Senescent cells exacerbate COVID-19: Cellular senescence is a state elicited in response to stress signals and is associated with a damaging secretory phenotype. The number of senescent cells increases with advanced age and this in turn drives age-related diseases. Camell et al. show that senescent cells have an amplified inflammatory response to severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) (see the Perspective by Cox and Lord). This response is communicated to nonsenescent cells, suppressing viral defense mechanisms and increasing the expression of viral entry proteins. In old mice infected with a SARS-CoV-2–related virus, treatment with senolytics to reduce the senolytic cell burden reduced mortality and increased antiviral antibodies. Science , abe4832, this issue p. eabe4832 ; see also abi4474, p. 281

OBJECTIVE Emerging epidemiological evidence suggests that higher magnesium intake may reduce diabetes incidence. We aimed to examine the association between magnesium intake and risk of type 2 diabetes by conducting a meta-analysis of prospective cohort studies. RESEARCH DESIGN AND METHODS We conducted a PubMed database search through January 2011 to identify prospective cohort studies of magnesium intake and risk of type 2 diabetes. Reference lists of retrieved articles were also reviewed. A random-effects model was used to compute the summary risk estimates. RESULTS Meta-analysis of 13 prospective cohort studies involving 536,318 participants and 24,516 cases detected a significant inverse association between magnesium intake and risk of type 2 diabetes (relative risk [RR] 0.78 [95% CI 0.73–0.84]). This association was not substantially modified by geographic region, follow-up length, sex, or family history of type 2 diabetes. A significant inverse association was observed in overweight (BMI ≥25 kg/m²) but not in normal-weight individuals (BMI <25 kg/m²), although test for interaction was not statistically significant (P_interaction = 0.13). In the dose-response analysis, the summary RR of type 2 diabetes for every 100 mg/day increment in magnesium intake was 0.86 (95% CI 0.82–0.89). Sensitivity analyses restricted to studies with adjustment for cereal fiber intake yielded similar results. Little evidence of publication bias was observed. CONCLUSIONS This meta-analysis provides further evidence supporting that magnesium intake is significantly inversely associated with risk of type 2 diabetes in a dose-response manner.

Background: The associations of egg consumption with cardiovascular disease (CVD) and diabetes are still unclear.Objective: We aimed to quantitativel

OBJECTIVE To investigate the long-term associations of magnesium intake with incidence of diabetes, systemic inflammation, and insulin resistance among young American adults. RESEARCH DESIGN AND METHODS A total of 4,497 Americans, aged 18–30 years, who had no diabetes at baseline, were prospectively examined for incident diabetes based on quintiles of magnesium intake. We also investigated the associations between magnesium intake and inflammatory markers, i.e., high-sensitivity C-reactive protein (hs-CRP), interleukin-6 (IL-6), and fibrinogen, and the homeostasis model assessment of insulin resistance (HOMA-IR). RESULTS During the 20-year follow-up, 330 incident cases of diabetes were identified. Magnesium intake was inversely associated with incidence of diabetes after adjustment for potential confounders. The multivariable-adjusted hazard ratio of diabetes for participants in the highest quintile of magnesium intake was 0.53 (95% CI, 0.32–0.86; P_trend < 0.01) compared with those in the lowest quintile. Consistently, magnesium intake was significantly inversely associated with hs-CRP, IL-6, fibrinogen, and HOMA-IR, and serum magnesium levels were inversely correlated with hs-CRP and HOMA-IR. CONCLUSIONS Magnesium intake was inversely longitudinally associated with incidence of diabetes in young American adults. This inverse association may be explained, at least in part, by the inverse correlations of magnesium intake with systemic inflammation and insulin resistance.

Background: It has been hypothesized that monosodium glutamate (MSG), a flavor enhancer, is positively associated with weight gain, which influences

A meta-analysis of cross-sectional studies found that shorter-time sleep was correlated with increased risk of obesity in children. However, findings from prospective cohort studies were inconsistent. PubMed and other data resources were searched through May 2015. Twenty-five eligible studies were identified including 56,584 children and adolescents with an average 3.4-year follow-up. Compared with children having the longest sleep duration (~12.2 hours), kids with the shortest sleep duration (~10.0 hours) were 76% more likely to be overweight/obese (pooled odds ratio [OR]: 1.76; 95% confidence interval [CI]: 1.39, 2.23); and had relatively larger annual BMI gain (pooled β coefficient: 0.13; 95% CI: 0.01, 0.25 kg/m²). With every 1 hour/day increment in sleep duration, the risk of overweight/obesity was reduced by 21% (OR: 0.79; 95% CI: 0.70, 0.89); and the annual BMI gain declined by 0.05 kg/m² (β = −0.05; 95% CI: −0.09, −0.01). The observed associations were not appreciably modified by region, baseline age or the length of follow-up. Accumulated literature indicates a modest inverse association between sleep duration and the risk of childhood overweight/obesity. Further research is needed to determine the age and gender specified optimal hours of sleep and ideal sleep pattern with respect to obesity prevention in children.