Alcohol drinking and heart defects
About 1.35 million babies are born with heart defects every year, making this the most common type of birth defect. Congenital heart defects are associated with high perinatal mortality (infant death within labor or a week of birth). They also cause a higher chance of cardiovascular disease in later life despite being corrected by surgery.Babies with FASD also had heart anomalies in a quarter of cases, indicating a strong link between alcohol exposure during pregnancy and congenital heart disease. Alcohol is thus a specific teratogen for heart defects. The novelty in the current study is the revelation that preconceptional alcohol ingestion by fathers is also apparently linked to defects of the developing heart in the fetus.
The current study used data on almost 42,000 babies born with heart defects from 1991 to 2019, drawn from 55 studies. These studies also supplied data on almost 300,000 babies without heart defects. Careful analysis of the data showed that the amount and frequency of drinking by the parents were directly proportional in a non-linear fashion to the risk of congenital heart disease. Thus, the lowest percentile of drinking carried a very low, statistically insignificant risk of this condition, but the risk slowly rose with increasingly heavy drinking by one or both parents.
The study also noted that mothers who drank had babies with a 20% higher risk of a specific and serious heart defect called the tetralogy of Fallot when compared to women who avoided alcohol before and during pregnancy.
Limitations
The observational nature of the study means there is a link between the two conditions, but nobody knows how alcohol causes congenital heart defects, or even if it does. The study cannot prove that drinking by the father is more toxic to the baby’s developing heart than by the mother. Thirdly, the study cannot provide a safe limit for alcohol consumption in pregnancy.The underlying mechanisms connecting parental alcohol and congenital heart diseases are uncertain and warrant further research. Although our analysis has limitations - for example the type of alcohol was not recorded - it does indicate that men and women planning a family should give up alcohol.”
Jiabi Qin
Other things to avoid
The referenced study concludes that expectant fathers should not smoke, drink or eat too much junk food. These are known to cause epigenetic changes or changes in the DNA that do not affect the code sequence but do alter the way the function of the molecule is regulated.
Most alterations of DNA function occurring in mice born to older male parents led to their being learning and memory-impaired, with a shorter lifespan and less capability of reproduction. The mechanism is likely to be the methylation of, or addition of methyl groups, to the DNA units.
Stress also may induce heritable DNA changes, while lack of food in early life, before adolescence set in, caused decreased mouse susceptibility to cardiovascular disease in the offspring, while those who had grandparents with exposure to poor nutrition had a reduced incidence of diabetes. However, offspring born to fathers who were previously food-deprived showed lower blood glucose levels.
Other more psychological stressors like fear-inducing smells or habitat changes reflected as lower responses to stress in the offspring, hinting that behavior was affected in a transmissible way from parents to offspring.
Smoking causes sperm mutations, as is already known, while 75% of babies with FASD have fathers with a drinking problem. Here again, DNA methylation is suspected to be the culprit. Offspring of mice fed alcohol have a higher incidence of low birth weight, learning deficits, and mobility issues. Thus fathers should also take care to avoid exposure to a wide range of teratogens as these experiences are also transmissible via epigenetics to the offspring.
Journal reference:
1Zhang S, Wang L, Yang T, et al. Parental alcohol consumption and the risk of congenital heart diseases in offspring: An updated systematic review and meta-analysis. Eur J Prev Cardiol. 2019. doi:10.1177/2047487319874530. https://journals.sagepub.com/doi/10.1177/2047487319874530
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