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The intergenerational transmission of smoking in adulthood: a 25-year study of maternal and offspring maladaptive attributes.

ABSTRACT: While smoking is a major cause of mortality and morbidity, and maternal smoking is a risk factor for smoking among their offspring, the mechanisms involved in the intergenerational transmission of smoking are not well understood. This study examines the pathways from maternal and adolescent child factors, and the parent-child relationship, to smoking among the adult offspring, approximately 25 years later. Data for the present analysis were based on time waves 2 (T2; 1983) and 7 (T7; 2007-2009) of an on-going study of a community sample of mothers and their children. Offspring and mother X¯ ages were 14.1 and 40.0 years, respectively, at T2, and 36.6 and 65.0 years, respectively, at T7. At T2, trained interviewers administered individual structured interviews. Psychosocial questionnaires were self-administered at T7. Structural equation modeling (SEM) was used to analyze the interrelationships among maternal and offspring attributes (T2 and T7). SEM results indicated a satisfactory model fit (RMSEA=0.052; CFI=0.91; SRMR=0.057), and confirmed hypothesized pathways. One pathway linked maternal maladaptive attributes (T2) to the mother-adolescent child attachment relationship (T2), which was associated with the offspring's maladaptive attributes over time (T2 to T7), which then predicted the adult offspring's smoking (T7). Other pathways highlighted the stability of maternal smoking, the continuity of maladaptive attributes, and less offspring educational attainment as predictors of offspring smoking at T7. Findings suggest the importance of early interventions to treat maternal smoking, maternal and offspring maladaptive attributes, and the mother-child relationship in order to reduce risk factors for the intergenerational transmission of smoking behavior. Interventions which enhance educational success should also prove effective in reducing smoking.

SUBMITTER: Brook JS

PROVIDER: S-EPMC3634878 | biostudies-literature | 2013 Jul

REPOSITORIES: biostudies-literature

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The intergenerational transmission of smoking in adulthood: a 25-year study of maternal and offspring maladaptive attributes.

Brook Judith S JS Rubenstone Elizabeth E Zhang Chenshu C Finch Stephen J SJ Brook David W DW

Addictive behaviors 20130321 7

While smoking is a major cause of mortality and morbidity, and maternal smoking is a risk factor for smoking among their offspring, the mechanisms involved in the intergenerational transmission of smoking are not well understood. This study examines the pathways from maternal and adolescent child factors, and the parent-child relationship, to smoking among the adult offspring, approximately 25 years later. Data for the present analysis were based on time waves 2 (T2; 1983) and 7 (T7; 2007-2009) ...[more]

PMID: 23602938

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Project description:The prevalence of inflammatory bowel disease (IBD) is increasing worldwide and correlates with dysregulated immune response because of gut microbiota dysbiosis. Some adverse early life events influence the establishment of the gut microbiota and act as risk factors for IBD. Prenatal maternal stress (PNMS) induces gut dysbiosis and perturbs the neuroimmune network of offspring. In this study, we aimed to investigate whether PNMS increases the susceptibility of offspring to colitis in adulthood. The related index was assessed during the weaning period and adulthood. We found that PNMS impaired the intestinal epithelial cell proliferation, goblet cell and Paneth cell differentiation, and mucosal barrier function in 3-week-old offspring. PNMS induced low-grade intestinal inflammation, but no signs of microscopic inflammatory changes were observed. Although there was no pronounced difference between the PNMS and control offspring in terms of their overall measures of alpha diversity for the gut microbiota, distinct microbial community changes characterized by increases in Desulfovibrio, Streptococcus, and Enterococcus and decreases in Bifidobacterium and Blautia were induced in the 3-week-old PNMS offspring. Notably, the overgrowth of Desulfovibrio persisted from the weaning period to adulthood, consistent with the results observed using fluorescence in situ hybridization in the colon mucosa. Mechanistically, the fecal microbiota transplantation experiment showed that the gut microbiota from the PNMS group impaired the intestinal barrier function and induced low-grade inflammation. The fecal bacterial solution from the PNMS group was more potent than that from the control group in inducing inflammation and gut barrier disruption in CaCo-2 cells. After treatment with a TNF-α inhibitor (adalimumab), no statistical difference in the indicators of inflammation and intestinal barrier function was observed between the two groups. Finally, exposure to PNMS remarkably increased the values of the histopathological parameters and the inflammatory cytokine production in a mouse model of experimental colitis in adulthood. These findings suggest that PNMS can inhibit intestinal development, impair the barrier function, and cause gut dysbiosis characterized by the persistent overgrowth of Desulfovibrio in the offspring, resulting in exacerbated experimental colitis in adulthood.

Dataset Information

The intergenerational transmission of smoking in adulthood: a 25-year study of maternal and offspring maladaptive attributes.

Publications

The intergenerational transmission of smoking in adulthood: a 25-year study of maternal and offspring maladaptive attributes.

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