Mother's Smoking May Affect Child's Craving for Fat

Norra MacReady

September 04, 2012

September 4, 2012 — A new study adds to the growing body of evidence that prenatal exposure to maternal cigarette smoking (PEMCS) may be a factor in the worldwide epidemic of obesity.

Adolescents whose mothers smoked while pregnant had a higher body mass index (BMI), had more total body fat, and reported a higher intake of dietary fat than the children of nonsmoking mothers, lead author Amirreza Haghighi, MD, and colleagues report in an article published online September 3 in the Archives of General Psychiatry.

There was also a correlation between smaller amygdala volume and higher fat intake among patients in the PEMCS group, but not in the control group.

The findings suggest that "PEMCS may increase the risk for obesity by enhancing dietary intake of fat, and that this effect may be mediated in part through subtle changes in brain structures involved in reward processing," the investigators write.

Dr. Haghighi, from the Hospital for Sick Children, University of Toronto, Ontario, Canada, and coauthors studied adolescents aged 13 to 19 years who were recruited from high schools in the Saguenay Lac St. Jean region of Quebec, Canada, as part of the ongoing Saguenay Youth Study. Only adolescents at Tanner stages 4 and 5 were included.

The 180 PEMCS participants were compared with 198 control patients matched for age, school attended, and maternal education to minimize the potential confounding influence of socioeconomic status (SES). Cigarette exposure was defined as "having a mother who smoked more than 1 cigarette per day during the second trimester of pregnancy and being nonexposed was defined as having a mother who did not smoke 1 year before (and throughout) the pregnancy," the authors explain. The mothers of exposed participants smoked an average of 11.1 (standard deviation [SD], 6.8) cigarettes daily throughout their pregnancies.

Dietary fat intake was determined through a 24-hour food recall interview conducted by a trained nutritionist on a Saturday morning. This was complemented by having the participants answer 6 questions about their eating habits, including fruit and vegetable consumption, for the previous 7 days. Brain structures were measured through magnetic resonance imaging of the left and right nucleus accumbens, as well as the left and right amygdala.

Exposed children weighed, on average, 301 g less at birth than the nonexposed children, and were breast-fed for an average of 4.5 weeks less (P < .001 for both comparisons). After adjusting for age, sex, and (when appropriate) height, the exposed children weighed an average of 1.7 kg more in adolescence, but this difference was not significant (P = .10). Their average BMI was 0.7 kg/m2 higher (P = .05).

These differences "remained virtually unchanged after additional adjusting for variables frequently associated with maternal cigarette smoking during pregnancy and implicated on their own in increasing the risk for obesity (ie, lower birth weight, shorter duration [or lack of] breastfeeding, and lower SES)," the authors write. "They also remained virtually unchanged after additional adjusting for maternal BMI, a known risk factor for offspring. Thus, it appears that the association between PEMCS and greater adiposity is independent of these factors and, as such, may be specific to maternal cigarette smoking."

Fat intake was 2.7% higher, as a percentage of energy intake, among the exposed than the nonexposed children (P =.001), a difference that remained significant (P < .001) after adjustment for birth weight, breast-feeding, and family income. Similarly, amygdala volume was 95 mm3 smaller among the exposed children (P < .001), again after adjustment for perinatal and socioeconomic factors, as well as maternal BMI. "In addition, amygdala volume correlated inversely with fat intake (r = −0.15; P = .006), and this correlation was seen in exposed (r = −0.16; P < .04) but not in nonexposed (r = −0.08; P = .29) participants."

The amygdala is part of the reward center in the brain, and lower amygdala volume has been associated with alcohol craving and addiction, the authors write. In animal studies, stimulation of the amygdala appears to decrease the preference for dietary fat.

The current research suggests that the smaller size or lower activity level of the amygdala may stimulate the craving for fat as well as increase the risk for addiction to substances such as alcohol. The reduction in amygdala size associated with PEMCS may help explain the higher fat intake and greater BMI of the PEMCS participants in this study, the authors point out.

These findings support the fetal-programming hypothesis of obesity, they conclude. The data "suggest that PEMCS may contribute in this context by modifying fat intake through neural mechanisms involving the amygdala."

The Saguenay Youth Study is funded by the Canadian Institutes of Health Research, the Heart and Stroke Foundation of Quebec, and the Canadian Foundation for Innovation. The authors have disclosed no relevant financial relationships.

Arch Gen Psychiatry. Published online September 3, 2012. Abstract

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