Pre-existing genetic variability or random mutations: a matter of priorities and choices


A matter of priorities: Bacteria evolved way to safeguard crucial genetic material

“The study, published online today in Nature, shows that bacteria have evolved a mechanism
that protects important genes from random mutation, effectively reducing the risk of self-destruction.”


My comments on what the actual article tells us in: Evidence of non-random mutation rates suggests an evolutionary risk management strategy

Non-random mutation, as evidenced by ‘hot’ and ‘cold’ genes involved in amino-acid biosynthesis, energy metabolism, and catabolism of specific compounds is compatible with a model where 1) nutrient chemicals calibrate intracellular signaling and stochastic gene expression, and 2) the metabolism of nutrients to pheromones standardizes and controls reproduction.

This is the model detailed in Human pheromones and food odors: epigenetic influences on the socioaffective nature of evolved behaviors. The honeybee is the invertebrate model organism that extends the common molecular biology across species from microbes to man, but additional support for my conceptualization can now be found in what was recently reported on threespine stickleback fish, a vertebrate model organism of speciation.

The study also shows that stickleback evolution is accelerated by the use of pre-existing genetic variation, instead of waiting for new, random mutations to arise, Wray explains.

Evolutionary theorists have been loudly shouting for years that “[RANDOM] Mutations are the reason each of us is unique. These changes to our genetic material are at the root of variation between individuals, and between cells within individuals.” Indeed, it seems that the theorists may continue to focus on non-random mutations instead of the more obvious scientifically established fact that pre-existing genetic variation enables adaptive evolution, and random mutation does not.

For example, the pre-existing genetic variation that allows a cell to adapt to changes in the availability of nutrients from its environment appears to have be programmed into the first living cell(s). Receptor-mediated cellular changes in metabolism of the nutrients enable cell to cell signaling that varies with the metabolism of nutrients to pheromones.

This fact can be  explained to a general audience by saying that food odors cause us to eat what causes us to produce pheromones that cause us to associate, or not associate, with other people. In this context, pheromones are social odors.

A matter of choices:

Pre-existing genetic variations across species makes food choice essential to individual survival, and it makes mate choice essential to species survival in species that sexually reproduce. An organism that eats the wrong food may not live to reproduce. Clearly, the pre-existing genetic variations make the RNA-mediated effects of different foods on hormones that affect our behavior a key indicator of how pre-existing genetic variability can effect hormones and their metabolism to pheromones that cause changes in sexual behavior.

The allegorical representation of this newly established scientific truth occurs in Genesis with a story indicating that what Eve decided to eat epigenetically altered events across Creation (i.e.,  based on pre-existing genetic variability, not random mutations).   Nevertheless, incorporating similar important choices into thoughts and decisions about what we eat and our mate choice may be easier for those who continue to think the development of their behavior was determined by random mutations. After all, who’s going to hold them accountable for not recognizing the truth about the difference between pre-existing genetic variations and random mutations?

About James V. Kohl 1308 Articles
James Vaughn Kohl was the first to accurately conceptualize human pheromones, and began presenting his findings to the scientific community in 1992. He continues to present to, and publish for, diverse scientific and lay audiences, while constantly monitoring the scientific presses for new information that is relevant to the development of his initial and ongoing conceptualization of human pheromones. Recently, Kohl integrated scientific evidence that pinpoints the evolved neurophysiological mechanism that links olfactory/pheromonal input to genes in hormone-secreting cells of tissue in a specific area of the brain that is primarily involved in the sensory integration of olfactory and visual input, and in the development of human sexual preferences. His award-winning 2007 article/book chapter on multisensory integration: The Mind’s Eyes: Human pheromones, neuroscience, and male sexual preferences followed an award winning 2001 publication: Human pheromones: integrating neuroendocrinology and ethology, which was coauthored by disinguished researchers from Vienna. Rarely do researchers win awards in multiple disciplines, but Kohl’s 2001 award was for neuroscience, and his 2007 “Reiss Theory” award was for social science. Kohl has worked as a medical laboratory scientist since 1974, and he has devoted more than twenty-five years to researching the relationship between the sense of smell and the development of human sexual preferences. Unlike many researchers who work with non-human subjects, medical laboratory scientists use the latest technology from many scientific disciplines to perform a variety of specialized diagnostic medical testing on people. James V. Kohl is certified with: * American Society for Clinical Pathology * American Medical Technologists James V. Kohl is a member of: * Society for Neuroscience * Society for Behavioral Neuroendocrinology * Association for Chemoreception Sciences * Society for the Scientific Study of Sexuality * International Society for Human Ethology * American Society for Clinical Laboratory Science * Mensa, the international high IQ society