Can fetal alcohol damage be passed down to grandchildren?

Fetal alcohol damage, primarily caused by prenatal alcohol exposure, can have profound effects not only on the individual directly exposed in utero but may also influence subsequent generations, including grandchildren. This phenomenon is linked to the concept of *transgenerational epigenetic inheritance*, where environmental factors such as alcohol exposure alter gene expression patterns without changing the underlying DNA sequence, potentially passing these changes down through multiple generations.

**Medical and Scientific Basis**

When a pregnant woman consumes alcohol, the developing fetus is exposed to ethanol and its toxic metabolites, which can disrupt normal development, leading to fetal alcohol spectrum disorders (FASD). These disorders include a range of physical, cognitive, and behavioral impairments. The damage is primarily due to alcohol’s interference with cellular processes during critical periods of embryonic and fetal growth.

Recent research has expanded understanding beyond direct fetal effects to consider whether these alcohol-induced changes can be inherited by the next generation. Studies using animal models and human epidemiological data suggest that alcohol exposure can cause epigenetic modifications—such as DNA methylation, histone modification, and changes in non-coding RNA—that affect gene regulation in germ cells (sperm or eggs). These epigenetic marks can be stable enough to be transmitted to offspring, potentially affecting the health and development of grandchildren.

For example, a study presented at the DOHaD (Developmental Origins of Health and Disease) 2025 conference examined the transgenerational effects of grandparental alcohol consumption on birthweight and other developmental outcomes in grandchildren using Mendelian randomization techniques in the Norwegian HUNT cohort. This study provided evidence supporting the adverse impact of grandparental drinking on the birthweight of grandchildren, indicating that the effects of alcohol exposure can extend beyond the directly exposed generation[1].

**Mechanisms of Transgenerational Transmission**

The key mechanism involves epigenetic reprogramming during gametogenesis and early embryonic development. Normally, epigenetic marks are largely erased and reset between generations to ensure totipotency of the embryo. However, some alcohol-induced epigenetic changes may escape this reprogramming, leading to persistent alterations in gene expression patterns in descendants.

Animal studies have demonstrated that paternal alcohol exposure can alter sperm DNA methylation patterns, which correlate with cognitive and behavioral deficits in offspring and even grand-offspring. Similarly, maternal alcohol exposure can affect the epigenome of oocytes and the developing embryo, influencing multiple generations.

**Implications for Public Health and Prevention**

Understanding that fetal alcohol damage can potentially be passed down to grandchildren underscores the importance of preventing alcohol consumption not only during pregnancy but also in individuals planning to conceive. It also highlights the need for long-term monitoring and support for families affected by FASD, as the consequences may ripple through generations.

The National Health and Medical Research Council (NHMRC) emphasizes the importance of epigenetic research in understanding how environmental exposures like alcohol affect health across generations. Their ongoing projects aim to capture high-resolution epigenomic changes to better understand and eventually reverse such damage, particularly in neurological disease states[2].

**Limitations and Ongoing Research**

While evidence is growing, the exact extent and mechanisms of transgenerational inheritance of fetal alcohol damage in humans remain under investigation. Human studies face challenges such as controlling for confounding factors and the long timescales involved. Animal models provide controlled environments to study mechanisms but may not fully replicate human complexity.

Further research is needed to clarify how epigenetic changes induced by alcohol exposure are maintained or modified across