Evaluating Stress during Pregnancy: Do We Have the Right Conceptions and the Correct Tools to Assess It?

Figure 3

Schemes that illustrate the hypothetical process underlying the transgenerational epigenetic inheritance of stress susceptibility and stress-related diseases via the paternal lineage. (a) When an “unstressed healthy couple” decides to become pregnant, the “biological future” of their child (and indeed of their lineage) might be deeply influenced by the circumstances that surround their pregnancy. In the case where the pregnant mother (F0) experiences stress, the ontogenetic trajectory of the fetus may deviate his/her phenotype to an alternative form that renders the child, and later the adult, susceptible to develop degenerative diseases (see Figure 2) and altered HPA axis physiology (see Figure 1), respectively. The alternative phenotype, however, features increased susceptibility to develop not only stress-related diseases and “stress hypersensitivity” but also spermatogonia that kept a record of the prenatal stress episode in their genome through epigenetic memories. (b) When the spermatozoids derived from the stress-modified precursors of the F1 male fertilize the oocyte of a “naïve” woman, even if the pregnancy proceeds under “no-stress conditions,” the conceived child (F2) inherits the “stressful phenotype” due to the permanence of the F-1 stress-related, gametic epigenetic memory. (c) A similar process takes place in subsequent generations. There is information supporting that this may happens for at least five generations. Epigenetic gametic inheritance can also applied to the maternal lineage, and it is possible that if both members of the couple were exposed to stress during fetal life, their gametes could “double the dosage” of the stress-related epigenetic memories passed on to their descendants making them much more stress prone and stress susceptible throughout their lives.

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