venerdì 17 agosto 2012

Harms of inflammation - 2

(TESTO IN ITALIANO SOTTO)

Atherosclerosis has features of an inflammatory disease: this underlines the importance of anti-inflammatory approaches to the prevention of atherosclerosis.

This reminds us the importance of anti-inflammatory approaches to the diet too:

- reduction of insulin release through a right management of carbohydrates intake (expecially high-glycemic index ones)

- enough EPA and DHA intake (long-chain fish-oil omega3 fatty acids)

The use of fish-oil supplements purified through repeated molecular distillation is strongly recommended (check the bottle before buying it).


COMMENTO IN ITALIANO:
(e sotto)


Source:


Circulation. 2002 Apr 16;105(15):1816-23.
Cyclooxygenase-2 promotes early atherosclerotic lesion formation in LDL receptor-deficient mice.
Burleigh ME, Babaev VR, Oates JA, Harris RC, Gautam S, Riendeau D, Marnett LJ, Morrow JD, Fazio S, Linton MF.
Department of Pharmacology, Vanderbilt University Medical Center, Nashville, Tenn, USA.

Abstract

BACKGROUND:
Atherosclerosis has features of an inflammatory disease. Because cyclooxygenase (COX)-2 is expressed in atherosclerotic lesions and promotes inflammation, we tested the hypotheses that selective COX-2 inhibition would reduce early lesion formation in LDL receptor-deficient (LDLR-/-) mice and that macrophage COX-2 expression contributes to atherogenesis in LDLR-/- mice.

METHODS AND RESULTS:
Treatment of male LDLR-/- mice fed the Western diet with rofecoxib or indomethacin for 6 weeks resulted in significant reductions in atherosclerosis in the proximal aorta (25% and 37%) and in the aorta en face (58% and 57%), respectively. Rofecoxib treatment did not inhibit platelet thromboxane production, a COX-1-mediated process, but it significantly reduced the urinary prostacyclin metabolite 2,3-dinor-6-keto-PGF1alpha. Fetal liver cell transplantation was used to generate LDLR-/- mice null for expression of the COX-2 gene by macrophages. After 8 weeks on the Western diet, COX-2-/- --> LDLR-/- mice developed significantly less (33% to 39%) atherosclerosis than control COX-2+/+ --> LDLR-/- mice. In both the inhibitor studies and the transplant studies, serum lipids did not differ significantly between groups.

CONCLUSIONS:
The present studies provide strong pharmacological and genetic evidence that COX-2 promotes early atherosclerotic lesion formation in LDLR-/- mice in vivo. These results support the potential of anti-inflammatory approaches to the prevention of atherosclerosis.




TESTO IN ITALIANO:

Danni dell'infiammazione – 2

L'aterosclerosi è una malattia infiammatoria: questo sottolinea l'importanza degli approcci anti-infiammatori nella prevenzione dell'aterosclerosi.

Questo ci ricorda anche l'importanza dell'approccio anti-infiammatorio nella dieta:

- riduzione dell'increzione di insulina tramite una corretta gestione dell'apporto dei carboidrati (specialmente di quelli ad alto indice glicemico)

- sufficiente apporto di EPA e DHA (gli acidi grassi omega3 a lunga catena contenuti nell'olio di pesce)

Si consiglia vivamente l'uso di integratori di olio di pesce purificati mediante distillazione molecolare ripetuta (controllare bene la confezione prima di acquistare).


FONTE COMMENTATA:
Cyclooxygenase-2 promotes early atherosclerotic lesion formation in LDL receptor-deficient mice


martedì 14 agosto 2012

Harms of inflammation - 1

(TESTO IN ITALIANO SOTTO)

Pro-inflammatory cytokines and systemic inflammation initiate or worsen:
- Autoimmunity
- Alzheimer's disease
- atherosclerosis

The unregulated systemic inflammation has a critical importance in common neurological and cardiovascular disease that shortens the nominal longevity of humans.
So pay attention to foods that stimulate the synthesis of mediators of inflammation: high-glycemic index carbohydrates.

COMMENTO IN ITALIANO:
(e sotto)


Source:

Inflamm Res. 2000 Nov;49(11):561-70.
Unregulated inflammation shortens human functional longevity.
Brod SA.
University of Texas Health Science Center at Houston, Department of Neurology, 77225, USA. Staley.a.brod@uth.tmc.edu

Abstract
Systemic inflammation, represented in large part by the production of pro-inflammatory cytokines, is the response of humans to the assault of the non-self on the organism. Three distinct types of human ailments - namely autoimmunity, presenile dementia (Alzheimer's disease), or atherosclerosis - are initiated or worsened by systemic inflammation. Autoimmunity is unregulated hyperimmunity to organ-specific proteins, inducing rapid turnover of antigen-specific T cells of the acquired immune system with ultimate exhaustion and loss of acquired immunity IL-2 and IFN-gamma production and proliferative decline, conforming to the limited capacity of clonal division (Hayflick phenonmenon). In Alzheimer's disease (AD), the primary degenerative process of amyloid-beta (AJ3) protein precedes a cascade of events that ultimately leads to a local "brain inflammatory response". Unregulated systemic immune processes are secondary but important as a driving-force role in AD pathogenesis. Atherosclerosis, an underlying cause of myocardial infarction, stroke, and other cardiovascular diseases, consists of focal plaques characterized by cholesterol deposition, fibrosis, and inflammation. The presence of activated T lymphocytes and macrophages indicate a local immunologic activation in the atherosclerotic plaque that may be secondary to unregulated pro-inflammatory cytokines too. The premature hyperimmunity of autoimmunity, the local "brain inflammatory response" to A/3 protein in AD, and the immune response to fatty changes in vessels in atherosclerosis all signal the critical importance of unregulated systemic inflammation to common neurological and cardiovascular disease that shortens the nominal longevity of humans.




TESTO IN ITALIANO:

Danni dell'infiammazione – 1

Le citochine pro-infiammatorie e l'infiammazione sistemica causano o peggiorano:
- Le malattie autoimmunitarie
- Il morbo di Alzheimer
- L'aterosclerosi

L'infiammazione sistemica sregolata ha un'importanza critica nelle comuni malattie neurologiche e cardiovascolari che riducono la longevità degli uomini.
Attenzione, quindi, agli alimenti che stimolano la sintesi dei mediatori pro-infiammatori: i carboidrati ad alto indice glicemico.

FONTE COMMENTATA:
Unregulated inflammation shortens human functional longevity.

lunedì 13 agosto 2012

The insulin-pathologies connection

(TESTO IN ITALIANO SOTTO)

A daily intake of high glycemic index carbohydrates is associated with an increased risk of coronaropathy, obesity, diabetes and cardiovascular pathologies.
It seems that caloric restriction benefits could be associated with the insulin resistance prevention.
Impaired glucose tolerance is associated with carotid atherosclerosis and with high cardiovascular risk (while a normal glucose tolerance and a plasma glucose within the normal range are not).
Insulin/glycemia excess and insulin resistance are associated with coronary heart disease, carotid atherosclerosis and cardiovascular risk.
Insulin-resistance is associated with cardiovascular disease independently of all classic and several nontraditional risk factors.
Insulin-resistance could be an important target to reduce cardiovascular disease risk.
High glycemic index carbohydrates produce substantial increases in blood glucose and insulin levels after ingestion. Their insulin stimulation is so strong that after their ingestion blood sugar levels begin to decline rapidly due to an exaggerated increase in insulin secretion.

According to these data, we can conclude that the pluridecennial daily intake of high glycemic carbohydrates (that is typical of most people) could be strongly associated with these pathologies.
Furthermore a low-glycemic index carbohydrates based diet could be useful for their prevention and treatment.



COMMENTO IN ITALIANO:
(e sotto)


Sources:










Diabetes Care. 2007 Feb;30(2):318-24.
Insulin resistance as estimated by homeostasis model assessment predicts incident symptomatic cardiovascular disease in caucasian subjects from the general population: the Bruneck study.
Bonora E, Kiechl S, Willeit J, Oberhollenzer F, Egger G, Meigs JB, Bonadonna RC, Muggeo M.
Endocrinologia e Malattie del Metabolismo, Ospedale Maggiore, Piazzale Stefani 1, 37126 Verona, Italy. enzobonora@virgilio.it
Abstract

OBJECTIVE:
The purpose of this study was to evaluate whether insulin resistance is associated to cardiovascular disease (CVD) and to understand whether this association can be explained by traditional and novel CVD risk factors associated with this metabolic disorder.

RESEARCH DESIGN AND METHODS:
We examined a sample representative of the population of Bruneck, Italy (n = 919; aged 40-79 years). Insulin-resistant subjects were those with a score in the top quartile of the homeostasis model assessment (HOMA) for insulin resistance (HOMA-IR). Risk factors correlated with insulin resistance included BMI, A1C, HDL cholesterol, triglycerides, blood pressure, high-sensitivity C-reactive protein (hsCRP), fibrinogen, oxidized LDL, vascular cell adhesion molecule-1 (VCAM-1), and adiponectin. Subjects without CVD at baseline were followed up for 15 years for incident CVD, a composite end point including fatal and nonfatal myocardial infarction and stroke, transient ischemic attack, and any revascularization procedure.

RESULTS:
During follow-up, 118 subjects experienced a first symptomatic CVD event. Levels of HOMA-IR were higher at baseline among subjects who developed CVD (2.8) compared with those remaining free of CVD (2.5) (P < 0.05). Levels of HOMA-IR also were significantly correlated (P < 0.05) with most CVD risk factors we evaluated. In Cox proportional hazard models, insulin-resistant subjects had an age-, sex-, and smoking-adjusted 2.1-fold increased risk (95% CI 1.3-3.1) of incident symptomatic CVD relative to non-insulin-resistant subjects. After sequential adjustment for physical activity and classic risk factors (A1C, LDL cholesterol, and hypertension) as well as BMI, HDL cholesterol, triglycerides, and novel risk factors, including fibrinogen, oxidized LDL, hsCRP, VCAM-1, and adiponectin, the association between HOMA-IR and incident CVD remained significant and virtually unchanged (hazard ratio 2.2 [95% CI 1.4-3.6], P < 0.001).

CONCLUSIONS:
HOMA-estimated insulin resistance is associated with subsequent symptomatic CVD in the general population independently of all classic and several nontraditional risk factors. These data suggest that insulin resistance may be an important target to reduce CVD risk.



Diabetes Care. 2003 Apr;26(4):1251-7.
Carotid atherosclerosis and coronary heart disease in the metabolic syndrome: prospective data from the Bruneck study.
Bonora E, Kiechl S, Willeit J, Oberhollenzer F, Egger G, Bonadonna RC, Muggeo M; Bruneck study.
Division of Endocrinology and Metabolic Diseases, University of Verona Medical School, Verona, Italy. enzobonora@virgilio.it

Abstract

OBJECTIVE:
The present study aimed at prospectively evaluating carotid atherosclerosis and coronary heart disease (CHD) in subjects with the metabolic syndrome.

RESEARCH DESIGN AND METHODS:
Within a prospective population-based survey examining 888 subjects aged 40-79 years, 303 subjects were identified as fulfilling World Health Organization (WHO) criteria and 158 as fulfilling the National Cholesterol Education Program (NCEP)-Adult Treatment Panel (ATP)-III criteria for diagnosing the metabolic syndrome. The 5-year change in carotid status, as assessed by echo-duplex scanning, and incident fatal and nonfatal CHD, as assessed by medical history and death certificates, were compared in subjects with the metabolic syndrome and in the rest of the sample (control subjects).

RESULTS:
Compared with the control subjects, subjects with the metabolic syndrome by WHO criteria had an increased 5-year incidence and progression of carotid atherosclerosis: 51 vs. 35% developed new plaques (P = 0.021) and 34 vs. 19% developed carotid stenosis >40% (P = 0.002) after adjusting for several confounders. Subjects with the metabolic syndrome by these criteria also had an increased incidence of CHD during follow-up: 8 vs. 3% in control subjects (P = 0.012). Similar results were found when the NCEP-ATPIII criteria were used.

CONCLUSIONS:
Subjects with the metabolic syndrome are at increased risk for both progressive carotid atherosclerosis and CHD.



Crit Rev Food Sci Nutr. 2003;43(4):357-77.
Low-glycemic-load diets: impact on obesity and chronic diseases.
Bell SJ, Sears B.
Sears Labs, 222 Rosewood Drive, Suite 500, Danvers, Massachusetts 01923, USA. sbell@searslabs.com

Abstract
Historically, carbohydrates have been thought to play only a minor role in promoting weight gain and in predicting the risk of development of chronic disease. Most of the focus had been on reducing total dietary fat. During the last 20 years, fat intake decreased, while the number of individuals who were overweight or developed a chronic conditions have dramatically increased. Simultaneously, the calories coming from carbohydrate have also increased. Carbohydrates can be classified by their post-prandial glycemic effect, called the glycemic index or glycemic load. Carbohydrates with high glycemic indexes and high glycemic loads produce substantial increases in blood glucose and insulin levels after ingestion. Within a few hours after their consumption, blood sugar levels begin to decline rapidly due to an exaggerated increase in insulin secretion. A profound state of hunger is created. The continued intake of high-glycemic load meals is associated with an increased risk of chronic diseases such as obesity, cardiovascular disease, and diabetes. In this review, the terms glycemic index and glycemic load are defined, coupled with an overview of short- and long-term changes that occur from eating diets of different glycemic indexes and glycemic loads. Finally, practical strategies for how to design low-glycemic-load diets consisting primarily of low-glycemic carbohydrates are provided.



Diabetologia. 2000 Feb;43(2):156-64.
Impaired glucose tolerance, Type II diabetes mellitus and carotid atherosclerosis: prospective results from the Bruneck Study.
Bonora E, Kiechl S, Oberhollenzer F, Egger G, Bonadonna RC, Muggeo M, Willeit J.
Department of Endocrinology and Metabolic Diseases, University of Verona Medical School, Italy.

Abstract

AIMS/HYPOTHESIS:
Cardiovascular disease is a well-known severe complication of impaired glucose tolerance and Type II (non-insulin-dependent) diabetes mellitus. The independent contribution of glucose intolerance to cardiovascular disease and the underlying pathogenic mechanisms are still, however, not clear.

METHODS:
In this prospective population-based study, 826 subjects aged 40-79 years underwent high resolution duplex ultrasound examinations of carotid arteries and extensive clinical and laboratory screenings for potential vascular risk factors at baseline and 5 years later. The ultrasound protocol involved measurements of maximum axial diameter of atherosclerotic plaques, if any, in common and internal carotid arteries on both sides and enable differentiation of two main stages in carotid artery disease, termed early non-stenotic and advanced stenotic atherosclerosis. Intima-media thickness was assessed at the follow-up examination.

RESULTS:
Type II diabetes and, to a lesser extent, impaired glucose tolerance were found to be statistically significant risk predictors of 5-year changes in carotid atherosclerosis. These associations were in part independent of other vascular risk factors typically clustering with glucose intolerance. Both impaired glucose tolerance and Type II diabetes mellitus were not independently related to early non-stenotic atherosclerosis. In contrast, Type II diabetes mellitus was the strongest single risk predictor of advanced stenotic atherosclerosis [odds ratio 5.0 (95% confidence intervals 2.3-11.1)] and impaired glucose tolerance was of relevance as well [odds ratio 2.8 (1.2-6.4)] (p < 0.001).

CONCLUSION/INTERPRETATION:
Impaired glucose tolerance and, to a greater extent, Type II diabetes were strong independent predictors of advanced carotid atherosclerosis in our prospective population-based study.



Diabetes Care. 1999 Aug;22(8):1339-46.
Plasma glucose within the normal range is not associated with carotid atherosclerosis: prospective results in subjects with normal glucose tolerance from the Bruneck Study.
Bonora E, Kiechl S, Willeit J, Oberhollenzer F, Egger G, Bonadonna R, Muggeo M.
Department of Endocrinology and Metabolic Diseases, University of Verona Medical School, Italy.

Abstract

OBJECTIVE:
There is substantial evidence that glucose intolerance is associated with an increased risk of cardiovascular disease. However, it is not well established whether plasma glucose is independently related to atherosclerosis when glucose tolerance is normal and, if so, to which stage of the complex atherosclerotic process.

RESEARCH DESIGN AND METHODS:
We prospectively examined the status of carotid arteries in 625 subjects aged 40-79 years who were randomly selected from the general population and had normal glucose tolerance (according to World Health Organization criteria) both at baseline and at 5 years of follow-up. All subjects had high-resolution echo-duplex evaluation of the common and internal carotid arteries (eight regions of interest on both sides) in 1990 and 1995 to detect the change in carotid status over time. The occurrence of new plaques in previously normal segments was termed "incident nonstenotic" or "early atherosclerosis," and the occurrence of stenosis in >40% of previously normal segments was termed "incident stenotic" or "advanced atherosclerosis." In addition, we evaluated the changes in the atherosclerosis score (the sum of all plaques) during the follow-up, and we measured intimal-medial thickening (IMT) in the common carotid artery in 1995. In all subjects, several candidate risk factors were assessed: sex, age, BMI, waist-to-hip ratio, glucose, HbA1c, insulin, urate, lipids, apolipoproteins A1 and B, blood pressure, lipoprotein(a), fibrinogen, antithrombin III, factor V Leiden mutation, ferritin, leukocyte count, smoking, alcohol intake, physical activity, and socioeconomic status. Fasting plasma glucose (FPG), plasma glucose 2 hr after the glucose load (2-h PG), and HbA1c concentrations in 1990 and 1995 were averaged in each subject to obtain an estimate of long-term glucose exposure of the arterial wall.

RESULTS:
Linear or logistical regression analyses indicated that neither baseline glucose and HbA1c levels nor mean FPG, mean 2-h PG, or mean HbA1c in 1990 and 1995 were independently related to IMT, a 5-year change in the atherosclerotic score, incident nonstenotic (early) atherosclerosis, or incident stenotic (advanced) atherosclerosis. Likewise, subjects with FPG levels above the median and subjects in the new category of "impaired fasting glucose" did not have an increased occurrence or progression of atherosclerosis. All results were consistent before and after adjustment for other vascular risk factors and possible confounders.

CONCLUSIONS:
These results suggest that plasma glucose levels within the normal range (<7.8 mg/dl both at FPG and 2-h PG) are not independently related to any stage of atherosclerosis.



Diabetes. 1998 Oct;47(10):1643-9.
Prevalence of insulin resistance in metabolic disorders: the Bruneck Study.
Bonora E, Kiechl S, Willeit J, Oberhollenzer F, Egger G, Targher G, Alberiche M, Bonadonna RC, Muggeo M.
Division of Endocrinology and Metabolic Diseases, University of Verona Medical School and Azienda Ospedaliera di Verona, Italy.

Abstract
The prevalence of insulin resistance in the most common metabolic disorders is still an undefined issue. We assessed the prevalence rates of insulin resistance in subjects with impaired glucose tolerance (IGT), NIDDM, dyslipidemia, hyperuricemia, and hypertension as identified within the frame of the Bruneck Study. The study comprised an age- and sex-stratified random sample of the general population (n = 888; aged 40-79 years). Insulin resistance was estimated by homeostasis model assessment (HOMA(IR)), preliminarily validated against a euglycemic-hyperinsulinemic clamp in 85 subjects. The lower limit of the top quintile of HOMA(IR) distribution (i.e., 2.77) in nonobese subjects with no metabolic disorders (n = 225) was chosen as the threshold for insulin resistance. The prevalence of insulin resistance was 65.9% in IGT subjects, 83.9% in NIDDM subjects, 53.5% in hypercholesterolemia subjects, 84.2% in hypertriglyceridemia subjects, 88.1% in subjects with low HDL cholesterol, 62.8% in hyperuricemia subjects, and 58.0% in hypertension subjects. The prevalence of insulin resistance in subjects with the combination of glucose intolerance (IGT or NIDDM), dyslipidemia (hypercholesterolemia and/or hypertriglyceridemia and/or low HDL cholesterol), hyperuricemia, and hypertension (n = 21) was 95.2%. In isolated hypercholesterolemia, hypertension, or hyperuricemia, prevalence rates of insulin resistance were not higher than that in nonobese normal subjects. An appreciable number of subjects (n = 85, 9.6% of the whole population) was insulin resistant but free of IGT, NIDDM, dyslipidemia, hyperuricemia, and hypertension. These results from a population-based study documented that 1) in hypertriglyceridemia and a low HDL cholesterol state, insulin resistance is as common as in NIDDM, whereas it is less frequent in hypercholesterolemia, hyperuricemia, and hypertension; 2) the vast majority of subjects with multiple metabolic disorders are insulin resistant; 3) in isolated hypercholesterolemia, hyperuricemia, or hypertension, insulin resistance is not more frequent than can be expected by chance alone; and 4) in the general population, insulin resistance can be found even in the absence of any major metabolic disorders.



Stroke. 1997 Jun;28(6):1147-52.
Relationship between insulin and carotid atherosclerosis in the general population. The Bruneck Study.
Bonora E, Willeit J, Kiechl S, Oberhollenzer F, Egger G, Bonadonna R, Muggeo M.
Department of Endocrinology and Metabolie Diseases, University of Verona (Italy) Medical School, Italy.

Abstract

BACKGROUND AND PURPOSE:
Although several studies have investigated the association between insulin and coronary heart disease, the relationship between this hormone and carotid atherosclerosis is not well established.

METHODS:
As a part of a population-based survey on atherosclerosis and its risk factors, serum insulin was measured at fasting (n = 888) and at 2 hours after an oral glucose load (n = 811; known diabetic subjects were excluded). The study population comprised an age- and sex-stratified random sample of men and women aged 40 to 79 years. Atherosclerosis in the common and internal carotid arteries was assessed twice (in 1990 and 1995) by duplex sonography. Progression during the 5-years follow-up was defined by an increase in the atherosclerosis score of more than the doubled measurement error (> 27%) or by the occurrence of new plaques. Subjects were stratified in quintiles according to baseline serum insulin at fasting or 2 hours after glucose loading.

RESULTS:
Logistic regression analysis revealed a significant association of carotid atherosclerosis with both low and high insulin (U-shaped relation). This finding was found before and after adjustment for several covariates (sex, age, body mass index, glucose tolerance, triglycerides, apolipoproteins Al and B, fibrinogen, blood pressure status, behavioral variables, and socioeconomic status). This relation applied equally to fasting and postglucose insulin and was more pronounced in the prospective analysis than in the cross-sectional analysis.

CONCLUSIONS:
We conclude that both "hypoinsulinemia" and hyperinsulinemia are independent risk indicators of carotid atherosclerosis.



J Gerontol A Biol Sci Med Sci. 1995 May;50(3):B142-7.
Long-term dietary restriction in older-aged rhesus monkeys: effects on insulin resistance.
Bodkin NL, Ortmeyer HK, Hansen BC.
School of Medicine, Department of Physiology, University of Maryland at Baltimore, USA.

Abstract
Long-term dietary restriction to maintain constant body weight in adult rhesus monkeys prevents the development of impaired glucose tolerance, hyperglycemia, and noninsulin-dependent diabetes mellitus. We sought to determine whether these positive antidiabetogenic effects of reduced calorie intake with maintenance of normal lean body weight might be mediated through prevention of the development of insulin resistance. Insulin-stimulated glucose uptake was assessed by the euglycemic hyperinsulinemic clamp technique in seven older-aged rhesus monkeys (20.7 +/- 0.6 years) who had been dietary restricted for 9 +/- 2 years. Results were compared to seven ad libitum-fed nondiabetic monkeys of similar age (21.0 +/- 1.3 years). Results showed that the dietary restricted monkeys had significantly higher in vivo insulin action compared to the ad libitum-fed group (14.06 +/- 2.4 vs 7.75 +/- 0.9 mg/kg FFM/min, respectively; p < .03). We conclude that long-term dietary restriction is an effective means of mitigating the development of significant insulin resistance in older-aged rhesus monkeys, and may be the mechanism underlying the prevention of Type II diabetes in this model.



COMMENTO IN ITALIANO:

La connessione tra insulina e le patologie diffuse.

Un apporto giornaliero di carboidrati ad alto indice glicemico è associato con aumentato rischio di coronaropatia, obesità, diabete e patologie cardiovascolari.
Sembra che i benefici della restrizione calorica siano associati alla prevenzione dell'insulino-resistenza.
La ridotta tolleranza al glucosio è associata con aterosclerosi carotidea a con elevato rischio cardiovascolare (mentre la normale tolleranza al glucosio ed il livello di glucosio plasmatico nei limiti del range normale non lo sono).
L'eccesso di insulina/glicemia e la resistenza all'insulina sono associati con la malattia coronarica, l'aterosclerosi carotidea ed il rischio cardiovascolare.
L'insulinoresistenza è associata con la patologia cardiovascolare indipendentemente da tutti gli altri numerosi fattori di rischio classici e non tradizionali.
Agire sull'insulinoresistenza potrebbe essere un importante obiettivo per ridurre il rischio cardiovascolare.
I carboidrati ad alto indice glicemico producono un sostenziale incremento nei livelli ematici di glucosio ed insulina. La loro stimolazione insulinica è così forte che dopo l'ingestione di tali tipi di carboidrati i livelli ematici di glucosio iniziano a diminuire rapidamente.

In base a questi dati possiamo concludere che l'apporto quotidiano pluridecennale di carboidrati ad alto indice glicemico (che è tipico della maggior parte della popolazione) potrebbe essere fortemente associato con le suddette patologie.
Inoltre, un dieta basata su carboidrati a basso indice glicemico potrebbe essere molto utile per la prevenzione ed il trattamento di esse.