Is genetic risk due to mutations

A Surprising Genetic Risk Factor For Type 2 Diabetes Is Discovered

Excerpt: The gene is expressed in the liver and is involved in the transportation of metabolites that affect fat levels in cells. By altering the level of the gene variant’s proteins, researchers found that they were able to affect the amount of a type of fat that is linked to Type 2 diabetes.

My comment: The nutrient-dependent de novo creation of genes in different cell types was reported in the context of mutation-initiated natural selection in October 2012. Thus, the creation of genes is one of the holy grails of evolutionary biology that is frequently attributed to mutation-driven evolution. In this report, the genetic risk factor is reported as a gene variant, which moves us forward to understanding why Analysis of 6,515 exomes reveals the recent origin of most human protein-coding variants.  The findings confirm their earlier work suggesting that the majority of variants, including potentially harmful ones, were picked up during the past 5,000–10,000 years. Subsequently, one of the co-authors on that report was a co-author on this one: Exonic Transcription Factor Binding Directs Codon Choice and Affects Protein Evolution.

My comment to Science Magazine was published on 12/13/13 The lack of response to it suggests that most people would rather continue to believe in mutation-driven natural selection as our species eats itself to death.

Is the intrinsic flexibility attributed to exploitation by natural selection epigenetically-effected by nutrient uptake? If so, natural selection for nutrients via seemingly futile cycles of themodynamically constrained protein biosynthesis and degradation might enable transcription factor binding that is limited by non-random nutrient-dependent changes in base pairs. The changes in based pairs would be accompanied by alternative splicings and amino acid substitutions in cells that stochastically express genes, which are most beneficial to species-specific cell types in different tissues.

The metabolism of nutrients to species-specific pheromones that control the physiology of reproduction could then epigenetically control transcription and gene expression from the top down via reproduction. We might then expect to see seemingly futile cycles of thermodynamically controlled nutrient-dependent protein biosynthesis and degradation result in conservation of genes associated with increased fitness in one ecological niche that might not be conserved in an organism that was competing for survival in the same ecological niche.

Clearly, the organism that was most capable of nutrient acquisition, which enabled the thermodynamics of its intercellular signaling to result in better organism-level thermoregulation, would establish its social niche among equally successful conspecifics that adapted to their ecological niche and proliferated more rapidly.

Symbiotic relationships might then result from cooperation among heterospecifics in situations where the failure to cooperate with other organisms and live from a different nutrient source would mean death to a unicellular organism or to a multicellular vertebrate. However, organisms that managed to somehow acquire more than an appropriate share of nutrients would be subjected to conserved molecular mechanisms for species diversification that suddenly were no longer adaptive.

Nutrient stress linked to thermal stress via abundance, but not by starvation or social stress, would then be the most likely cause of mutations that are not eliminated by the finely-tuned molecular mechanisms of adaptation to the epigenetic landscape that occur via its incorporation into the physical landscape of DNA in the organized genomes of species from microbes to man.

I welcome comments from anyone who thinks this theory might benefit progress, since I cannot properly evaluate my own model.