Brain development: diet, amino acids, olfactory receptor genes, and mutations
October 16, 2013 | James Kohl
Excerpt: “What is exciting about this is if we can work out how it functions, a treatment might be asparagine supplementation in the diet.”
My comment: The implications are more profound. Dietary supplements already support a model of nutrient-dependent pheromone-controlled adaptive evolution that refutes the idea of mutation-initiated natural selection. In that model, nutrients are typically naturally selected, but supplements also help to enable ecological, social, neurogenic, and socio-cognitive niche construction via conserved molecular mechanisms in species from microbes to man. Examples of cause and effect sans mutations and sans supplements include a human population that adapted in what is now central China during the past ~30,000 years. The substitution of the amino acid alanine for valine appears to be involved in the brain development of the human population, which is linked to a change in a single base pair. Brain development is thereby also linked via an adaptive variant of a human ectodysplasin receptor to expression of phenotypic traits: differences in hair thickness, sweat glands, mammary tissue, and teeth. All phenotypic expression can also be linked to the de novo creation of species-specific pheromone blends.
Choline, for example, is a nutrient that links mice to man via its involvement in brain development and also in the production of species-specific pheromones associated with observed physical traits and sexual selection. See, for example: Nutrient-dependent/pheromone-controlled adaptive evolution: a model.
“The recently detailed mouse model (Li et al., 2013) builds on what is known about olfactory/pheromonal communication in species from microbes to man and incorporates works from mammals that elucidate the molecular mechanisms that are clearly involved. Sex-dependent production of a mouse ‘chemosignal’ with incentive salience appears to have arisen de novo via coincident adaptive evolution that involves an obvious two-step synergy between commensal bacteria and a sex-dependent liver enzyme that metabolizes the nutrient chemical choline.
The result of this synergy is (1) a liver enzyme that oxidizes trimethylamine to (2) an odor that causes (3) species-specific behaviors. Thus, the complex systems that biology required to get from nutrient acquisition and nutrient metabolism to species-specific odor-controlled behavior is exemplified by adaptive evolution of an attractive odor to mice that repels rats (see for review Li et al., 2013).
The mouse odor also repels humans. High excretion rates of trimethylamine-associated odor in humans cause ‘fish odor syndrome’. The aversive body odor has been attributed to a mutation (Dolphin, Janmohamed, Smith, Shephard, & Phillips, 1997). This attribution is not consistent with the portrayal of synergy in the mouse model, which enables both the production of the odor and the response to the odor.”
Deficiency of Asparagine Synthetase Causes Congenital Microcephaly and a Progressive Form of Encephalopathy
Highlights: 1) Recessive mutations in ASNS are responsible for a severe neurological condition; 2) Two of the identified mutations lead to a remarkable depletion of the ASNS protein 3) Asns-deficient mice have structural brain abnormalities and memory deficits 4) Asparagine synthesis is essential for the development and function of the brain
Obvioulsy, these mutations do not appear to be randomly linked to mutation-initiated natural selection for microcephaly. However, evolutionary theorists may still think that no past evidence or current evidence does not mean no evidence will ever be found for such a link. Indeed, it may just mean that so far there is no experimental evidence that supports the theory of mutation-driven evolution of the brain, or of behavior, or of anything else.
For contrast, see: Human olfaction: from genomic variation to phenotypic diversity. “Widespread phenotypic diversity in human olfaction is, in part, attributable to prevalent genetic variation in OR genes, owing to copy number variation, deletion alleles and deleterious single nucleotide polymorphisms.” Doron Lancet is one of the co-authors on this study and the asparagine-brain development study. One study attests to the importance of experience-dependent de novo creation of olfactory receptor (OR) genes, which I have placed into the context of ecological, social, neurogenic, and socio-cognitive niche construction in my model of adaptive evolution. The other study addresses the involvement of amino acid synthesis in brain development. Taken together, we have experimental evidence of nutrient-dependent amino acid substitutions associated with de novo creation of OR genes and the metabolism of nutrients that enables the de novo creation of species-specific blends of pheromones, which control the physiology of reproduction in species from microbes to man.
If not from Doron Lancet, we should soon be hearing from someone — besides me — that adaptive evolution of the human brain and behavior is clearly nutrient-dependent and pheromone-controlled. And, there’s a model for that!