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life is cancer

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  • Anna
    Evolution of Cancer -- A 1.6 Billion-Year-Old Accident Waiting to Happen (Today s Most Popular) Posted: 21 Aug 2013 08:32 AM PDT “Tumors are a re-emergence
    Message 1 of 5 , Aug 22, 2013
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      Evolution of Cancer --"A 1.6 Billion-Year-Old Accident Waiting to Happen" (Today's Most Popular)

      Posted: 21 Aug 2013 08:32 AM PDT

       

                   60

       

      “Tumors are a re-emergence of our inner Metazoan 1.0, a throwback to an ancient world when multicellular life was simpler,” says Paul Davies of Arizona State University’s Beyond Center for Fundamental Concepts in Science . “In that sense, cancer is an accident waiting to happen.”

      A new way to look at cancer — by tracing its deep evolutionary roots to the dawn of multicellularity more than a billion years ago — has been proposed by Davies in collaboration with Charles Lineweaver of the Australian National University. If their theory is correct, it promises to transform the approach to cancer therapy, and to link the origin of cancer to the origin of life and the developmental processes of embryos. Davies and Lineweaver are both theoretical physicists and cosmologists with experience in the field of astrobiology — the search for life beyond Earth.

      “Cancer is not a random bunch of selfish rogue cells behaving badly, but a highly-efficient pre-programmed response to stress, honed by a long period of evolution,” claims Davies, director of the BEYOND Center for Fundamental Concepts in Science at ASU and principal investigator of a major research program funded by the National Cancer Institute designed to bring insights from physical science to the problem of cancer.

      They say it’s because cancer revisits tried-and-tested genetic pathways going back a billion years, to the time when loose collections of cells began cooperating in the lead-up to fully developed multicellular life. Dubbed by the authors “Metazoa 1.0,” these early assemblages fell short of the full cell and organ differentiation associated with modern multicellular organisms – like humans.

      But according to Davies and Lineweaver, the genes for the early, looser assemblages – Metazoa 1.0 – are still there, forming an efficient toolkit. Normally it is kept locked, suppressed by the machinery of later genes used for more sophisticated body plans. If something springs the lock, the ancient genes systematically roll out the many traits that make cancer such a resilient form of life – and such a formidable adversary.

      They turned to cancer research only recently, in part because of the creation at Arizona State University of the Center for the Convergence of Physical Science and Cancer Biology. The center is one of twelve established by the National Cancer Institute to encourage physical scientists to lend their insights into tackling cancer.

      The new theory challenges the orthodox view that cancer develops anew in each host by a series of chance mutational accidents. Davies and Lineweaver claim that cancer is actually an organized and systematic response to some sort of stress or physical challenge. It might be triggered by a random accident, they say, but thereafter it more or less predictably unfolds.

      Their view of cancer is outlined in the article “Exposing cancer’s deep evolutionary roots,” written by Davies (available free with registration -see below). It appears in a special issue of Physics World devoted to the physics of cancer.

      “We envisage cancer as the execution of an ancient program pre-loaded into the genomes of all cells,” says Davies, an Arizona State University Regents’ Professor in ASU’s College of Liberal Arts and Sciences. “It is rather like Windows defaulting to ‘safe mode’ after suffering an insult of some sort.” As such, he describes cancer as a throwback to an ancestral phenotype.

      The new theory predicts that as cancer progresses through more and more malignant stages, it will express genes that are more deeply conserved among multicellular organisms, and so are in some sense more ancient. Davies and Lineweaver are currently testing this prediction by comparing gene expression data from cancer biopsies with phylogenetic trees going back 1.6 billion years.

      But if this is the case, then why hasn’t evolution eliminated the ancient cancer subroutine? “Because it fulfills absolutely crucial functions during the early stages of embryo development,” Davies explains. “Genes that are active in the embryo and normally dormant thereafter are found to be switched back on in cancer. These same genes are the ‘ancient’ ones, deep in the tree of multicellular life.”

      The link with embryo development has been known to cancer biologists for a long time, says Davies, but the significance of this fact is rarely appreciated. If the new theory is correct, researchers should find that the more malignant stages of cancer will re-express genes from the earliest stages of embryogenesis.

       

                   6a00d8341bf7f753ef0192ac09a8c1970d-500wi

       

      Davies adds that there is already some evidence for this in several experimental studies, including recent research at Harvard University and the Albert Einstein College of Medicine in New York.

      “As cancer progresses through its various stages within a single organism, it should be like running the evolutionary and developmental arrows of time backward at high speed,” says Davies. The image belwo shows that a typical four-week-old human embryo looks similar to fish embryos, with proto-gills and a tail.(credit: University of New South Wales).

      This could provide clues to future treatments. For example, when life took the momentous step from single cells to multicellular assemblages, Earth had low levels of oxygen. Sure enough, cancer reverts to an ancient form of metabolism called fermentation, which can supply energy with little need for oxygen, although it requires lots of sugar.

      Davies and Lineweaver predict that if cancer cells are saturated with oxygen but deprived of sugar, they will become more stressed than healthy cells, slowing them down or even killing them. ASU’s Center for the Convergence of Physical Science and Cancer Biology, of which Davies is principal investigator, is planning a workshop in November to examine the clinical evidence for this.

      “Like aging, cancer seems to be a deeply embedded part of the life process," says Davies. "Also like aging, cancer generally cannot be cured but its effects can certainly be mitigated, for example, by delaying onset and extending periods of dormancy. But we will learn to do this effectively only when we better understand cancer, including its place in the great sweep of evolutionary history.”

      Source: Paul Davies, Exposing cancer's deep evolutionary roots, Physics World, 2013 (requires free registration)

      The Daily Galaxy via Physics World and Arizona State University

    • james kohl
      Excerpts and my comments: “Cancer is not a random bunch of selfish rogue cells behaving badly, but a highly-efficient pre-programmed response to stress...
      Message 2 of 5 , Aug 22, 2013
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        "Excerpts" and my comments:

        Cancer is not a random bunch of selfish rogue cells behaving badly, but a highly-efficient pre-programmed response to stress..."

        JK: Non-random programmed response to stress (as in nutrient stress and social stress?)

        "They turned to cancer research only recently, in part because of the creation at Arizona State University of the Center for the Convergence of Physical Science and Cancer Biology."

        JK: We will next see creation of a Center for Evolutionary Medicine

        "The new theory challenges the orthodox view that cancer develops anew in each host by a series of chance mutational accidents. Davies and Lineweaver claim that cancer is actually an organized and systematic response to some sort of stress or physical challenge."

        JK: The response so obviously involves the conserved molecular mechanisms of thermodynamic regulation of intercellular signaling and intranuclear interactions that treatments have begun to address the role of sugar and its metabolism as if it cancer cell, like typical cell differentiation was nutrient-dependent (but not pheromone-controlled).

        "Sure enough, cancer reverts to an ancient form of metabolism called fermentation, which can supply energy with little need for oxygen, although it requires lots of sugar."

        JK: Who shall we thank for suppressing information on non-random thermodynamics and the required organism-level thermoregulation in accord with what is neuroscientifically known about nutrient-dependent pheromone-controlled adaptive evolution? Oh, you didn't realize you were delaying cancer treatments by touting mutation-driven evolution?

        No problem, unless you or your family has been affected by a cancer diagnosis at a time when the conserved molecular mechanisms of adaptive evolution have been revealed in study after study, and no results suggest mutation-driven evolution. Do they? That's a problem.

        Those who tout mutations theory are likely to be blamed for a deadly lack of scientific progress; be rooted out via NSA-funded monitoring of your newsgroup posts and charged with conspiracy to destroy human populations from within -- acts of terrorism with effects of stupidity (sans knowledge of epigenetic effects). On the other hand, maybe no one will notice you have changed your perspective on Darwin's works, and started to make sense. Why wait to do so. Admit it now, and you might make "the cut" when other academics are culled from the priesthood.
         
        James V. Kohl
        Medical laboratory scientist (ASCP)
        Independent researcher
        Kohl, J.V. (2013) Nutrient-dependent/pheromone-controlled adaptive evolution: a model. Socioaffective Neuroscience & Psychology, 3: 20553.
        Kohl, J.V. (2012) Human pheromones and food odors: epigenetic influences on the socioaffective nature of evolved behaviors. Socioaffective Neuroscience & Psychology, 2: 17338.


        From: Anna <pantheon@...>
        To: 4DWorldx@yahoogroups.com
        Sent: Thursday, August 22, 2013 4:35 AM
        Subject: [evol-psych] life is cancer

         
        Posted: 21 Aug 2013 08:32 AM PDT
         
                     60
         
        “Tumors are a re-emergence of our inner Metazoan 1.0, a throwback to an ancient world when multicellular life was simpler,” says Paul Davies of Arizona State University’s Beyond Center for Fundamental Concepts in Science . “In that sense, cancer is an accident waiting to happen.”
        A new way to look at cancer — by tracing its deep evolutionary roots to the dawn of multicellularity more than a billion years ago — has been proposed by Davies in collaboration with Charles Lineweaver of the Australian National University. If their theory is correct, it promises to transform the approach to cancer therapy, and to link the origin of cancer to the origin of life and the developmental processes of embryos. Davies and Lineweaver are both theoretical physicists and cosmologists with experience in the field of astrobiology — the search for life beyond Earth.
        “Cancer is not a random bunch of selfish rogue cells behaving badly, but a highly-efficient pre-programmed response to stress, honed by a long period of evolution,” claims Davies, director of the BEYOND Center for Fundamental Concepts in Science at ASU and principal investigator of a major research program funded by the National Cancer Institute designed to bring insights from physical science to the problem of cancer.
        They say it’s because cancer revisits tried-and-tested genetic pathways going back a billion years, to the time when loose collections of cells began cooperating in the lead-up to fully developed multicellular life. Dubbed by the authors “Metazoa 1.0,” these early assemblages fell short of the full cell and organ differentiation associated with modern multicellular organisms – like humans.
        But according to Davies and Lineweaver, the genes for the early, looser assemblages – Metazoa 1.0 – are still there, forming an efficient toolkit. Normally it is kept locked, suppressed by the machinery of later genes used for more sophisticated body plans. If something springs the lock, the ancient genes systematically roll out the many traits that make cancer such a resilient form of life – and such a formidable adversary.
        They turned to cancer research only recently, in part because of the creation at Arizona State University of the Center for the Convergence of Physical Science and Cancer Biology. The center is one of twelve established by the National Cancer Institute to encourage physical scientists to lend their insights into tackling cancer.
        The new theory challenges the orthodox view that cancer develops anew in each host by a series of chance mutational accidents. Davies and Lineweaver claim that cancer is actually an organized and systematic response to some sort of stress or physical challenge. It might be triggered by a random accident, they say, but thereafter it more or less predictably unfolds.
        Their view of cancer is outlined in the article “Exposing cancer’s deep evolutionary roots,” written by Davies (available free with registration -see below). It appears in a special issue of Physics World devoted to the physics of cancer.
        “We envisage cancer as the execution of an ancient program pre-loaded into the genomes of all cells,” says Davies, an Arizona State University Regents’ Professor in ASU’s College of Liberal Arts and Sciences. “It is rather like Windows defaulting to ‘safe mode’ after suffering an insult of some sort.” As such, he describes cancer as a throwback to an ancestral phenotype.
        The new theory predicts that as cancer progresses through more and more malignant stages, it will express genes that are more deeply conserved among multicellular organisms, and so are in some sense more ancient. Davies and Lineweaver are currently testing this prediction by comparing gene expression data from cancer biopsies with phylogenetic trees going back 1.6 billion years.
        But if this is the case, then why hasn’t evolution eliminated the ancient cancer subroutine? “Because it fulfills absolutely crucial functions during the early stages of embryo development,” Davies explains. “Genes that are active in the embryo and normally dormant thereafter are found to be switched back on in cancer. These same genes are the ‘ancient’ ones, deep in the tree of multicellular life.”
        The link with embryo development has been known to cancer biologists for a long time, says Davies, but the significance of this fact is rarely appreciated. If the new theory is correct, researchers should find that the more malignant stages of cancer will re-express genes from the earliest stages of embryogenesis.
         
                     6a00d8341bf7f753ef0192ac09a8c1970d-500wi
         
        Davies adds that there is already some evidence for this in several experimental studies, including recent research at Harvard University and the Albert Einstein College of Medicine in New York.
        “As cancer progresses through its various stages within a single organism, it should be like running the evolutionary and developmental arrows of time backward at high speed,” says Davies. The image belwo shows that a typical four-week-old human embryo looks similar to fish embryos, with proto-gills and a tail.(credit: University of New South Wales).
        This could provide clues to future treatments. For example, when life took the momentous step from single cells to multicellular assemblages, Earth had low levels of oxygen. Sure enough, cancer reverts to an ancient form of metabolism called fermentation, which can supply energy with little need for oxygen, although it requires lots of sugar.
        Davies and Lineweaver predict that if cancer cells are saturated with oxygen but deprived of sugar, they will become more stressed than healthy cells, slowing them down or even killing them. ASU’s Center for the Convergence of Physical Science and Cancer Biology, of which Davies is principal investigator, is planning a workshop in November to examine the clinical evidence for this.
        “Like aging, cancer seems to be a deeply embedded part of the life process," says Davies. "Also like aging, cancer generally cannot be cured but its effects can certainly be mitigated, for example, by delaying onset and extending periods of dormancy. But we will learn to do this effectively only when we better understand cancer, including its place in the great sweep of evolutionary history.”
        Source: Paul Davies, Exposing cancer's deep evolutionary roots, Physics World, 2013 (requires free registration)
        The Daily Galaxy via Physics World and Arizona State University


      • james kohl
        Stress-Induced Recruitment of Bone Marrow-Derived Monocytes to the Brain Promotes Anxiety-Like Behavior Abstract excerpt: ...monocyte recruitment to the brain
        Message 3 of 5 , Aug 22, 2013
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          Stress-Induced Recruitment of Bone Marrow-Derived Monocytes to the Brain Promotes Anxiety-Like Behavior

          Abstract excerpt: "...monocyte recruitment to the brain in response to social stress represents a novel cellular mechanism that contributes to the development of anxiety."

          My comment: In my model, nutrient stress and social stress, which are linked via the immune system to cancer, act via the same conserved molecular mechanisms.

          Article excerpt: Related to the points above, RSD increased mRNA expression of IL-1β in the HYPO, BG, and HPC, but did not change IL-1β in the CTX-R of CCR2KO and CX3CR1KO mice (Table 2). Reduced IL-1β expression in the CTX-R of CCR2KO and CX3CR1KO is likely related to impaired macrophage recruitment and suggests it is susceptible to stress-induced inflammatory signaling (Munhoz et al., 2006).

          My comment: RSD is repeated social defeat. The increased mRNA expression must be due to epigenetic effects of the sensory environment on the microRNA / messenger RNA balance because the perturbe balance is responsible for stress-induced inflammatory signaling associated with thermodynamic control of intercellular signaling and organism-level thermoregulation.

          Article excerpt: "These findings provide insight into how stress-associated recruitment of myeloid cells to the brain directly influences behavior."
           
          My comment: The findings also provide insight into how stress-associated change in the microRNA/messenger RNA balance influence manifestations of some cancers, associated with nutrient stress and/or social stress. I mention this primarily because Williams is pretending to know something about stress on the human ethology yahoo group, and few people know about stress induced changes associated with changes in the microRNA/messenger RNA balance and epigenetic effects on the immune system, hormones, and behavior.

          James V. Kohl
          Medical laboratory scientist (ASCP)
          Independent researcher
          Kohl, J.V. (2013) Nutrient-dependent/pheromone-controlled adaptive evolution: a model. Socioaffective Neuroscience & Psychology, 3: 20553.
          Kohl, J.V. (2012) Human pheromones and food odors: epigenetic influences on the socioaffective nature of evolved behaviors. Socioaffective Neuroscience & Psychology, 2: 17338.


          From: james kohl <jvkohl@...>
          To: "evolutionary-psychology@yahoogroups.com" <evolutionary-psychology@yahoogroups.com>
          Sent: Thursday, August 22, 2013 7:44 AM
          Subject: Re: [evol-psych] life is cancer

           
          "Excerpts" and my comments:

          Cancer is not a random bunch of selfish rogue cells behaving badly, but a highly-efficient pre-programmed response to stress..."

          JK: Non-random programmed response to stress (as in nutrient stress and social stress?)

          "They turned to cancer research only recently, in part because of the creation at Arizona State University of the Center for the Convergence of Physical Science and Cancer Biology."

          JK: We will next see creation of a Center for Evolutionary Medicine

          "The new theory challenges the orthodox view that cancer develops anew in each host by a series of chance mutational accidents. Davies and Lineweaver claim that cancer is actually an organized and systematic response to some sort of stress or physical challenge."

          JK: The response so obviously involves the conserved molecular mechanisms of thermodynamic regulation of intercellular signaling and intranuclear interactions that treatments have begun to address the role of sugar and its metabolism as if it cancer cell, like typical cell differentiation was nutrient-dependent (but not pheromone-controlled).

          "Sure enough, cancer reverts to an ancient form of metabolism called fermentation, which can supply energy with little need for oxygen, although it requires lots of sugar."

          JK: Who shall we thank for suppressing information on non-random thermodynamics and the required organism-level thermoregulation in accord with what is neuroscientifically known about nutrient-dependent pheromone-controlled adaptive evolution? Oh, you didn't realize you were delaying cancer treatments by touting mutation-driven evolution?

          No problem, unless you or your family has been affected by a cancer diagnosis at a time when the conserved molecular mechanisms of adaptive evolution have been revealed in study after study, and no results suggest mutation-driven evolution. Do they? That's a problem.

          Those who tout mutations theory are likely to be blamed for a deadly lack of scientific progress; be rooted out via NSA-funded monitoring of your newsgroup posts and charged with conspiracy to destroy human populations from within -- acts of terrorism with effects of stupidity (sans knowledge of epigenetic effects). On the other hand, maybe no one will notice you have changed your perspective on Darwin's works, and started to make sense. Why wait to do so. Admit it now, and you might make "the cut" when other academics are culled from the priesthood.
           
          James V. Kohl
          Medical laboratory scientist (ASCP)
          Independent researcher
          Kohl, J.V. (2013) Nutrient-dependent/pheromone-controlled adaptive evolution: a model. Socioaffective Neuroscience & Psychology, 3: 20553.
          Kohl, J.V. (2012) Human pheromones and food odors: epigenetic influences on the socioaffective nature of evolved behaviors. Socioaffective Neuroscience & Psychology, 2: 17338.


          From: Anna <pantheon@...>
          To: 4DWorldx@yahoogroups.com
          Sent: Thursday, August 22, 2013 4:35 AM
          Subject: [evol-psych] life is cancer

           
          Posted: 21 Aug 2013 08:32 AM PDT
           
                       60
           
          “Tumors are a re-emergence of our inner Metazoan 1.0, a throwback to an ancient world when multicellular life was simpler,” says Paul Davies of Arizona State University’s Beyond Center for Fundamental Concepts in Science . “In that sense, cancer is an accident waiting to happen.”
          A new way to look at cancer — by tracing its deep evolutionary roots to the dawn of multicellularity more than a billion years ago — has been proposed by Davies in collaboration with Charles Lineweaver of the Australian National University. If their theory is correct, it promises to transform the approach to cancer therapy, and to link the origin of cancer to the origin of life and the developmental processes of embryos. Davies and Lineweaver are both theoretical physicists and cosmologists with experience in the field of astrobiology — the search for life beyond Earth.
          “Cancer is not a random bunch of selfish rogue cells behaving badly, but a highly-efficient pre-programmed response to stress, honed by a long period of evolution,” claims Davies, director of the BEYOND Center for Fundamental Concepts in Science at ASU and principal investigator of a major research program funded by the National Cancer Institute designed to bring insights from physical science to the problem of cancer.
          They say it’s because cancer revisits tried-and-tested genetic pathways going back a billion years, to the time when loose collections of cells began cooperating in the lead-up to fully developed multicellular life. Dubbed by the authors “Metazoa 1.0,” these early assemblages fell short of the full cell and organ differentiation associated with modern multicellular organisms – like humans.
          But according to Davies and Lineweaver, the genes for the early, looser assemblages – Metazoa 1.0 – are still there, forming an efficient toolkit. Normally it is kept locked, suppressed by the machinery of later genes used for more sophisticated body plans. If something springs the lock, the ancient genes systematically roll out the many traits that make cancer such a resilient form of life – and such a formidable adversary.
          They turned to cancer research only recently, in part because of the creation at Arizona State University of the Center for the Convergence of Physical Science and Cancer Biology. The center is one of twelve established by the National Cancer Institute to encourage physical scientists to lend their insights into tackling cancer.
          The new theory challenges the orthodox view that cancer develops anew in each host by a series of chance mutational accidents. Davies and Lineweaver claim that cancer is actually an organized and systematic response to some sort of stress or physical challenge. It might be triggered by a random accident, they say, but thereafter it more or less predictably unfolds.
          Their view of cancer is outlined in the article “Exposing cancer’s deep evolutionary roots,” written by Davies (available free with registration -see below). It appears in a special issue of Physics World devoted to the physics of cancer.
          “We envisage cancer as the execution of an ancient program pre-loaded into the genomes of all cells,” says Davies, an Arizona State University Regents’ Professor in ASU’s College of Liberal Arts and Sciences. “It is rather like Windows defaulting to ‘safe mode’ after suffering an insult of some sort.” As such, he describes cancer as a throwback to an ancestral phenotype.
          The new theory predicts that as cancer progresses through more and more malignant stages, it will express genes that are more deeply conserved among multicellular organisms, and so are in some sense more ancient. Davies and Lineweaver are currently testing this prediction by comparing gene expression data from cancer biopsies with phylogenetic trees going back 1.6 billion years.
          But if this is the case, then why hasn’t evolution eliminated the ancient cancer subroutine? “Because it fulfills absolutely crucial functions during the early stages of embryo development,” Davies explains. “Genes that are active in the embryo and normally dormant thereafter are found to be switched back on in cancer. These same genes are the ‘ancient’ ones, deep in the tree of multicellular life.”
          The link with embryo development has been known to cancer biologists for a long time, says Davies, but the significance of this fact is rarely appreciated. If the new theory is correct, researchers should find that the more malignant stages of cancer will re-express genes from the earliest stages of embryogenesis.
           
                       6a00d8341bf7f753ef0192ac09a8c1970d-500wi
           
          Davies adds that there is already some evidence for this in several experimental studies, including recent research at Harvard University and the Albert Einstein College of Medicine in New York.
          “As cancer progresses through its various stages within a single organism, it should be like running the evolutionary and developmental arrows of time backward at high speed,” says Davies. The image belwo shows that a typical four-week-old human embryo looks similar to fish embryos, with proto-gills and a tail.(credit: University of New South Wales).
          This could provide clues to future treatments. For example, when life took the momentous step from single cells to multicellular assemblages, Earth had low levels of oxygen. Sure enough, cancer reverts to an ancient form of metabolism called fermentation, which can supply energy with little need for oxygen, although it requires lots of sugar.
          Davies and Lineweaver predict that if cancer cells are saturated with oxygen but deprived of sugar, they will become more stressed than healthy cells, slowing them down or even killing them. ASU’s Center for the Convergence of Physical Science and Cancer Biology, of which Davies is principal investigator, is planning a workshop in November to examine the clinical evidence for this.
          “Like aging, cancer seems to be a deeply embedded part of the life process," says Davies. "Also like aging, cancer generally cannot be cured but its effects can certainly be mitigated, for example, by delaying onset and extending periods of dormancy. But we will learn to do this effectively only when we better understand cancer, including its place in the great sweep of evolutionary history.”
          Source: Paul Davies, Exposing cancer's deep evolutionary roots, Physics World, 2013 (requires free registration)
          The Daily Galaxy via Physics World and Arizona State University




        • anonymous_9001
          What on Earth are you talking about? ... Those who tout mutations theory are likely to be blamed for a deadly lack of scientific progress; be rooted out via
          Message 4 of 5 , Aug 22, 2013
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            What on Earth are you talking about?

            --- In evolutionary-psychology@yahoogroups.com, james kohl <jvkohl@...> wrote:

            Those who tout mutations theory are likely to be blamed for a deadly lack of scientific progress; be rooted out via NSA-funded monitoring of your newsgroup posts and charged with conspiracy to destroy human populations from within
          • james kohl
            From: anonymous_9001 ... From: anonymous_9001 To: evolutionary-psychology@yahoogroups.com Sent: Friday, August 23, 2013 12:35 AM
            Message 5 of 5 , Aug 23, 2013
            • 0 Attachment


              From: anonymous_9001
              To: evolutionary-psychology@yahoogroups.com
              Sent: Friday, August 23, 2013 12:35 AM
              Subject: Re: [evol-psych] life is cancer

              What on Earth are you talking about?

              JK: Why do you ask? When you going to address the accurate representations of fact I have provided. As we've seen, you certainly are capable of responding to my nonsense.
              James V. Kohl
              Medical laboratory scientist (ASCP)
              Independent researcher
              Kohl, J.V. (2013) Nutrient-dependent/pheromone-controlled adaptive evolution: a model. Socioaffective Neuroscience & Psychology, 3: 20553.
              Kohl, J.V. (2012) Human pheromones and food odors: epigenetic influences on the socioaffective nature of evolved behaviors. Socioaffective Neuroscience & Psychology, 2: 17338.


              --- In evolutionary-psychology@yahoogroups.com, james kohl wrote:

              Those who tout mutations theory are likely to be blamed for a deadly lack of scientific progress; be rooted out via NSA-funded monitoring of your newsgroup posts and charged with conspiracy to destroy human populations from within



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