Science Gazette

Alcohol abuse by fathers raises the likelihood of fetal development problems

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Prenatal visits have typically focused almost entirely on the conduct of mothers, but new study from Texas A&M University’s College of Veterinary Medicine & Biomedical Sciences (CVMBS) suggests that scientists should pay greater attention to the behavior of dads as well.

Dr. Michael Golding, an associate professor in the Department of Veterinary Physiology & Pharmacology (VTPP) at the CVMBS, has spent years researching the father’s involvement in embryonic development, particularly as it pertains to drugs and alcohol.

According to Golding, a number of studies have demonstrated that men pass down more than simply their DNA, but the specific mechanism and effects of this process are still unclear.

“There’s significant indication that there’s something beyond simply genetics being passed from the male,” Golding said. “So, if that data is reliable, we need to start paying more attention to male behavior.

“For example, if a parent has been exposed to famine, they may pass on a trait known as ‘thriftiness,’ in which their children may get more nourishment from less food,” he said. “That may be a plus if they grow up in a similar setting, or it could be a negative if they grow up in a period when hunger isn’t a problem, making them more prone to obesity and metabolic disorders. This kind of information may be found in human clinical data.”

Epigenetics is Golding’s study of how variables other than genes, including as behavior and environment, influence development, and one of the key challenges in the hunt for answers on how male prenatal behavior affects fetal growth has been how these epigenetic influences appear.

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At this point, there is at least one solution.

The epigenetic component of prenatal alcohol exposure in men may emerge in the placenta, according to Golding’s team, who published their findings in the FASEB Journal in November.

According to Kara Thomas, a VTPP graduate student and the paper’s primary author, their findings reveal that children of alcoholic dads have a variety of placental-related issues, including fetal growth limitation, larger placentas, and lower placental efficiency in mice.

“Because the placenta is responsible for supplying nutrients to the developing baby, fetal growth limitation may be linked to a less effective placenta. This is why placental efficiency is so crucial: it informs us how many grams of fetus are generated per gram of placenta “Thomas stated his opinion. “Paternal alcohol consumption causes placentas to overgrow in an attempt to compensate for their inability to provide nutrition to the baby.”

The mystery, on the other hand, grew.

These increases were common in male progeny, although the frequency varied widely depending on the mother; nevertheless, they were much less common in female offspring. Although the information is handed down from the father, Golding thinks that the mother’s genetics and the sex of the child also have a role.

“This is a surprising observation because it implies that there is some complication here,” Golding said. “Yes, males may pass on things other than genetics to their kid, but the mother’s genetics might read epigenetic factors differently, which affects the way the placenta operates.”

These findings do not draw a clear line in terms of how human male drinking before conception affects fetal development, but they do indicate that it is an issue that needs to be investigated.

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Golding hopes that physicians and society as a whole will start asking more questions regarding male prenatal behavior so that more data may be gathered.

“What I want to alter in the end is the stigma that surrounds the development of birth abnormalities,” Golding added. “There’s information in sperm that has an influence on the kids but isn’t linked to the genetic code; it’s in your epigenetic code, which is very vulnerable to environmental exposures, so the birth abnormalities we find could not be the mother’s responsibility; they might equally be the father’s or both.

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