Nutrient-dependent “tweaking” of immense gene networks (revisited)
Posted on February 22, 2013 by James Kohl.
- Karen K. Ryan and
- Randy J. Seeley
Science 22 February 2013: 339 (6122), 918-919. [DOI:10.1126/science.1234062]
Excerpt: “…understanding our diets as a collection of signaling molecules, having hormone-like actions via cell-surface and nuclear receptor signaling, may provide new insights into the relationship between what we eat and metabolic disease.”
I detailed the epigenetic effects of food odors associated with nutrient-dependent pheromone-controlled species diversity in Kohl, J.V. (2012) Human pheromones and food odors: epigenetic influences on the socioaffective nature of evolved behaviors. Socioaffective Neuroscience & Psychology, 2: 17338. My conclusion was based on the concept of the epigenetic “tweaking” of immense gene networks and extension of the honeybee model organism of cause and effect. Simply put, “Olfaction and odor receptors provide a clear evolutionary trail that can be followed from unicellular organisms to insects to humans.”
The clarity that Ryan and Seely add to the complex systems biology of adaptive evolution can now be addressed by further examination of other recent works. On Feb 14, 2013 two published papers in “Cell” focus on data that they use to eloquently elucidate virtually all of what is currently known about natural selection for nutrient-dependent adaptively evolved pheromone-controlled sexual selection in a human population. Taken together, Kamberov et al, and Grossman et al., have extended a mammalian model to humans in which a change in a single base pair results in an amino acid substitution with downstream effects on the thermodynamic regulation of organism-level survival.
The change is manifested in increased eccrine and apocine gland density and hair thickness that enables sexual selection for species-specific pheromone production via the actions of microbes on the glandular secretion of nutrient metabolites associated with sexually dimorphic visually appealing physical characteristics. This occurs in the same context as our development of food preferences, which is driven by chemical appeal, not by visual appeal.
Everything I know about animal models places nutrient-dependent pheromone-controlled adaptive evolution at the forefront of cause and effect, with effects on hormones that affect behavior. However, the link to nutrient-dependent disease processes is clearer in Ryan and Seely. I think they have made it more likely that people will compare what’s adaptive and maladaptive in terms of hormone-organized and hormone-activated evolved behavior via ecological, social, neurogenic, and socio-cognitive niche construction in vertebrates and invertebrates. Can we expect that the nutrient-dependent pheromone-controlled development of our socio-cognitive niche will enable us — like the honeybee — to make the best choices for our survival? If not, may God help us all.
Retired medical laboratory scientist
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