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Docosahexaenoic acid vs. creative use of mutations in natural selection

Posted on September 20, 2012 by James Kohl.

The authors posit that advantageous mutations in a particular gene cluster led to the ability to use long chain polyunsaturated fatty acids, like docosahexaenoic acid (DHA) in the development of human brain structure and function. Re: Adaptive Evolution of the FADS Gene Cluster within Africa

My comment: In my model, nutrient chemicals such as DHA elicit epigenetic effects on intracellular signaling and stochastic gene expression. The changes in gene expression include de novo gene expression for receptor proteins that enable receptor-mediated events in cells. These events facilitate increased de novo receptor protein production via gene duplication, which is how nutrient chemicals are directly responsible for developmental changes in brain structure and function. Nutrient chemicals metabolize to species-specific pheromones that also epigenetically effect brain development.

I wrote: “Just as the influence of diet and pheromones can be in the larval stages or in other developmental stages of insects, it can also be in the pre- and postconception stages of mammals, including humans (Fowden et al., 2006; Mennella, Jagnow, & Beauchamp, 2001). For example, pheromones and nutrition could alter levels of maternal hormones, gestational events, and postnatal outcomes via their direct effect on maternal GnRH and the placenta. The outcomes might not always be positive, which means the possible effects should not be ignored. That would be like ignoring the likely effects of docosahexaenoic acid in the maternal and postnatal diet on LH and on neuronal development in the mammalian brain (Lassek & Gaulin, 2011).”

The difference in what I conveyed using what is currently known about the basic principles of biology and levels of biological organization is the focus of others on ‘mutation’.  Thus, human brain evolution via mutation shows up in interpretations for the lay audience. See: “Genetic mutation may have allowed early humans to migrate throughout Africa.” September 19th, 2012.

Excerpt: “… a critical genetic variant arose in a key gene cluster… more than 85,000 years ago. This variation… allowed early humans to convert plant-based polyunsaturated fatty acids (PUFAs) to brain PUFAs necessary for increased brain size, complexity and function.”

My Comment:  Is the genetic variant (above) a mutation? Starting from the epigenetic effect of glucose on gene duplication that benefits yeast cells by increasing glucose uptake, it is possible to move from microbes to man via the honeybee model organism of nutrient-chemical dependent brain development. In the honeybee, it is also metabolism of nutrient chemicals to species-specific pheromones that help to determines difference in the neuroanatomy of the bees’ brains.

If only nutrient chemicals were involved in brain development, researchers might continue to suggest without peril that the epigenetic effects were due to chemically induced mutations. The mutations might even be considered to be random. Any organism may or may not be exposed to a new nutrient chemical in its sensory environment.

Here’s the paradigm shift.  When others realize that nutrient chemicals metabolize to species-specific pheromones that control reproduction in species from microbes to man, the “Just-So” story line about random mutations or the effect of any mutation on adaptive evolution changes. The change is from one event that might be considered capable of causing a random mutation that is beneficial to the requirement for two concurrent events. The concurrent events involve the pairing of the epigenetic effect of the nutrient chemical with the change in the pheromone production that epigenetically controls reproduction. With that change, we have nutrient-chemical-dependent AND pheromone-dependent reproduction across all species.  What that means in the context of my model is that “Olfaction and odor receptors provide a clear evolutionary trail that can be followed from unicellular organisms to insects to humans.

The likelihood that two requirements for speciation, namely food and reproduction would unequivocally be required in all species due to random mutations seems incalculable. The calculation would require inclusion of all possible combinations of nutrients that could metabolize to all combinations of pheromones in all organisms that evolved across the continuum of evolution that enabled development of the human brain.

Do you believe that occurred due to random mutations? Is that what those who think  mutations cause adaptive evolution would like you to believe? Is there a model for that? Or, do they take us all to be the fools that some of us obviously are?



James Kohl
Retired medical laboratory scientist

James Kohl

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