The purpose of the study was to evaluate how prenatal stress affects sexual hormones, sperm quality, quantity of ovarian follicles, and fertility. The stressor was immersion in cold water of the female rats in their last week of pregnancy (day 15-21). After birth, the offspring were weaned, weighed, and isolated into males and females. The offspring were weighed at birth, weaning, and adulthood. Body weight gain was lower in male and female offspring that were exposed to stress at all evaluated stages. The HPA axis being stimulated by stress explains the lower body weight regardless of having food accessible. This could also be due to CRH, leptin, and other food-intake controlling hormones being altered. Additionally, dams’ corticosterone levels were evaluated, and the results had shown nearly three orders of magnitude higher levels of stressed dams compared to control. Offspring count did not show significance in the study, as the control and stressed group had similar numbers. However, vaginal smears of stressed female offspring compared to control offspring showed significant results of estrous cyclicity (p = 0.0001). Stressed female offspring had longer estrous cycles or had incomplete cycles. This also correlated with lower levels of estradiol, and low serum progesterone (p = 0.003). Specifically with male offspring, testicular relative weight was lower in stressed males compared to the control males (p = 0.004). This could be due to higher apoptosis index in germinal cells. Thus, sperm quality was lower in stressed male offspring as well. (P = 0.05). The sperm quality could be observed by abnormality in the head and/or tail. This ties into only 70% of stressed males impregnating control females whereas 100% of control male impregnated control females. When both stressed male and female were introduced, only 50% were impregnated (p = 0.0024). In conclusion, prenatal stress does cause alteration in females and male progeny. Alterations specifically in weight, sperm quality, testicular cell death, infertility, and lower levels of hormones.
García-Vargas D, Juárez-Rojas L, Rojas Maya S, Retana-Márquez S. Prenatal stress decreases sperm quality, mature follicles and fertility in rats. Syst Biol Reprod Med. 2019 Jun;65(3):223-235. doi: 10.1080/19396368.2019.1567870. Epub 2019 Jan 28. PMID: 30689429.
Epigenetic inheritance continues to be an interesting subject, as the extent to which a phenotype can be altered through behavior seems to be quite significant. Perhaps more negatively, however, this research may potentially compound the responsibility that we as a society place on pregnant mothers. Therefore, out of ethical consideration for women of child-bearing capacity, it would be incumbent upon the medical and scientific communities to establish a clear causational relationship between prenatal stress and negative alterations in progeny. I only bring this up because I found a similar yet slightly contradictory study on prenatal stress and its effect on male rat offspring. In a study by Khazaleh et al., researchers found that 50% maternal water restriction, from day ten of pregnancy onwards, had a negative effect on some reproductive characteristics (i.e. intromission latency, intromission frequency, and post-ejaculation interval), but it did not severely affect reproductive performance or reproductive hormones in male rat offspring (Khazaleh et al., 2020). This was contrary to your study, in which sperm quality was found to be lower in the stressed male offspring, which led to a decrease in successful impregnation; this was not the case in Khazaleh et al., as all hormonal concentrations, sperm count, and vitality were not significantly affected. Overall, I think such discrepancies can cast doubt on the degree to which behavior affects heritability. That said, I am excited to see where the research takes us!
ReplyDeleteKhazaleh, J. A.-, Kridli, R., Obeidat, B., Zaitoun, S., & Abdelqader, A. (2020). Effect of Maternal Water Restriction on Sexual Behavior, Reproductive Performance, and Reproductive Hormones of Male Rat Offspring. Animals (Basel), 10(3). https://doi-org.dml.regis.edu/10.3390/ani10030379