BackgroundStudies reveal that electronic cigarette (e-cigarette) and hookah use are increasing among adolescents and young adults. However, the long-term health effects are unknown, especially with regards to pregnancy. Because of the increased use in women of reproductive age, and the unknown long-term health risks, our primary objectives were to determine the perceived risks of e-cigarette and hookah use in pregnancy, and learn common colloquial terms associated with e-cigarettes. Furthermore, we sought to determine if there is a stigma associated with e-cigarette use in pregnancy.MethodsEleven focus groups including 87 participants were conducted immediately following regularly scheduled CenteringPregnancy® prenatal care with women at three different clinics in the greater Houston area. A minimum of two facilitators led the groups, using ten lead-in prompts, with Spanish translation as necessary. Facilitators took notes which were compared immediately following each group discussion and each group was audio recorded and transcribed. Three facilitators utilized NVivo 9.0 software to organize the transcribed data into nodes to identify major themes. To increase rigor, transcripts were further analyzed by two obstetricians who were instructed to find the major themes.ResultsAnalyses revealed contradicting themes concerning e-cigarette use. In general, e-cigarettes were perceived as safer alternatives to regular tobacco cigarettes, especially if used as smoking cessation devices. A major theme is that use in pregnancy is harmful to the fetus. However, it was perceived that use for smoking cessation in pregnancy may have fewer side effects. We found that a common term for e-cigarettes is “Blu.” In our discussion of hookah use, participants perceived use as popular among teenagers and that use in pregnancy is dangerous for the fetus.ConclusionsAlthough a strong theme emerged against hookah use, we found contradicting themes in our discussions on e-cigarette use in pregnancy. It is possible that e-cigarette use will not carry the same stigma as regular cigarette smoking in pregnancy. In addition, the impression of e-cigarettes as a healthier alternative to smoking may influence use in pregnancy. Clinicians need to be prepared for questions of e-cigarette safety and efficacy as smoking cessation devices from their pregnant patients who smoke, and women who smoke and are planning to become pregnant.
Background Gestational diabetes mellitus (GDM) is one of most common complications of pregnancy, with incidence rates varying by maternal age, race/ethnicity, obesity, parity, and family history. Given its increasing prevalence in recent decades, co-variant environmental and sociodemographic factors may be additional determinants of GDM occurrence. Objectives We hypothesized that environmental risk factors, in particular measures of the food environment, may be a diabetes contributor. We employed geospatial modeling in a populous U.S. county to characterize the association of the relative availability of fast food restaurants and supermarkets to GDM. Study Design Utilizing a perinatal database with over 4900 encoded antenatal and outcome variables inclusive of zip code data, 8912 consecutive pregnancies were analyzed for correlations between GDM and food environment based on county-wide food permit registration data. Linkage between pregnancies and food environment was achieved on the basis of validated 5 digit zip code data. The prevalence of supermarkets and fast food restaurants per 100,000 inhabitants for each zip code were gathered from publicly available food permit sources. In order to independently authenticate our findings with objective data, we measured hemoglobin A1c (HbA1c) levels as a function of geospatial distribution of food environment in a matched subset (n=80). Results Residence in neighborhoods with a high prevalence of fast food restaurants (fourth quartile) was significantly associated with an increased risk of developing GDM (relative to first quartile, aOR: 1.63 [95% CI 1.21–2.19]). In multivariate analysis, this association held true after controlling for potential confounders (p=0.002). Measurement of HbA1c levels in a matched subset were significantly increased in association with residence in a zip code with a higher fast food/supermarket ratio (n=80, r=0.251 p<0.05). Conclusions As demonstrated by geospatial analysis, a relationship of food environment and risk for gestational diabetes was identified.
Background Fetal exposure to nicotine is not limited to maternal tobacco smoke, as electronic cigarettes have an increased prevalence of use among reproductive aged women. Animal models have shown that nicotine exposure in utero is associated with increased risk of asthma and cognitive deficits, as well as increased expression of the hippocampal glucocorticoid receptor. We hypothesized that in utero nicotine exposure is associated with epigenetic changes in the offspring lung and brain which may contribute to a memory of this exposure. Methods Sprague-Dawley rat dams received either saline or 2mg/kg of nicotine by intraperitoneal injection once daily from embryonic day 6 (e6) to e22. Pups were sacrificed on day 1 of life, and brain and lung tissues were harvested (N=3/ group). Results We found that nicotine exposed offspring have altered histone modifications in the brain. Dimethylation of lysine 9 of histone H3 is decreased (0.43-fold, p=0.03) while acetylation is increased (1.79-fold, p=0.031). Histone deacetylase (HDAC) activity is significantly decreased with nicotine exposure in brain and lung (0.11-fold, p<0.001; 0.12-fold, p<0.001, respectively). Expression of splice variant 1.7 of the glucocorticoid receptor is reduced in the nicotine exposed offspring lung (0.25-fold, p=0.038). Conclusions We conclude that nicotine exposure is associated with epigenetic alterations in the offspring and may lead to susceptibility to adult disease,. Our finding that in utero exposure to nicotine is associated with inhibition of HDAC activity in the brain of offspring is of importance as a similar inhibition has been suggested as a mechanism for the potentiation of addiction.
Highlights d SCA7 mice display increased histone H3 promoter Ac in DNA repair genes in cerebellum d DNA damage is elevated in SCA7 cells, primary neurons, and patient stem cell neurons d DNA repair assays in cells expressing polyQ-ataxin-7 show deficits in specific pathways d LAM-HTGTS identifies altered repair processes on endogenous DNA in SCA7 cell models
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