This randomized trial in free-living adults with T2D showed that the incorporation of approximately 46 g/d of peanuts into an ADA meal plan yielded a higher P:S ratio and higher intake of MUFA, PUFA, α-tocopherol, niacin and magnesium as compared to a peanut-free control diet, which are important cardioprotective nutrients for persons with T2D. As expected, the peanut intervention yielded similar reductions in weight, BMI and WC as compared to the peanut-free intervention, and all of the blood lipids and lipid ratios improved in a favorable direction in both groups during the study.
Similar to the blood lipid findings of our recent pooled analysis of 25 nut (walnut, almond, macadamia, pistachio, hazelnut, pecan and peanut) intervention trials (583 men and women with normolipidemia and hypercholesterolemia who were not taking lipid-lowering medications) , age and gender did not modify the effect of peanuts on the blood lipids and lipid ratios. Contrary to the findings of the aforementioned pooled analysis, BMI did not influence the blood lipid results, perhaps due to the narrower range of BMIs, smaller sample size, and the presence of T2D among the participants in the current study.
The clinically relevant reduction in LDL-C:HDL-C observed in the peanut group and the increase in HDL-C are worth noting in the context of our primarily overweight or obese study population. We have previously cited several reasons for the decreased blood lipid responsiveness to nut enriched diets in overweight and obese individuals . Specifically, obesity is associated with reduced intestinal cholesterol absorption ; hence the cholesterol lowering effects from the plant sterols in nuts will be blunted when cholesterol absorption rates are low. Insulin resistant states, the hallmark of overweight and obese persons with T2D, increase cholesterol synthesis and also reduce intestinal absorption . Therefore, enhanced cholesterol flux in hepatocytes down-regulates LDL-C receptors and makes them refractory to changes in dietary fatty acids, and a decreased cholesterol flux through enterocytes reduces the cholesterol-raising response to dietary cholesterol and enhances the aforementioned cholesterol-lowering effect of plant stanols.
Several studies have been performed to determine the influence between specific nuts and blood lipids and glycemic control in persons with T2D. Scott et al.  compared an American Heart Association diet [30% fat (15% MUFA), 55% carbohydrate, 15% protein] with an almond enriched high protein diet [40% fat (22% MUFA), 35% carbohydrate, 25% protein] in 7 patients with T2D (unknown degree of lipid lowering medication usage) and observed no between-treatment effects on LDL-C, TG and FBG, which is consistent with our null findings for these measurements. However, these investigators reported that weight loss was a potential confounding factor in the analysis. As a known confounder for influencing WC and biological measurements, the inclusion of weight change was added into our mixed models. As expected, each kilogram of weight loss was associated with significant reductions in WC, FBG and HbA1c among the cohort of study participants (P < 0.01-P = 0.01) (Table 4), which demonstrates that regardless of either dietary approach the key to improvements in these measurements is mediated through successful weight loss.
More recently, Jenkins et al.  evaluated the effects of a 3 month dietary intervention using a parallel study design in 117 subjects with T2D using a full dose of mixed nuts (mean intake 73 g/d), muffins, or half portions of muffins and mixed nuts, hence replacing mixed nuts for carbohydrates in the ADA diet. In contrast to our null findings, this team reported an absolute −0.21% reduction in HbA1c (P = 0.001), a 5% decrease in TC (P < 0.001), a 8% decrease in LDL-C (P < 0.001), a 8% decrease in TC:HDL-C (P = 0.006), and a 9% decrease in LDL-C:HDL-C (P = 0.002) in the full dose nut group (n = 40) as compared to the muffin group (n = 39).
Our study is not without limitations. The nutrient intake data was obtained from self-reported 24-hour dietary recalls and we did not have a biomarker of dietary adherence. Hence, self-reporting errors in the treatment diet may partially explain the dissociation between the superior nutrient profile of the peanut diet and the lack of difference in cardiovascular disease risk factors. Additionally, we did not obtain 2-hour postprandial blood glucose measurements or utilize a continuous glucose monitoring system to assess the degree of blood glucose variability in the study participants, the latter being associated with oxidative stress and endothelial dysfunction independent of HbA1c .