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The menopausal transition period in aging women is strongly associated with weight gain. Evidence shows that weight changes during menopause increases the risk of developing cardiovascular disease (CVD) in postmenopausal women. However, the potential mechanisms that cause weight gain and adverse changes to body composition specifically during the menopausal transition period remain to be elucidated. In this contemporary review, we examined recent evidence for adverse changes in body composition at midlife during the menopausal transition and the link to increased CVD risk and described factors that may contribute to these changes, including normal chronological aging, hormonal factors (decreased estrogen, etc.), behavioral factors (changes in diet, physical activity), or other emerging factors ( e.g. , sleep). This review focused on identifying factors that make the menopausal transition period a critical window for prevention of CVD. Future study is needed to decipher the extent to which hormonal changes, age-related factors, and behavioral factors interact with and contribute to increased CVD risk in women undergoing menopause. Understanding the causes of weight gain during the menopausal transition may help to inform strategies to mitigate adverse CVD outcomes for women transitioning through menopause.

Poor sleep is a determinant of obesity; with overconsumption of energy contributing to this relationship. Eating behavior characteristics are predictive of energy intake and weight change and may underlie observed associations of sleep with weight status and obesity risk factors. However; relationships between sleep and dimensions of eating behavior; as well as possible individual differences in these relations; are not well characterized. Therefore; the aim of this study was to evaluate whether sleep behaviors; including duration; timing; quality; and regularity relate to dietary restraint; disinhibition; and tendency towards hunger and to explore whether these associations differ by sex. This cross-sectional study included 179 adults aged 20–73 years (68.7% women; 64.8% with BMI ≥ 25 kg/m2). Sleep was evaluated by accelerometry over 2 week. Eating behavior dimensions were measured with the Three-Factor Eating Questionnaire. Prolonged wake after sleep onset (WASO) (0.029 ± 0.011; p = 0.007), greater sleep fragmentation index (0.074 ± 0.036; p = 0.041), and lower sleep efficiency (−0.133 ± 0.051; p = 0.010) were associated with higher dietary restraint. However; higher restraint attenuated associations of higher WASO and sleep fragmentation with higher BMI (p-interactions < 0.10). In terms of individual differences; sex influenced associations of sleep quality measures with tendency towards hunger (p-interactions < 0.10). Stratified analyses showed that; in men only; higher sleep fragmentation index; longer sleep onset latency; and lower sleep efficiency were associated with greater tendency towards hunger (β = 0.115 ± 0.037; p = 0.003; β = 0.169 ± 0.072; p = 0.023; β = −0.150 ± 0.055; p = 0.009; respectively). Results of this analysis suggest that the association of poor sleep on food intake could be exacerbated in those with eating behavior traits that predispose to overeating; and this sleep-eating behavior relation may be sex-dependent. Strategies to counter overconsumption in the context of poor quality sleep should be evaluated in light of eating behavior traits

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Background: Sleeping less than 7 h per night is a risk factor for positive energy balance and weight gain. While the effect of short sleep on energy intake has been extensively studied, its influence on physical activity (PA), a key determinant of energy expenditure, is not well characterized. To date, no study has evaluated sedentary and PA patterns in response to chronic mild short sleep, which is experienced by up to one-third of US adults. Hypothesis: Sedentary behavior will be higher and PA (light intensity [LIPA] and moderate-vigorous intensity [MVPA]) will be lower during 6 wk of mild sleep restriction (SR) relative to maintenance of adequate sleep (AS). Methods: Data are presented from 76 participants (age: 34.2±12.4 y; BMI: 25.6±3.4 kg/m 2 ; n=55 women) from two randomized crossover trials with identical sleep interventions. Men and women with adequate habitual sleep duration ≥7 h/ night underwent two 6-wk sleep conditions, AS and SR, separated by a 6-wk washout period. During AS, participants were instructed to maintain average nightly bed and wake times determined from 2 wk screening with wrist-actigraphy and sleep logs. In SR, total sleep time was curtailed by 1.5 h per night by delaying bedtimes. Nightly sleep diaries and 24-h wrist actigraphy confirmed adherence to the protocol, which was verified weekly. Daily wrist actigraphy data were used to determine time spent in sedentary behavior and PA. Linear mixed models were used to test whether sleep condition (SR vs AS) influenced sedentary behavior or PA, adjusting for time in bed. Results: Across the full sample, sedentary time was significantly greater in SR than in AS (39.8±13.6 min/d, P<0.01). Similar results were observed in analyses stratified by sex; compared to AS, in SR, sedentary time was 53.0±16.5 min/d higher in women (P=0.001) with a trend towards significance in men (20.3±11.3, P=0.07). Although a slight increase in LIPA over 6 wk was observed in SR relative to AS in the full sample (2.9±0.8 min/d, P<0.001) and in men (3.7±1.2 min/d, P<0.01), overall, time spent in LIPA across weeks was significantly lower in SR relative to AS. This main effect of SR on LIPA was observed in the full sample (SR vs AS: -44.6±3.3 min/d, P<0.0001) and separately in women (SR vs AS: -38.2±10.5 min/d, P<0.001) and men (SR vs AS: -9.4±4.6 min/d, P=0.04). In men only, the slope of change in MVPA over 6 wk differed slightly in SR vs AS (2.6±1.1, P=0.02). However, across weeks, time in MVPA was significantly lower in SR compared to HS (-12.4±4.2 min/d, P=0.003). Conclusions: We provide some of the first evidence of an adverse impact of chronic short sleep on PA patterns in men and women. Greater sedentary time and lower PA levels can promote positive energy balance and may underlie associations of short sleep with risk for cardiometabolic diseases. Results further highlight the importance of achieving adequate sleep to promote cardiovascular health.