Effects of one serving of mixed nuts on serum lipids, insulin resistance and inflammatory markers in patients with the metabolic syndrome☆

Abstract 

Background and aims

Knowledge of the effect of nut consumption on metabolic syndrome (MetS) components is limited. We assessed the effects of nut intake on adiposity, serum lipids, insulin resistance, and inflammatory biomarkers in patients with MetS.

Methods and results

In a randomized, parallel-group, 12-week feeding trial, 50 patients with MetS were given recommendations for a healthy diet with or without supplementation with 30g/day of raw nuts (15g walnuts, 7.5g almonds and 7.5g hazelnuts) (Nut and Control diet groups, respectively). Adiposity measures, serum lipids, insulin, Homeostasis Model Assessment (HOMA), interleukin-6 (IL-6) and other inflammatory biomarkers, and 48-h fecal fat were determined basally and at study's completion. Moderate weight loss, decreased adiposity, and lower blood pressure occurred similarly after both diets. The Control, but not the Nut diet, was associated with significant (P<0.05) reduction of LDL-cholesterol, with mean changes of −0.36 versus −0.13mmol/L, respectively (between-group differences, P=0.154). The Nut diet reduced fasting insulin by 2.60μU/mL (95% CI, −4.62 to −0.59) and HOMA-insulin resistance by 0.72 (−1.28 to −0.16) (P<0.05 versus Control diet; both). Among inflammatory markers, the Nut diet resulted in changes of median plasma IL-6 of −1.1ng/L (−2.7 to −0.1; P=0.035 versus Control diet), but adjustment for weight loss attenuated the significance of the association. Stool fat decreased with the Control diet and slightly increased with the Nut diet (P<0.05 for between-group differences).

Conclusion

Patients with MetS show decreased lipid responsiveness but improved insulin sensitivity after daily intake of 30g of mixed nuts.

Keywords: Nuts, Metabolic syndrome, Insulin resistance, Lipid profile, Inflammation, Interleukin-6

Abbreviations: MetS, metabolic syndrome, HOMA, Homeostasis Model Assessment, CVD, cardiovascular disease, ATP III, Adult Treatment Panel III, REE, resting energy expenditure, O₂, oxygen, CO₂, carbon dioxide, SFA, saturated fatty acid, CRP, C-reactive protein, IL-6, interleukin-6, MCP-1, monocyte chemotactic protein-1, PAI-1, plasminogen activator inhibitor-1, IL-18, interleukin-18, ANCOVA, analysis of covariance, MUFA, monounsaturated fatty acid, PUFA, polyunsaturated fatty acid