Chronic inflammation and gut barrier breakdown contribute to the progression of metabolic syndrome and affect the development of cardiometabolic diseases, especially in persons consuming low-quality diets with limited bioactive compounds. Almonds are a rich source of bioactive compounds with antioxidant and anti-inflammatory properties. We hypothesize almond consumption can help disrupt metabolic syndrome progression by improving gut and cardiometabolic health and decreasing inflammation and oxidative stress. To test this hypothesis, adults with metabolic syndrome were randomized to consume either almonds (2 oz, whole, dry roasted, n = 38) or crackers (control, equal caloric content, n = 39), as a daily snack for 12 weeks, and samples were collected (0, 4, and 12 weeks). Compared with participants consuming crackers, almond consumption resulted in lower plasma total and low-density lipoprotein-cholesterol concentrations, a modest improvement in waist circumference (week 4), and improved dietary intakes of α-tocopherol, soluble fiber, copper, biotin, magnesium, polyunsaturated fatty acids, and monounsaturated fatty acids. Almond consumption raised plasma α-tocopherol concentrations (relative to cholesterol concentrations) and increased excretion of a vitamin E biomarker (α-CEHC). Almond consumption improved biomarkers of gut barrier function and intestinal inflammation (fecal calprotectin, myeloperoxidase) in participants with elevated inflammation at baseline. Total body weight, caloric intake, and markers of carbohydrate metabolism (glucose, insulin), systemic inflammation (plasma interleukin-6, C-reactive protein, lipopolysaccharide-binding protein, CD14), and oxidative damage (malondialdehyde) were not altered by almond consumption. In conclusion, daily almond snacking improves nutrient intake and decreases gut inflammation in participants with metabolic syndrome. These beneficial dietary and inflammatory changes may contribute to the improvements in cardiovascular health observed.
Keywords: Alpha-tocopherol; Calprotectin; Metabolic syndrome; Myeloperoxidase; Obesity.
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