Abstract
Prenatal exposure to an adverse uterine environment can have long lasting effects on adult offspring through DNA methylation, histone acetylation, and other epigenetic effects that alter gene expression and physiology. It is well-known that consumption of CNS stimulants such as caffeine, nicotine, amphetamines, and cocaine during pregnancy can adversely impact the offspring. However, most work in this area has focused on neurological and behavioral outcomes and has been limited to assessments in young offspring. The impact of prenatal exposure to these agents on the adult cardiovascular system has received relatively little attention. Evidence from both animal and human studies indicate that exposure to CNS stimulants during the gestational period can negatively impact the adult heart and vasculature, potentially leading to cardiovascular diseases later in life. This review discusses our current understanding of the impact of prenatal exposure to cocaine, methamphetamine, nicotine, and caffeine on the adult cardiovascular system.
Highlights
Drug and alcohol use during pregnancy is a significant public health concern
The purpose of this review is to summarize our current understanding of the impact of prenatal exposure to CNS stimulants on adult cardiovascular function
Similar to Zhang’s work with prenatal cocaine [28, 45], we found that PKCε expression was significantly decreased in adult rats that had been prenatally exposed to methamphetamine, suggesting that prenatal exposure to these drugs might alter myocardial sensitivity to ischemia in the adult heart through a similar (PKC-ε-dependent) mechanism
Summary
Drug and alcohol use during pregnancy is a significant public health concern. The 2018 National Survey on Drug Use and Health estimated that 5 % of pregnant women used an illicit drug within the past month [1]. Use of tobacco products (12%) and binge consumption of alcohol (5%) are common among pregnant women [1] Prenatal exposure to these substances can have a profound impact on adult offspring. It is well-established that substance use during pregnancy can negatively impact cognition [2, 3], the stress response [4], anxiety [5, 6], and susceptibility to drug addiction [7, 8] in the adult offspring These transgenerational effects involve epigenetic mechanisms (DNA methylation, histone acetylation, micro RNA) [9,10,11] as well as drug-induced changes in endocrine function [12, 13], receptor expression [14,15,16], and structural changes within the brain [17, 18] that can have pathological consequences extending into adulthood
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