For over 25 years, there have been studies seeking to understand if paternal drinking affects fetal and infant health and FASD in particular. Finding that 75% of children born with FASD had fathers who were alcoholics, Abel et al. conducted a number of animal studies that described negative effects from paternal alcohol consumption but without clear or satisfactory links to humans . Consequently, FASD prevention programs have primarily focused on pregnant women, where the evidence was certain, and treated paternal drinking as largely a risk factor for maternal drinking rather than a risk factor for FASD itself.
Now, with advances in epigenetic research, two recent analyses of studies are showing that paternal factors, and alcohol use, in particular, play a larger role in fetal/child health than just passing along genes. Each study analysis systematically reviewed findings about the role of paternal alcohol consumption on conception, pregnancy, and fetal and infant health. One analysis used a paternal-alcohol consumption lens, while the other used a birth-defect lens. These results provide evidence to expand prevention efforts to men, especially in the preconception period, and to continue research in the field of epigenetics and alcohol-exposed pregnancy. (To learn about epigenetics click here.)
The first review by McBride and Johnson looked at 150 research studies and distilled them down to 11 good-quality studies. The associated effects of paternal drinking fell into three themes: impact on maternal drinking, sperm health, and fetal/infant health. Two studies showed an association between low levels of paternal drinking with lowered sperm count, as well as underdeveloped sperm leading to conception problems and miscarriage. Seven studies showed an increased risk of miscarriage when men drank 10 drinks or more per week in the preconception period, and one study found an association of all cases of ventricle malformation (heart defect) with daily paternal alcohol consumption during the preconception period .
The second study review by Day and Savani et al. focused on birth defects and links to paternal alcohol consumption, age and environmental factors. The authors explore the evidence for how these factors impact sperm DNA and, therefore, how the developing cells of an embryo “read” and “express” genetic instructions. For example, genes that are normally “silenced” may be “activated”. Paternal alcohol consumption epigenetically impacts the “gene expression governing individual organ development” that can adversely affect fetal development, in the immediate instance and in future generations . Deficiencies in brain size, heart formation, and cognitive and motor abilities (noted as being symptoms of FASD) were linked to paternal alcohol use even when there was no maternal alcohol consumption.
Both of these study analyses contend that more research is needed in order to understand the full impact of alcohol and epigenetics, and the interplay between maternal and paternal factors. Still, this latest research supports the need for health promotion policies and practices that address men’s alcohol use, not only as an influence on women’s alcohol use, and to benefit men’s health, but also for its potential adverse effect on fetal/child health.
For more on men and FASD prevention, see earlier posts:
- How Do Partners Affect Women’s Alcohol Use During Pregnancy?, August 11, 2014
- How Men Can Help Prevent FASD, March 11, 2014
- Pregnant Pause Campaign for Aussie Dads, October 1, 2013
- FASD Prevention in Australia’s Ord Valley, October 13, 2011
- Getting Fathers Involved, January 4, 2011
Abel, E., Paternal contribution to fetal alcohol syndrome. Addiction Biology, 2004. 9(2): p. 127-133. (Link here)
McBride, N. and S. Johnson, Fathers’ role in alcohol-exposed pregnancies: Systematic review of human studies. American Journal of Preventive Medicine, Article in Press.
Day, J., et al., Influence of paternal preconception exposures on their offspring: Through epigentics to phenotype. American Journal of Stem Cells, 2016. 5(1): p. 11-18.