Tree Nut Consumption and Adipose Tissue Mass: Mechanisms of Action.

There is concern that tree nuts may cause weight gain due to their energy density, yet evidence shows that tree nuts do not adversely affect weight status. Epidemiologic and experimental studies have shown a reduced risk of chronic diseases with tree nut consumption without an increased risk of weight gain. In fact, tree nuts may protect against weight gain and benefit weight-loss interventions. However, the relation between tree nut consumption and adiposity is not well understood at the mechanistic level. This review summarizes the proposed underlying mechanisms that might account for this relation. Evidence suggests that tree nuts may affect adiposity through appetite control, displacement of unfavorable nutrients, increased diet-induced thermogenesis, availability of metabolizable energy, antiobesity action of bioactive compounds, and improved functionality of the gut microbiome. The gut microbiome is a common factor among these mechanisms and may mediate, in part, the relation between tree nut consumption and reduced adiposity. Further research is needed to understand the impact of tree nuts on the gut microbiome and how the gut microbial environment affects the nutrient absorption and metabolism of tree nuts. The evidence to date suggests that tree nut consumption favorably affects body composition through different mechanisms that involve the gut microbiome. A better understanding of these mechanisms will contribute to the evolving science base that addresses the causes and treatments for overweight and obesity.

Coronary Exercise Hyperemia Is Impaired in Patients with Peripheral Arterial Disease.

BACKGROUND: Peripheral arterial disease (PAD) is an atherosclerotic vascular disease that affects over 200 million people worldwide. The hallmark of PAD is ischemic leg pain and this condition is also associated with an augmented blood pressure response to exercise, impaired vascular function, and high risk of myocardial infarction and cardiovascular mortality. In this study, we tested the hypothesis that coronary exercise hyperemia is impaired in PAD. METHODS: Twelve patients with PAD and no overt coronary disease (65 ± 2 years, 7 men) and 15 healthy control subjects (64 ± 2 years, 9 men) performed supine plantar flexion exercise (30 contractions/min, increasing workload). A subset of subjects (n = 7 PAD, n = 8 healthy) also performed isometric handgrip exercise (40% of maximum voluntary contraction to fatigue). Coronary blood velocity in the left anterior descending artery was measured by transthoracic Doppler echocardiography; blood pressure and heart rate were monitored continuously. RESULTS: Coronary blood velocity responses to 4 min of plantar flexion exercise (PAD: Δ2.4 ± 1.2, healthy: Δ6.0 ± 1.6 cm/sec, P = 0.039) and isometric handgrip exercise (PAD: Δ8.3 ± 4.2, healthy: Δ16.9 ± 3.6, P = 0.033) were attenuated in PAD patients. CONCLUSION: These data indicate that coronary exercise hyperemia is impaired in PAD, which may predispose these patients to myocardial ischemia.