strategie nutrizionali per migliorare il glucosio post-prandiale

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mi permetto di postare questo studio, non tanto per le "novità" in esso contenuto quanto per il fatto che ritengo possa essere utilizzato come riferimento da mostrare a chi inizia ad avvicinarsi a questo tipo di studi o semplicemente a chi dovesse farne richiesta nella sezione alimentazione.


particolarmente interessanti i riferimenti a:
- aceto (vinegar)
- olio, frutta secca, olio di pesce
- proteine e curva glicemica
- perdita di peso

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Dietary Strategies for Improving Post-Prandial Glucose, Lipids, Inflammation, and Cardiovascular Health
James H. O’Keefe MD, a, , Neil M. Gheewala MSa and Joan O. O’Keefe RDa
aMid America Heart Institute and University of Missouri–Kansas City, Kansas City, Missouri.


Received 16 August 2007;
revised 5 October 2007;
accepted 7 October 2007.
Available online 16 January 2008.

The highly processed, calorie-dense, nutrient-depleted diet favored in the current American culture frequently leads to exaggerated supraphysiological post-prandial spikes in blood glucose and lipids. This state, called post-prandial dysmetabolism, induces immediate oxidant stress, which increases in direct proportion to the increases in glucose and triglycerides after a meal. The transient increase in free radicals acutely triggers atherogenic changes including inflammation, endothelial dysfunction, hypercoagulability, and sympathetic hyperactivity. Post-prandial dysmetabolism is an independent predictor of future cardiovascular events even in nondiabetic individuals. Improvements in diet exert profound and immediate favorable changes in the post-prandial dysmetabolism. Specifically, a diet high in minimally processed, high-fiber, plant-based foods such as vegetables and fruits, whole grains, legumes, and nuts will markedly blunt the post-meal increase in glucose, triglycerides, and inflammation. Additionally, lean protein, vinegar, fish oil, tea, cinnamon, calorie restriction, weight loss, exercise, and low-dose to moderate-dose alcohol each positively impact post-prandial dysmetabolism. Experimental and epidemiological studies indicate that eating patterns, such as the traditional Mediterranean or Okinawan diets, that incorporate these types of foods and beverages reduce inflammation and cardiovascular risk. This anti-inflammatory diet should be considered for the primary and secondary prevention of coronary artery disease and diabetes.

Dietary Strategies for Improving Post-Prandial Glucose, Lipids, Inflammation, and Cardiovascular Health
James H. O’Keefe, Neil M. Gheewala, Joan O. O’Keefe
Exaggerated post-prandial spikes in blood glucose and lipids induce proportional increases in oxidant stress, which acutely trigger inflammation and endothelial dysfunction and increased risk of future cardiovascular events even in nondiabetic individuals. Improvements in diet exert profound and immediate favorable changes in these post-prandial disturbances. Low glycemic index vegetables and fruits, nuts, lean protein, vinegar, tea, fish oil, calorie restriction, weight loss, and moderate- to low-dose alcohol each significantly improve post-meal inflammation. This anti-inflammatory diet should be considered for the primary and secondary prevention of coronary artery disease and diabetes.

Abbreviations: CAD, coronary artery disease; CV, cardiovascular

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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).

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Post-Prandial Hyperlipemia

Recent studies of healthy individuals indicate that a single meal high in saturated fat will cause immediate increases in triglycerides, oxidative stress, and inflammation, which causes corresponding post-meal worsening of endothelial dysfunction, vasoconstriction, and systolic blood pressure ([11] and [12]). Post-prandial hyperlipemia, manifest as elevated levels of triglycerides, chylomicrons, and remnant lipoproteins, causes oxidative stress and inflammation, and independently potentiates the adverse effects of post-prandial hyperglycemia (13). These elevated and protracted post-meal lipid levels are common manifestations of insulin resistance and the metabolic syndrome (14).
Triglycerides are traditionally measured in the fasting state—typically the lowest triglyceride level of the day. Two large recently published cohort studies involving over 40,000 individuals found that post-prandial hypertriglyceridemia was associated with increased risk of CV events, whereas fasting triglyceride level was not ([15] and [16]). Post-prandial triglyceride levels are also directly related to angiographic progression of coronary and carotid atherosclerosis (3). Subanalyses of 3 randomized trials showed that lowering levels of elevated triglycerides by 20% to 40% reduced CAD rates by approximately 30% to 40% (15).
How the Modern Diet Causes Inflammation

Excessive ingestion of calorie-dense, easily digestible foods causes abnormal surges in blood glucose and triglyceride levels (11 F. Jakulj, K. Zernicke and S. Bacon et al., A high fat meal increases cardiovascular reactivity to psychological stress in healthy young adults, J Nutr 137 (2007), pp. 935–939. View Record in Scopus | Cited By in Scopus (6)[11], [12] and [13]). This bolus of energetic substrate overwhelms the metabolic capabilities of the mitochondria in the overnourished muscle and adipose tissues. Glucose and free fatty acids flood the Krebs cycle, stimulating an excess of the reduced form of nicotinamide adenine dinucleotide production, which outstrips the capacity of oxidative phosphorylation and drives the transfer of single electrons to oxygen, creating free radicals such as superoxide anion (17). Post-prandial glucose excursion correlates directly with the ensuing increase in free radicals (Fig. 2). This post-prandial oxidant stress acutely triggers atherogenic changes, including increases in low-density lipoprotein oxidation, sympathetic tone, vasoconstriction, and thrombogenicity ([5] and [17]). Meal-induced inflammation is evidenced by immediate increases in C-reactive protein, cytokines, and endothelin-1 (Fig. 3) ([3] and [17]). Even hyperglycemic spikes induced artificially using intravenous glucose infusions in lean nondiabetic individuals have been shown to markedly increase free radical generation (18).


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Figure 2. Glucose Excursion Directly Related to Oxidant Stress
Linear correlation between post-prandial glucose excursions and urinary excretion of 8-iso prostaglandin F2α (PGF2α), a measure of oxidant stress. Reprinted with permission (17).


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Figure 3. Post-Prandial Stress
The immediate deleterious effects of a beverage containing 75 g glucose mixed with 700 kcal/m2 of whipping cream. Within 2 to 4 h glucose and triglyceride levels double, causing immediate oxidant stress (nitrotyrosine), inflammation (C-reactive protein [CRP]), resulting in deterioration in endothelial function. FMD % = percent flow-mediated dilation. Data from Ceriello et al. (41 J.A. Byrans, P.A. Judd and P.R. Ellis, The effect of consuming instant black tea on postprandial plasma glucose and insulin concentrations in healthy humans, J Am Coll Nutr 26 (2007), pp. 471–477.41).

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Therapies for Post-Prandial Dysmetabolism

Promising pharmacologic approaches to the normalization of post-prandial dysmetabolism are evolving. However, resorting to drug therapy for an epidemic caused by a maladaptive diet is less rational than simply realigning our eating habits with our physiological needs (2). The traditional Mediterranean and the Okinawan diets, which are rich in minimally processed natural foods that are low in caloric density but high in nutrient density, have been associated with improved CV health and longevity ([1] and [19]). These diets are closer to the ancestral hunter-gatherer eating patterns for which modern humans remain genetically adapted (20). Specifically, diets that include large amounts of fresh unprocessed plants, with moderate levels of lean protein and beneficial fats (such as omega-3 and monounsaturated fats) and low levels of processed carbohydrates and saturated and trans fats, and that are rich in antioxidants substantially improve post-prandial glucose and lipid levels (19 A. Lichtenstein, L. Appel and M. Brands et al., Diet and lifestyle recommendations revision 2006: a scientific statement from the American Heart Association Nutrition Committee, Circulation 114 (2006), pp. 82–96. View Record in Scopus | Cited By in Scopus (328)19).
Type and Amount of Carbohydrate Consumed

The amount and type of carbohydrate consumed with a meal is a major determinant of the post-prandial glucose excursion (21). The glycemic index of a food is defined as the incremental increase in the area under the post-prandial glucose curve after ingestion of 50 g of a specific food compared with that noted after ingestion of 50 g of oral glucose. A meal such as white bread and jelly with a glycemic index of 80 will result in a 2-fold higher incremental increase in glucose compared with an isocaloric meal of whole-grain bread and peanut butter with a glycemic index of 40. Most studies show that diets rich in high-glycemic-index, low-fiber foods independently increase the risk of both CV disease and type 2 diabetes ([19] and [21]).
Minimally processed plants such as vegetables, fruits, nuts, seeds, and grains generally increase post-prandial glucose and triglycerides to a lesser degree than do processed foods (22). Ideal carbohydrate foods for improving post-prandial dysmetabolism include green leafy vegetables such as broccoli and spinach, or fruits such as grapefruits and cherries. Their lower caloric density and glycemic indexes and higher fiber and water content induce less glucose excursion after a meal, whereas their antioxidant phytonutrients dampen down the oxidant stress that is inherently generated when glucose or fatty acids are burned in the Krebs cycle (2). Dietary antioxidants such as those present in deeply pigmented plant-based foods and drinks such as berries, red wine, dark chocolate, tea, and pomegranates help to protect the vascular endothelium from post-prandial oxidant stress and inflammation independently of their effects on post-prandial glucose and triglyceride levels ([2] and [23]). Cinnamon is a calorie-free herb rich in antioxidants that, when added to a high-glycemic-index meal, significantly reduces the post-prandial glucose excursion, partly by slowing gastric emptying (24).
Excess intake of processed carbohydrates sets up a vicious cycle whereby the transient spikes in blood glucose and insulin early after a meal trigger reactive hypoglycemia and hunger (25). The chronic consumption of a diet high in processed carbohydrates leads to excess visceral fat, which increases both insulin resistance and inflammation and predisposes to diabetes, hypertension, and CV disease (25). In contrast, restriction of refined carbohydrates will improve the post-prandial levels of both glucose and triglycerides and can reduce intra-abdominal fat, particularly in individuals with insulin resistance (25).
The amount of carbohydrate consumed is equally important as the glycemic index. Small quantities of high glycemic index foods such as white rice, glucose, or potatoes will have a proportionally smaller effect on post-prandial glucose spikes than larger quantities of these foods (26). On the other hand, even low glycemic index foods such as legumes (e.g., lentils) when consumed in large quantities can cause substantial post-prandial glucose spikes (26). Thus, portion control is of fundamental importance to the short- and long-term health effects of any diet. The portion size inflation that has transpired in American restaurants in recent decades is not just contributing to the obesity crisis but also is causing immediate toxic effects throughout the vascular system in the person who consumes such a meal (16).
Dietary fiber is effective at delaying gastric emptying, slowing digestion, and reducing post-prandial excursions of both glucose and triglycerides (27). Minimally processed plant-based foods are natural sources of soluble and insoluble fiber that improve post-prandial dysmetabolism, reduce oxidant stress and inflammation, and lower the risks of CAD and diabetes ([19], [22] and [27]).

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Nuts, Olive Oil, and Fish Oil

Nuts, when consumed with a meal, will significantly reduce the post-prandial glucose excursion by slowing digestion. Recent studies show that almonds, pistachios, or peanuts, when eaten along with high glycemic index carbohydrates such as white bread or mashed potatoes, will reduce the post-prandial glucose area under the curve by approximately 30% to 50% (28) (Fig. 4). Importantly, nuts also decrease meal-induced oxidative protein damage because they lower post-prandial oxidative stress and additionally provide antioxidants (29 D. Jenkins, C. Kendall and A. Josse et al., Almonds decrease post-prandial glycemia, insulinemia, and oxidative damage in healthy individuals, J Nutr 136 (2006), pp. 2987–2992. View Record in Scopus | Cited By in Scopus (20)29).


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Figure 4. Almonds Reduce Post-Prandial Glucose
The post-prandial increase in the area under the curve for glucose was reduced by 58% when 90 g of almonds were added to a high glycemic index meal (p = 0.009). Data from Josse et al. (28 A. Josse, C. Kendall, L. Augustin, P. Ellis and D. Jenkins, Almonds and post-prandial glycemia—a dose-response study, Metabolism 56 (2007), pp. 400–404. Abstract | Article | PDF (239 K) | View Record in Scopus | Cited By in Scopus (13)28).


A recent trial randomized 772 subjects at high risk for CAD to a low-fat diet or a Mediterranean-style diet supplemented with either walnuts (30 g/day) or virgin olive oil (1 l/week). This trial found that after 3 months the Mediterranean diets supplemented with either nuts or olive oil produced clinically significant reductions in systolic blood pressure, fasting glucose, and inflammatory biomarkers compared with the low-fat diet (1).
Epidemiologic studies consistently indicate that consumption of nuts at least 5 times per week will reduce CAD and diabetes risks by 20% to 50% (29). Tree nuts are comprised predominantly of monounsaturated fats and are a rich source of antioxidants, fiber, phytosterols, magnesium, and folic acid, which might beneficially influence CV risk. Replacing refined carbohydrates with monounsaturated fats (using nuts and/or olive oil) will reduce post-prandial hyperglycemia and hypertriglyceridemia, increase high-density lipoprotein, and decrease oxidative stress ([1] and [2]). One practical way to accomplish this is to substitute nuts (all of which have very low glycemic indexes) for the sugary and starchy snack foods that are staples in the American diet.
Fish oil (omega-3 fatty acids) lowers post-prandial triglyceride levels by 16% to 40% in a dose-dependent fashion, in part by upregulating lipoprotein lipase activity and accelerating the clearance of chylomicrons (30). Thus, some of the documented anti-inflammatory and cardioprotective activities of omega-3 fatty acids may be conferred in part by significant improvements in post-meal lipid levels (31).