No abstract

The Mediterranean diet (MD) may provide metabolic benefits but no systematic review to date has examined its effect on a multitude of outcomes related to metabolic health. This systematic review with meta-analysis (International Prospective Register of Systematic Reviews, PROSPERO; number CRD42019141459) aimed to examine the MD’s effect on metabolic syndrome (MetSyn) incidence, components and risk factors (primary outcomes), and incidence and/or mortality from MetSyn-related comorbidities and receipt of pharmacologic treatment for MetSyn components and comorbidities (secondary outcomes). We searched Pubmed, Embase, Cumulative Index to Nursing and Allied Health Literature (CINAHL), and Web of Science for controlled trials published until June 2019, comparing the MD with no treatment, usual care, or different diets in adults. Studies not published in English and not promoting the whole MD were excluded. Two authors independently extracted data and assessed risk of bias using the Cochrane Collaboration’s and Risk of Bias in non-randomised studies (ROBINS-I) tools. Reporting followed the Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) guidelines. Random-effects meta-analyses, subgroup analyses and meta-regressions were performed, and heterogeneity was quantified using the I2 statistic. We identified 2654 reports and included 84 articles reporting 57 trials (n = 36,983). In random effects meta-analyses, the MD resulted in greater beneficial changes in 18 of 28 MetSyn components and risk factors (body weight, body mass index, waist circumference, systolic and diastolic blood pressure, glucose, insulin, homeostatic model assessment of insulin resistance (HOMA-IR) index, total-, low-density lipoprotein (LDL)- and high-density lipoprotein (HDL)-cholesterol, triglycerides, alanine transaminase, hepatic fat mass, C-reactive protein, interleukin-6, tumour necrosis factor-a, and flow-mediated dilatation) and lower risk of cardiovascular disease incidence (risk ratio (RR) = 0.61, 95% confidence intervals (CI) 0.42–0.80; I2 = 0%), and stroke (RR = 0.67, 95% CI 0.35–0.98; I2 = 0%). Only six studies reported effects on pharmacotherapy use, and pooled analysis indicated no differences between diet groups. Lack of consistency in comparator groups and other study characteristics across studies resulted in high heterogeneity for some outcomes, which could not be considerably explained by meta-regressions. However, a consistent direction of beneficial effect of the MD was observed for the vast majority of outcomes examined. Findings support MD’s beneficial effect on all components and most risk factors of the MetSyn, in addition to cardiovascular disease and stroke incidence. More studies are needed to establish effects on other clinical outcomes and use of pharmacotherapy for MetSyn components and comorbidities. Despite the high levels of heterogeneity for some outcomes, this meta-analysis enabled the comparison of findings across studies and the examination of consistency of effects. The consistent direction of effect, suggesting the MD’s benefits on metabolic health, supports the need to promote this dietary pattern to adult populations.

Aims GLP‐1 analogs have recently risen to the forefront as effective medications for lowering weight through actions in the central nervous system (CNS). However, their actions in the CNS have not yet been studied in the human brain after longer‐term administration at the highest dose approved for obesity (liraglutide 3.0 mg). Materials and Methods A total of 20 participants with obesity were treated with placebo and liraglutide (3.0 mg) in the context of a randomized, placebo‐controlled, double‐blind, cross‐over trial after 5 weeks of dose escalation. Neurocognitive and neuroimaging (fMRI) responses to food cues were examined at the clinical research center of Beth Israel Deaconess Medical Center. Results While using liraglutide, patients lost more weight (placebo‐subtracted −2.7%; P < .001), had decreased fasting glucose (P < .001) and showed improved cholesterol levels. In an uncontrolled analysis, brain activation in response to food images was not altered by liraglutide vs placebo. When controlled for BMI/weight, liraglutide increased activation of the right orbitofrontal cortex (OFC) in response to food cues (P < .016, corrected for multiple comparisons). Conclusions In contrast to prior studies, we demonstrate for the first time that liraglutide treatment, administered over a longer period at the highest doses approved for obesity, does not alter brain activation in response to food cues. A counter‐regulatory increase in reward‐related OFC activation in response to food cues can be observed when neuroimaging data are controlled for BMI changes, indicating changes in CNS that could lead to later plateaus of weight loss. These data point to a promising focus for additional interventions which, by contributing to the CNS reward system, could provide tangible benefits in reversing the plateauing phenomenon and promoting further weight loss.

The discovery of leptin, an adipocyte-secreted hormone, set the stage for unraveling the mechanisms dictating energy homeostasis, revealing adipose tissue as an endocrine system that regulates appetite and body weight. Fluctuating leptin levels provide molecular signals to the brain regarding available energy reserves modulating energy homeostasis and neuroendocrine response in states of leptin deficiency and to a lesser extent in hyperleptinemic states. While leptin replacement therapy fails to provide substantial benefit in common obesity, it is an effective treatment for congenital leptin deficiency and states of acquired leptin deficiency such as lipodystrophy. Current evidence suggests that regulation of eating behavior in humans is not limited to homeostatic mechanisms and that the reward, attention, memory and emotion systems are involved, participating in a complex central nervous system network. It is critical to study these systems for the treatment of typical obesity. Although progress has been made, further studies are required to unravel the physiology, pathophysiology and neurobehavioral mechanisms underlying potential treatments for weight-related problems in humans.

No abstract

No abstract

Objective The 6 Minute Walk Test (6MWT) is a measure that is routinely used to assess a response to treatment for cardiopulmonary diseases such as pulmonary fibrosis and congestive heart failure. The measure has never been verified as a valid measure of exercise capacity in the highly prevalent patient population of type 2 diabetes (T2DM). This study investigated the correlation between the 6MWT and graded exercise testing (GXT) in an effort to validate the 6MWT as a quality tool for assessing exercise capacity in adults with T2DM. Research Design and Method This is a secondary data analysis of Program ACTIVE II, a randomized controlled trial designed to assess the effectiveness of two behavioral interventions on depression and glycemic outcomes in adults with T2DM. The correlation of 6MWT and predicted VO2 max (PVO2M) using GXT was examined in a subsample of participants at the time of study enrollment and at post-intervention. Results PVO2M showed a significant correlation with 6MWT distance both at baseline (r=0.57, p=0.014) and post-intervention (r = 0.66, p = 0.037). The regression analysis of baseline data revealed that 6MWT distance alone explained 45% (F = 13.03, p = .0024) of the variability in PVO2M. When combined with the SF-12 physical health component score (PCS), 6MWT explained 66% (F = 13.62, p < .001) of the variance in PVO2M. After adjusting for PCS, 6MWT distance explained an additional 30% variability in PVO2M. Conclusions Findings from this study indicate that the 6MWT and predicted exercise capacity are significantly correlated. The 6MWT can be used to estimate exercise capacity in adults with T2DM.

No abstract