Article Outline

Post-Prandial Hyperglycemia Post-Prandial Hyperlipemia How the Modern Diet Causes Inflammation Therapies for Post-Prandial Dysmetabolism Type and Amount of Carbohydrate Consumed Nuts, Olive Oil, and Fish Oil Vinegar High-Biological-Quality Protein Calorie Restriction and Weight Loss Light to Moderate Alcohol Consumption Exercise Summary and RecommendationsAcknowledgementsReferences
Systemic inflammation is increasingly recognized as an important mediator of coronary artery disease (CAD) and other common chronic degenerative diseases such as diabetes and Alzheimer dementia (1). In many individuals a maladaptive diet is a major underlying cause of this chronic inflammation ([1] and [2]). High-calorie meals rich in processed, easily digestible, quickly absorbable foods and drinks can lead to exaggerated post-prandial elevations in blood glucose and triglycerides (3). Accumulating data from multiple lines of evidence suggests that this condition, termed post-prandial dysmetabolism, is an important and largely unrecognized fundamental disturbance involved in the genesis of inflammation and atherosclerosis (3).
Exaggerated post-prandial spikes in glucose and lipids generate excess free radicals (or reactive oxygen species) that can trigger a biochemical cascade resulting in inflammation, endothelial dysfunction, and sympathetic hyperactivity ([4] and [5]). These post-prandial changes when repeated multiple times daily eventually lead to atherosclerotic risk factors and CAD. Dietary and lifestyle factors play a central role in the etiology of post-prandial dysmetabolism (3). The hypothesis of this review is that specific dietary strategies can dramatically and immediately improve post-prandial glucose and lipid levels, inflammation, and endothelial function, and if used in the long-term will also improve cardiovascular (CV) health.
Post-Prandial Hyperglycemia

Recent studies indicate that about one-third of American adults and two-thirds of CAD patients have abnormal glucose homeostasis ([6] and [7]). A significant proportion of these at-risk individuals will have a fasting glucose level in the nondiabetic range (<126 mg/dl) but would show hyperglycemia diagnostic of impaired glucose tolerance (>140 mg/dl) or diabetes (>200 mg/dl) after an oral glucose tolerance test or a meal.
Continuous linear direct relationships exist between glucose levels after a glucose challenge and the risks of both CV death and all-cause mortality (8). At only 80 mg/dl the CV risk of post-prandial or post-challenge glycemia begins to increase; by 140 mg/dl, the point at which we traditionally only begin to classify patients as glucose intolerant or pre-diabetic, the risk is already increased by 58% ([9] and 10 P. Mellen, W. Cefalu and D. Herrington, Diabetes, the metabolic syndrome, and angiographic progression of coronary artery disease in postmenopausal women, Arterioscler Thromb Vasc Biol 26 (2006), pp. 189–193. View Record in Scopus | Cited By in Scopus (12)[10]) (Fig. 1).

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Figure 1. Post-Challenge Glucose and Coronary Atherosclerosis Progression

Patients with normal glucose tolerance who had a post-prandial glucose level of <87 mg/dl had coronary regression. The remaining patients had coronary progression in proportion to the increase in post-prandial glucose. Data from Mellen et al. (10 P. Mellen, W. Cefalu and D. Herrington, Diabetes, the metabolic syndrome, and angiographic progression of coronary artery disease in postmenopausal women, Arterioscler Thromb Vasc Biol 26 (2006), pp. 189–193. View Record in Scopus | Cited By in Scopus (12)10).