Passing On Stress

By: James V. Kohl | Published on: May 22, 2012

Exposure to an environmental toxin can affect future generations’ ability to handle stressful conditions.

Excerpt: “We are now in the third human generation since the start of the chemical revolution, since humans have been exposed to these kinds of toxins,” David Crews, a zoologist at the University of Texas, at Austin and one of the paper’s lead authors, said in a press release. “This is the animal model of that.”
My comment:
It is now clearer how olfactory/pheromonal input causes beneficial transgenerational epigenetic effects via direct effects of nutrient chemicals on food preferences, and the role that nutrient chemicals play in sexual reproduction via their metabolism to pheromones. From the article: “How an ancestral environmental exposure modifies the germline epigenome and promotes epigenetic transgenerational inheritance is critical in any consideration of tissue function.”  This is the gene, cell, tissue… organ (the brain) organ-system model exemplified in the honeybee model of food odors, pheromones and brain development.
In species from microbes to man receptor-mediated changes caused by nutrient chemicals and pheromones alter intracellular signaling and stochastic gene expression. Thus, olfaction and odor receptors provide a clear evolutionary trail that can be followed from unicellular organisms to insects to humans. Nutrient chemicals are responsible for the ecological niche, and their metabolism is responsible for the social niche. The ecological and social niche cause the adaptive evolution of the neurogenic niche responsible for invertebrate and vertebrate food choice and mate choice.
I was happy to see the authors express the fact that: “Although no direct epigenetic measurements were made in the current study, the epigenetic model and role of epigenetics in development provides the molecular basis of the observations presented.” Perhaps others will now proceed based on the epigenetic effects of nutrient chemicals and pheromones that have been modeled in species from microbes to man.
Clearly, this is the right model, and it’s time to use it to explain biologically based cause and effect, and to dispense with theories that cannot be modeled using the molecular biology that is common to species from microbes to man.

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