Smoking during pregnancy may lead to later substance use in the child

Charlotte Cecil, King’s College London

Smoking during pregnancy is a well-known risk factor for many health problems in children, including low birth weight, heart defects and asthma. In our latest study, we show that smoking in pregnancy also increases the risk for children’s later tobacco smoking, as well as alcohol and cannabis use. This effect may be partly explained by so-called epigenetic changes at birth, in genes important for brain function and development.

Substance abuse and addiction are among the biggest causes of death worldwide, damaging individuals, their families and entire communities. While most teens who begin experimenting with substances during adolescence do not go on to develop an addiction, some seem to be more at risk than others. Because addiction is difficult to treat, it is important to understand how it develops, so that we may prevent it in the first place.

So far, most studies looking at what predicts substance use have focused on teens and adults. These have shown that substance use runs in families, so that genetic factors seem to be important. At the same time, environmental factors also seem to be important, such as the amount of stress teens may be exposed to, or whether they hang out with friends who use substances.

More recently, studies have begun to wind back the clock by examining the role of events that happened early in life – beginning in the womb. This is because new evidence suggests that what mothers experience during pregnancy (diet, smoking, stress) can affect fetal development in a way that shapes a child’s future health and behaviour. A key mechanism through which this is thought to happen is epigenetics.

Epigenetics: how genes ‘talk’ with the environment

Our genes and our environment can “communicate” with one another through epigenetics. We can think of epigenetic processes as a biological switch that turns genes on and off. In other words, although our genes do not change across our lifespan, the way our genes are expressed (switched on) does. This allows our body to use our genetic information more flexibly, and to adapt to our changing environment. Although epigenetic changes have been observed both in relation to prenatal events (such as smoking) and substance use in adults, no one has yet examined whether these things may be linked.

To address this gap, we carried out a study examining the relationship between prenatal events, epigenetic changes in early life, and substance use in adolescence. The study was based on 244 youths from the Avon Longitudinal Study of Parents and Children (ALSPAC), who have been followed from pregnancy to early adulthood.

We found that prenatal smoking was associated with epigenetic changes at birth, which in turn were linked to higher substance use (and an earlier age of onset) in adolescence. These changes were located in genes important for many functions, including brain development. One of the biggest changes happened in PACSIN1, a gene that plays a key role in how neurons branch and communicate with one another.

Our findings add to our understanding of the effects of prenatal smoking on child health and show that this link may be partly explained by epigenetic changes in the child. Together, these findings suggest that interventions that help reduce smoking in pregnancy may not only promote children’s healthy development, but also reduce vulnerability to substance use.

Substance abuse and addiction are very complex issues, so our findings are only part of a bigger picture that still needs to be fully mapped out. For example, maternal smoking is likely to work alongside a host of other risks, which will also need to be examined in future. Because our study is based on associations and involved a relatively small number of children, findings will also need to be replicated in larger studies that can test causation. Finally, it will be important to understand exactly how the epigenetic changes found here increase risk for substance use.

The Conversation

Charlotte Cecil, ESRC FRL Fellow, King’s College London

This article was originally published on The Conversation. Read the original article.


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