Effects of Dietary Pulses on Lipids and Oxidative Stress as Risk Factors of Cardiovascular Disease
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Modulation of diet is the primary lifestyle approach for reducing cardiovascular disease (CVD) risk, with a major focus of current guidelines being to lower LDL cholesterol by reducing intake of saturated fatty acids. However, dietary effects on lipid-related CVD risk factors extend beyond LDL cholesterol, with growing emphasis on the prevention and management of atherogenic dyslipidemia, which includes elevated triglyceride, small dense LDL, and reduced HDL cholesterol, and which is associated with excess adiposity and insulin resistance. We here review recent studies of dietary macronutrient effects on CVD risk that may act through effects on plasma lipid and lipoprotein metabolism.Effects of reducing saturated fatty acids on CVD risk have been evaluated both in terms of the replacement macronutrient(s) and the food and dietary context in which the macronutrients are consumed. Although weight loss remains the most important goal for reducing cardiometabolic risk among overweight and obese individuals, a variety of lines of evidence support limitation of added sugars and processed starches for improving features of atherogenic dyslipidemia.Increasing understanding of the complexity of nutrient-disease relationships has shifted the framework for CVD prevention from a focus on macronutrient content of diets to foods and dietary patterns.
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Background: Foods that have similar carbohydrate content can differ in the amount they raise blood glucose. The effects of this property, called the glycemic index (GI), on risk factors for cardiovascular disease and diabetes, are not well understood, especially in the context of a healthful dietary pattern that itself improves risk factors. Aims: To study the effects of the amount of dietary carbohydrate (40% vs 58% energy) and GI (40% vs 65% on the glucose scale) on insulin sensitivity (determined by glucose and insulin levels during a 2 hour oral glucose tolerance test), systolic blood pressure (SBP), and fasting lipids (LDL-C, HDL-C, and TG) in non-diabetic, overweight adults with SBP 120 - 159 mmHg. Methods: We randomized 163 adults, mean age 53 y, in a 4 period crossover feeding study. The 4 diets, each studied for 5 weeks, were (1) higher-carbohydrate, higher-GI; (2) higher-carbohydrate, lower-GI; (3) lower-carbohydrate, higher-GI; and (4) lower-carbohydrate, lower-GI. All diets were based on a healthful DASH-type dietary pattern. At the end of each feeding period in a subsample of participants (N=51-57) we obtained hourly blood samples for glucose, insulin, and TG over 12 hours while participants ate the day’s meals in the research facility. Results: The four study diets did not significantly differentially affect insulin sensitivity, LDL-C, or SBP. The lower-carbohydrate or lower-GI diets increased HDL-C by about 4% (with between diet P-values <0.016) and lowered TG by 20% (P<0.031, compared to the higher-carbohydrate, higher-GI diet. Most of these effects were accounted for by lower amount of carbohydrate rather than lower GI. Similarly, the lower carbohydrate or lower GI diets lowered 12-hour blood glucose by an average of 20% (P<0.031) compared to the higher carbohydrate, higher GI diet. The lower-carbohydrate, lower-GI diet reduced 12-hour serum insulin levels the most by 17% (P=0.032). Compared to levels measured when the participants were eating their own diets, all study diets lowered SBP by an average of 9 mm (7%) and LDL-C by 13 mg/dL (9%). Conclusions: In the context of healthful dietary patterns, varying the amount of carbohydrate or its GI in non-diabetic overweight adults does not affect fasting insulin sensitivity, SBP or LDL-C over 5 weeks. HDL-C and triglycerides improved on the lower carbohydrate diets but were not affected by GI. However, postprandial glycemia is reduced either by lowering GI or amount of carbohydrate, and hyperinsulinemia is reduced by the combination of low GI and low carbohydrate. We speculate that consistent associations in populations of reduced CVD event rates with lower intakes of carbohydrate and GI, if causal, result more from reduced postprandial glycemia and hyperinsulinemia than from lower BP and improved lipid risk factors.
Crossover study
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Oxidative stress can be defined as a situation of imbalance in which the levels of pro-oxidants, referred to as reactive oxygen species (ROS) present in tissues, by far outweigh the amounts of neutralizing substances, otherwise known as antioxidants, as previously discussed [1]. There is overwhelming evidence in the literature to show that this phenomenon is associated with both type 1 and type 2 diabetes [1–7]. Many experimental approaches have been used to demonstrate the association of oxidative stress with diabetes. Some investigators have examined levels of ROS or their degradation products, while others have assessed tissue and blood levels of micronutrient antioxidants and/or the levels and activities of antioxidant enzymes in experimental animals and in individuals afflicted with diabetes. While it has been fairly accepted that oxidative stress may play a role in the etiology of type 1 diabetes [4,8,9], it is presently not clear that it plays any role in the pathogenesis of type 2 diabetes. Previous studies had suggested that oxidative stress is a consequence of type 2 diabetes and may be primarily involved in the development of secondary complications of the disease [10–15]. However, there is a growing body of evidence to show that it 412may actually play a role, even if secondary, in the pathogenesis of the disease [1–3,6,7,16–20]. In this chapter, we will review the literature to determine the relationship between oxidative stress and type 2 diabetes, with particular attention to the role played by oxidative stress in the pathogenesis of the disease. We will then determine if there is a valid scientific basis for a beneficial role of antioxidant supplementation in the prevention and as adjunct therapy for glycemic control in human subjects afflicted with type 2 diabetes, as reported in some studies.
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