Offspring from families at high risk for alcohol dependence: Increased body mass index in association with prenatal exposure to cigarettes but not alcohol

Abstract

The prevalence of overweight and obese children is increasing, a tendency that can be expected to increase the risk of adverse outcomes in adulthood. The aim of this study was to determine if prenatal exposure to alcohol, cigarettes, and street drugs would be associated with differences in body mass index (BMI) in childhood and adolescence in offspring from families at high and low genetic risk for developing alcohol dependence. Annual follow-up of offspring (N =288) provided 1200 height and weight assessments for analysis. Maternal substance use data were available for 235 offspring from families stratified for familial/genetic risk for alcohol dependence (high or low risk), providing the opportunity to assess prenatal exposure and familial/genetic risk in relation to BMI in the offspring. When data were grouped by the presence or absence of any prenatal cigarette exposure, a significant difference in offspring BMI was seen for 8-to 11-year-olds. Significant group differences were also seen at ages 12-15 and 16-18 years. A dose-response relationship between cigarette use by the mother and offspring BMI was also seen. With the strong tendency for individuals who are overweight in childhood and adolescence to become overweight adults, prenatal exposure to nicotine may be a harbinger of increased risk for numerous adultonset, weight-related health problems.

Association between Prenatal Tobacco Exposure and Outcome of Neonates Born to Opioid-Maintained Mothers

“…Somm et al [9] showed in a recent publication that prenatal nicotine exposure caused alterations in pancreatic islet development, which can lead to the metabolic syndrome in offspring with early signs of adipose tissue dysregulation. These results suggest a direct association between maternal nicotine consumption and the impaired control of body weight and glucose metabolism in neonates [10] . Nicotine also causes neurotoxic effects that can potentially contribute to abnormalities in synaptic activity [3] and damage the central nervous system of the child [11] .…”

Endocrine-Disrupting Organotin Compounds Are Potent Inducers of Adipogenesis in Vertebrates

“…Environmental estrogens such as bisphenol A and nonylphenol, for instance, can promote adipocyte differentiation or proliferation in murine cell lines (70,71). Furthermore, epidemiological studies link maternal smoking during pregnancy to an elevated risk of childhood obesity (72)(73)(74)(75)(76).…”

Maternal nicotine exposure leads to higher liver oxidative stress and steatosis in adult rat offspring

“…Also tobacco exposure can contribute to obesity development since several epidemiological studies have reported that maternal smoking during pregnancy and/or lactation can be a risk factor for child and teenager obesity and hypertension (Gao et al, 2005;Goldani et al, 2007;Hill et al, 2005;Von Kries et al, 2002;Wideroe et al, 2003). The relationship between environmental, nutritional and hormonal influences at critical windows of plasticity and several chronic adult diseases is named programming (Barker, 2003;de Moura et al, 2008).…”