Introduction: Low-Saturated Fat, High-Carbohydrate Diets: Effects on Triglyceride and LDL Synthesis, the LDL Receptor, and Cardiovascular Disease Risk

Author(s):  
Robert H. Knopp
2002 ◽  
Vol 63 (1) ◽  
pp. 20-32 ◽  
Author(s):  
John L. Sievenpiper ◽  
Alexandra L. Jenkins ◽  
Dana L. Whitham ◽  
Vladimir Vuksan

Insulin resistance is a prevalent condition, in which insulin loses its normal physiological action. Since people were first classified as insulin resistant over 60 years ago, one of the main discoveries has been that insulin resistance clusters with other risk factors such as obesity, elevated triglycerides, and low high-density lipoprotein cholesterol, increasing cardiovascular disease risk. Although insulin resistance appears to manifest first in the periphery and then in the liver, other sites, such as the brain and the pancreatic β-cell, may play pathogenic roles. Factors contributing to insulin resistance at these sites include perturbations in free fatty acids, glucose, and hormone-signalling, some of which may be linked to various genetic polymorphisms. Appropriate nutritional treatment for insulin resistance is controversial. Two main approaches are drawn from diabetes recommendations: i) a high-carbohydrate, low-fat, highfibre diet emphasizing low glycemic-index foods and ii) sharing calories between monounsaturated fat and complex carbohydrate at the expense of saturated fat. Recent interest in insulin resistance has prompted the development of new guidelines. Promising data have also emerged, showing that a high-carbohydrate, high-fibre, low-fat diet plus exercise programs maintained through intensive counselling can decrease diabetes risk by over 40%. Additional research is required to confirm the sustainability of this approach and sort out the determinants of insulin resistance so that more effective nutritional interventions will result.


2020 ◽  
Vol 79 (OCE2) ◽  
Author(s):  
Marie-Pierre St-Onge ◽  
Ayanna Campbell ◽  
Arindam RoyChoudhury

AbstractNut consumers have lower body weight and are at lower cardiovascular disease risk than non-consumers. Interestingly, minority adults, who have the highest prevalence of obesity and are at disproportionate risk of cardiovascular disease, have low nut intakes. The goal of this study was to test whether consumption of almonds, compared to low-fat/high-carbohydrate cereal bars (LF-HC), as a supplement for 24 wk, would improve appetite regulation and body composition in Blacks and Hispanics. Twenty-nine adults, BMI > 25 kg/m2, age 30–65 y, were recruited and randomized to consume either almonds or LF-HC providing 17.5% of their estimated energy requirements as part of their regular diet. A total of 17 adults completed the study, 9 men and 8 women; 7 of whom were randomized to almond consumption (4 men, 3 women), and 10 to LF-HC consumption (5 men, 5 women). Outcome variables included appetite-regulating hormones and inflammatory markers, which were measured from fasting blood samples taken at baseline, week 12, and endpoint. Body composition was measured by magnetic resonance imaging at baseline and endpoint. Data were analyzed using linear mixed model with treatment, time, and their interaction as predictor variables; age, race, sex, and baseline BMI as covariates; and participant ID as a random effect variable. Peptide YY concentrations were higher in the almond group compared to LF-HC (time x treatment interaction at 12 wk, P < 0.001; 24 wk, P = 0.13). Glucagon-like peptide 1 concentrations were higher in the almond group compared to LF-HC (time x treatment interaction at 12 wk, P = 0.10; 24 wk, P = 0.015). Ghrelin levels decreased in LF-HC compared to the almond group at 12 wk but not 24 wk (time x treatment interaction at 12 wk, P = 0.017; 24 wk, P = 0.23). There was a slight trend for a time x treatment interaction on body weight (P = 0.14; change in almond = 0.6 ± 1.8 kg; LF-HC = 1.9 ± 2.7 kg). There was a time x treatment interaction on intermuscular adipose tissue (P = 0.013; change in almond = -0.10 ± 0.14 cm3; LF-HC = 0.04 ± 0.07 cm3). None of the measured inflammatory markers (C reactive protein, interleukin-6, and tumor necrosis factor) were affected by the dietary interventions. Despite the lack of profound body composition changes, daily almond intake for 24 wk, within the usual diet, ameliorated satiety and ectopic fat deposition, suggesting a potential role of nut consumption in the context of a weight reduction program in minority adults. Our data support further exploration of the health effects of nut consumption in this population.


2020 ◽  
Vol 16 ◽  
Author(s):  
Stephen J. Roy ◽  
Hirofumi Tanaka

: Lifestyle modifications in the form of diet and exercise are generally a first-line approach to reduce hypertensive risk and overall cardiovascular disease (CVD) risk. Accumulating research evidence has revealed that consumption of non- and low-fat dairy products incorporated into the routine diet is an effective means to reduce elevated blood pressure and improve vascular functions. However, the idea of incorporating whole-fat or full-fat dairy products in the normal routine diet as a strategy to reduce CVD risk has been met with controversy. The aim of this review is to review both sides of the argument surrounding saturated fat intake and CVD risk from the standpoint of dairy intake. Throughout the review, we examined observational studies on relationships between CVD risk and dairy consumption, dietary intervention studies using non-fat and whole-fat dairy, and mechanistic studies investigating physiological mechanisms of saturated fat intake that may help to explain increases in cardiovascular disease risk. Currently available data have demonstrated that whole-fat dairy is unlikely to augment hypertensive risk when added to the normal routine diet but may negatively impact CVD risk. In conclusion, whole-fat dairy may not be a recommended alternative to non- or low-fat dairy products as a means to reduce hypertensive or overall CVD risk.


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