Inherited Fears

Mice appear to pass certain fears onto their offspring, according to a new study.

By | December 2, 2013

WIKIMEDIAMice trained to fear the smell of a cherry-and-almond-scented chemical called acetophenone passed their anxieties onto their pups, according to a study published this week (December 1) in Nature Neuroscience. Compared to control mice, mice born to acetophenone-fearing fathers shuddered more in response to the scent the very first time they smelled it, and the same was true for a third generation of mice. The researchers provide evidence to suggest that the effect may be mediated by epigenetic changes, but the field is divided.

“The claims they make are so extreme they kind of violate the principle that extraordinary claims require extraordinary proof,” Columbia University molecular biologist Timothy Bestor told Nature.

Others are more convinced. Neurobiologist David Sweatt of the University of Alabama at Birmingham told Nature that the manuscript is “the most rigorous and convincing set of studies published to date demonstrating acquired transgenerational epigenetic effects in a laboratory model.”

For example, the researchers, Kerry Ressler and Brian Dias of Emory University in Atlanta, Georgia, noted differences in the numbers of neurons that produce an acetophenone-detecting receptor protein in mice trained to fear the scent, as well as their descendants, as compared to control mice. And the brain structures that receive projections from these neurons and help process smells were also bigger in acetophenone-fearing mice. Furthermore, the sperm of these mice displayed fewer methylation tags on the Olfr151 gene, which encodes an acetophenone-sensitive receptor, suggesting epigenetics as a possible mechanism for the inheritance of fear. Those methylation marks presumably fell within the body of the gene, however, not the promoter, leading Bestor to question their role in regulating the expression of Olfr151.

“I don’t see any way by which that gene could be directly regulated by methylation,” Bestor told National Geographic’s Only Human.

But evidence that epigenetics can influence behavior across generations seems to be accumulating. In people, children conceived in the midst of famine in a war-torn Netherlands in the 1940s have been noted for an increased risk of diabetes, heart disease, and other conditions, for example, and some researchers suspect that a parent’s anxiety can influence their children or children’s children via epigenetic changes to receptors for stress hormones.

More work is needed to nail down the epigenetic pathways that might orchestrate such changes, however. “Until someone can really explain it in a molecular way,” skepticism will persist, Ressler told Nature. “Unfortunately, it’s probably going to be complicated and it’s probably going to take a while.”

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Avatar of: James V. Kohl

James V. Kohl

Posts: 475

December 3, 2013

Re: “I don’t see any way by which that gene could be directly regulated by methylation,” Bestor told National Geographic’s Only Human."

National Geographic and Nature block my comments on journalist's posts and research reports. Otherwise, it would already be clear that the epigenetic effects of odors associated with nutrient uptake and ingestion of methyl groups links food odors to transgenerational epigenetic effects on memory via conserved molecular mechanisms.

The epigenetic effects of nutrient metabolism to species-specific pheromones, which control the physiology of reproduction, also link nutrient-dependent methylation to memory and social preferences that are established via ecological, social, neurogenic, and socio-cognitive niche construction associated with the thermodynamics and organism-level thermoregulation of increased organismal complexity in species from microbes to man.

Unfortunately, the physical constraints and the biological complexity required to link epigenetic information to memory and behavior seem to be hidden from the majority of researchers who establish popular opinion and often academically suppress new ideas. They tout mutations theory while avoiding discussion of nutrient-dependent pheromone-controlled adaptive evolution in the context of Darwin's 'conditions of life.' They ignore the requirement of species-wide epistasis that Dobzhansky (1973)  came very close to explaining via nutrient-dependent amino acid substitutions, before attributing the substitutions to mutations as others have since continued to do. See, for example:

Jay R. Feierman: I am absolutely certain that if you showed this statement to any professor of biology or genetics in any accredited university anywhere in the world that 100% of them would say that “Random mutations are the substrate upon which directional natural selection acts” is a correct and true statement.... You really want us to believe that you are the expert on this topic when 100% of university level biology textbooks for Biology 101 and all biology and genetics professors will say the exact same sentence or something almost identical.

Whether or not anyone believes that I am an expert on this topic, I have published a series of works that with and  without co-authors establish the obvious facts that Darwin tried to establish. Life is nutrient-dependent. Had Darwin suspected that speciation was controlled by the metabolism of nutrients to species-specific pheromones, we could have avoided more that 80 years of the nonsense about natural selection that was added after Haldane suggested the idea of mutation-driven evolution.

See for review: Nutrient-dependent/pheromone-controlled adaptive evolution: a model. Those who decide to stick with the popular theory, like Feierman has done, may never be held accountable for ignoring biological facts, like Feierman has done while he also blocks most of my posts. But I would not stake my career in academia on that, if I had one, or had ever wanted one.

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