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Re: [evol-psych] An on-off switch for eating (addendum)

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  • james kohl
    Addendum Deciphering the Cell Embracing complexity 3,000,000,000 base pairs of DNA 3 metres of DNA 20,000-25,000 genes 10,000-20,000 protein species 4,000,000
    Message 1 of 2 , Sep 28, 2013
      Addendum

      Deciphering the Cell
      Embracing complexity
      3,000,000,000 base pairs of DNA
      3 metres of DNA
      20,000-25,000 genes
      10,000-20,000 protein species
      4,000,000 ribosomes
      60,000,000 tRNA molecules
      300,000 mRNA molecules
      10,000,000,000 protein molecules
      1,000 miRNA species
      50,000,000,000,000 cells in body
      80,000,000,000 neurons in brain

      The on-off switch is not likely to have adaptively evolved to end up in neurons of the bed nucleus of the stria terminalis. What kind of idiot suggests the report below is "good neuroscience?" That was a rhetorical  question.
       
      James V. Kohl
      Medical laboratory scientist (ASCP)
      Independent researcher
      Kohl, J.V. (2013) Nutrient-dependent/pheromone-controlled adaptive evolution: a model. Socioaffective Neuroscience & Psychology, 3: 20553.
      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: evolutionary-psychology@yahoogroups.com
      Sent: Saturday, September 28, 2013 9:29 PM
      Subject: [evol-psych] An on-off switch for eating

       

      Excerpt: These neurons reside in a brain locale called the bed nucleus of the stria terminalis, or BNST. Some of the message-sending arms of these neurons reach into the lateral hypothalamus, a brain region known to play a big role in feeding.

      On the human ethology group, an anonymous fool wrote:

      Good neuroscience here. Interesting to see the ol' LH making a comeback in food-intake regulation. Still, it is unlikely to be the whole story. The story goes that there two systems with one (involving the LH) being involved in homeostasis-driven processes and the other having more to do with "reward" (involving the VTA, basal ganglia, PFC etc.) that is thought to subvert the evolved "simple" homeostatic processes. I doubt that it is this simple or that the LH is disconnected from "food reward." But...only time will tell. And, here there is actually a goodchance of making headway as the cognitivists have sort of kept their nose out of this issue and, hence, have not ruined it.

      My comment:
      In the context of experiments in rats with vaginocervical stimulation to see how it might affect neuronal activity, Barry Komisaruk reported that Phil Teitelbaum once said "...he kicked himself all around the room when he was scooped by Brobeck on the critical role of the lateral hypothalamus in feeding behavior."  Teitelbaum did not realize that his rats were dying because they were starving to death. However, Komisaruk had already unknowingly been scooped by Kohl (2012) on the epigenetic effects of glucose and pheromones on other behavioral traits linked to the lateral hypothalamus. The vaginocervical stimulation strongly inhibited the firing activity of neurons in the lateral hypothalamus, which indicated its involvement in locomotion. Another effect of the vaginocervical stimulation was a sudden lordosis response, that occurred even after removal of the ovaries and pituitary (i.e., independent of hormone activation). The third effect was that vaginocervical stimulation with a probe caused immobilization. That affect on behavior can be compared the response of sows to the epigenetic effects of the pig pheromones, androstenone and androstenol on luteinizing hormone, lordosis, and the behavior they exhibit called "standing," which facilitates artificial insemination.

      That affect on behavior also links the critical role of the lateral hypothalmus (LH) to the critical role of nutrient-dependent pheormone-controlled hypothalamic secretion of gonadotropin releasing hormone (GnRH) and secretion of luteinizing hormone in my model. Unfortunately,  until you realize that the abreviation for luteinizing hormone (LH) is the same as the abreviation for the lateral hypothalamus (LH), you might never make the connection between olfactory/pheromonal input, classically conditioned hormone-organized and hormone-activated responses to mammalian pheromones, and the obvious affects of changes in hormone secretion on behavior that no longer requires the presence of food odors or pheromones because the response had been classically conditioned. Thus, brain imagery (in cases that propose an on-off switch for eating) is used to examine what appears to be cause and effect relationships in the context of hormones and behavior, but outside the context of nutrient-dependent pheromone-controlled adaptive evolution, which is why relatively meaningless results of brain imaging do not link sensory cause directly to behavioral affect are meaningfully reported. See, for example: "The Inhibitory Circuit Architecture of the Lateral Hypothalamus Orchestrates Feeding" in the context of Blackshaw's neurogenic niche construction.
        


       
      James V. Kohl
      Medical laboratory scientist (ASCP)
      Independent researcher
      Kohl, J.V. (2013) Nutrient-dependent/pheromone-controlled adaptive evolution: a model. Socioaffective Neuroscience & Psychology, 3: 20553.
      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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