Smoking cessation, weight gain, and risk of stroke among postmenopausal women.

The relationship between smoking cessation, concurrent weight gain, and stroke events is not yet understood. Thus, we examined the association between smoking cessation and subsequent stroke risk and whether the association was modified by concurrent weight gain. In 2017, we analyzed data from 109,498 postmenopausal US women enrolled in the Women's Health Initiative from 1993 to 1998. Women with a history of cancer or cardiovascular disease events were excluded. The median length of follow-up time was 14.01 years. Variables of primary focus were smoking cessation, weight change, and clinically confirmed incident cases of hemorrhagic and ischemic stroke. Hazard ratios were estimated for stroke incidences (all, ischemic, and hemorrhagic) associated with smoking cessation using Cox regression. The exposure-outcome relationship of smoking cessation and risk of stroke was evaluated for effect modification by weight change. Recent quitters between baseline and year 3 had a significantly lower risk for all stroke and ischemic stroke, but not hemorrhagic stroke, when compared to the reference group of continuing smokers. In the multivariable-adjusted model for ischemic stroke, the hazard ratio for recent quitters was 0.66 (95% CI: 0.46, 0.95). In the model for hemorrhagic stroke, the hazard ratio for recent quitters was 0.76 (95% CI: 0.36, 1.61). The association between recent quitting and stroke risk was not significantly modified by weight change. Smoking cessation was associated with a significant reduction in stroke risk. The benefit of smoking cessation on the risk of stroke was not attenuated by concurrent weight gain.

Assessment of the influence of food attributes on meal choice selection by socioeconomic status and race/ethnicity among women living in Chicago, USA: A discrete choice experiment.

Large and persistent obesity disparities exist in the US by socioeconomic status (SES) and race/ethnicity, and weight loss interventions have traditionally been less effective in these populations. Thus, a better understanding is needed of the behavioral, economic, and geographic factors that influence obesity risk factors such as eating behaviors. We used a discrete choice experiment to evaluate the impact of different meal attributes on meal choice and to test whether the relative importance of these attributes varied by SES and race/ethnicity. Study participants (n = 228) were given a series of 10 choice tasks and asked to choose among 4 meals, each rated based on the following attributes: taste; healthfulness; preparation time; travel time to food outlet for meal/ingredients; and price. SES was measured using education and self-reported difficulty paying for basics. Race/ethnicity was categorized as Hispanic/Latina, non-Hispanic black, non-Hispanic white, and non-Hispanic other. Data were analyzed using mixed logit regression models with interaction terms to determine whether meal attributes influenced meal choices differentially by SES and race/ethnicity. Healthfulness and taste were the most important attributes for all participants. Price was a more important attribute among those in the lowest SES group compared with those in the higher SES groups. Travel was the least important attribute for low SES participants, and it was not significantly related to meal choice in these groups. Discrete choice experiments as illustrated here may help pinpoint the most salient targets for interventions to improve eating behaviors and reduce obesity disparities. Specifically, our findings suggest interventions should incorporate strategies to target the pricing of healthy and unhealthy food options.

Circadian disruption, clock genes, and metabolic health.

A growing body of research has identified circadian-rhythm disruption as a risk factor for metabolic health. However, the underlying biological basis remains complex, and complete molecular mechanisms are unknown. There is emerging evidence from animal and human research to suggest that the expression of core circadian genes, such as circadian locomotor output cycles kaput gene (CLOCK), brain and muscle ARNT-Like 1 gene (BMAL1), period (PER), and cyptochrome (CRY), and the consequent expression of hundreds of circadian output genes are integral to the regulation of cellular metabolism. These circadian mechanisms represent potential pathophysiological pathways linking circadian disruption to adverse metabolic health outcomes, including obesity, metabolic syndrome, and type 2 diabetes. Here, we aim to summarize select evidence from in vivo animal models and compare these results with epidemiologic research findings to advance understanding of existing foundational evidence and potential mechanistic links between circadian disruption and altered clock gene expression contributions to metabolic health-related pathologies. Findings have important implications for the treatment, prevention, and control of metabolic pathologies underlying leading causes of death and disability, including diabetes, cardiovascular disease, and cancer.

Insulin resistance since early adulthood and appendicular lean mass in middle-aged adults without diabetes: 20 years of the CARDIA study.

AIMS: To determine the association between 20-year trajectories in insulin resistance (IR) since young adulthood and appendicular lean mass (ALM) at middle-age in adults without diabetes. METHODS: A prospective cohort study was designed among young and middle-aged US men (n = 925) and women (n = 1193). Fasting serum glucose and insulin were measured five times in 1985-2005. IR was determined using the homeostasis model assessment (HOMA). ALM was measured in 2005 and ALM adjusted for BMI (ALM/BMI) was the outcome. Sex-specific analyses were performed. RESULTS: Three HOMA-IR trajectories were identified. Compared to the low-stable group, the adjusted ALM/BMI difference was -0.041 (95% CI: -0.060 to -0.022) and -0.114 (-0.141 to -0.086) in men, and -0.052 (-0.065 to -0.039) and -0.043 (-0.063 to -0.023) in women, respectively, for the medium-increase and high-increase groups. Further adjusting for the treadmill test duration attenuated these estimates to -0.022 (-0.040 to -0.004) and -0.061 (-0.089 to -0.034) in men and -0.026 (-0.038 to -0.014) and -0.007 (-0.026 to 0.012) in women. CONCLUSIONS: Compared to the low-stable insulin resistance trajectory between early and middle adulthood, the high-increase trajectory was associated with lower ALM/BMI in middle-aged men, but not women, without diabetes, after adjusting for cardiorespiratory fitness.