Objective: The recent obesity epidemic has been accompanied by a parallel growth in chronic sleep deprivation. Physiologic studies suggest sleep deprivation may influence weight through effects on ...appetite, physical activity, and/or thermoregulation. This work reviews the literature regarding short sleep duration as an independent risk factor for obesity and weight gain.
Methods and Procedures: A literature search was conducted for all articles published between 1966 and January 2007 using the search “sleep” and (“duration” or “hour” or “hours”) and (“obesity” or “weight”) in the MEDLINE database. Additional references were identified by reviewing bibliographies and contacting experts in the field. Studies reporting the association between sleep duration and at least one measure of weight were included.
Results: Thirty‐six publications (31 cross‐sectional, 5 prospective, and 0 experimental) were identified. Findings in both cross‐sectional and cohort studies of children suggested short sleep duration is strongly and consistently associated with concurrent and future obesity. Results from adult cross‐sectional analyses were more mixed with 17 of 23 studies supporting an independent association between short sleep duration and increased weight. In contrast, all three longitudinal studies in adults found a positive association between short sleep duration and future weight. This relationship appeared to wane with age.
Discussion: Short sleep duration appears independently associated with weight gain, particularly in younger age groups. However, major study design limitations preclude definitive conclusions. Further research with objective measures of sleep duration, repeated assessments of both sleep and weight, and experimental study designs that manipulate sleep are needed to better define the causal relationship of sleep deprivation on obesity.
IMPORTANCE: It is crucial to incorporate quality and types of carbohydrate and fat when investigating the associations of low-fat and low-carbohydrate diets with mortality. OBJECTIVE: To investigate ...the associations of low-carbohydrate and low-fat diets with total and cause-specific mortality among US adults. DESIGN, SETTING, AND PARTICIPANTS: This prospective cohort study used data from the US National Health and Nutrition Examination Survey from 1999 to 2014 from 37 233 adults 20 years or older with 24-hour dietary recall data. Data were analyzed from July 5 to August 27, 2019. EXPOSURES: Overall, unhealthy, and healthy low-carbohydrate-diet and low-fat-diet scores based on the percentage of energy as total and subtypes of carbohydrate, fat, and protein. MAIN OUTCOMES AND MEASURES: All-cause mortality from baseline until December 31, 2015, linked to National Death Index mortality data. RESULTS: A total of 37 233 US adults (mean SD age, 49.7 18.3 years; 19 598 52.6% female) were included in the present analysis. During 297 768 person-years of follow-up, 4866 total deaths occurred. Overall low-carbohydrate-diet and low-fat-diet scores were not associated with total mortality. The multivariable-adjusted hazard ratios for total mortality per 20-percentile increase in dietary scores were 1.07 (95% CI, 1.02-1.11; P = .01 for trend) for unhealthy low-carbohydrate-diet score, 0.91 (95% CI, 0.87-0.95; P < .001 for trend) for healthy low-carbohydrate-diet score, 1.06 (95% CI, 1.01-1.12; P = .04 for trend) for unhealthy low-fat-diet score, and 0.89 (95% CI, 0.85-0.93; P < .001 for trend) for healthy low-fat-diet score. The associations remained similar in the stratification and sensitivity analyses. CONCLUSIONS AND RELEVANCE: In this study, overall low-carbohydrate-diet and low-fat-diet scores were not associated with total mortality. Unhealthy low-carbohydrate-diet and low-fat-diet scores were associated with higher total mortality, whereas healthy low-carbohydrate-diet and low-fat-diet scores were associated with lower total mortality. These findings suggest that the associations of low-carbohydrate and low-fat diets with mortality may depend on the quality and food sources of macronutrients.
AbstractObjectiveTo examine how a healthy lifestyle is related to life expectancy that is free from major chronic diseases.DesignProspective cohort study.Setting and participantsThe Nurses’ Health ...Study (1980-2014; n=73 196) and the Health Professionals Follow-Up Study (1986-2014; n=38 366).Main exposuresFive low risk lifestyle factors: never smoking, body mass index 18.5-24.9, moderate to vigorous physical activity (≥30 minutes/day), moderate alcohol intake (women: 5-15 g/day; men 5-30 g/day), and a higher diet quality score (upper 40%).Main outcomeLife expectancy free of diabetes, cardiovascular diseases, and cancer.ResultsThe life expectancy free of diabetes, cardiovascular diseases, and cancer at age 50 was 23.7 years (95% confidence interval 22.6 to 24.7) for women who adopted no low risk lifestyle factors, in contrast to 34.4 years (33.1 to 35.5) for women who adopted four or five low risk factors. At age 50, the life expectancy free of any of these chronic diseases was 23.5 (22.3 to 24.7) years among men who adopted no low risk lifestyle factors and 31.1 (29.5 to 32.5) years in men who adopted four or five low risk lifestyle factors. For current male smokers who smoked heavily (≥15 cigarettes/day) or obese men and women (body mass index ≥30), their disease-free life expectancies accounted for the lowest proportion (≤75%) of total life expectancy at age 50.ConclusionAdherence to a healthy lifestyle at mid-life is associated with a longer life expectancy free of major chronic diseases.
Dietary interventions in patients with type 2 diabetes (T2D) are important for preventing long-term complications. Although a healthy diet is crucial, there is still uncertainty about the optimal ...macronutrient composition. We performed a meta-analysis comparing diets high in cis-monounsaturated fatty acids (MUFA) to diets high in carbohydrates (CHO) or in polyunsaturated fatty acids (PUFA) on metabolic risk factors in patients with T2D.
We systematically reviewed PubMed, MEDLINE, and Cochrane databases and prior systematic reviews and meta-analyses to identify interventions assessing HbA1c, fasting plasma glucose and insulin, LDL and HDL cholesterol, triglycerides, body weight, or systolic/diastolic blood pressure. Meta-analyses were conducted using both fixed- and random-effects models to calculate the weighted mean difference (WMD) and 95% CI.
We identified 24 studies totaling 1,460 participants comparing high-MUFA to high-CHO diets and 4 studies totaling 44 participants comparing high-MUFA to high-PUFA diets. When comparing high-MUFA to high-CHO diets, there were significant reductions in fasting plasma glucose (WMD -0.57 mmol/L 95% CI -0.76, -0.39), triglycerides (-0.31 mmol/L -0.44, -0.18), body weight (-1.56 kg -2.89, -0.23), and systolic blood pressure (-2.31 mmHg -4.13, -0.49) along with significant increases in HDL cholesterol (0.06 mmol/L 0.02, 0.10). When high-MUFA diets were compared with high-PUFA diets, there was a significant reduction in fasting plasma glucose (-0.87 mmol/L -1.67, -0.07). All of the outcomes had low to medium levels of heterogeneity, ranging from 0.0 to 69.5% for diastolic blood pressure (Phet = 0.011).
Our meta-analysis provides evidence that consuming diets high in MUFA can improve metabolic risk factors among patients with T2D.
BACKGROUND—The prevalence of smoking in diabetic patients remains high, and reliable quantification of the excess mortality and morbidity risks associated with smoking is important for diabetes ...management. We performed a systematic review and meta-analysis of prospective cohort studies to evaluate the relation of active smoking with risk of total mortality and cardiovascular events among diabetic patients.
METHODS AND RESULTS—We searched Medline and Embase databases through May 2015, and multivariate-adjusted relative risks were pooled by using random-effects models. A total of 89 cohort studies were included. The pooled adjusted relative risk (95% confidence interval) associated with smoking was 1.55 (1.46–1.64) for total mortality (48 studies with 1 132 700 participants and 109 966 deaths), and 1.49 (1.29–1.71) for cardiovascular mortality (13 studies with 37 550 participants and 3163 deaths). The pooled relative risk (95% confidence interval) was 1.44 (1.34–1.54) for total cardiovascular disease (16 studies), 1.51 (1.41–1.62) for coronary heart disease (21 studies), 1.54 (1.41–1.69) for stroke (15 studies), 2.15 (1.62–2.85) for peripheral arterial disease (3 studies), and 1.43 (1.19–1.72) for heart failure (4 studies). In comparison with never smokers, former smokers were at a moderately elevated risk of total mortality (1.19; 1.11–1.28), cardiovascular mortality (1.15; 1.00–1.32), cardiovascular disease (1.09; 1.05–1.13), and coronary heart disease (1.14; 1.00–1.30), but not for stroke (1.04; 0.87–1.23).
CONCLUSIONS—Active smoking is associated with significantly increased risks of total mortality and cardiovascular events among diabetic patients, whereas smoking cessation is associated with reduced risks in comparison with current smoking. The findings provide strong evidence for the recommendation of quitting smoking among diabetic patients.
The relation between sugar-sweetened beverages (SSBs) and body weight remains controversial.
We conducted a systematic review and meta-analysis to summarize the evidence in children and adults.
We ...searched PubMed, EMBASE, and Cochrane databases through March 2013 for prospective cohort studies and randomized controlled trials (RCTs) that evaluated the SSB-weight relation. Separate meta-analyses were conducted in children and adults and for cohorts and RCTs by using random- and fixed-effects models.
Thirty-two original articles were included in our meta-analyses: 20 in children (15 cohort studies, n = 25,745; 5 trials, n = 2772) and 12 in adults (7 cohort studies, n = 174,252; 5 trials, n = 292). In cohort studies, one daily serving increment of SSBs was associated with a 0.06 (95% CI: 0.02, 0.10) and 0.05 (95% CI: 0.03, 0.07)-unit increase in BMI in children and 0.22 kg (95% CI: 0.09, 0.34 kg) and 0.12 kg (95% CI: 0.10, 0.14 kg) weight gain in adults over 1 y in random- and fixed-effects models, respectively. RCTs in children showed reductions in BMI gain when SSBs were reduced random and fixed effects: -0.17 (95% CI: -0.39, 0.05) and -0.12 (95% CI: -0.22, -0.2), whereas RCTs in adults showed increases in body weight when SSBs were added (random and fixed effects: 0.85 kg; 95% CI: 0.50, 1.20 kg). Sensitivity analyses of RCTs in children showed more pronounced benefits in preventing weight gain in SSB substitution trials (compared with school-based educational programs) and among overweight children (compared with normal-weight children).
Our systematic review and meta-analysis of prospective cohort studies and RCTs provides evidence that SSB consumption promotes weight gain in children and adults.
To examine and quantify the potential dose-response relationship between red and processed meat consumption and risk of all-cause, cardiovascular and cancer mortality.
We searched MEDLINE, Embase, ...ISI Web of Knowledge, CINHAL, Scopus, the Cochrane library and reference lists of retrieved articles up to 30 November 2014 without language restrictions. We retrieved prospective cohort studies that reported risk estimates for all-cause, cardiovascular and cancer mortality by red and/or processed meat intake levels. The dose-response relationships were estimated using data from red and processed meat intake categories in each study. Random-effects models were used to calculate pooled relative risks and 95 % confidence intervals and to incorporate between-study variations.
Nine articles with seventeen prospective cohorts were eligible in this meta-analysis, including a total of 150 328 deaths. There was evidence of a non-linear association between processed meat consumption and risk of all-cause and cardiovascular mortality, but not for cancer mortality. For processed meat, the pooled relative risk with an increase of one serving per day was 1·15 (95 % CI 1·11, 1·19) for all-cause mortality (five studies; P<0·001 for linear trend), 1·15 (95 % CI 1·07, 1·24) for cardiovascular mortality (six studies; P<0·001) and 1·08 (95 % CI 1·06, 1·11) for cancer mortality (five studies; P<0·001). Similar associations were found with total meat intake. The association between unprocessed red meat consumption and mortality risk was found in the US populations, but not in European or Asian populations.
The present meta-analysis indicates that higher consumption of total red meat and processed meat is associated with an increased risk of total, cardiovascular and cancer mortality.
IMPORTANCE: The 2015-2020 Dietary Guidelines for Americans recommend multiple healthy eating patterns. However, few studies have examined the associations of adherence to different dietary patterns ...with long-term risk of cardiovascular disease (CVD). OBJECTIVE: To examine the associations of dietary scores for 4 healthy eating patterns with risk of incident CVD. DESIGN, SETTING, AND PARTICIPANTS: Prospective cohort study of initially healthy women from the Nurses’ Health Study (NHS) (1984-2016) and the NHS II (1991-2017) and men from the Health Professionals Follow-up Study (HPFS) (1986-2012). The dates of analysis were July 25 to December 4, 2019. EXPOSURES: Healthy Eating Index–2015 (HEI-2015), Alternate Mediterranean Diet Score (AMED), Healthful Plant-Based Diet Index (HPDI), and Alternate Healthy Eating Index (AHEI). MAIN OUTCOMES AND MEASURES: Cardiovascular disease events, including fatal and nonfatal coronary heart disease (CHD) and stroke. RESULTS: The final study sample included 74 930 women in the NHS (mean SD baseline age, 50.2 7.2 years), 90 864 women in the NHS II (mean SD baseline age, 36.1 4.7 years), and 43 339 men in the HPFS (mean SD baseline age, 53.2 9.6 years). During a total of 5 257 190 person-years of follow-up, 23 366 incident CVD cases were documented (18 092 CHD and 5687 stroke) (some individuals were diagnosed as having both CHD and stroke). Comparing the highest with the lowest quintiles, the pooled multivariable-adjusted hazard ratios (HRs) of CVD were 0.83 (95% CI, 0.79-0.86) for the HEI-2015, 0.83 (95% CI, 0.79-0.86) for the AMED, 0.86 (95% CI, 0.82-0.89) for the HPDI, and 0.79 (95% CI, 0.75-0.82) for the AHEI (P for trend <.001 for all). In addition, a 25-percentile higher dietary score was associated with 10% to 20% lower risk of CVD (pooled HR, 0.80 95% CI, 0.77-0.83 for the HEI-2015; 0.90 95% CI, 0.87-0.92 for the AMED; 0.86 95% CI, 0.82-0.89 for the HPDI; and 0.81 95% CI, 0.78-0.84 for the AHEI). These dietary scores were statistically significantly associated with lower risk of both CHD and stroke. In analyses stratified by race/ethnicity and other potential risk factors for CVD, the inverse associations between these scores and risk of CVD were consistent in most subgroups. CONCLUSIONS AND RELEVANCE: In 3 large prospective cohorts with up to 32 years of follow-up, greater adherence to various healthy eating patterns was consistently associated with lower risk of CVD. These findings support the recommendations of the 2015-2020 Dietary Guidelines for Americans that multiple healthy eating patterns can be adapted to individual food traditions and preferences.
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