A new comparative analysis across mammals brings order to previously ambiguous results on the effects that maternal stress has on the developing offspring. Different studies (often on the same species) have reported that early adversity enhances, hampers, or has no effect on offspring development and performance. Researchers from the German Primate Center and Universities of Göttingen and New Mexico have now proposed a hypothesis that largely predicts such highly variable patterns in the growth rates of disadvantaged offspring across 719 studies on 21 mammal species.
“The idea is that prenatal stress affects offspring in two different ways depending on the timing of the stressor during pregnancy – yielding different outcomes before birth, after birth, and after weaning” says Andreas Berghänel, the lead author of the study. The study was published in the journal PNAS.
For example, prenatal maternal stress late in gestation causes mothers to invest less energy in their unborn offspring, which leads to slower intrauterine and early postnatal growth rates. Once offspring have reached nutritional independence, however, they are no longer affected directly by their mother’s provisioning, and consequently grow at the same rate as non-disadvantaged offspring. Thus, maternal stress late in gestation leads to slow growth during dependent phases and unchanged growth later.
By contrast, prenatal maternal stress early in gestation causes the fetus to be entirely reprogrammed to deal with a reduced life expectancy. To “make the best of a bad job”, the early challenged offspring switches to an accelerated pace of life and grows and matures faster than unchallenged offspring to ensure that it reproduces before it dies. Once set on the fast track, the offspring under early prenatal maternal stress remain on this trajectory even after weaning and therefore overshoot the usual body size for age throughout development.
In combination, an infant’s acceleration of their developmental processes together with a deceleration due to reduced maternal investment could then cancel each other out during phases of intense maternal investment (gestation and lactation). It is not until the infant is nutritionally independent that the programming effects become clear. This new comparative study finds all of these predictions are supported in a large sample of studies that each measured the effects of prenatal stress on offspring size and growth compared to an unchallenged control group. All stressors seem to have the same effect, and the results are stable across a variety of experiments. Whether mothers were exposed directly to stressors (via food restriction or other adversities) or were experimentally manipulated to increase their “stress hormones” (for example, cortisol), the patterns of offspring growth across developmental stage relative to the timing of the stressor remained the same.
Previous evolutionary hypotheses about prenatal maternal stress effects also invoked the idea of fetal programming, but most assumed that any fitness benefits to the offspring were the result of enhanced environmental matching between the mother and offspring rather than an offspring strategy specifically to counteract the deleterious effects of reduced maternal investment. These new results may bear some translational value for understanding why girls reach menarche earlier in poorer neighborhoods, why teenage pregnancies are more frequent in disadvantaged families, and why adverse conditions during early development (particularly in formula-fed children) often lead to obesity and other metabolic health problems later in life.