Loading ...
Sorry, an error occurred while loading the content.

Re: [evol-psych] Adaptive evolution via the nutrient-dependent pheromone-controlled microRNA/messenger RNA balance

Expand Messages
  • David Leake
    Thanks for asking. It s not something that I can explain outside the context of the model, which details how olfaction and odor receptors enable
    Message 1 of 15 , Feb 8, 2013
    • 0 Attachment
      Thanks for asking. It's not something that I can explain outside the context of the model, which details how olfaction and odor receptors enable nutrient-dependent pheromone-controlled adaptive evolution. Once others understand something about the common molecular mechanisms that establish that fact, I may be able to explain microRNA-facilitated alternative splicings and their impact on intracellular signaling, stochastic gene expression and the control of de novo protein synthesis via changes in the microRNA/messenger RNA balance. But there must be a starting point, as detailed in  Human pheromones and food odors: epigenetic influences on the socioaffective nature of evolved behaviors.
      Jam
      es, I obtained the paper through the link you gave, however the discussion is all about epigenetic processes and there is nothing about how these might lead to changes in genomic DNA as required for evolution to occur. Do you have a concise description of your model for that?

      -----Original Message-----
      From: james kohl <jvkohl@...>
      To: David Leake <dwleake@...>; evolutionary-psychology <evolutionary-psychology@yahoogroups.com>; human-ethology <human-ethology@yahoogroups.com>
      Sent: Wed, Feb 6, 2013 5:42 pm
      Subject: Re: [evol-psych] Adaptive evolution via the nutrient-dependent pheromone-controlled microRNA/messenger RNA balance

       
      Thanks for asking. It's not something that I can explain outside the context of the model, which details how olfaction and odor receptors enable nutrient-dependent pheromone-controlled adaptive evolution. Once others understand something about the common molecular mechanisms that establish that fact, I may be able to explain microRNA-facilitated alternative splicings and their impact on intracellular signaling, stochastic gene expression and the control of de novo protein synthesis via changes in the microRNA/messenger RNA balance. But there must be a starting point, as detailed in  Human pheromones and food odors: epigenetic influences on the socioaffective nature of evolved behaviors.

      As you may know, I have had no success whatsoever in getting anyone to acknowledge how ridiculous random mutations theory is. I think the problem is because they won't read my most recent published work, or any others, and that means they will continue to fall further and further behind the neuroscientific progress exemplified by the paper I just cited. For example, if I told you that miRNAs serve a role in synaptic tagging and capture by providing synapse-specific sequestration of relevant mRNAs being trafficked down dendrites, it would be relatively meaningless, wouldn't it?   And yet, that is one way that the nutrient-dependent pheromone-controlled miRNA/mRNA balance converts genomic DNA to brain structure and function, which includes epigenetic effects of food odors and pheromones on learning and memory. On the other hand, if I could place the nutrient-dependent pheromone-controlled miRNA/mRNA balance in the context of hormone-organized and hormone-activated genetically predisposed behavior, I might be able to take a step-by-step approach that not possible with anyone who still thinks that mutations cause adaptive evolution.
       
      James V. Kohl
      Medical laboratory scientist (ASCP)
      Independent researcher




      From: David Leake <dwleake@...>
      To: evolutionary-psychology@yahoogroups.com; human-ethology@yahoogroups.com; jvkohl@...
      Sent: Wed, February 6, 2013 7:09:27 PM
      Subject: Re: [evol-psych] Adaptive evolution via the nutrient-dependent pheromone-controlled microRNA/messenger RNA balance

      Excerpt:"In conclusion, alternative splicing coupled with RNA QC appears to function in the NS as a prevalent gene regulation strategy. We predict that future work in this area will yield additional important insights into molecular mechanisms that allow the information stored in the form of genomic DNA to be converted into brain structure and function."
       
      In my model, the microRNA/messenger RNA balance is nutrient-dependent and pheromone-controlled, which is how it enables adaptive evolution via ecological, social, neurogenic, and socio-cognitive niche construction. Of course, that makes the theory of mutation-caused evolution appear to be even more ridiculous than it has ever seemed to be. But the real question about mutation-caused adaptive evolution remains: "Is there a model for that?"
      The excerpt refers to information stored in genomic DNA. Can you briefly explain how niche construction leads to changes in the information stored in genomic DNA (which is certainly a requirement for evolution to happen)?

      Dave Leake

      -----Original Message-----
      From: james kohl <jvkohl@...>
      To: human-ethology <human-ethology@yahoogroups.com>
      Cc: evolutionary-psychology <evolutionary-psychology@yahoogroups.com>
      Sent: Wed, Feb 6, 2013 2:00 pm
      Subject: [evol-psych] Adaptive evolution via the nutrient-dependent pheromone-controlled microRNA/messenger RNA balance

       
      Regulation of gene expression in mammalian nervous system through alternative pre-mRNA splicing coupled with RNA quality control mechanisms   Original Research Article 
      Molecular and Cellular Neuroscience, Available online 25 January 2013, Pages 
      Karen Yap, Eugene V. Makeyev
       
      Excerpt:"In conclusion, alternative splicing coupled with RNA QC appears to function in the NS as a prevalent gene regulation strategy. We predict that future work in this area will yield additional important insights into molecular mechanisms that allow the information stored in the form of genomic DNA to be converted into brain structure and function."
       
      In my model, the microRNA/messenger RNA balance is nutrient-dependent and pheromone-controlled, which is how it enables adaptive evolution via ecological, social, neurogenic, and socio-cognitive niche construction. Of course, that makes the theory of mutation-caused evolution appear to be even more ridiculous than it has ever seemed to be. But the real question about mutation-caused adaptive evolution remains: "Is there a model for that?"
       

       
      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.
    • james kohl
      David, thanks for your additional interest Here is a link to the diagram: Human Pheromones: Epigenetic Effects of Odors and Their Affects on Behavior The
      Message 2 of 15 , Feb 8, 2013
      • 0 Attachment
        David,
        thanks for your additional interest

        Here is a link to the diagram:
        Human Pheromones: Epigenetic Effects of Odors and Their Affects on Behavior

        The epigenetic effects that lead to changes in genomic DNA -- as required for adaptive evolution to occur -- are detailed in the following context.


        This model of systems biology represents the conservation of bottom-up organization and top-down activation via:
        1.Nutrient-dependent stress-induced and social stress-induced intracellular changes in the homeostatic balance of microRNA(miRNA) and messenger RNA (mRNA);
        2.Intermolecular changes in DNA (genes);
        3.Non-random experience-dependent stochastic variations in de novo gene expression for odor receptors;
        4.The required gene-cell-tissue-organ-organ system pathway that links sensory input directly to gene activation in neurosecretory cells of the brain;
        5.The required reciprocity that links gene expression to behavior that alters gene expression (i.e., from genes to behavior and back).

        I'm rather certain you can see why I asked that you read the published work first. Those who cannot accept the fact that adaptive evolution is nutrient-dependent and pheromone-controlled (as exemplified in model organisms like the honeybee) are not likely to look further at the molecular mechanisms above. And there is at least one more level of complexity that has recently been added to these 5 steps, that more specifically addresses the nutrient-dependent alternative splicings required for sex differences and for species diversity controlled by pheromones, which also are exemplified in animal models.

        Small intranuclear proteins also participate in generating alternative splicing techniques of pre-mRNA and, by this mechanism, contribute to sexual differentiation in at least two species, Drosophila melanogaster and Caenorhabditis elegans.... That similar proteins perform functions in humans suggests the possibility that some human sex differences may arise from alternative splicings of otherwise identical genes. Diamond, Binstock and Kohl (1996)

        Note: Jay Feierman announced that he is going to write about learning and memory after I mentioned this (below) "....nutrient-dependent pheromone-controlled miRNA/mRNA balance converts genomic DNA to brain structure and function, which includes epigenetic effects of food odors and pheromones on learning and memory." It will be interesting to see how much of my model is included in his approach.

        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: David Leake <DWLeake@...>
        To: evolutionary-psychology@yahoogroups.com; human-ethology@yahoogroups.com
        Sent: Fri, February 8, 2013 3:11:06 PM
        Subject: [human-ethology] Re: [evol-psych] Adaptive evolution via the nutrient-dependent pheromone-controlled microRNA/messenger RNA balance

         

        Thanks for asking. It's not something that I can explain outside the context of the model, which details how olfaction and odor receptors enable nutrient-dependent pheromone-controlled adaptive evolution. Once others understand something about the common molecular mechanisms that establish that fact, I may be able to explain microRNA-facilitated alternative splicings and their impact on intracellular signaling, stochastic gene expression and the control of de novo protein synthesis via changes in the microRNA/messenger RNA balance. But there must be a starting point, as detailed in  Human pheromones and food odors: epigenetic influences on the socioaffective nature of evolved behaviors.
        James, I obtained the paper through the link you gave, however the discussion is all about epigenetic processes and there is nothing about how these might lead to changes in genomic DNA as required for evolution to occur. Do you have a concise description of your model for that?

        -----Original Message-----
        From: james kohl <jvkohl@...>
        To: David Leake <dwleake@...>; evolutionary-psychology <evolutionary-psychology@yahoogroups.com>; human-ethology <human-ethology@yahoogroups.com>
        Sent: Wed, Feb 6, 2013 5:42 pm
        Subject: Re: [evol-psych] Adaptive evolution via the nutrient-dependent pheromone-controlled microRNA/messenger RNA balance

         
        Thanks for asking. It's not something that I can explain outside the context of the model, which details how olfaction and odor receptors enable nutrient-dependent pheromone-controlled adaptive evolution. Once others understand something about the common molecular mechanisms that establish that fact, I may be able to explain microRNA-facilitated alternative splicings and their impact on intracellular signaling, stochastic gene expression and the control of de novo protein synthesis via changes in the microRNA/messenger RNA balance. But there must be a starting point, as detailed in  Human pheromones and food odors: epigenetic influences on the socioaffective nature of evolved behaviors.

        As you may know, I have had no success whatsoever in getting anyone to acknowledge how ridiculous random mutations theory is. I think the problem is because they won't read my most recent published work, or any others, and that means they will continue to fall further and further behind the neuroscientific progress exemplified by the paper I just cited. For example, if I told you that miRNAs serve a role in synaptic tagging and capture by providing synapse-specific sequestration of relevant mRNAs being trafficked down dendrites, it would be relatively meaningless, wouldn't it?   And yet, that is one way that the nutrient-dependent pheromone-controlled miRNA/mRNA balance converts genomic DNA to brain structure and function, which includes epigenetic effects of food odors and pheromones on learning and memory. On the other hand, if I could place the nutrient-dependent pheromone-controlled miRNA/mRNA balance in the context of hormone-organized and hormone-activated genetically predisposed behavior, I might be able to take a step-by-step approach that not possible with anyone who still thinks that mutations cause adaptive evolution.
         
        James V. Kohl
        Medical laboratory scientist (ASCP)
        Independent researcher




        From: David Leake <dwleake@...>
        To: evolutionary-psychology@yahoogroups.com; human-ethology@yahoogroups.com; jvkohl@...
        Sent: Wed, February 6, 2013 7:09:27 PM
        Subject: Re: [evol-psych] Adaptive evolution via the nutrient-dependent pheromone-controlled microRNA/messenger RNA balance

        Excerpt:"In conclusion, alternative splicing coupled with RNA QC appears to function in the NS as a prevalent gene regulation strategy. We predict that future work in this area will yield additional important insights into molecular mechanisms that allow the information stored in the form of genomic DNA to be converted into brain structure and function."
         
        In my model, the microRNA/messenger RNA balance is nutrient-dependent and pheromone-controlled, which is how it enables adaptive evolution via ecological, social, neurogenic, and socio-cognitive niche construction. Of course, that makes the theory of mutation-caused evolution appear to be even more ridiculous than it has ever seemed to be. But the real question about mutation-caused adaptive evolution remains: "Is there a model for that?"
        The excerpt refers to information stored in genomic DNA. Can you briefly explain how niche construction leads to changes in the information stored in genomic DNA (which is certainly a requirement for evolution to happen)?

        Dave Leake

        -----Original Message-----
        From: james kohl <jvkohl@...>
        To: human-ethology <human-ethology@yahoogroups.com>
        Cc: evolutionary-psychology <evolutionary-psychology@yahoogroups.com>
        Sent: Wed, Feb 6, 2013 2:00 pm
        Subject: [evol-psych] Adaptive evolution via the nutrient-dependent pheromone-controlled microRNA/messenger RNA balance

         
        Regulation of gene expression in mammalian nervous system through alternative pre-mRNA splicing coupled with RNA quality control mechanisms   Original Research Article 
        Molecular and Cellular Neuroscience, Available online 25 January 2013, Pages 
        Karen Yap, Eugene V. Makeyev
         
        Excerpt:"In conclusion, alternative splicing coupled with RNA QC appears to function in the NS as a prevalent gene regulation strategy. We predict that future work in this area will yield additional important insights into molecular mechanisms that allow the information stored in the form of genomic DNA to be converted into brain structure and function."
         
        In my model, the microRNA/messenger RNA balance is nutrient-dependent and pheromone-controlled, which is how it enables adaptive evolution via ecological, social, neurogenic, and socio-cognitive niche construction. Of course, that makes the theory of mutation-caused evolution appear to be even more ridiculous than it has ever seemed to be. But the real question about mutation-caused adaptive evolution remains: "Is there a model for that?"
         

         
        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.
      • David Leake
        Thanks James. Your visual model reflects what was described in the article, with a focus on gene activation/expression, but the model still does not specify
        Message 3 of 15 , Feb 9, 2013
        • 0 Attachment
          Thanks James.

          Your visual model reflects what was described in the article, with a focus on gene activation/expression, but the model still does not specify how this leads to heritable DNA changes. Your model seems in tune with evo-devo (evolution of development) in terms of concern with changes in regulatory processes, new uses for existing proteins, role of miRNA and mRNA, etc. etc., but evo-devo still relies on mutations to explain adaptive evolution.

          It would be very useful to people trying to understand your model if you could clearly describe how it might work in the adaptive evolution of a single  behavior. For example, based on your extensive knowledge of Apis mellifera, you might explain how age polyethism (workers begin life as nurses and transition with age to foragers) might have evolved without mutations. You could just take one of the well-studied mechanisms of age polyethism and explain how your model would apply. Or any other honeybee behavior you want, that's just an example.....

          Cheers,
          David

          -----Original Message-----
          From: james kohl <jvkohl@...>
          To: human-ethology <human-ethology@yahoogroups.com>
          Cc: evolutionary-psychology <evolutionary-psychology@yahoogroups.com>
          Sent: Fri, Feb 8, 2013 5:41 pm
          Subject: Re: [human-ethology] Re: [evol-psych] Adaptive evolution via the nutrient-dependent pheromone-controlled microRNA/messenger RNA balance

           
          David,
          thanks for your additional interest

          Here is a link to the diagram:
          Human Pheromones: Epigenetic Effects of Odors and Their Affects on Behavior

          The epigenetic effects that lead to changes in genomic DNA -- as required for adaptive evolution to occur -- are detailed in the following context.


          This model of systems biology represents the conservation of bottom-up organization and top-down activation via:
          1.Nutrient-dependent stress-induced and social stress-induced intracellular changes in the homeostatic balance of microRNA(miRNA) and messenger RNA (mRNA);
          2.Intermolecular changes in DNA (genes);
          3.Non-random experience-dependent stochastic variations in de novo gene expression for odor receptors;
          4.The required gene-cell-tissue-organ-organ system pathway that links sensory input directly to gene activation in neurosecretory cells of the brain;
          5.The required reciprocity that links gene expression to behavior that alters gene expression (i.e., from genes to behavior and back).

          I'm rather certain you can see why I asked that you read the published work first. Those who cannot accept the fact that adaptive evolution is nutrient-dependent and pheromone-controlled (as exemplified in model organisms like the honeybee) are not likely to look further at the molecular mechanisms above. And there is at least one more level of complexity that has recently been added to these 5 steps, that more specifically addresses the nutrient-dependent alternative splicings required for sex differences and for species diversity controlled by pheromones, which also are exemplified in animal models.

          Small intranuclear proteins also participate in generating alternative splicing techniques of pre-mRNA and, by this mechanism, contribute to sexual differentiation in at least two species, Drosophila melanogaster and Caenorhabditis elegans.... That similar proteins perform functions in humans suggests the possibility that some human sex differences may arise from alternative splicings of otherwise identical genes. Diamond, Binstock and Kohl (1996)

          Note: Jay Feierman announced that he is going to write about learning and memory after I mentioned this (below) "....nutrient-dependent pheromone-controlled miRNA/mRNA balance converts genomic DNA to brain structure and function, which includes epigenetic effects of food odors and pheromones on learning and memory." It will be interesting to see how much of my model is included in his approach.

          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: David Leake <DWLeake@...>
          To: evolutionary-psychology@yahoogroups.com; human-ethology@yahoogroups.com
          Sent: Fri, February 8, 2013 3:11:06 PM
          Subject: [human-ethology] Re: [evol-psych] Adaptive evolution via the nutrient-dependent pheromone-controlled microRNA/messenger RNA balance

           
          Thanks for asking. It's not something that I can explain outside the context of the model, which details how olfaction and odor receptors enable nutrient-dependent pheromone-controlled adaptive evolution. Once others understand something about the common molecular mechanisms that establish that fact, I may be able to explain microRNA-facilitated alternative splicings and their impact on intracellular signaling, stochastic gene expression and the control of de novo protein synthesis via changes in the microRNA/messenger RNA balance. But there must be a starting point, as detailed in  Human pheromones and food odors: epigenetic influences on the socioaffective nature of evolved behaviors.
          James, I obtained the paper through the link you gave, however the discussion is all about epigenetic processes and there is nothing about how these might lead to changes in genomic DNA as required for evolution to occur. Do you have a concise description of your model for that?

          -----Original Message-----
          From: james kohl <jvkohl@...>
          To: David Leake <dwleake@...>; evolutionary-psychology <evolutionary-psychology@yahoogroups.com>; human-ethology <human-ethology@yahoogroups.com>
          Sent: Wed, Feb 6, 2013 5:42 pm
          Subject: Re: [evol-psych] Adaptive evolution via the nutrient-dependent pheromone-controlled microRNA/messenger RNA balance

           
          Thanks for asking. It's not something that I can explain outside the context of the model, which details how olfaction and odor receptors enable nutrient-dependent pheromone-controlled adaptive evolution. Once others understand something about the common molecular mechanisms that establish that fact, I may be able to explain microRNA-facilitated alternative splicings and their impact on intracellular signaling, stochastic gene expression and the control of de novo protein synthesis via changes in the microRNA/messenger RNA balance. But there must be a starting point, as detailed in  Human pheromones and food odors: epigenetic influences on the socioaffective nature of evolved behaviors.

          As you may know, I have had no success whatsoever in getting anyone to acknowledge how ridiculous random mutations theory is. I think the problem is because they won't read my most recent published work, or any others, and that means they will continue to fall further and further behind the neuroscientific progress exemplified by the paper I just cited. For example, if I told you that miRNAs serve a role in synaptic tagging and capture by providing synapse-specific sequestration of relevant mRNAs being trafficked down dendrites, it would be relatively meaningless, wouldn't it?   And yet, that is one way that the nutrient-dependent pheromone-controlled miRNA/mRNA balance converts genomic DNA to brain structure and function, which includes epigenetic effects of food odors and pheromones on learning and memory. On the other hand, if I could place the nutrient-dependent pheromone-controlled miRNA/mRNA balance in the context of hormone-organized and hormone-activated genetically predisposed behavior, I might be able to take a step-by-step approach that not possible with anyone who still thinks that mutations cause adaptive evolution.
           
          James V. Kohl
          Medical laboratory scientist (ASCP)
          Independent researcher




          From: David Leake <dwleake@...>
          To: evolutionary-psychology@yahoogroups.com; human-ethology@yahoogroups.com; jvkohl@...
          Sent: Wed, February 6, 2013 7:09:27 PM
          Subject: Re: [evol-psych] Adaptive evolution via the nutrient-dependent pheromone-controlled microRNA/messenger RNA balance

          Excerpt:"In conclusion, alternative splicing coupled with RNA QC appears to function in the NS as a prevalent gene regulation strategy. We predict that future work in this area will yield additional important insights into molecular mechanisms that allow the information stored in the form of genomic DNA to be converted into brain structure and function."
           
          In my model, the microRNA/messenger RNA balance is nutrient-dependent and pheromone-controlled, which is how it enables adaptive evolution via ecological, social, neurogenic, and socio-cognitive niche construction. Of course, that makes the theory of mutation-caused evolution appear to be even more ridiculous than it has ever seemed to be. But the real question about mutation-caused adaptive evolution remains: "Is there a model for that?"
          The excerpt refers to information stored in genomic DNA. Can you briefly explain how niche construction leads to changes in the information stored in genomic DNA (which is certainly a requirement for evolution to happen)?

          Dave Leake

          -----Original Message-----
          From: james kohl <jvkohl@...>
          To: human-ethology <human-ethology@yahoogroups.com>
          Cc: evolutionary-psychology <evolutionary-psychology@yahoogroups.com>
          Sent: Wed, Feb 6, 2013 2:00 pm
          Subject: [evol-psych] Adaptive evolution via the nutrient-dependent pheromone-controlled microRNA/messenger RNA balance

           
          Regulation of gene expression in mammalian nervous system through alternative pre-mRNA splicing coupled with RNA quality control mechanisms   Original Research Article 
          Molecular and Cellular Neuroscience, Available online 25 January 2013, Pages 
          Karen Yap, Eugene V. Makeyev
           
          Excerpt:"In conclusion, alternative splicing coupled with RNA QC appears to function in the NS as a prevalent gene regulation strategy. We predict that future work in this area will yield additional important insights into molecular mechanisms that allow the information stored in the form of genomic DNA to be converted into brain structure and function."
           
          In my model, the microRNA/messenger RNA balance is nutrient-dependent and pheromone-controlled, which is how it enables adaptive evolution via ecological, social, neurogenic, and socio-cognitive niche construction. Of course, that makes the theory of mutation-caused evolution appear to be even more ridiculous than it has ever seemed to be. But the real question about mutation-caused adaptive evolution remains: "Is there a model for that?"
           

           
          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.
        • clarence_sonny_williams
          David, I m so busy that I have not visited the site in some time, but I am closely following your valiant attempts to wring a cogent explanation out of Mr.
          Message 4 of 15 , Feb 10, 2013
          • 0 Attachment
            David,

            I'm so busy that I have not visited the site in some time, but I am
            closely following your valiant attempts to wring a cogent explanation
            out of Mr. Kohl for how his form of "directed evolution" works. The
            many writings of other creationists and believers in intelligent design
            (Mr. Kohl is a creationist by his own admission) offer similar efforts
            at explanations. They, however, usually omit the "olfactory
            connection," perhaps because, unlike Mr. Kohl, they do not own a
            "pheromone" product for sale to anyone who wants to enhance their sex
            life.

            Perhaps you've also found, as I did, that Mr. Kohl's explanation
            contains a lot of scientific terms, but their connection escapes me
            (e.g. I do not understand his term, "neurogenic" niche, although I know
            a great deal about genes, neurons, and niche construction). Your
            discussion, however, is easy to follow and is very informative; thanks
            for that.

            Many before you have also made the attempt to have this creationist and
            pheromone salesman explain his "model" of "adaptive evolution" (I
            presume he means natural selection) that "destroys" the role of random
            mutations . Good luck.

            Finally, David, have you read James Shapiro's "Evolution: A View from
            the 21st Century"? His form of near-creationism (he denies the label)
            relies on the CRISPR system/pathways recently discovered in bacteria.
            That is an interesting natural phenomenon that begs the question of
            random mutations.

            --- In evolutionary-psychology@yahoogroups.com, David Leake wrote:
            >
            > Thanks James.
            >
            >
            > Your visual model reflects what was described in the article, with a
            focus on gene activation/expression, but the model still does not
            specify how this leads to heritable DNA changes. Your model seems in
            tune with evo-devo (evolution of development) in terms of concern with
            changes in regulatory processes, new uses for existing proteins, role of
            miRNA and mRNA, etc. etc., but evo-devo still relies on mutations to
            explain adaptive evolution.
            >
            >
            > It would be very useful to people trying to understand your model if
            you could clearly describe how it might work in the adaptive evolution
            of a single behavior. For example, based on your extensive knowledge of
            Apis mellifera, you might explain how age polyethism (workers begin life
            as nurses and transition with age to foragers) might have evolved
            without mutations. You could just take one of the well-studied
            mechanisms of age polyethism and explain how your model would apply. Or
            any other honeybee behavior you want, that's just an example.....
            >
            >
            > Cheers,
            > David
            >
            >
            > -----Original Message-----
            > From: james kohl
            > To: human-ethology
            > Cc: evolutionary-psychology
            > Sent: Fri, Feb 8, 2013 5:41 pm
            > Subject: Re: [human-ethology] Re: [evol-psych] Adaptive evolution via
            the nutrient-dependent pheromone-controlled microRNA/messenger RNA
            balance
            >
            >
            >
            >
            >
            >
            > David,
            > thanks for your additional interest
            >
            > Here is a link to the diagram:
            > Human Pheromones: Epigenetic Effects of Odors and Their Affects on
            Behavior
            >
            > The epigenetic effects that lead to changes in genomic DNA -- as
            required for adaptive evolution to occur -- are detailed in the
            following context.
            >
            > This model of systems biology represents the conservation of bottom-up
            organization and top-down activation via:
            > 1.Nutrient-dependent stress-induced and social stress-induced
            intracellular changes in the homeostatic balance of microRNA(miRNA) and
            messenger RNA (mRNA);
            > 2.Intermolecular changes in DNA (genes);
            > 3.Non-random experience-dependent stochastic variations in de novo
            gene expression for odor receptors;
            > 4.The required gene-cell-tissue-organ-organ system pathway that links
            sensory input directly to gene activation in neurosecretory cells of the
            brain;
            > 5.The required reciprocity that links gene expression to behavior that
            alters gene expression (i.e., from genes to behavior and back).
            >
            > I'm rather certain you can see why I asked that you read the published
            work first. Those who cannot accept the fact that adaptive evolution is
            nutrient-dependent and pheromone-controlled (as exemplified in model
            organisms like the honeybee) are not likely to look further at the
            molecular mechanisms above. And there is at least one more level of
            complexity that has recently been added to these 5 steps, that more
            specifically addresses the nutrient-dependent alternative splicings
            required for sex differences and for species diversity controlled by
            pheromones, which also are exemplified in animal models.
            >
            > Small intranuclear proteins also participate in generating alternative
            splicing techniques of pre-mRNA and, by this mechanism, contribute to
            sexual differentiation in at least two species, Drosophila melanogaster
            and Caenorhabditis elegans.... That similar proteins perform functions
            in humans suggests the possibility that some human sex differences may
            arise from alternative splicings of otherwise identical genes. Diamond,
            Binstock and Kohl (1996)
            >
            > Note: Jay Feierman announced that he is going to write about learning
            and memory after I mentioned this (below) "....nutrient-dependent
            pheromone-controlled miRNA/mRNA balance converts genomic DNA to brain
            structure and function, which includes epigenetic effects of food odors
            and pheromones on learning and memory." It will be interesting to see
            how much of my model is included in his approach.
            >
            > 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: David Leake
            > To: evolutionary-psychology@yahoogroups.com;
            human-ethology@yahoogroups.com
            > Sent: Fri, February 8, 2013 3:11:06 PM
            > Subject: [human-ethology] Re: [evol-psych] Adaptive evolution via the
            nutrient-dependent pheromone-controlled microRNA/messenger RNA balance
            >
            >
            >
            >
            > Thanks for asking. It's not something that I can explain outside the
            context of the model, which details how olfaction and odor receptors
            enable nutrient-dependent pheromone-controlled adaptive evolution. Once
            others understand something about the common molecular mechanisms that
            establish that fact, I may be able to explain microRNA-facilitated
            alternative splicings and their impact on intracellular signaling,
            stochastic gene expression and the control of de novo protein synthesis
            via changes in the microRNA/messenger RNA balance. But there must be a
            starting point, as detailed in Human pheromones and food odors:
            epigenetic influences on the socioaffective nature of evolved behaviors.
            > James, I obtained the paper through the link you gave, however the
            discussion is all about epigenetic processes and there is nothing about
            how these might lead to changes in genomic DNA as required for evolution
            to occur. Do you have a concise description of your model for that?
            >
            >
            > -----Original Message-----
            > From: james kohl
            > To: David Leake ; evolutionary-psychology ; human-ethology
            > Sent: Wed, Feb 6, 2013 5:42 pm
            > Subject: Re: [evol-psych] Adaptive evolution via the
            nutrient-dependent pheromone-controlled microRNA/messenger RNA balance
            >
            >
            >
            >
            >
            >
            >
            > Thanks for asking. It's not something that I can explain outside the
            context of the model, which details how olfaction and odor receptors
            enable nutrient-dependent pheromone-controlled adaptive evolution. Once
            others understand something about the common molecular mechanisms that
            establish that fact, I may be able to explain microRNA-facilitated
            alternative splicings and their impact on intracellular signaling,
            stochastic gene expression and the control of de novo protein synthesis
            via changes in the microRNA/messenger RNA balance. But there must be a
            starting point, as detailed in Human pheromones and food odors:
            epigenetic influences on the socioaffective nature of evolved behaviors.
            >
            > As you may know, I have had no success whatsoever in getting anyone to
            acknowledge how ridiculous random mutations theory is. I think the
            problem is because they won't read my most recent published work, or any
            others, and that means they will continue to fall further and further
            behind the neuroscientific progress exemplified by the paper I just
            cited. For example, if I told you that miRNAs serve a role in synaptic
            tagging and capture by providing synapse-specific sequestration of
            relevant mRNAs being trafficked down dendrites, it would be relatively
            meaningless, wouldn't it? And yet, that is one way that the
            nutrient-dependent pheromone-controlled miRNA/mRNA balance converts
            genomic DNA to brain structure and function, which includes epigenetic
            effects of food odors and pheromones on learning and memory. On the
            other hand, if I could place the nutrient-dependent
            pheromone-controlled miRNA/mRNA balance in the context of
            hormone-organized and hormone-activated genetically predisposed
            behavior, I might be able to take a step-by-step approach that not
            possible with anyone who still thinks that mutations cause adaptive
            evolution.
            >
            >
            > James V. Kohl
            > Medical laboratory scientist (ASCP)
            > Independent researcher
            >
            >
            >
            >
            >
            >
            >
            > From: David Leake
            > To: evolutionary-psychology@yahoogroups.com;
            human-ethology@yahoogroups.com; jvkohl@...
            > Sent: Wed, February 6, 2013 7:09:27 PM
            > Subject: Re: [evol-psych] Adaptive evolution via the
            nutrient-dependent pheromone-controlled microRNA/messenger RNA balance
            >
            >
            >
            > Excerpt:"In conclusion, alternative splicing coupled with RNA QC
            appears to function in the NS as a prevalent gene regulation strategy.
            We predict that future work in this area will yield additional important
            insights into molecular mechanisms that allow the information stored in
            the form of genomic DNA to be converted into brain structure and
            function."
            >
            > In my model, the microRNA/messenger RNA balance is nutrient-dependent
            and pheromone-controlled, which is how it enables adaptive evolution via
            ecological, social, neurogenic, and socio-cognitive niche construction.
            Of course, that makes the theory of mutation-caused evolution appear to
            be even more ridiculous than it has ever seemed to be. But the real
            question about mutation-caused adaptive evolution remains: "Is there a
            model for that?"
            >
            > The excerpt refers to information stored in genomic DNA. Can you
            briefly explain how niche construction leads to changes in the
            information stored in genomic DNA (which is certainly a requirement for
            evolution to happen)?
            >
            >
            > Dave Leake
            >
            >
            > -----Original Message-----
            > From: james kohl
            > To: human-ethology
            > Cc: evolutionary-psychology
            > Sent: Wed, Feb 6, 2013 2:00 pm
            > Subject: [evol-psych] Adaptive evolution via the nutrient-dependent
            pheromone-controlled microRNA/messenger RNA balance
            >
            >
            >
            >
            >
            >
            >
            >
            >
            > Regulation of gene expression in mammalian nervous system through
            alternative pre-mRNA splicing coupled with RNA quality control
            mechanisms Original Research Article
            > Molecular and Cellular Neuroscience, Available online 25 January 2013,
            Pages
            > Karen Yap, Eugene V. Makeyev
            >
            >
            > Excerpt:"In conclusion, alternative splicing coupled with RNA QC
            appears to function in the NS as a prevalent gene regulation strategy.
            We predict that future work in this area will yield additional important
            insights into molecular mechanisms that allow the information stored in
            the form of genomic DNA to be converted into brain structure and
            function."
            >
            > In my model, the microRNA/messenger RNA balance is nutrient-dependent
            and pheromone-controlled, which is how it enables adaptive evolution via
            ecological, social, neurogenic, and socio-cognitive niche construction.
            Of course, that makes the theory of mutation-caused evolution appear to
            be even more ridiculous than it has ever seemed to be. But the real
            question about mutation-caused adaptive evolution remains: "Is there a
            model for that?"
            >
            >
            >
            > 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.
            >
          • james kohl
            From: David Leake Your visual model reflects what was described in the article, with a focus on gene activation/expression, but the model
            Message 5 of 15 , Feb 10, 2013
            • 0 Attachment
              From: David Leake <DWLeake@...>
              Your visual model reflects what was described in the article, with a focus on gene activation/expression, but the model still does not specify how this leads to heritable DNA changes. Your model seems in tune with evo-devo (evolution of development) in terms of concern with changes in regulatory processes, new uses for existing proteins, role of miRNA and mRNA, etc. etc., but evo-devo still relies on mutations to explain adaptive evolution.

              JK: Thanks for the synopsis of the diagram/article/model.

              It would be very useful to people trying to understand your model if you could clearly describe how it might work in the adaptive evolution of a single  behavior. For example, based on your extensive knowledge of Apis mellifera, you might explain how age polyethism (workers begin life as nurses and transition with age to foragers) might have evolved without mutations.

              JK: Excellent suggestion. In the diagram of my model, you can "picture" what happens, because there is no stage of life in mammals where epigenesis and epistasis are not epigenetically effected by food odors and pheromones.

              You could just take one of 
              the well-studied mechanisms of age polyethism and explain how your model would apply. Or any other honeybee behavior you want, that's just an example.....

              JK: This was already done. As detailed in From fertilization to adult sexual behavior, the mammalian model was extended to invertebrates "from egg to adult" in Organizational and activational effects of hormones on insect behavior. The beauty of your suggestion to apply my model to
              well-studied mechanisms of age polyethism lies in the context of Honey bees as a model for understanding mechanisms of life history transitions. "In this review we discuss the physiological and genetic mechanisms of this behavioral transition, which include large scale changes in hormonal activity, metabolism, flight ability, circadian rhythms, sensory perception and processing, neural architecture, learning ability, memory and gene expression."  

              Note: No one else seems willing to enter discussion about the only existing model of adaptive evolution, which includes life history transitions and epigenetic effects on gene expression.

              You write: "...
              but the model still does not specify how this leads to heritable DNA changes." That's another excellent point. Because it is the only model, it must explain how alternative splicings lead to heritable changes in gene expression, and it does. See below: "That similar proteins perform functions in humans suggests the possibility that some human sex differences may arise from alternative splicings of otherwise identical genes."

              Natural selection for nutrients results in nutrient-dependent sex differences in pheromones that enable sexual selection for nutrient-dependent fitness in species from microbes to man.  Berreby wrote: Research in behavioral epigenetics is seeking evidence that links experience to biochemistry to gene expression and back out again. Also: "
              It needs, and doesn’t yet have, at least one slam-dunk demonstration of all the links in a chain from behavior to neural activity to gene expression and back out again. How, for example, do biochemical events at a neuron’s nucleus affect the synaptic signaling between neurons that is the basis for all behavior?"

              I have since detailed how the required changes in gene expression occur but the details are not discussed. One antagonist continues to deny there is sufficient evidence of transgenerational epigenetic inheritance to dispense with the mutations theory. Others think that auditory and visual input directly activate

              "the physiological and genetic mechanisms of ... behavioral transition[s], which include large scale changes in hormonal activity, metabolism, flight ability, circadian rhythms, sensory perception and processing, neural architecture, learning ability, memory and gene expression."

              All others need to do is what you have done. Tell me
              what's missing from my model. But what if it's not, as I have detailed in a series of published works! What if, for example, as I concluded: "Olfaction and odor receptors provide a clear evolutionary trail that can be followed from unicellular organisms to insects to humans."

              Thanks again for your interest and pertinent comments and questions. You exemplify how science progresses.


              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.



              -----Original Message-----
              From: james kohl <jvkohl@...>
              To: human-ethology <human-ethology@yahoogroups.com>
              Cc: evolutionary-psychology <evolutionary-psychology@yahoogroups.com>
              Sent: Fri, Feb 8, 2013 5:41 pm
              Subject: Re: [human-ethology] Re: [evol-psych] Adaptive evolution via the nutrient-dependent pheromone-controlled microRNA/messenger RNA balance

               
              David,
              thanks for your additional interest

              Here is a link to the diagram:
              Human Pheromones: Epigenetic Effects of Odors and Their Affects on Behavior

              The epigenetic effects that lead to changes in genomic DNA -- as required for adaptive evolution to occur -- are detailed in the following context.


              This model of systems biology represents the conservation of bottom-up organization and top-down activation via:
              1.Nutrient-dependent stress-induced and social stress-induced intracellular changes in the homeostatic balance of microRNA(miRNA) and messenger RNA (mRNA);
              2.Intermolecular changes in DNA (genes);
              3.Non-random experience-dependent stochastic variations in de novo gene expression for odor receptors;
              4.The required gene-cell-tissue-organ-organ system pathway that links sensory input directly to gene activation in neurosecretory cells of the brain;
              5.The required reciprocity that links gene expression to behavior that alters gene expression (i.e., from genes to behavior and back).

              I'm rather certain you can see why I asked that you read the published work first. Those who cannot accept the fact that adaptive evolution is nutrient-dependent and pheromone-controlled (as exemplified in model organisms like the honeybee) are not likely to look further at the molecular mechanisms above. And there is at least one more level of complexity that has recently been added to these 5 steps, that more specifically addresses the nutrient-dependent alternative splicings required for sex differences and for species diversity controlled by pheromones, which also are exemplified in animal models.

              Small intranuclear proteins also participate in generating alternative splicing techniques of pre-mRNA and, by this mechanism, contribute to sexual differentiation in at least two species, Drosophila melanogaster and Caenorhabditis elegans.... That similar proteins perform functions in humans suggests the possibility that some human sex differences may arise from alternative splicings of otherwise identical genes. Diamond, Binstock and Kohl (1996)

              Note: Jay Feierman announced that he is going to write about learning and memory after I mentioned this (below) "....nutrient-dependent pheromone-controlled miRNA/mRNA balance converts genomic DNA to brain structure and function, which includes epigenetic effects of food odors and pheromones on learning and memory." It will be interesting to see how much of my model is included in his approach.

              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: David Leake <DWLeake@...>
              To: evolutionary-psychology@yahoogroups.com; human-ethology@yahoogroups.com
              Sent: Fri, February 8, 2013 3:11:06 PM
              Subject: [human-ethology] Re: [evol-psych] Adaptive evolution via the nutrient-dependent pheromone-controlled microRNA/messenger RNA balance

               
              Thanks for asking. It's not something that I can explain outside the context of the model, which details how olfaction and odor receptors enable nutrient-dependent pheromone-controlled adaptive evolution. Once others understand something about the common molecular mechanisms that establish that fact, I may be able to explain microRNA-facilitated alternative splicings and their impact on intracellular signaling, stochastic gene expression and the control of de novo protein synthesis via changes in the microRNA/messenger RNA balance. But there must be a starting point, as detailed in  Human pheromones and food odors: epigenetic influences on the socioaffective nature of evolved behaviors.
              James, I obtained the paper through the link you gave, however the discussion is all about epigenetic processes and there is nothing about how these might lead to changes in genomic DNA as required for evolution to occur. Do you have a concise description of your model for that?

              -----Original Message-----
              From: james kohl <jvkohl@...>
              To: David Leake <dwleake@...>; evolutionary-psychology <evolutionary-psychology@yahoogroups.com>; human-ethology <human-ethology@yahoogroups.com>
              Sent: Wed, Feb 6, 2013 5:42 pm
              Subject: Re: [evol-psych] Adaptive evolution via the nutrient-dependent pheromone-controlled microRNA/messenger RNA balance

               
              Thanks for asking. It's not something that I can explain outside the context of the model, which details how olfaction and odor receptors enable nutrient-dependent pheromone-controlled adaptive evolution. Once others understand something about the common molecular mechanisms that establish that fact, I may be able to explain microRNA-facilitated alternative splicings and their impact on intracellular signaling, stochastic gene expression and the control of de novo protein synthesis via changes in the microRNA/messenger RNA balance. But there must be a starting point, as detailed in  Human pheromones and food odors: epigenetic influences on the socioaffective nature of evolved behaviors.

              As you may know, I have had no success whatsoever in getting anyone to acknowledge how ridiculous random mutations theory is. I think the problem is because they won't read my most recent published work, or any others, and that means they will continue to fall further and further behind the neuroscientific progress exemplified by the paper I just cited. For example, if I told you that miRNAs serve a role in synaptic tagging and capture by providing synapse-specific sequestration of relevant mRNAs being trafficked down dendrites, it would be relatively meaningless, wouldn't it?   And yet, that is one way that the nutrient-dependent pheromone-controlled miRNA/mRNA balance converts genomic DNA to brain structure and function, which includes epigenetic effects of food odors and pheromones on learning and memory. On the other hand, if I could place the nutrient-dependent pheromone-controlled miRNA/mRNA balance in the context of hormone-organized and hormone-activated genetically predisposed behavior, I might be able to take a step-by-step approach that not possible with anyone who still thinks that mutations cause adaptive evolution.
               
              James V. Kohl
              Medical laboratory scientist (ASCP)
              Independent researcher




              From: David Leake <dwleake@...>
              To: evolutionary-psychology@yahoogroups.com; human-ethology@yahoogroups.com; jvkohl@...
              Sent: Wed, February 6, 2013 7:09:27 PM
              Subject: Re: [evol-psych] Adaptive evolution via the nutrient-dependent pheromone-controlled microRNA/messenger RNA balance

              Excerpt:"In conclusion, alternative splicing coupled with RNA QC appears to function in the NS as a prevalent gene regulation strategy. We predict that future work in this area will yield additional important insights into molecular mechanisms that allow the information stored in the form of genomic DNA to be converted into brain structure and function."
               
              In my model, the microRNA/messenger RNA balance is nutrient-dependent and pheromone-controlled, which is how it enables adaptive evolution via ecological, social, neurogenic, and socio-cognitive niche construction. Of course, that makes the theory of mutation-caused evolution appear to be even more ridiculous than it has ever seemed to be. But the real question about mutation-caused adaptive evolution remains: "Is there a model for that?"
              The excerpt refers to information stored in genomic DNA. Can you briefly explain how niche construction leads to changes in the information stored in genomic DNA (which is certainly a requirement for evolution to happen)?

              Dave Leake

              -----Original Message-----
              From: james kohl <jvkohl@...>
              To: human-ethology <human-ethology@yahoogroups.com>
              Cc: evolutionary-psychology <evolutionary-psychology@yahoogroups.com>
              Sent: Wed, Feb 6, 2013 2:00 pm
              Subject: [evol-psych] Adaptive evolution via the nutrient-dependent pheromone-controlled microRNA/messenger RNA balance

               
              Regulation of gene expression in mammalian nervous system through alternative pre-mRNA splicing coupled with RNA quality control mechanisms   Original Research Article 
              Molecular and Cellular Neuroscience, Available online 25 January 2013, Pages 
              Karen Yap, Eugene V. Makeyev
               
              Excerpt:"In conclusion, alternative splicing coupled with RNA QC appears to function in the NS as a prevalent gene regulation strategy. We predict that future work in this area will yield additional important insights into molecular mechanisms that allow the information stored in the form of genomic DNA to be converted into brain structure and function."
               
              In my model, the microRNA/messenger RNA balance is nutrient-dependent and pheromone-controlled, which is how it enables adaptive evolution via ecological, social, neurogenic, and socio-cognitive niche construction. Of course, that makes the theory of mutation-caused evolution appear to be even more ridiculous than it has ever seemed to be. But the real question about mutation-caused adaptive evolution remains: "Is there a model for that?"
               

               
              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.
            • james kohl
              I think William s obvious, ongoing, confusion is due in part to his inability to pose questions about the content of my model. But, for example, if you don t
              Message 6 of 15 , Feb 10, 2013
              • 0 Attachment
                I think William's obvious, ongoing, confusion is due in part to his inability to pose questions about the content of my model. But, for example, if you don't know what a neurogenic niche is, you probably wouldn't understand how natural variation in neurogenetic networks are involved in olfactory behavior. Thus, the suggestion is often made by Williams that others look at works that lack the explanatory power of my model, if only because he's not capable of understanding the basic principle of biology and levels of biological organization required to link sensory input to adaptive evolution of species from microbes to man.
                 
                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: clarence_sonny_williams <clarencew@...>
                To: evolutionary-psychology@yahoogroups.com
                Sent: Sun, February 10, 2013 7:50:45 AM
                Subject: [human-ethology] Re: [evol-psych] Adaptive evolution via the nutrient-dependent pheromone-controlled microRNA/messenger RNA balance

                 

                David,

                I'm so busy that I have not visited the site in some time, but I am
                closely following your valiant attempts to wring a cogent explanation
                out of Mr. Kohl for how his form of "directed evolution" works. The
                many writings of other creationists and believers in intelligent design
                (Mr. Kohl is a creationist by his own admission) offer similar efforts
                at explanations. They, however, usually omit the "olfactory
                connection," perhaps because, unlike Mr. Kohl, they do not own a
                "pheromone" product for sale to anyone who wants to enhance their sex
                life.

                Perhaps you've also found, as I did, that Mr. Kohl's explanation
                contains a lot of scientific terms, but their connection escapes me
                (e.g. I do not understand his term, "neurogenic" niche, although I know
                a great deal about genes, neurons, and niche construction). Your
                discussion, however, is easy to follow and is very informative; thanks
                for that.

                Many before you have also made the attempt to have this creationist and
                pheromone salesman explain his "model" of "adaptive evolution" (I
                presume he means natural selection) that "destroys" the role of random
                mutations . Good luck.

                Finally, David, have you read James Shapiro's "Evolution: A View from
                the 21st Century"? His form of near-creationism (he denies the label)
                relies on the CRISPR system/pathways recently discovered in bacteria.
                That is an interesting natural phenomenon that begs the question of
                random mutations.

                --- In evolutionary-psychology@yahoogroups.com, David Leake wrote:
                >
                > Thanks James.
                >
                >
                > Your visual model reflects what was described in the article, with a
                focus on gene activation/expression, but the model still does not
                specify how this leads to heritable DNA changes. Your model seems in
                tune with evo-devo (evolution of development) in terms of concern with
                changes in regulatory processes, new uses for existing proteins, role of
                miRNA and mRNA, etc. etc., but evo-devo still relies on mutations to
                explain adaptive evolution.
                >
                >
                > It would be very useful to people trying to understand your model if
                you could clearly describe how it might work in the adaptive evolution
                of a single behavior. For example, based on your extensive knowledge of
                Apis mellifera, you might explain how age polyethism (workers begin life
                as nurses and transition with age to foragers) might have evolved
                without mutations. You could just take one of the well-studied
                mechanisms of age polyethism and explain how your model would apply. Or
                any other honeybee behavior you want, that's just an example.....
                >
                >
                > Cheers,
                > David
                >
                >
                > -----Original Message-----
                > From: james kohl
                > To: human-ethology
                > Cc: evolutionary-psychology
                > Sent: Fri, Feb 8, 2013 5:41 pm
                > Subject: Re: [human-ethology] Re: [evol-psych] Adaptive evolution via
                the nutrient-dependent pheromone-controlled microRNA/messenger RNA
                balance
                >
                >
                >
                >
                >
                >
                > David,
                > thanks for your additional interest
                >
                > Here is a link to the diagram:
                > Human Pheromones: Epigenetic Effects of Odors and Their Affects on
                Behavior
                >
                > The epigenetic effects that lead to changes in genomic DNA -- as
                required for adaptive evolution to occur -- are detailed in the
                following context.
                >
                > This model of systems biology represents the conservation of bottom-up
                organization and top-down activation via:
                > 1.Nutrient-dependent stress-induced and social stress-induced
                intracellular changes in the homeostatic balance of microRNA(miRNA) and
                messenger RNA (mRNA);
                > 2.Intermolecular changes in DNA (genes);
                > 3.Non-random experience-dependent stochastic variations in de novo
                gene expression for odor receptors;
                > 4.The required gene-cell-tissue-organ-organ system pathway that links
                sensory input directly to gene activation in neurosecretory cells of the
                brain;
                > 5.The required reciprocity that links gene expression to behavior that
                alters gene expression (i.e., from genes to behavior and back).
                >
                > I'm rather certain you can see why I asked that you read the published
                work first. Those who cannot accept the fact that adaptive evolution is
                nutrient-dependent and pheromone-controlled (as exemplified in model
                organisms like the honeybee) are not likely to look further at the
                molecular mechanisms above. And there is at least one more level of
                complexity that has recently been added to these 5 steps, that more
                specifically addresses the nutrient-dependent alternative splicings
                required for sex differences and for species diversity controlled by
                pheromones, which also are exemplified in animal models.
                >
                > Small intranuclear proteins also participate in generating alternative
                splicing techniques of pre-mRNA and, by this mechanism, contribute to
                sexual differentiation in at least two species, Drosophila melanogaster
                and Caenorhabditis elegans.... That similar proteins perform functions
                in humans suggests the possibility that some human sex differences may
                arise from alternative splicings of otherwise identical genes. Diamond,
                Binstock and Kohl (1996)
                >
                > Note: Jay Feierman announced that he is going to write about learning
                and memory after I mentioned this (below) "....nutrient-dependent
                pheromone-controlled miRNA/mRNA balance converts genomic DNA to brain
                structure and function, which includes epigenetic effects of food odors
                and pheromones on learning and memory." It will be interesting to see
                how much of my model is included in his approach.
                >
                > 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: David Leake
                > To: evolutionary-psychology@yahoogroups.com;
                human-ethology@yahoogroups.com
                > Sent: Fri, February 8, 2013 3:11:06 PM
                > Subject: [human-ethology] Re: [evol-psych] Adaptive evolution via the
                nutrient-dependent pheromone-controlled microRNA/messenger RNA balance
                >
                >
                >
                >
                > Thanks for asking. It's not something that I can explain outside the
                context of the model, which details how olfaction and odor receptors
                enable nutrient-dependent pheromone-controlled adaptive evolution. Once
                others understand something about the common molecular mechanisms that
                establish that fact, I may be able to explain microRNA-facilitated
                alternative splicings and their impact on intracellular signaling,
                stochastic gene expression and the control of de novo protein synthesis
                via changes in the microRNA/messenger RNA balance. But there must be a
                starting point, as detailed in Human pheromones and food odors:
                epigenetic influences on the socioaffective nature of evolved behaviors.
                > James, I obtained the paper through the link you gave, however the
                discussion is all about epigenetic processes and there is nothing about
                how these might lead to changes in genomic DNA as required for evolution
                to occur. Do you have a concise description of your model for that?
                >
                >
                > -----Original Message-----
                > From: james kohl
                > To: David Leake ; evolutionary-psychology ; human-ethology
                > Sent: Wed, Feb 6, 2013 5:42 pm
                > Subject: Re: [evol-psych] Adaptive evolution via the
                nutrient-dependent pheromone-controlled microRNA/messenger RNA balance
                >
                >
                >
                >
                >
                >
                >
                > Thanks for asking. It's not something that I can explain outside the
                context of the model, which details how olfaction and odor receptors
                enable nutrient-dependent pheromone-controlled adaptive evolution. Once
                others understand something about the common molecular mechanisms that
                establish that fact, I may be able to explain microRNA-facilitated
                alternative splicings and their impact on intracellular signaling,
                stochastic gene expression and the control of de novo protein synthesis
                via changes in the microRNA/messenger RNA balance. But there must be a
                starting point, as detailed in Human pheromones and food odors:
                epigenetic influences on the socioaffective nature of evolved behaviors.
                >
                > As you may know, I have had no success whatsoever in getting anyone to
                acknowledge how ridiculous random mutations theory is. I think the
                problem is because they won't read my most recent published work, or any
                others, and that means they will continue to fall further and further
                behind the neuroscientific progress exemplified by the paper I just
                cited. For example, if I told you that miRNAs serve a role in synaptic
                tagging and capture by providing synapse-specific sequestration of
                relevant mRNAs being trafficked down dendrites, it would be relatively
                meaningless, wouldn't it? And yet, that is one way that the
                nutrient-dependent pheromone-controlled miRNA/mRNA balance converts
                genomic DNA to brain structure and function, which includes epigenetic
                effects of food odors and pheromones on learning and memory. On the
                other hand, if I could place the nutrient-dependent
                pheromone-controlled miRNA/mRNA balance in the context of
                hormone-organized and hormone-activated genetically predisposed
                behavior, I might be able to take a step-by-step approach that not
                possible with anyone who still thinks that mutations cause adaptive
                evolution.
                >
                >
                > James V. Kohl
                > Medical laboratory scientist (ASCP)
                > Independent researcher
                >
                >
                >
                >
                >
                >
                >
                > From: David Leake
                > To: evolutionary-psychology@yahoogroups.com;
                human-ethology@yahoogroups.com; jvkohl@...
                > Sent: Wed, February 6, 2013 7:09:27 PM
                > Subject: Re: [evol-psych] Adaptive evolution via the
                nutrient-dependent pheromone-controlled microRNA/messenger RNA balance
                >
                >
                >
                > Excerpt:"In conclusion, alternative splicing coupled with RNA QC
                appears to function in the NS as a prevalent gene regulation strategy.
                We predict that future work in this area will yield additional important
                insights into molecular mechanisms that allow the information stored in
                the form of genomic DNA to be converted into brain structure and
                function."
                >
                > In my model, the microRNA/messenger RNA balance is nutrient-dependent
                and pheromone-controlled, which is how it enables adaptive evolution via
                ecological, social, neurogenic, and socio-cognitive niche construction.
                Of course, that makes the theory of mutation-caused evolution appear to
                be even more ridiculous than it has ever seemed to be. But the real
                question about mutation-caused adaptive evolution remains: "Is there a
                model for that?"
                >
                > The excerpt refers to information stored in genomic DNA. Can you
                briefly explain how niche construction leads to changes in the
                information stored in genomic DNA (which is certainly a requirement for
                evolution to happen)?
                >
                >
                > Dave Leake
                >
                >
                > -----Original Message-----
                > From: james kohl
                > To: human-ethology
                > Cc: evolutionary-psychology
                > Sent: Wed, Feb 6, 2013 2:00 pm
                > Subject: [evol-psych] Adaptive evolution via the nutrient-dependent
                pheromone-controlled microRNA/messenger RNA balance
                >
                >
                >
                >
                >
                >
                >
                >
                >
                > Regulation of gene expression in mammalian nervous system through
                alternative pre-mRNA splicing coupled with RNA quality control
                mechanisms Original Research Article
                > Molecular and Cellular Neuroscience, Available online 25 January 2013,
                Pages
                > Karen Yap, Eugene V. Makeyev
                >
                >
                > Excerpt:"In conclusion, alternative splicing coupled with RNA QC
                appears to function in the NS as a prevalent gene regulation strategy.
                We predict that future work in this area will yield additional important
                insights into molecular mechanisms that allow the information stored in
                the form of genomic DNA to be converted into brain structure and
                function."
                >
                > In my model, the microRNA/messenger RNA balance is nutrient-dependent
                and pheromone-controlled, which is how it enables adaptive evolution via
                ecological, social, neurogenic, and socio-cognitive niche construction.
                Of course, that makes the theory of mutation-caused evolution appear to
                be even more ridiculous than it has ever seemed to be. But the real
                question about mutation-caused adaptive evolution remains: "Is there a
                model for that?"
                >
                >
                >
                > 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.
                >

              • Nils K.
                Dear All! ... David, I m so busy that I have not visited the site in some time, but I am closely following your valiant attempts to wring a cogent explanation
                Message 7 of 15 , Feb 10, 2013
                • 0 Attachment
                  Dear All!

                  --- In evolutionary-psychology@yahoogroups.com, "clarence_sonny_williams" wrote:

                  David,

                  I'm so busy that I have not visited the site in some time, but I am
                  closely following your valiant attempts to wring a cogent explanation
                  [...]

                  NKO:
                  .... not visited the site AND closely following ...
                  The language here does not point to "busy" but to other causes.
                  I've my own thoughts about the other causes based on the verbal
                  forms of the earlier messages ... Is Edgar also "busy"?. And a third
                  man is also "busy"? -- he explained away a genetic illness by
                  blaming the Neanderthals, and later on disappeared from our
                  discussions. Hope all is well with all three guys. Lastly, by the way,
                  as a person who is researching biological evolution from an advanced
                  standpoint, I've concluded long ago that geniunely random mutations +
                  more or less random selection (which is the way natural selection is
                  happening) are absolutely unable to explain evolution.
                  Using Popper's discovery that we can disprove a scientific theory, it
                  is not difficult to show mathematically that the random mutation
                  theory is impossible. Clarence, you was back again with a lie in your
                  opening message: JV Kohl is NOT a creationist.

                  Best,
                  NKO
                • David Leake
                  James, I followed the links you provided, my comments are in red below.....David ... From: james kohl Sent: Sun, Feb 10, 2013 1:36 pm
                  Message 8 of 15 , Feb 11, 2013
                  • 0 Attachment
                    James, I followed the links you provided, my comments are in red below.....David

                    -----Original Message-----
                    From: james kohl <jvkohl@...>
                    Sent: Sun, Feb 10, 2013 1:36 pm
                    Subject: Re: [psychiatry-research] Communication Disorders and Cellular Machinery

                     
                    A correspondent noted that my model seems to be in tune with evo-devo (evolution of development) in the context of changes in regulatory processes, epigenesis, and the role of miRNA and mRNA etc, but that evo-devo relies on mutations to explain adaptive evolution.

                    After correctly summarizing its content, he asked that I specify how my model of nutrient-dependent pheromone-controlled adaptive evolution leads to heritable DNA changes. He suggested that it would be useful if I clearly described the adaptive evolution of a single behavior or how age polyethism in
                    Apis mellifera evolved sans mutations.

                    JK: Excellent suggestion. In the diagram of my model, you can "picture" what happens, because there is no stage of life in mammals where epigenesis and epistasis are not epigenetically effected by food odors and pheromones.


                    Correspondent: "You could just take one of the well-studied mechanisms of age polyethism and explain how your model would apply. Or any other honeybee behavior you want, that's just an example....."

                    JK: This was already done. As detailed in From fertilization to adult sexual behavior, the mammalian model was extended to invertebrates "from egg to adult" in Organizational and activational effects of hormones on insect behavior. The beauty of your suggestion to apply my model to
                    well-studied mechanisms of age polyethism lies in the context of Honey bees as a model for understanding mechanisms of life history transitions. "In this review we discuss the physiological and genetic mechanisms of this behavioral transition, which include large scale changes in hormonal activity, metabolism, flight ability, circadian rhythms, sensory perception and processing, neural architecture, learning ability, memory and gene expression."  

                    DL: The article linked certainly has a wealth of detail on changes in gene expression that underlie age polyethism in bees. However doing a search within the article for "evol" (to find "evolve" or "evolution" etc) and "herit" (to find "inherit" or "heritable" etc) and "select" (to find terms related to selective forces) and "splic" (to find "alternative splicing/splice") all fail to locate anywhere in the article where the authors discuss how change in gene expression or anything else might be transmitted to the next generation. As the authors argue, bees are certainly a great model organism for understanding the mechanisms of life history transitions within the lifetimes of worker bees (e.g., from being nurses that can barely fly to foragers that are great fliers), but that doesn't address mechanisms of adaptive evolution. I noticed in another email you state that this article's authors "Elekonich and Robinson used my model" but for some reason they do not cite "Kohl" in this article.

                    Note: No one else seems willing to enter discussion about the only existing model of adaptive evolution, which includes life history transitions and epigenetic effects on gene expression.

                    DL: Life history transitions can be understood from the evo-devo perspective as having evolved to promote the adaptation of species members to their physical and social environments by properly timing and orchestrating developmental stages, which involves epigenetic processes that are consistently and reliably passed on to offspring. However, your frequent highlighting of "epigenetic effects on gene expression" is not accompanied by further explanation of how the different gene expression is presumably transmitted to the next generation. Does your model say that epigenetic effects actually change the genes? There's some evidence that epigenetic marks might be transmitted to offspring or maybe even another generation or two, but that evidence is rare and contested (it seems rarer than the rate of potentially beneficial mutations). If epigenetic effects are at the heart of adaptive evolution, why isn't there abundant evidence of this? It should be there, because biologists can currently identify and track epigenetic methyl and acetyl marks on genes in detail.

                    You write: "...
                    but the model still does not specify how this leads to heritable DNA changes." That's another excellent point. Because it is the only model, it must explain how alternative splicings lead to heritable changes in gene expression, and it does. See in From fertilization to adult sexual behavior,: "That similar proteins perform functions in humans suggests the possibility that some human sex differences may arise from alternative splicings of otherwise identical genes." 

                    DL: I used the same search terms within this Milton Diamond article and once again found that the various epigenetic influences and alternative gene splicings described only had to do with development over the course of a lifetime.....there's nothing at all about how these lead to adaptive evolution. It's beginning to sound like one key process for adaptive evolution in your model is the "alternative splicings of otherwise identical genes." Does that mean that the solitary bees that gave rise to eusocial bees have essentially the same genes but the genes operate differently due to epigenetic marks and alternative splicings that have been acquired and passed on to successive generations?

                    Natural selection for nutrients results in nutrient-dependent sex differences in pheromones that enable sexual selection for nutrient-dependent fitness in species from microbes to man.  Berreby wrote: Research in behavioral epigenetics is seeking evidence that links experience to biochemistry to gene expression and back out again. Also: "
                    It needs, and doesn’t yet have, at least one slam-dunk demonstration of all the links in a chain from behavior to neural activity to gene expression and back out again. How, for example, do biochemical events at a neuron’s nucleus affect the synaptic signaling between neurons that is the basis for all behavior?" 

                    DL: Although you use the Berreby article to support your model, the article actually seems to oppose it in the way it clarifies what "modern" epigenetics is about. Regarding what researchers in this field do, Berreby writes: "C.H. Waddington’s founding definition of epigenetics—transgenerational inheritance that isn’t dependent on DNA sequence—doesn’t fit what they do......Szyf thinks questions of heritability narrowly spotlight a single epigenetic time scale (what happens between generations), while methylation and demethylation occur at time scales ranging from seconds to hours (supporting short-term memories) to decades (supporting long-term memories), as well as generations. The emphasis on heritability is a cumbersome holdover from genetics, he says, 'because in genetics, of course, everything is heritable. Do we want epigenetics to look like genetics? Why should we?'"

                    I have since detailed how the required changes in gene expression occur but the details are not discussed. One antagonist continues to deny there is sufficient evidence of transgenerational epigenetic inheritance to dispense with the mutations theory. Others think that auditory and visual input directly activate
                    "the physiological and genetic mechanisms of ... behavioral transition[s], which include large scale changes in hormonal activity, metabolism, flight ability, circadian rhythms, sensory perception and processing, neural architecture, learning ability, memory and gene expression." In this group, the idiot Moonbat poses ridiculous questions that show he knows nothing about the topic and that he has not read any of my published works.

                    All others need to do is what you have done. Tell me
                    what's missing from my model. But what if it's not! What if, for example, as I concluded: "Olfaction and odor receptors provide a clear evolutionary trail that can be followed from unicellular organisms to insects to humans."

                    DL: Shouldn't we expect that there must be an evolutionary trail from the common ancestor of all life, not only for olfaction and odor receptors but for all the other processes necessary for survival?

                    Thanks again for your interest and pertinent comments and questions. You exemplify how science progresses. Moonbat exemplifies how antagonist retard scientific progress by inferring that I have a communications disorder when all that's required is to read what I've published.
                     
                    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: M <moontopia@...>
                    To: Dr Smellgood <jvkohl@...>; Psychiatry Research <psychiatry-research@yahoogroups.com>
                    Cc: gmsizemore2@...; SEATTLE_ROBOTICS@yahoogroups.com; INTRODUCTORY-MACHINE-PSYCHOLOGY@yahoogroups.com; PSYCHOROBOTICS@yahoogroups.com; Robert Karl Stonjek <stonjek@...>; MITOCW <mit-opencourseware-discussion@yahoogroups.com>; Logic-Language-Learning@yahoogroups.com; Astropsychology <astropsychology@yahoogroups.com>
                    Sent: Sun, February 10, 2013 5:23:34 PM
                    Subject: [psychiatry-research] Communication Disorders and Cellular Machinery

                     
                    
                    NOBODY on PR questioned your ability to communicate with other test tune specialists. Otherwise, you would not be published in their peer-reviewed journals.
                     
                    This is a PR list. What everyone here has in common is an interest in behaviour. Few are chemists.
                     
                    I am pleading for one person to come forward and say they understand what you have communicated with respect to the following specifics:
                     
                    (1) In what specific way does JVK make an ORIGINAL contribution as a first discoverer in cell chemistry, as Watson and Crick were first to discover the double-helix structure of DNA for which they received a Nobel Prize? For example, did he discover chemical X or Y?
                     
                    (2) Has he proven that this original and uniquely-his discovery dwarfs the importance of DNA as a master control in the cell (in effect a biocomputer)? What are the specific details of that proof of master controller as someone might point to wrinkled and smooth peas in a test of Mendelian-DNA genetics?
                     
                    Is there anything about my two questions which is not clear to everybody on PR? 
                     
                    If we get these two clear and specific answers here I see no reason why Marc A at Harvard would not publish due recognition in his journal.
                     
                    Moonbat
                     
                    I have posted in complete sincerity that if JVK has made a uniquely-his discovery in the chemistry of the cell which dwarfs the importance of DNA as a master controller he deserves a Nobel Prize. As I understand it, DNA is generally accepted as the master controller which, for example, explains at a chemical level the wrinkled and smooth peas and other unit factors in the experiments of Mendel. It took almost a century for science to work out the genotype chemical details behind those Mendel-observed phenotypes to give the Mendelian-DNA model which is standard in the teaching of introductory psychology .... pending JVK correction?
                     
                    So why would JVK not deserve a Nobel Prize for being the first to discover the proof of a chemical control system which dwarfs in importance the Mendelian-DNA model of master controller?
                     
                    It would be unfortunate if we who make a living in talk-therapy and related activities were to discredit him because he is afflicted with a communication disorder.
                    ----- Original Message -----
                    Sent: Saturday, February 02, 2013 5:04 PM
                    Subject: Re: [psychiatry-research] Mutation in humans? Adaptive evolution in mice?

                     
                    What makes you think I have not learned how to communicate my knowledge?
                  • charles beck
                    David Thank you for your dedication in performing this professional service. Your avoiding ad hominem remarks is much appreciated. Charles From:
                    Message 9 of 15 , Feb 11, 2013
                    • 0 Attachment

                      David

                      Thank you for your dedication in performing this professional service. Your avoiding ad hominem remarks is much appreciated.

                      Charles

                       

                      From: evolutionary-psychology@yahoogroups.com [mailto:evolutionary-psychology@yahoogroups.com] On Behalf Of David Leake
                      Sent: Monday, February 11, 2013 1:55 AM
                      To: human-ethology@yahoogroups.com; evolutionary-psychology@yahoogroups.com
                      Subject: [evol-psych] Re: Adaptive evolution via the nutrient-dependent pheromone-controlled microRNA/messenger RNA balance

                       




                      James, I followed the links you provided, my comments are in red below.....David

                      -----Original Message-----
                      From: james kohl <jvkohl@...>
                      Sent: Sun, Feb 10, 2013 1:36 pm
                      Subject: Re: [psychiatry-research] Communication Disorders and Cellular Machinery

                       

                      A correspondent noted that my model seems to be in tune with evo-devo (evolution of development) in the context of changes in regulatory processes, epigenesis, and the role of miRNA and mRNA etc, but that evo-devo relies on mutations to explain adaptive evolution.

                      After correctly summarizing its content, he asked that I specify how my model of nutrient-dependent pheromone-controlled adaptive evolution leads to heritable DNA changes. He suggested that it would be useful if I clearly described the adaptive evolution of a single behavior or how age polyethism in Apis mellifera evolved sans mutations.


                      JK: Excellent suggestion. In the diagram of my model, you can "picture" what happens, because there is no stage of life in mammals where epigenesis and epistasis are not epigenetically effected by food odors and pheromones.

                      Correspondent: "You could just take one of the well-studied mechanisms of age polyethism and explain how your model would apply. Or any other honeybee behavior you want, that's just an example....."

                      JK: This was already done. As detailed in From fertilization to adult sexual behavior, the mammalian model was extended to invertebrates "from egg to adult" in Organizational and activational effects of hormones on insect behavior. The beauty of your suggestion to apply my model to well-studied mechanisms of age polyethism lies in the context of Honey bees as a model for understanding mechanisms of life history transitions. "In this review we discuss the physiological and genetic mechanisms of this behavioral transition, which include large scale changes in hormonal activity, metabolism, flight ability, circadian rhythms, sensory perception and processing, neural architecture, learning ability, memory and gene expression."  

                       

                      DL: The article linked certainly has a wealth of detail on changes in gene expression that underlie age polyethism in bees. However doing a search within the article for "evol" (to find "evolve" or "evolution" etc) and "herit" (to find "inherit" or "heritable" etc) and "select" (to find terms related to selective forces) and "splic" (to find "alternative splicing/splice") all fail to locate anywhere in the article where the authors discuss how change in gene expression or anything else might be transmitted to the next generation. As the authors argue, bees are certainly a great model organism for understanding the mechanisms of life history transitions within the lifetimes of worker bees (e.g., from being nurses that can barely fly to foragers that are great fliers), but that doesn't address mechanisms of adaptive evolution. I noticed in another email you state that this article's authors "Elekonich and Robinson used my model" but for some reason they do not cite "Kohl" in this article.

                       

                      Note: No one else seems willing to enter discussion about the only existing model of adaptive evolution, which includes life history transitions and epigenetic effects on gene expression.

                      DL: Life history transitions can be understood from the evo-devo perspective as having evolved to promote the adaptation of species members to their physical and social environments by properly timing and orchestrating developmental stages, which involves epigenetic processes that are consistently and reliably passed on to offspring. However, your frequent highlighting of "epigenetic effects on gene expression" is not accompanied by further explanation of how the different gene expression is presumably transmitted to the next generation. Does your model say that epigenetic effects actually change the genes? There's some evidence that epigenetic marks might be transmitted to offspring or maybe even another generation or two, but that evidence is rare and contested (it seems rarer than the rate of potentially beneficial mutations). If epigenetic effects are at the heart of adaptive evolution, why isn't there abundant evidence of this? It should be there, because biologists can currently identify and track epigenetic methyl and acetyl marks on genes in detail.


                      You write: "...
                      but the model still does not specify how this leads to heritable DNA changes." That's another excellent point. Because it is the only model, it must explain how alternative splicings lead to heritable changes in gene expression, and it does. See in From fertilization to adult sexual behavior,: "That similar proteins perform functions in humans suggests the possibility that some human sex differences may arise from alternative splicings of otherwise identical genes." 


                      DL: I used the same search terms within this Milton Diamond article and once again found that the various epigenetic influences and alternative gene splicings described only had to do with development over the course of a lifetime.....there's nothing at all about how these lead to adaptive evolution. It's beginning to sound like one key process for adaptive evolution in your model is the "alternative splicings of otherwise identical genes." Does that mean that the solitary bees that gave rise to eusocial bees have essentially the same genes but the genes operate differently due to epigenetic marks and alternative splicings that have been acquired and passed on to successive generations?

                      Natural se
                      lection for nutrients results in nutrient-dependent sex differences in pheromones that enable sexual selection for nutrient-dependent fitness in species from microbes to man.  Berreby wrote: Research in behavioral epigenetics is seeking evidence that links experience to biochemistry to gene expression and back out again. Also: "It needs, and doesn’t yet have, at least one slam-dunk demonstration of all the links in a chain from behavior to neural activity to gene expression and back out again. How, for example, do biochemical events at a neuron’s nucleus affect the synaptic signaling between neurons that is the basis for all behavior?" 

                       

                      DL: Although you use the Berreby article to support your model, the article actually seems to oppose it in the way it clarifies what "modern" epigenetics is about. Regarding what researchers in this field do, Berreby writes: "C.H. Waddington’s founding definition of epigenetics—transgenerational inheritance that isn’t dependent on DNA sequence—doesn’t fit what they do......Szyf thinks questions of heritability narrowly spotlight a single epigenetic time scale (what happens between generations), while methylation and demethylation occur at time scales ranging from seconds to hours (supporting short-term memories) to decades (supporting long-term memories), as well as generations. The emphasis on heritability is a cumbersome holdover from genetics, he says, 'because in genetics, of course, everything is heritable. Do we want epigenetics to look like genetics? Why should we?'"


                      I have since detailed how the required changes in gene expression occur but the details are not discussed. One antagonist continues to deny there is sufficient evidence of transgenerational epigenetic inheritance to dispense with the mutations theory. Others think that auditory and visual input directly activate
                      "the physiological and genetic mechanisms of ... behavioral transition[s], which include large scale changes in hormonal activity, metabolism, flight ability, circadian rhythms, sensory perception and processing, neural architecture, learning ability, memory and gene expression." In this group, the idiot Moonbat poses ridiculous questions that show he knows nothing about the topic and that he has not read any of my published works.

                      All others need to do is what you have done. Tell me
                      what's missing from my model. But what if it's not! What if, for example, as I concluded: "Olfaction and odor receptors provide a clear evolutionary trail that can be followed from unicellular organisms to insects to humans."

                       

                      DL: Shouldn't we expect that there must be an evolutionary trail from the common ancestor of all life, not only for olfaction and odor receptors but for all the other processes necessary for survival?

                      Thanks again for your interest and pertinent comments and questions. You exemplify how science progresses. Moonbat exemplifies how antagonist retard scientific progress by inferring that I have a communications disorder when all that's required is to read what I've published.

                       

                      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.

                       

                    • David Leake
                      Thanks Charles! I have only occasionally glanced at Mr Kohl s posts and there are certainly plenty of ad hominem remarks from both sides. His explanations seem
                      Message 10 of 15 , Feb 11, 2013
                      • 0 Attachment
                        Thanks Charles! I have only occasionally glanced at Mr Kohl's posts and there are certainly plenty of ad hominem remarks from both sides. His explanations seem hard for everyone else to understand, my "dedication" is aimed at trying to see if there's something really there, otherwise go back to deleting his posts! 

                        David

                        -----Original Message-----
                        From: charles beck <cbeck@...>
                        To: evolutionary-psychology <evolutionary-psychology@yahoogroups.com>
                        Sent: Mon, Feb 11, 2013 1:49 pm
                        Subject: RE: [evol-psych] Re: Adaptive evolution via the nutrient-dependent pheromone-controlled microRNA/messenger RNA balance

                         
                        David
                        Thank you for your dedication in performing this professional service. Your avoiding ad hominem remarks is much appreciated.
                        Charles
                         
                        From: evolutionary-psychology@yahoogroups.com [mailto:evolutionary-psychology@yahoogroups.com] On Behalf Of David Leake
                        Sent: Monday, February 11, 2013 1:55 AM
                        To: human-ethology@yahoogroups.com; evolutionary-psychology@yahoogroups.com
                        Subject: [evol-psych] Re: Adaptive evolution via the nutrient-dependent pheromone-controlled microRNA/messenger RNA balance
                         



                        James, I followed the links you provided, my comments are in red below.....David
                        -----Original Message-----
                        From: james kohl <jvkohl@...>
                        Sent: Sun, Feb 10, 2013 1:36 pm
                        Subject: Re: [psychiatry-research] Communication Disorders and Cellular Machinery
                         
                        A correspondent noted that my model seems to be in tune with evo-devo (evolution of development) in the context of changes in regulatory processes, epigenesis, and the role of miRNA and mRNA etc, but that evo-devo relies on mutations to explain adaptive evolution.

                        After correctly summarizing its content, he asked that I specify how my model of nutrient-dependent pheromone-controlled adaptive evolution leads to heritable DNA changes. He suggested that it would be useful if I clearly described the adaptive evolution of a single behavior or how age polyethism in Apis mellifera evolved sans mutations.

                        JK: Excellent suggestion. In the diagram of my model, you can "picture" what happens, because there is no stage of life in mammals where epigenesis and epistasis are not epigenetically effected by food odors and pheromones.

                        Correspondent: "You could just take one of the well-studied mechanisms of age polyethism and explain how your model would apply. Or any other honeybee behavior you want, that's just an example....."

                        JK: This was already done. As detailed in From fertilization to adult sexual behavior, the mammalian model was extended to invertebrates "from egg to adult" in Organizational and activational effects of hormones on insect behavior. The beauty of your suggestion to apply my model to well-studied mechanisms of age polyethism lies in the context of Honey bees as a model for understanding mechanisms of life history transitions. "In this review we discuss the physiological and genetic mechanisms of this behavioral transition, which include large scale changes in hormonal activity, metabolism, flight ability, circadian rhythms, sensory perception and processing, neural architecture, learning ability, memory and gene expression."  
                         
                        DL: The article linked certainly has a wealth of detail on changes in gene expression that underlie age polyethism in bees. However doing a search within the article for "evol" (to find "evolve" or "evolution" etc) and "herit" (to find "inherit" or "heritable" etc) and "select" (to find terms related to selective forces) and "splic" (to find "alternative splicing/splice") all fail to locate anywhere in the article where the authors discuss how change in gene expression or anything else might be transmitted to the next generation. As the authors argue, bees are certainly a great model organism for understanding the mechanisms of life history transitions within the lifetimes of worker bees (e.g., from being nurses that can barely fly to foragers that are great fliers), but that doesn't address mechanisms of adaptive evolution. I noticed in another email you state that this article's authors "Elekonich and Robinson used my model" but for some reason they do not cite "Kohl" in this article.
                         
                        Note: No one else seems willing to enter discussion about the only existing model of adaptive evolution, which includes life history transitions and epigenetic effects on gene expression.
                        DL: Life history transitions can be understood from the evo-devo perspective as having evolved to promote the adaptation of species members to their physical and social environments by properly timing and orchestrating developmental stages, which involves epigenetic processes that are consistently and reliably passed on to offspring. However, your frequent highlighting of "epigenetic effects on gene expression" is not accompanied by further explanation of how the different gene expression is presumably transmitted to the next generation. Does your model say that epigenetic effects actually change the genes? There's some evidence that epigenetic marks might be transmitted to offspring or maybe even another generation or two, but that evidence is rare and contested (it seems rarer than the rate of potentially beneficial mutations). If epigenetic effects are at the heart of adaptive evolution, why isn't there abundant evidence of this? It should be there, because biologists can currently identify and track epigenetic methyl and acetyl marks on genes in detail.

                        You write: "...
                        but the model still does not specify how this leads to heritable DNA changes." That's another excellent point. Because it is the only model, it must explain how alternative splicings lead to heritable changes in gene expression, and it does. See in From fertilization to adult sexual behavior,: "That similar proteins perform functions in humans suggests the possibility that some human sex differences may arise from alternative splicings of otherwise identical genes." 

                        DL: I used the same search terms within this Milton Diamond article and once again found that the various epigenetic influences and alternative gene splicings described only had to do with development over the course of a lifetime.....there's nothing at all about how these lead to adaptive evolution. It's beginning to sound like one key process for adaptive evolution in your model is the "alternative splicings of otherwise identical genes." Does that mean that the solitary bees that gave rise to eusocial bees have essentially the same genes but the genes operate differently due to epigenetic marks and alternative splicings that have been acquired and passed on to successive generations?

                        Natural se
                        lection for nutrients results in nutrient-dependent sex differences in pheromones that enable sexual selection for nutrient-dependent fitness in species from microbes to man.  Berreby wrote: Research in behavioral epigenetics is seeking evidence that links experience to biochemistry to gene expression and back out again. Also: "It needs, and doesn’t yet have, at least one slam-dunk demonstration of all the links in a chain from behavior to neural activity to gene expression and back out again. How, for example, do biochemical events at a neuron’s nucleus affect the synaptic signaling between neurons that is the basis for all behavior?" 
                         
                        DL: Although you use the Berreby article to support your model, the article actually seems to oppose it in the way it clarifies what "modern" epigenetics is about. Regarding what researchers in this field do, Berreby writes: "C.H. Waddington’s founding definition of epigenetics—transgenerational inheritance that isn’t dependent on DNA sequence—doesn’t fit what they do......Szyf thinks questions of heritability narrowly spotlight a single epigenetic time scale (what happens between generations), while methylation and demethylation occur at time scales ranging from seconds to hours (supporting short-term memories) to decades (supporting long-term memories), as well as generations. The emphasis on heritability is a cumbersome holdover from genetics, he says, 'because in genetics, of course, everything is heritable. Do we want epigenetics to look like genetics? Why should we?'"

                        I have since detailed how the required changes in gene expression occur but the details are not discussed. One antagonist continues to deny there is sufficient evidence of transgenerational epigenetic inheritance to dispense with the mutations theory. Others think that auditory and visual input directly activate
                        "the physiological and genetic mechanisms of ... behavioral transition[s], which include large scale changes in hormonal activity, metabolism, flight ability, circadian rhythms, sensory perception and processing, neural architecture, learning ability, memory and gene expression." In this group, the idiot Moonbat poses ridiculous questions that show he knows nothing about the topic and that he has not read any of my published works.

                        All others need to do is what you have done. Tell me
                        what's missing from my model. But what if it's not! What if, for example, as I concluded: "Olfaction and odor receptors provide a clear evolutionary trail that can be followed from unicellular organisms to insects to humans."
                         
                        DL: Shouldn't we expect that there must be an evolutionary trail from the common ancestor of all life, not only for olfaction and odor receptors but for all the other processes necessary for survival?

                        Thanks again for your interest and pertinent comments and questions. You exemplify how science progresses. Moonbat exemplifies how antagonist retard scientific progress by inferring that I have a communications disorder when all that's required is to read what I've published.
                         
                        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.
                         
                      • james kohl
                        From: David Leake To: human-ethology@yahoogroups.com; evolutionary-psychology@yahoogroups.com Sent: Mon, February 11, 2013 8:27:39 AM Subject: [human-ethology]
                        Message 11 of 15 , Feb 11, 2013
                        • 0 Attachment
                          From: David Leake
                          To: human-ethology@yahoogroups.com; evolutionary-psychology@yahoogroups.com
                          Sent: Mon, February 11, 2013 8:27:39 AM
                          Subject: [human-ethology] Re: Adaptive evolution via the nutrient-dependent pheromone-controlled microRNA/messenger RNA balance

                          James, I followed the links you provided, my comments are in red below.....David

                          Thanks, David. I've reformatted this to proceed as if it was an interview and avoid incongruities and unnecessary repetition. I apologize for the length and applaud you for your efforts to help me clarify this.

                          DL noted that my model seems to be in tune with evo-devo (evolution of development) in the context of changes in regulatory processes, epigenesis, and the role of miRNA and mRNA etc, but that evo-devo relies on mutations to explain adaptive evolution. After correctly summarizing its content, he asked that I specify how my model of nutrient-dependent pheromone-controlled adaptive evolution leads to heritable DNA changes. He suggested it would be useful if I clearly described how age polyethism in Apis mellifera evolved sans mutations. I noted that the adaptive evolution of age-related differentiation of behavior (i.e., polyethism) had been detailed in accord with my published works.

                          JK: In the diagram of my model, you can "picture" what happens in vertebrates. There is no stage of life in mammals where epigenesis and epistasis are not epigenetically effected by food odors and pheromones. As detailed in From fertilization to adult sexual behavior, the mammalian model of hormone-organized and hormone-activated behavior was extended to invertebrates "from egg to adult" in Organizational and activational effects of hormones on insect behavior. Extension of the mammalian model to insects now includes well-studied�mechanisms of age polyethism in the context of Honey bees as a model for understanding mechanisms of life history transitions. The link is to a review article that discusses physiological and genetic mechanisms of hormone-organized and hormone-activated behavioral transitions that include “…large scale changes in hormonal activity, metabolism, flight ability, circadian rhythms, sensory perception and processing, neural architecture, learning ability, memory and gene expression." Gene expression in hormone-secreting nerve cells of brain tissue is the key indicator of cause and effect in my model.

                          DL: The article linked certainly has a wealth of detail on changes in gene expression that underlie age polyethism in bees. However doing a search within the article for "evol" (to find "evolve" or "evolution" etc) and "herit" (to find "inherit" or "heritable" etc) and "select" (to find terms related to selective forces) and "splic" (to find "alternative splicing/splice") all fail to locate anywhere in the article where the authors discuss how change in gene expression or anything else might be transmitted to the next generation. As the authors argue, bees are certainly a great model organism for understanding the mechanisms of life history transitions within the lifetimes of worker bees (e.g., from being nurses that can barely fly to foragers that are great fliers), but that doesn't address mechanisms of adaptive evolution.�I noticed in another email you state that this article's authors "Elekonich and Robinson used my model" but for some reason they do not cite "Kohl" in this article.

                          JK: Diamond, Binstock, and Kohl (1996) “From fertilization to adult sexual behavior” is consecutively cited twice in their “Background and history section” as Diamond et al., (1996)

                          1) "The development of species-typical and sex-specific adult behaviors in vertebrate animals is influenced by gonadal steroid hormones, non-gonadal hormones, and non-hormonal factors working on the underlying neural circuitry (reviewed in Diamond et al., 1996; Kawata, 1995; Schlinger, 1998)."

                          2) “Effects of hormones on brain and behavior occur through three mechanisms: (1) behaviors both organized and activated by hormones, (2) behaviors only organized by hormones, and (3) behaviors only activated by hormones (reviewed in Arnold and Breedlove, 1985; Diamond et al., 1996)." Simply put, Gene Robinson et al., have since offered us a model organism in a series of articles that link nutrient-dependent pheromone-controlled development of behavior in all species.

                          DL: Life history transitions can be understood from the evo-devo perspective as having evolved to promote the adaptation of species members to their physical and social environments by properly timing and orchestrating developmental stages, which involves epigenetic processes that are consistently and reliably passed on to offspring. However, your frequent highlighting of "epigenetic effects on�gene expression" is not accompanied by further explanation of how the different gene expression is presumably transmitted to the next generation. Does your model say that epigenetic effects actually change the genes? There's some evidence that epigenetic marks might be transmitted to offspring or maybe even another generation or two, but that evidence is rare and contested (it seems rarer than the rate of potentially beneficial mutations). If epigenetic effects are at the heart of adaptive evolution, why isn't there abundant evidence of this? It should be there, because biologists can currently identify and track epigenetic methyl and acetyl marks on genes in detail.

                          JK: �Kohl (2012) incorporates the abundant evidence in species from microbes to man. For example, in Diamond, Binstock, and Kohl (1996), we indicated that alternative splicing was responsible for genetically predisposed nutrient-dependent pheromone-controlled Sexual Selection in our section on Molecular Epigenetics. This extends Natural Selection for nutrients to Sexual Selection for pheromones, as follows: “Yet another kind of epigenetic imprinting occurs in species as diverse as yeast, Drosophila, mice, and humans and is based upon small DNA-binding proteins called “chromo domain” proteins, e.g., polycomb. These proteins affect chromatin structure, often in telomeric regions, and thereby affect transcription and silencing of various genes (Saunders, Chue, Goebl, Craig, Clark, Powers, Eissenberg, Elgin, Rothfield, and Earnshaw, 1993; Singh, Miller, Pearce, Kothary, Burton, Paro, James, and Gaunt, 1991; Trofatter, Long, Murrell, Stotler, Gusella, and Buckler, 1995). Small intranuclear proteins also participate in generating alternative splicing techniques of pre-mRNA and, by this mechanism, contribute to sexual differentiation in at least two species, Drosophila melanogaster and Caenorhabditis elegans (Adler and Hajduk, 1994; de Bono, Zarkower, and Hodgkin, 1995; Ge, Zuo, and Manley, 1991; Green, 1991; Parkhurst and Meneely, 1994; Wilkins, 1995; Wolfner, 1988). That similar proteins perform functions in humans suggests the possibility that some human sex differences may arise from alternative splicings of otherwise identical genes.”

                          The small intranuclear proteins are now called microRNAs, and more than 2000 of them have been indentified. It is the effects of the microRNAs on pre-RNA and sex differences, which appear to “…arise from alternative splicings of otherwise identical genes” that links nutrient-dependent pheromone-controlled adaptive evolution from the advent of sexual reproduction in yeasts to human sexual reproduction sans mutations theory.

                          This is where evolutionary theory and mutations theory has failed. There is no indication from theory of how sex differences adaptively evolved. Perhaps I did not address this thoroughly when I indicated that my model “…must explain how alternative splicings lead to heritable changes in gene expression, and it does. See in From fertilization to adult sexual behavior,: "That similar proteins perform functions in humans suggests the possibility that some human sex differences may arise from alternative splicings of otherwise identical genes."� If an alternative suggestion for the advent of sexual reproduction (and sexual orientation) has been proposed by evolutionary theorists, I haven't learned of it.

                          DL: I used the same search terms within this Milton Diamond article and once again found that the various epigenetic influences and alternative gene splicings described only had to do with development over the course of a lifetime.....there's nothing at all about how these lead to adaptive evolution.

                          JK: That review article is 16 years old; there are now more than 10,000 papers published on microRNAs, starting in 2002. Nevertheless, we clearly indicated it is the nutrient-dependent development of the sex differences over the course of a lifetime that leads to nutrient-dependent pheromone-controlled reproduction and transgenerational genetic predispositions in offspring, which are the result of transgenerational epigenetic inheritance of genotypes that develop into activity-dependent stochastically determined phenotypes via alternative splicings. For comparison, there is no indication from evolutionary theory of how mutations are selected that lead to sexual selection or to benefits in offspring.

                          DL: It's beginning to sound like one key process for adaptive evolution in your model is the "alternative splicings of otherwise identical genes." Does that mean that the solitary bees that gave rise to eusocial bees have essentially the same genes but the genes operate differently due to epigenetic marks and alternative splicings that have been acquired and passed on to successive generations?

                          JK: Yes! Thanks for posing that as a question, since you obviously knew the answer. I wrote: Natural selection for nutrients results in nutrient-dependent sex differences in pheromones that enable sexual selection for nutrient-dependent fitness in species from microbes to man.� Berreby wrote: Research in behavioral epigenetics is seeking evidence that links experience to biochemistry to gene expression and back out again. Also: "It needs, and doesn’t yet have, at least one slam-dunk demonstration of all the links in a chain from behavior to neural activity to gene expression and back out again. How, for example, do biochemical events at a neuron’s nucleus affect the synaptic signaling between neurons that is the basis for all behavior?" I'll make sense of this after I address your next comments and question.

                          DL: Although you use the Berreby article to support your model, the article actually seems to oppose it in the way it clarifies what "modern" epigenetics is about. Regarding what researchers in this field do, Berreby writes: "C.H. Waddington’s founding definition of epigenetics—transgenerational inheritance that isn’t dependent on DNA sequence—doesn’t fit what they do......Szyf thinks questions of heritability narrowly spotlight a single epigenetic time scale (what happens between generations), while methylation and demethylation occur at time scales ranging from seconds to hours (supporting short-term memories) to decades (supporting long-term memories), as well as generations. The emphasis on heritability is a cumbersome holdover from genetics, he says, 'because in genetics, of course, everything is heritable. Do we want epigenetics to look like genetics? Why should we?'"

                          JK: What I want is for people to examine gene -x- environment interactions and realize that adaptive evolution is unequivocally dependent on genetically predisposed nutrient uptake/intake and the metabolism of nutrients to species-specific pheromones, which is the only way the required reciprocity is established that links genes to behavior and back across species and transgenerationally – via the epigenetic effects of nutrients on Natural Selection and the epigenetic effects of pheromones on Sexual Selection. The epigenetic effects in vertebrates and invertebrates are hormone-organized and hormone-activated by food odors and pheromones.

                          Berreby asks: “How, for example, do biochemical events at a neuron’s nucleus affect the synaptic signaling between neurons that is the basis for all behavior?"�In mammals, it is clear that MicroRNA-182 Regulates Amygdala-Dependent Memory Formation and that De novo mRNA synthesis is required for both consolidation and reconsolidation of fear memories in the amygdala. It is also clear that the molecular mechanisms for learning and memory are nutrient-dependent and pheromone-controlled in species where the microRNA / messenger RNA balance determines survival (e.g., epistasis). Simply put, if organisms cannot learn the difference between a food source and a conspecific, their species is not going to survive.

                          I wrote: I have since detailed how the required changes in gene expression occur but the details are not discussed. One antagonist continues to deny there is sufficient evidence of transgenerational epigenetic inheritance, and that we can therefore dispense with the mutations theory. Others think that auditory and visual input directly activate "the physiological and genetic mechanisms of ... behavioral transition[s], which include large scale changes in hormonal activity, metabolism, flight ability, circadian rhythms, sensory perception and processing, neural architecture, learning ability, memory and gene expression." In the Psychiatry Research group, Moonbat, poses ridiculous questions that show he knows nothing about the topic and that he has not read any of my published works. All others need to do is what you have done. Tell me what's missing from my model. But what if it's not! What if, for example, as I concluded: "Olfaction and odor receptors provide a clear evolutionary trail that can be followed from unicellular organisms to insects to humans."

                          DL: Shouldn't we expect that there must be an evolutionary trail from the common ancestor of all life, not only for olfaction and odor receptors but for all the other processes necessary for survival?

                          JK: Nutrients are required for individual survival, and nutrient-dependent pheromone production is required for reproduction and survival of species; for diversification of species via ecological and social niche construction, and for adaptively evolved intelligence via neurogenic and socio-cognitive niche construction. The evolutionary trail incorporates non-essential aspects of survival (e.g., visual input) because other sensory input is associated with the epigenetic effects of food odors and pheromones. The associations are beneficial or species would not have incorporated them during adaptive evolution. However, in cave fish, when the visual association is no longer required, eye regression is the clearest indicator of the fact that visual input is not required for species survival in any species from microbes to man. Need I mention anything further about why “The Blind Watchmaker” theory of mutations and evolution seems ridiculous given the continuum of olfactory/pheromonal involvement but no continuum that includes eyes (or ears)?

                          Thanks again for facilitating answers to intelligent questions so others who are interested in comparing biological facts to theory might be encouraged to also ask intelligent questions. Clarence “Sonny” Williams will no doubt continue to advise others not to read my works, but to read others works instead. Jay Feierman will continue to ignore my posts and block many of my responses on the ISHE human ethology group. John Angel and Glen Sizemore will do their best to berate me and promote animal training without acknowledging any current perspective on what is neuroscientifically known about classical conditioning compared to operant conditioining. And Moonbat will always be the anonymous fool. These are not ad hominem attacks; they are a response to their ad hominem attacks.

                          It will be interesting to see if anyone else asks questions about my model or the content of my published works in the context of scientific progress and epigenetic influences on the socioaffective nature of evolved behaviors, so that we can move forward from here. In addition, I look forward to any more questions you might have for me, and hope you will keep them coming.


                          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.


                          -----Original Message-----
                          From: james kohl <jvkohl@...>
                          Sent: Sun, Feb 10, 2013 1:36 pm
                          Subject: Re: [psychiatry-research] Communication Disorders and Cellular Machinery

                          A correspondent noted that my model seems to be in tune with evo-devo (evolution of development) in the context of changes in regulatory processes, epigenesis, and the role of miRNA and mRNA etc, but that evo-devo relies on mutations to explain adaptive evolution.

                          After correctly summarizing its content, he asked that I specify how my model of nutrient-dependent pheromone-controlled adaptive evolution leads to heritable DNA changes. He suggested that it would be useful if I clearly described the adaptive evolution of a single behavior or how age polyethism in
                          Apis mellifera evolved sans mutations.

                          JK: Excellent suggestion. In the diagram of my model, you can "picture" what happens, because there is no stage of life in mammals where epigenesis and epistasis are not epigenetically effected by food odors and pheromones.


                          Correspondent: "You could just take one of�the well-studied�mechanisms of age polyethism and explain how your model would apply. Or any other honeybee behavior you want, that's just an example....."

                          JK: This was already done. As detailed in From fertilization to adult sexual behavior, the mammalian model was extended to invertebrates "from egg to adult" in Organizational and activational effects of hormones on insect behavior. The beauty of your suggestion to apply my model to
                          well-studied�mechanisms of age polyethism lies in the context of Honey bees as a model for understanding mechanisms of life history transitions. "In this review we discuss the physiological and genetic mechanisms of this behavioral transition, which include large scale changes in hormonal activity, metabolism, flight ability, circadian rhythms, sensory perception and processing, neural architecture, learning ability, memory and gene expression."

                          DL: The article linked certainly has a wealth of detail on changes in gene expression that underlie age polyethism in bees. However doing a search within the article for "evol" (to find "evolve" or "evolution" etc) and "herit" (to find "inherit" or "heritable" etc) and "select" (to find terms related to selective forces) and "splic" (to find "alternative splicing/splice") all fail to locate anywhere in the article where the authors discuss how change in gene expression or anything else might be transmitted to the next generation. As the authors argue, bees are certainly a great model organism for understanding the mechanisms of life history transitions within the lifetimes of worker bees (e.g., from being nurses that can barely fly to foragers that are great fliers), but that doesn't address mechanisms of adaptive evolution.�I noticed in another email you state that this article's authors "Elekonich and Robinson used my model" but for some reason they do not cite "Kohl" in this article.

                          Note: No one else seems willing to enter discussion about the only existing model of adaptive evolution, which includes life history transitions and epigenetic effects on gene expression.

                          DL: Life history transitions can be understood from the evo-devo perspective as having evolved to promote the adaptation of species members to their physical and social environments by properly timing and orchestrating developmental stages, which involves epigenetic processes that are consistently and reliably passed on to offspring. However, your frequent highlighting of "epigenetic effects on�gene expression" is not accompanied by further explanation of how the different gene expression is presumably transmitted to the next generation. Does your model say that epigenetic effects actually change the genes? There's some evidence that epigenetic marks might be transmitted to offspring or maybe even another generation or two, but that evidence is rare and contested (it seems rarer than the rate of potentially beneficial mutations). If epigenetic effects are at the heart of adaptive evolution, why isn't there abundant evidence of this? It should be there, because biologists can currently identify and track epigenetic methyl and acetyl marks on genes in detail.

                          You write: "...
                          but the model still does not specify how this leads to heritable DNA changes." That's another excellent point. Because it is the only model, it must explain how alternative splicings lead to heritable changes in gene expression, and it does. See in From fertilization to adult sexual behavior,: "That similar proteins perform functions in humans suggests the possibility that some human sex differences may arise from alternative splicings of otherwise identical genes."�

                          DL: I used the same search terms within this Milton Diamond article and once again found that the various epigenetic influences and alternative gene splicings described only had to do with development over the course of a lifetime.....there's nothing at all about how these lead to adaptive evolution. It's beginning to sound like one key process for adaptive evolution in your model is the "alternative splicings of otherwise identical genes." Does that mean that the solitary bees that gave rise to eusocial bees have essentially the same genes but the genes operate differently due to epigenetic marks and alternative splicings that have been acquired and passed on to successive generations?

                          Natural selection for nutrients results in nutrient-dependent sex differences in pheromones that enable sexual selection for nutrient-dependent fitness in species from microbes to man.� Berreby wrote: Research in behavioral epigenetics is seeking evidence that links experience to biochemistry to gene expression and back out again. Also: "
                          It needs, and doesn’t yet have, at least one slam-dunk demonstration of all the links in a chain from behavior to neural activity to gene expression and back out again. How, for example, do biochemical events at a neuron’s nucleus affect the synaptic signaling between neurons that is the basis for all behavior?"�

                          DL: Although you use the Berreby article to support your model, the article actually seems to oppose it in the way it clarifies what "modern" epigenetics is about. Regarding what researchers in this field do, Berreby writes: "C.H. Waddington’s founding definition of epigenetics—transgenerational inheritance that isn’t dependent on DNA sequence—doesn’t fit what they do......Szyf thinks questions of heritability narrowly spotlight a single epigenetic time scale (what happens between generations), while methylation and demethylation occur at time scales ranging from seconds to hours (supporting short-term memories) to decades (supporting long-term memories), as well as generations. The emphasis on heritability is a cumbersome holdover from genetics, he says, 'because in genetics, of course, everything is heritable. Do we want epigenetics to look like genetics? Why should we?'"

                          I have since detailed how the required changes in gene expression occur but the details are not discussed. One antagonist continues to deny there is sufficient evidence of transgenerational epigenetic inheritance to dispense with the mutations theory. Others think that auditory and visual input directly activate
                          "the physiological and genetic mechanisms of ... behavioral transition[s], which include large scale changes in hormonal activity, metabolism, flight ability, circadian rhythms, sensory perception and processing, neural architecture, learning ability, memory and gene expression." In this group, the idiot Moonbat poses ridiculous questions that show he knows nothing about the topic and that he has not read any of my published works.

                          All others need to do is what you have done. Tell me what's missing from my model. But what if it's not! What if, for example, as I concluded: "Olfaction and odor receptors provide a clear evolutionary trail that can be followed from unicellular organisms to insects to humans."

                          DL: Shouldn't we expect that there must be an evolutionary trail from the common ancestor of all life, not only for olfaction and odor receptors but for all the other processes necessary for survival?

                          Thanks again for your interest and pertinent comments and questions. You exemplify how science progresses. Moonbat exemplifies how antagonist retard scientific progress by inferring that I have a communications disorder when all that's required is to read what I've published.
                          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: M <moontopia@...>
                          To: Dr Smellgood <jvkohl@...>; Psychiatry Research <psychiatry-research@yahoogroups.com>
                          Cc: gmsizemore2@...; SEATTLE_ROBOTICS@yahoogroups.com; INTRODUCTORY-MACHINE-PSYCHOLOGY@yahoogroups.com; PSYCHOROBOTICS@yahoogroups.com; Robert Karl Stonjek <stonjek@...>; MITOCW <mit-opencourseware-discussion@yahoogroups.com>; Logic-Language-Learning@yahoogroups.com; Astropsychology <astropsychology@yahoogroups.com>
                          Sent: Sun, February 10, 2013 5:23:34 PM
                          Subject: [psychiatry-research] Communication Disorders and Cellular Machinery

                          
                          NOBODY on PR questioned your ability to communicate with other test tune specialists. Otherwise, you would not be published in their peer-reviewed journals.
                          This is a PR list. What everyone here has in common is an interest in behaviour. Few are chemists.
                          I�am pleading for�one person�to come forward and say they understand what you have communicated with respect to the following specifics:
                          (1) In what specific�way does JVK make an ORIGINAL contribution as a first�discoverer in cell chemistry, as Watson and Crick were first to�discover the double-helix structure of DNA for which they received a Nobel Prize? For example, did he discover chemical X or Y?
                          (2) Has he proven that this original and uniquely-his discovery dwarfs the importance of DNA as a master control in the cell (in effect a biocomputer)? What are the specific details of that proof of master controller as someone might point to wrinkled and smooth peas in a test of Mendelian-DNA genetics?
                          Is there anything about my two questions which is not clear to everybody on�PR?�
                          If we get these two clear and specific�answers here I see no reason why Marc A at Harvard would not publish due recognition in his journal.
                          Moonbat
                          I have posted in complete sincerity that if JVK has made a uniquely-his discovery in the chemistry of the cell which dwarfs the importance of DNA as a master controller he deserves a Nobel Prize. As I understand it, DNA is generally accepted as the master controller which, for example, explains at a chemical level the wrinkled and smooth peas and other unit factors in the experiments of Mendel.�It took almost a century for science to work out the genotype�chemical details behind those Mendel-observed phenotypes to give the Mendelian-DNA model which is standard in the teaching of introductory psychology .... pending JVK correction?
                          So why would JVK not deserve a Nobel Prize for being the first to discover the�proof of�a chemical control system which dwarfs in importance the�Mendelian-DNA model of master controller?
                          It would be unfortunate if we who make a living in talk-therapy and related activities were to discredit him because he is afflicted with a communication disorder.
                          ----- Original Message -----
                          Sent: Saturday, February 02, 2013 5:04 PM
                          Subject: Re: [psychiatry-research] Mutation in humans? Adaptive evolution in mice?

                          What makes you think I have not learned how to communicate my knowledge?
                        • james kohl
                          I think we have seen that the reason for the ad hominem remarks is that they help others avoid discussion of the biological facts. We now see what happens when
                          Message 12 of 15 , Feb 11, 2013
                          • 0 Attachment
                            I think we have seen that the reason for the ad hominem remarks is that they help others avoid discussion of the biological facts. We now see what happens when someone who is more familiar with the basic principles of biology and levels of biological organization required to link sensory input directly to genes and behavior and back enters discussion of the model and model organism that does so.
                             
                            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: charles beck <cbeck@...>
                            To: evolutionary-psychology@yahoogroups.com
                            Sent: Mon, February 11, 2013 6:49:44 PM
                            Subject: RE: [evol-psych] Re: Adaptive evolution via the nutrient-dependent pheromone-controlled microRNA/messenger RNA balance

                             

                            David

                            Thank you for your dedication in performing this professional service. Your avoiding ad hominem remarks is much appreciated.

                            Charles

                             

                            From: evolutionary-psychology@yahoogroups.com [mailto:evolutionary-psychology@yahoogroups.com] On Behalf Of David Leake
                            Sent: Monday, February 11, 2013 1:55 AM
                            To: human-ethology@yahoogroups.com; evolutionary-psychology@yahoogroups.com
                            Subject: [evol-psych] Re: Adaptive evolution via the nutrient-dependent pheromone-controlled microRNA/messenger RNA balance

                             




                            James, I followed the links you provided, my comments are in red below.....David

                            -----Original Message-----
                            From: james kohl <jvkohl@...>
                            Sent: Sun, Feb 10, 2013 1:36 pm
                            Subject: Re: [psychiatry-research] Communication Disorders and Cellular Machinery

                             

                            A correspondent noted that my model seems to be in tune with evo-devo (evolution of development) in the context of changes in regulatory processes, epigenesis, and the role of miRNA and mRNA etc, but that evo-devo relies on mutations to explain adaptive evolution.

                            After correctly summarizing its content, he asked that I specify how my model of nutrient-dependent pheromone-controlled adaptive evolution leads to heritable DNA changes. He suggested that it would be useful if I clearly described the adaptive evolution of a single behavior or how age polyethism in Apis mellifera evolved sans mutations.


                            JK: Excellent suggestion. In the diagram of my model, you can "picture" what happens, because there is no stage of life in mammals where epigenesis and epistasis are not epigenetically effected by food odors and pheromones.

                            Correspondent: "You could just take one of the well-studied mechanisms of age polyethism and explain how your model would apply. Or any other honeybee behavior you want, that's just an example....."

                            JK: This was already done. As detailed in From fertilization to adult sexual behavior, the mammalian model was extended to invertebrates "from egg to adult" in Organizational and activational effects of hormones on insect behavior. The beauty of your suggestion to apply my model to well-studied mechanisms of age polyethism lies in the context of Honey bees as a model for understanding mechanisms of life history transitions. "In this review we discuss the physiological and genetic mechanisms of this behavioral transition, which include large scale changes in hormonal activity, metabolism, flight ability, circadian rhythms, sensory perception and processing, neural architecture, learning ability, memory and gene expression."  

                             

                            DL: The article linked certainly has a wealth of detail on changes in gene expression that underlie age polyethism in bees. However doing a search within the article for "evol" (to find "evolve" or "evolution" etc) and "herit" (to find "inherit" or "heritable" etc) and "select" (to find terms related to selective forces) and "splic" (to find "alternative splicing/splice") all fail to locate anywhere in the article where the authors discuss how change in gene expression or anything else might be transmitted to the next generation. As the authors argue, bees are certainly a great model organism for understanding the mechanisms of life history transitions within the lifetimes of worker bees (e.g., from being nurses that can barely fly to foragers that are great fliers), but that doesn't address mechanisms of adaptive evolution. I noticed in another email you state that this article's authors "Elekonich and Robinson used my model" but for some reason they do not cite "Kohl" in this article.

                             

                            Note: No one else seems willing to enter discussion about the only existing model of adaptive evolution, which includes life history transitions and epigenetic effects on gene expression.

                            DL: Life history transitions can be understood from the evo-devo perspective as having evolved to promote the adaptation of species members to their physical and social environments by properly timing and orchestrating developmental stages, which involves epigenetic processes that are consistently and reliably passed on to offspring. However, your frequent highlighting of "epigenetic effects on gene expression" is not accompanied by further explanation of how the different gene expression is presumably transmitted to the next generation. Does your model say that epigenetic effects actually change the genes? There's some evidence that epigenetic marks might be transmitted to offspring or maybe even another generation or two, but that evidence is rare and contested (it seems rarer than the rate of potentially beneficial mutations). If epigenetic effects are at the heart of adaptive evolution, why isn't there abundant evidence of this? It should be there, because biologists can currently identify and track epigenetic methyl and acetyl marks on genes in detail.


                            You write: "...
                            but the model still does not specify how this leads to heritable DNA changes." That's another excellent point. Because it is the only model, it must explain how alternative splicings lead to heritable changes in gene expression, and it does. See in From fertilization to adult sexual behavior,: "That similar proteins perform functions in humans suggests the possibility that some human sex differences may arise from alternative splicings of otherwise identical genes." 


                            DL: I used the same search terms within this Milton Diamond article and once again found that the various epigenetic influences and alternative gene splicings described only had to do with development over the course of a lifetime.....there's nothing at all about how these lead to adaptive evolution. It's beginning to sound like one key process for adaptive evolution in your model is the "alternative splicings of otherwise identical genes." Does that mean that the solitary bees that gave rise to eusocial bees have essentially the same genes but the genes operate differently due to epigenetic marks and alternative splicings that have been acquired and passed on to successive generations?

                            Natural se
                            lection for nutrients results in nutrient-dependent sex differences in pheromones that enable sexual selection for nutrient-dependent fitness in species from microbes to man.  Berreby wrote: Research in behavioral epigenetics is seeking evidence that links experience to biochemistry to gene expression and back out again. Also: "It needs, and doesn’t yet have, at least one slam-dunk demonstration of all the links in a chain from behavior to neural activity to gene expression and back out again. How, for example, do biochemical events at a neuron’s nucleus affect the synaptic signaling between neurons that is the basis for all behavior?" 

                             

                            DL: Although you use the Berreby article to support your model, the article actually seems to oppose it in the way it clarifies what "modern" epigenetics is about. Regarding what researchers in this field do, Berreby writes: "C.H. Waddington’s founding definition of epigenetics—transgenerational inheritance that isn’t dependent on DNA sequence—doesn’t fit what they do......Szyf thinks questions of heritability narrowly spotlight a single epigenetic time scale (what happens between generations), while methylation and demethylation occur at time scales ranging from seconds to hours (supporting short-term memories) to decades (supporting long-term memories), as well as generations. The emphasis on heritability is a cumbersome holdover from genetics, he says, 'because in genetics, of course, everything is heritable. Do we want epigenetics to look like genetics? Why should we?'"


                            I have since detailed how the required changes in gene expression occur but the details are not discussed. One antagonist continues to deny there is sufficient evidence of transgenerational epigenetic inheritance to dispense with the mutations theory. Others think that auditory and visual input directly activate
                            "the physiological and genetic mechanisms of ... behavioral transition[s], which include large scale changes in hormonal activity, metabolism, flight ability, circadian rhythms, sensory perception and processing, neural architecture, learning ability, memory and gene expression." In this group, the idiot Moonbat poses ridiculous questions that show he knows nothing about the topic and that he has not read any of my published works.

                            All others need to do is what you have done. Tell me
                            what's missing from my model. But what if it's not! What if, for example, as I concluded: "Olfaction and odor receptors provide a clear evolutionary trail that can be followed from unicellular organisms to insects to humans."

                             

                            DL: Shouldn't we expect that there must be an evolutionary trail from the common ancestor of all life, not only for olfaction and odor receptors but for all the other processes necessary for survival?

                            Thanks again for your interest and pertinent comments and questions. You exemplify how science progresses. Moonbat exemplifies how antagonist retard scientific progress by inferring that I have a communications disorder when all that's required is to read what I've published.

                             

                            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.

                             

                          Your message has been successfully submitted and would be delivered to recipients shortly.