Pheromones, Reciprocity, and Prosocial Behavior
Posted on September 4, 2012 by James Kohl.
“Research shows reciprocity an important component of prosocial behavior.” September 3rd, 2012.
Excerpt: “…that the capuchins responded similarly to in-group and out-group partners has implications for the commonly held view that humans are unique in their ability to cooperate with strangers,” de Waal explained.”
The literature on prosocial behavior can be succinctly summarized. Simply put, the required reciprocity is that of the evolved gene, cell, tissue, organ, organ system pathway in vertebrates. This organized pathway allows nutrient chemicals and social odors (called pheromones) to activate it. In this context, organization equals genetically predisposed nature and activation equals nurture that involves sensory stimuli from the environment, which epigenetically effect genetically predisposed behaviors (see for review Kohl ,2012).
In my review, the epigenetic effects of nutrient chemicals and pheromones are conserved across species from microbes to man. They enable adaptive evolution via ecological, social, neurogenic, and socio-cognitive niche construction. Adaptive evolution requires conservation of molecular biology as everyone knows; the molecular biology of life does not change from one species to the next. That’s why, in primate species, we see the same reciprocity as is seen in the molecular mechanisms for nutrient acquisition and pheromone-controlled species survival in every other species.
For example, conspecifics in the social niche exhibit prosocial and antisocial behaviors that help to enable nutrient acquisition. Antisocial behavior may include ingestion of heterospecifics to facilitate species survival in ‘hard’ times when the decline of prosocial behaviors may even lead to cannibalism as part of the continuum of evolved prosocial and antisocial behaviors that led to primate prosociality.
“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.”
The key to this concept is the conservation of the GnRH molecule across 400 million years of vertebrate evolution from its origins as the yeast alpha-mating pheromone at the advent of sexual reproduction in unicellular organisms. That “key” is also why it is important for proponents of random mutations theory to attempt to explain-away both the conservation of the GnRH ligand and the diversification of its receptor, which underlies self / non-self recognition that is due to primate neuroimmune system evolution as well as the evolution of the primate neuroendocrine system, which is responsible for nutrient-dependent sexual reproduction.
I have not seen anything that suggests how random mutations could lead to the apparent design in biology of an evolved gene, cell, tissue, organ, organ system pathway. Similarly, no evidence suggests that random mutations link sensory input to transgenerational epigenetic inheritance and effects on vertebrate neuroendocrine and neuroimmune systems via adaptive evolution of ecological, social , neurogenic, and socio-cognitive niche construction.
There is, however, evidence that group selection in microbes is dependent on circumstances in which one species ingests the other. This leads to the advent of multicellularity and increased ability of the newly evolved multicellular organism to ingest more nutrients (supplied through additional ingestion of the other species).
In this context, the survival of both species depends on their nutrient-dependent production of pheromones that enable quorum sensing. The pheromones of the species that is eaten signal the species that eats it. The signal indicates that there are a sufficient number to be eaten so that the heterospecific organism does not exhaust its food supply, which might lead to extinction. The pheromones of the heterospecific multicellular organism also regulate its nutrient-dependent reproduction.
Microbes use quorum sensing to help ensure they do not reproduce beyond the availability of nutrient chemicals to sustain colony growth. Quorum sensing may occur in two species that share the same ecological niche. At the advent of mulicellularity, the pheromones of both species control how many of one species are ingested by the other. That’s how nutrient chemicals and pheromones have established the evolutionary origin of multicellularity and of group selection. The evidence for group selection via nutrient-chemical metabolism to pheromones also is found in ants, and the pheromones are important to speciation in bees.
The moderator of the human ethology yahoo group, Jay Feierman, was the only person to ever ask me the question “What about birds.” Recently, he told the group: “You can’t model altruism and cooperation among non-relatives by inclusive fitness theory (kin-selection theory).”
My response is that the behavioral development of the birds and the bees must be modeled using ethological facts (not inclusive fitness theory or any other theory). I’ve detailed the ethological facts in a series of published works that refute some well-established, but factually baseless, theories.
There are many species that cooperate with non-relatives and relatives alike, so that they can share a particular ecological niche. Cooperation, like altruism, is based on species-specific pheromones that also signal fitness and kinship, which means that olfaction and the evolution of odor receptors can be used to model altruism and cooperation across species using the same molecular mechanisms of reciprocity that I have detailed.
Retired medical laboratory scientist
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