Human pheromones: an epigenetic continuum from microbes to mammals
Posted on September 11, 2012 by James Kohl.
Different noses for different mice and men Review by Andreas Keller (2012). Excerpt: “We are only just beginning to understand the causes and consequences of the unusual genetic and functional variability of large chemosensory receptor gene repertoires in different species.
My comment: I have detailed the causes and the consequences across species from microbes to man. Only by modeling the common molecular biology can cause and effect be understood, so I modeled it!
Personal receptor repertoires: olfaction as a model (reviewed): Excerpt: “…the effective size of the functional human OR repertoire is much higher than the number of intact loci, implying considerable enhancement of the potential of human smell perception diversity.
My comment: Of course the effective size and its genetically predisposed variability is much higher than was claimed, and it is precisely the size required for our species survival as is the effective size of the olfactory receptor repertoire that is required for the survival of other species. If this calibration of the precision did not continue to occur in each species, extinction would occur (as it does when species cannot locate sufficient nutrient chemicals that support pheromone controlled reproduction).
Genomic variation in the vomeronasal receptor gene repertoires of inbred mice (reviewed) Excerpt: “We describe complex patterns of non-random sequence variation that indicate these receptors are under divergent selective pressures that correlate with proposed ligand, phylogeny, chromosomal clustering, and protein domain.”
My comment: What they are saying is that complex patterns of non-random sequence variation result from the combination of genetic predisposition and experience with ligand-specific, de novo receptor gene-mediated beneficial changes in nutrient chemical-dependent behavior that enables adaptive evolution via ecological, social, neurogenic, and socio-cognitive niche construction. Simply put, adaptive evolution via speciation is controlled by the metabolism of nutrient chemicals to pheromones — species specific chemicals that control reproduction in species from microbes to man. For science journalists and laypeople, I’m simply saying that what you eat determines the pheromones that you produce, which determine your social and sexual success. That is what I detailed in Human pheromones and food odors: epigenetic influences on the socioaffective nature of evolved behaviors Review by Kohl (2012)
Excerpt from the section An epigenetic continuum from microbes to humans: from theory to facts, paragraph 2)
“A gene that codes for the mammalian olfactory receptor, OR7D4, links food odors to human hunger, dietary restraint, and adiposity (Choquette et al., 2012). OR7D4 exemplifies a direct link1 from human social odors to their perception (Keller, Zhuang, Chi, Vosshall, & Matsunami, 2007) and to unconscious affects2 on human behavior associated with human olfactory-visual integration (Zhou, Hou, Zhou, & Chen, 2011); human brain activation associated with sexual preferences (Savic, Heden-Blomqvist, & Berglund, 2009), human learned odor hedonics; and motor function (Boulkroune, Wang, March, Walker, & Jacob, 2007).”
1This ‘direct link’ is between the ligand: androstadienone, and the OR7D4 receptor.
2‘Effect(s)’ and ‘affect(s)’. In context, sensory input effects hormones that affect behavior. An effect of sensory input on hormones can result in behavioral affects/affects on behavior.
Though the concept is technical, there are people who are familiar with the basic principles of biology and levels of biological organization that are required to link sensory cause to hormones and their behavioral affects in mammals like mice and men. To some, it has now become clear or it will soon become clearer that random mutations theory has no explanatory power when attempts are made to link adaptive evolution via ecological, social, neurogenic, and socio-cognitive niche construction as detailed in my model. Random mutations do not cause adaptive evolution. That’s a ridiculous theory. It is, nevertheless, one that many scientists will continue to incorporate into their works until they know more about cause and effect.
In my model, for comparison, “The concept that is extended is the epigenetic tweaking of immense gene networks in ‘superorganisms’ (Lockett, Kucharski, & Maleszka, 2012) that ‘solve problems through the exchange and the selective cancellation and modification of signals (Bear, 2004, p. 330)’. It is now clearer how an environmental drive probably evolved from that of food ingestion in unicellular organisms to that of socialization in insects. It is also clear that, in mammals, food odors and pheromones cause changes in hormones such as LH, which has developmental affects on sexual behavior in nutrient-dependent, reproductively fit individuals across species of vertebrates.”
It is the change in luteinizing hormone (LH) that epigenetically links olfactory/pheromonal input to the biological core of evolved mammalian behavior via conservation of an evolved gene, cell, tissue, organ, organ system pathway that organizes and activates behavioral reciprocity. The only explanation for adaptive evolution with any across-species explanatory power is found in my details of the epigenetic effects of olfactory/pheromonal input on intracellular signaling and stochastic gene expression, which leads to de novo expression of olfactory receptor genes. Thus, when someone like Andreas Keller says “We are only just beginning to understand the causes and consequences of the unusual genetic and functional variability of large chemosensory receptor gene repertoires in different species.” –The collective, We, should not be used.
Instead, minimally, others could comment on my model, and perhaps tell me what I don’t understand.
Retired medical laboratory scientist
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