n-3 Fatty Acids; Ventricular Arrhythmia-Related Events; and Fatal Myocardial Infarction in Postmyocardial Infarction Patients With Diabetes
OBJECTIVE: We carried out a secondary analysis in high-risk patients with a previous myocardial infarction (MI) and diabetes in the Alpha Omega Trial. We tested the hypothesis that in these patients an increased intake of the n-3 fatty acids eicosapentaenoic acid (EPA); docosahexaenoic acid (DHA); and a-linolenic acid (ALA) will reduce the incidence of ventricular arrhythmias and fatal MI. RESEARCH DESIGN AND METHODS: A subgroup of 1;014 post-MI patients with diabetes aged 60-80 years was randomly allocated to receive one of four trial margarines; three with an additional amount of n-3 fatty acids and one placebo for 40 months. The end points were ventricular arrhythmia-related events and fatal MI. The data were analyzed according to the intention-to-treat principle; using multivariable Cox proportional hazards models. RESULTS The patients consumed on average 18.6 g of margarine per day; which resulted in an additional intake of 223 mg EPA plus 149 mg DHA and/or 1.9 g ALA in the active treatment groups. During follow-up; 29 patients developed a ventricular arrhythmia-related events and 27 had a fatal MI. Compared with placebo patients; the EPA-DHA plus ALA group experienced less ventricular arrhythmia-related events (hazard ratio 0.16; 95% CI 0.04-0.69). These n-3 fatty acids also reduced the combined end-point ventricular arrhythmia-related events and fatal MI (0.28; 0.11-0.71). CONCLUSIONS: Our results suggest that low-dose supplementation of n-3 fatty acids exerts a protective effect against ventricular arrhythmia-related events in post-MI patients with diabetes.
The role of diet in the prevention of type 2 diabetes
Type 2 diabetes mellitus is an important preventable disease and a growing public health problem. Epidemiologic and interventional studies suggest that weight loss is the main driving force to reduce diabetes risk. Landmark clinical trials of lifestyle changes in subjects with prediabetes have shown that diet and exercise leading to weight loss consistently reduce the incidence of diabetes. However; from these studies it cannot be established whether dietary changes alone play a significant role in preventing diabetes. Here we review epidemiologic and clinical trial evidence relating nutrients; foods and dietary patterns to diabetes risk and the possible mechanisms involved. The differential effects of carbohydrate and fat quantity and quality; and those of specific foods and whole diets are discussed. Importantly; most dietary components influencing diabetes risk have similar effects on biomarkers of cardiovascular risk and inflammation. The conclusion is that there is no universal dietary strategy to prevent diabetes or delay its onset. Together with the maintenance of ideal body weight; the promotion of the so-called prudent diet (characterized by a higher intake of food groups that are generally recommended for health promotion; particularly plant-based foods; and a lower intake of red meat; meat products; sweets; high-fat dairy and refined grains) or a Mediterranean dietary pattern rich in olive oil; fruits and vegetables; including whole grains; pulses and nuts; low-fat dairy; and moderate alcohol consumption (mainly red wine) appears as the best strategy to decrease diabetes risk; especially if dietary recommendations take into account individual preferences; thus enabling long-time adherence.
Nuts as a replacement for carbohydrates in the diabetic diet
OBJECTIVE Fat intake; especially monounsaturated fatty acid (MUFA); has been liberalized in diabetic diets to preserve HDL cholesterol and improve glycemic control; yet the exact sources have not been clearly defined. Therefore; we assessed the effect of mixed nut consumption as a source of vegetable fat on serum lipids and HbA(1c) in type 2 diabetes. RESEARCH DESIGN AND METHODS A total of 117 type 2 diabetic subjects were randomized to one of three treatments for 3 months. Supplements were provided at 475 kcal per 2;000-kcal diet as mixed nuts (75 g/day); muffins; or half portions of both. The primary outcome was change in HbA(1c). RESULTS The relative increase in MUFAs was 8.7% energy on the full-nut dose compared with muffins. Using an intention-to-treat analysis (n = 117); full-nut dose (mean intake 73 g/day) reduced HbA(1c) (-0.21% absolute HbA(1c) units; 95% CI -0.30 to -0.11; P < 0.001) with no change after half-nut dose or muffin. Full-nut dose was significantly different from half-nut dose (P = 0.004) and muffin (P = 0.001); but no difference was seen between half-nut dose and muffins. LDL cholesterol also decreased significantly after full-nut dose compared with muffin. The LDL cholesterol reduction after half-nut dose was intermediate and not significantly different from the other treatments. Apolipoprotein (apo) B and the apoB:apoA1 ratio behaved similarly. Nut intake related negatively to changes in HbA(1c) (r = -0.20; P = 0.033) and LDL cholesterol (r = -0.24; P = 0.011). CONCLUSIONS Two ounces of nuts daily as a replacement for carbohydrate foods improved both glycemic control and serum lipids in type 2 diabetes.
The glycemic effect of nut-enriched meals in healthy and diabetic subjects
BACKGROUND AND AIMS: The intake of nuts has been linked to a reduced risk of cardiovascular disease (CVD) and diabetes in large cohort studies. One potential contributing mechanism may be the ability of nuts to improve post-meal glycemic response. We; therefore; examined the effect of nuts alone and in combination with white bread on postprandial glycemia. METHODS AND RESULTS: 30; 60 and 90 g (approximately 1; 2 and 3 ounces) of mixed nuts were consumed with and without 50 g available carbohydrate from white bread by 10-14 normoglycemic and 5-10 type 2 diabetic subjects. Glycemic response (GR) was assessed by calculating the incremental area under the 2 h blood glucose curve. All three doses of mixed nuts; when fed alone; significantly reduced the glycemic response in both normoglycemic and diabetic patients. Furthermore; in the normoglycemic subjects; adding nuts to white bread progressively reduced the GR of the meal by 11.2 ± 11.6%; 29.7 ± 12.2% and 53.5 ± 8.5% for the 30; 60; and 90 g doses (P = 0.354; P = 0.031 and P < 0.001; respectively); while in subjects with type 2 diabetes; the effect was half of that seen in the non-diabetic subjects (P = 0.474; P = 0.113 and P = 0.015; respectively). CONCLUSION: Nuts alone have little effect on post-meal blood glucose response. Furthermore; when taken with bread; nuts progressively reduce the glycemic response in a dose-dependent manner. While these findings support a short-term benefit for nuts in postprandial glucose response; more studies are required to determine whether these acute benefits result in long-term improvements in glycemic control.
Glycemic and insulinemic responses to different preexercise snacks in participants with impaired fasting glucose.
PURPOSE: To compare serum glucose and insulin responses to 3 preexercise snacks before; during; and after exercise in individuals with impaired fasting glucose (IFG) and healthy (H) men. In addition; in an IFG population; the authors sought to determine whether a natural fruit snack (i.e.; raisins) yields more desirable glucose and insulin concentrations than an energy bar or a glucose solution. METHODS: The IFG (n = 11; age = 54.5 ± 1.3 yr; fasting blood glucose [BG] = 6.3 ± 0.1 mmol/L) and H groups (n = 9; age = 48.0 ± 3.1 yr; fasting BG = 4.9 ± 0.1 mmol/L) cycled at 50% of VO2peak for 45 min on 4 occasions after consuming water or 50 g of carbohydrate from raisins (R); an energy bar (EB); or a glucose beverage (GLU). Metabolic markers were measured before; during; and after exercise. RESULTS: In all nutritional conditions; glucose concentrations of the IFG group were consistently higher than in the H group. Differences between IFG and H groups in insulin concentrations were sporadic and isolated. In the IFG group; preexercise glucose concentration was lower in the R condition than in GLU. Ten and 20 min into exercise; glucose concentrations in the R and EB conditions were lower than in GLU. Insulin concentrations were lower in the R condition than in EB and GLU immediately before exercise and at Minute 10 but at 20 min R remained lower than only GLU. CONCLUSION: Glucose concentrations were higher in the IFG group regardless of preexercise snack. Compared with the glucose solution; raisins lowered both the postprandial glycemic and insulinemic responses; whereas the energy bar reduced glycemia but not insulinemia.
Almond ingestion at mealtime reduces postprandial glycemia and chronic ingestion reduces hemoglobin A1c in individuals with well-controlled type 2 diabetes mellitus.
Abstract: Cohort studies are equivocal regarding a relationship between regular nut consumption and reduced risk of type 2 diabetes mellitus. Although acute trials show reductions in postprandial glycemia in healthy individuals ingesting 60 to 90 g almonds; trials have not been conducted using a single serving of almonds (28 g) in individuals with type 2 diabetes mellitus. This randomized crossover trial examined the impact of one serving of almonds at mealtime on postprandial glycemia; insulinemia; and plasma glucagon-like peptideÂ1 in healthy individuals and individuals with type 2 diabetes mellitus. On 2 occasions separated by at least 1 week; 19 adults (including 7 adults with type 2 diabetes mellitus) consumed a standardized evening meal and fasted overnight before ingesting the test meal (bagel; juice; and butter) with or without almonds. A small pilot study (6-7 subjects per group) was also conducted to observe whether chronic almond ingestion (1 serving 5 d/wk for 12 weeks) lowered hemoglobin A1c in individuals with type 2 diabetes mellitus. A standard serving of almonds reduced postprandial glycemia significantly in participants with diabetes (-30%; P = .043) but did not influence glycemia in participants without diabetes (-7%; P = .638). Insulinemia and glucagon-like peptideÂ1 at 30 minutes postmeal were not impacted by almond ingestion for either group. In the pilot study; regular almond ingestion for 12 weeks reduced hemoglobin A1c by 4% (P = .045 for interaction) but did not influence fasting glucose concentrations. These data show that modest almond consumption favorably improves both short-term and long-term markers of glucose control in individuals with uncomplicated type 2 diabetes mellitus.
The impact of pistachio intake alone or in combination with high-carbohydrate foods on post-prandial glycemia
Background/Objectives: Dietary strategies that reduce post-prandial glycemia are important in the prevention and treatment of diabetes and coronary heart disease (CHD). This may be achieved by addition of high-quality protein and fat contained in pistachio nuts; to carbohydrate-containing foods or meals.Subjects/Methods:A total of 10 healthy volunteers (3 males; 7 females); aged 48.3±6.4 years; Body mass index (BMI) 28.0±4.8 kg/m(2) participated in two studies. Study 1 assessed the dose-response effect of 28; 56 and 84 g pistachios consumed alone or co-ingested with white bread (50 g available carbohydrate); Study 2 assessed the effective dose (56 g) of pistachios on post-prandial glycemia consumed with different commonly consumed carbohydrate foods (50 g available carbohydrate). Relative glycemic responses (RGRs) of study meals compared with white bread; were assessed over the 2 h post-prandial period.Results:The RGRs of pistachios consumed alone expressed as a percentage of white bread (100%) were: 28 g (5.7±1.8%); 56 g (3.8±1.8%); 84 g (9.3±3.2%); P<0.001. Adding pistachios to white bread resulted in a dose-dependent reduction in the RGR of the composite meal; 28 g (89.1±6.0; P=0.100); 56 g (67.3±9.8; P=0.009); 84 g (51.5±7.5; P<0.001). Addition of 56 g pistachios to carbohydrate foods significantly reduced the RGR: parboiled rice (72.5±6.0) versus rice and pistachios (58.7±5.1) (P=0.031); pasta (94.8±11.4) versus pasta and pistachios (56.4±5.0) (P=0.025); whereas for mashed potatoes (109.0±6.6) versus potatoes and pistachios; (87.4±8.0) (P=0.063) the results approached significance.Conclusions:Pistachios consumed alone had a minimal effect on post-prandial glycemia and when taken with a carbohydrate meal attenuated the RGR. The beneficial effects of pistachios on post-prandial glycemia could; therefore; be part of the mechanism by which nuts reduce the risk of diabetes and CHD.
Acute and second-meal effects of almond form in impaired glucose tolerant adults: a randomized crossover trial.
BACKGROUND: Nut consumption may reduce the risk of developing type 2 diabetes. The aim of the current study was to measure the acute and second-meal effects of morning almond consumption and determine the contribution of different nut fractions. METHODS: Fourteen impaired glucose tolerant (IGT) adults participated in a randomized; 5-arm; crossover design study where whole almonds (WA); almond butter (AB); defatted almond flour (AF); almond oil (AO) or no almonds (vehicle - V) were incorporated into a 75 g available carbohydrate-matched breakfast meal. Postprandial concentrations of blood glucose; insulin; non-esterified free fatty acids (NEFA); glucagon-like peptide-1 (GLP-1) and appetitive sensations were assessed after treatment breakfasts and a standard lunch. RESULTS: WA significantly attenuated second-meal and daylong blood glucose incremental area under the curve (AUCI) and provided the greatest daylong feeling of fullness. AB and AO decreased blood glucose AUCI in the morning period and daylong blood glucose AUCI was attenuated with AO. WA and AO elicited a greater second-meal insulin response; particularly in the early postprandial phase; and concurrently suppressed the second-meal NEFA response. GLP-1 concentrations did not vary significantly between treatments. CONCLUSIONS: Inclusion of almonds in the breakfast meal decreased blood glucose concentrations and increased satiety both acutely and after a second-meal in adults with IGT. The lipid component of almonds is likely responsible for the immediate post-ingestive response; although it cannot explain the differential second-meal response to AB versus WA and AO.