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Re: [human-ethology] Williams: Nonsense vs missense "mutations" and human breath analysis

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  • james kohl
    I mentioned this when I first responded to the Science site. Here it is again in the context of Williams nonsense.... [and my model of genes with large
    Message 1 of 2 , Apr 5, 2013
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      I mentioned this when I first responded to the Science site. Here it is again in the context of Williams' nonsense.... [and my model of genes with large effects]
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      Your comment on Adaptive Evolution of Multiple Traits Through Multiple
      Mutations at a Single Gene has been approved and is now live at
      http://comments.sciencemag.org/content/10.1126/science.1233213,

      In the context of adaptive evolution, Linnen et al.,reminds us to look at
      models of genes with large effects for comparison to random mutations theory.
      For example, using the molecular mechanisms common to all species and
      exemplified in the mouse, the time from pleiotropy to epistasis in a human
      population appears to be approximately 30,000 years (Kamberov et al., 2013;
      Grossman et al., 2013). Perhaps epistasis requires only one
      nutrient-dependent pheromone-controlled amino acid substitution. That
      likelihood led me to look at pleiotropy, amino acid substitutions, and
      epistasis in several different model organisms via the common molecular
      mechanisms of "Nutrient-dependent / Pheromone-controlled thermodynamics and
      thermoregulation" (posted to figshare).

      I moved quickly from microbes to nematodes, insects, and mammals.
      Receptor-mediated mouse to human examples of how nutrient-dependent amino
      acid substitutions can be readily linked to pheromone-controlled reproduction
      via common molecular mechanisms become as clear as they are in the honeybee
      model organism. What the queen eats determines her pheromone production and
      everything else about the interactions in the colony, including the
      development of the worker bees brain. The epigenetic effects occur sans
      mutations, which tends to refute the multiple mutations approach to adaptive
      evolution and replace theory with a model. In the model, natural selection is
      for nutrients that metabolize to pheromones. The pheromones control
      reproduction and link epigenetic effects on the microRNA/messenger RNA
      balance from stochastic gene expression to behavior and back.

       
      James V. Kohl
      Medical laboratory scientist (ASCP)
      Independent researcher
      Kohl, J.V. (2012) Human pheromones and food odors: epigenetic influences on the socioaffective nature of evolved behaviors. Socioaffective Neuroscience & Psychology, 2: 17338.



      From: james kohl <jvkohl@...>
      To: human-ethology@yahoogroups.com
      Cc: evolutionary-psychology@yahoogroups.com
      Sent: Fri, April 5, 2013 5:25:32 PM
      Subject: [human-ethology] Williams: Nonsense vs missense "mutations" and human breath analysis

       

      Human Breath Analysis May Support the Existence of Individual Metabolic Phenotypes

       

      My comment to The Scientist site (4/5/13):

      Sex-dependent production of a mouse “chemosignal” with incentive salience appears to have arisen de novo via coincident adaptive evolution that involves an obvious two-step synergy between commensal bacteria and a sex-dependent liver enzyme that metabolizes the nutrient chemical choline. The result of this synergy is 1) a liver enzyme that oxidizes trimethylamine to 2) an odor that causes 3) species-specific behaviors. Thus, the complex systems biology required to get from nutrient acquisition and nutrient metabolism to species-specific odor-controlled behavior is exemplified by adaptive evolution of an attractive odor to mice that repels rats (see for review Li et al., 2013).  

      The mouse odor also repels humans. High excretion rates of trimethylamine-associated odor in humans cause "fish odor syndrome." The aversive body odor has been attributed to a missense "mutation" (Dolphin, Janmohamed, Smith, Shephard, & Phillips, 1997). This attribution is not consistent with the portrayal of synergy in the mouse model, which enables both the production of the odor and the response to the odor. This synergy requires at least two things to simultaneously happen: for example, 1) natural selection for nutrient chemicals and 2) sexual selection for odor production. Sexual selection for nutrient-dependent odor production is not likely to be achieved via one missense "mutation" involved in nutrient acquisition and another missense "mutation" that is involved in odor production because two mutations are not likely to simultaneously occur.

      In my model, the adaptive evolution of nutrient-dependent pheromones controls reproduction and non-random species divergence. Is there a reason for use of the term “breathprint” in humans, or does “breathprint” intentionally infer that human pheromones do not exist? Would it not be unusual for chemical signals that control reproduction in species from microbes to man, to not exist in the context of human pheromones?


      James V. Kohl
      Medical laboratory scientist (ASCP)
      Independent researcher
      Kohl, J.V. (2012) Human pheromones and food odors: epigenetic influences on the socioaffective nature of evolved behaviors. Socioaffective Neuroscience & Psychology, 2: 17338.

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