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1.
Gastroenterol Clin North Am ; 52(2): 347-362, 2023 06.
Artigo em Inglês | MEDLINE | ID: mdl-37197878

RESUMO

The obesity epidemic is caused by the misalignment between human biology and the modern food environment, which has led to unhealthy eating patterns and behaviors and an increase in metabolic diseases. This has been caused by the shift from a "leptogenic" to an "obesogenic" food environment, characterized by the availability of unhealthy food and the ability to eat at any time of day due to advances in technology. Binge Eating Disorder (BED) is the most commonly diagnosed eating disorder, characterized by recurrent episodes of binge eating and a sense of loss of control over eating, and is treated with cognitive-behavioral therapy-enhanced (CBT-E). Shift work, especially night shift work, can disrupt the body's natural circadian rhythms and increase the risk of obesity and other negative health consequences, such as cardiovascular disease and metabolic syndrome. One dietary approach to address circadian dysregulation is time-restricted eating (TRE), which involves restricting food intake to specific periods of the day to synchronize the body's internal clock with the external environment. TRE has been found to cause modest weight loss and improve metabolic outcomes such as insulin sensitivity and blood pressure, but the extent to which it is beneficial may depend on adherence and other factors such as caloric restriction.


Assuntos
Terapia Cognitivo-Comportamental , Obesidade , Humanos , Obesidade/terapia , Obesidade/epidemiologia , Comportamento Alimentar/fisiologia , Dieta , Ritmo Circadiano/fisiologia
2.
Heart Mind (Mumbai) ; 6(4): 254-261, 2022.
Artigo em Inglês | MEDLINE | ID: mdl-36994354

RESUMO

Background: Ischemic heart disease (IHD) risk in women includes biomedical, behavioral, and psychosocial contributors. The purpose of this study was to build upon previous research suggesting that in women, somatic symptoms (SS) of depression may be important to the development of IHD risk factors and major adverse cardiovascular events (MACE). Based on previous findings, we hypothesized that: (1) SS would be associated with robust biomedical predictors of heart disease and functional capacity, while cognitive symptoms (CS) of depression would not, and (2) SS would independently predict adverse health outcomes while CS would not. Methods: We examined the relationships between symptoms of depression (SS/CS), metabolic syndrome (MetS), inflammatory markers (IM), coronary artery disease (CAD) severity, and functional capacity in two independent cohorts of women with suspected IHD. In the Women's Ischemia Syndrome Evaluation (WISE), we also examined these variables as predictors of all-cause mortality (ACM) + MACE over a median 9.3-year follow-up. The WISE sample included 641 women with suspected ischemia with or without obstructive CAD. The WISE-Coronary Vascular Dysfunction (WISE-CVD) sample consisted of 359 women with suspected ischemia and no obstructive CAD. All study measures were collected uniformly at baseline. Depressive symptoms were measured via the Beck Depression Inventory. MetS was assessed according to Adult Treatment Panel III (ATP-III) criteria. Results: In both studies, SS was associated with MetS (Cohen's d = 0.18, 0.26, P < 0.05, respectively), while CS was not. Within WISE, using Cox Proportional Hazard Regression, SS (Hazard ratio [HR] = 1.08, 95% confidence interval [CI] = 1.01-1.15; HR = 1.07, 95% CI = 1.00-1.13) and MetS (HR = 1.89, 95% CI = 1.16-3.08; HR = 1.74, 95% CI=1.07-2.84) were independent predictors of ACM + MACE after controlling for demographics, IM, and CAD severity, while CS was not. Conclusions: In two independent samples of women undergoing coronary angiography due to suspected ischemia, SS but not CS of depression were associated with MetS, and both SS and MetS independently predicted ACM and MACE. These results add to previous studies suggesting that SS of depression may warrant specific attention in women with elevated cardiovascular disease (CVD) risk. Future research evaluating the biobehavioral basis of the relationship between depression, MetS, and CVD is needed.

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