intelligence. The expansion of the brain over the course of human evolution is herein regarded as one of several components of an interrelated complex including protracted physical development, reduced reproductive receptivity, and increased longevity. These cardinal phenotypic features, herein referred to as the Quadripartite Complex, were ostensibly selected for their adaptiveness amidst the environmental alteration that ensued during the formative phase of human evolution – the Plio-Pleistocene period. This interval of environmental alteration eventuated in ecological upheaval and dietary diminution. Intriguingly, experimentally imposed dietary restriction routinely results in protracted physical development, reduced reproductive receptivity, increased longevity, and proportionately increased brain size relative to body size. Thus, dietary restriction would seem to induce identical adaptations, whether experienced ontogenetically or evolutionarily. Several experiments have determined that dietary restriction promotes the preservation and production of neurons via induction of neurotrophic factors. Inasmuch as neurogenesis is a molecular mediator of mental acuity, it is evident that energy intake and cognition are intimately intertwined. Extrapolating to an evolutionary context, increased intelligence ought logically to confer advantages to organisms enduring dietary deprivation insofar as increased intelligence should ensure more facile food acquisition. This reasoning underlies the nutritional neurotrophic neoteny (N3) theory, which holds that humans exhibit an altered pattern of neurotrophin expression resulting from positive selection for heightened intelligence amidst environmental alteration and consequent dietary deficiency. The altered pattern of neurotrophin expression exhibited by humans, it is deduced, results in a protracted phase of developmental neurogenesis and a resultant retention of neurons that would otherwise be extirpated due to programmed cell death. Importantly, during neonatal neurogenesis mammals produce an excess number of neurons whose survival or destruction is decisively determined by the availability and action of neurotrophic factors. An altered pattern of neurotrophin expression during neurogenesis (as N3 avows) could therefore furnish a larger adult brain. As to how humans could afford to accrete exorbitant neural tissue under conditions of chronic food scarcity the homo hypothalamic hypometabolic (H3) theory offers a plausible postulate: reduced rates of growth and reduced reproductive receptivity, mediated by the hypothalamus and its associated endocrine effectors, offset the energetic costs of increased encephalization in humans. H3 is herein presented as a general theory of human evolution while N3 may be regarded as a special theory of human encephalization and intelligence.
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Abbreviations
- AOHP:
-
Amen optimal health protocol
- ATP:
-
Adenosine triphosphate
- BDNF:
-
Brain-derived neurotrophic factor
- CREB:
-
Cyclic adenosine monophosphate (cAMP) response element-binding protein
- ETH:
-
Expensive tissue hypothesis
- H3 :
-
Homo hypothalamic hypometabolic
- N3 :
-
Nutritional neurotrophic neoteny
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Amen-Ra, N.SS. (2011). The Nutritional Neurotrophic Neoteny Theory: Evolutionary Interactions Among Diet, Brain, and Behavior. In: Preedy, V., Watson, R., Martin, C. (eds) Handbook of Behavior, Food and Nutrition. Springer, New York, NY. https://doi.org/10.1007/978-0-387-92271-3_30
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