Increases heart attack risk, due to high glycemic index diet

Editorial Note

Article originally published in the past and updated with scientific and divulgative criteria. The text presented here summarizes peer-reviewed scientific evidence and does not replace the advice of your treating physician. For individual questions, please consult a healthcare professional.

IN BRIEF

• A diet with a high glycemic index (GI) and high glycemic load (GL) is associated, in large-scale observational studies, with an increased risk of major cardiovascular events and mortality in various geographical and socioeconomic contexts.
• Experimental evidence in people with diabetes shows that reducing the glycemic index or load improves some parameters of glycemic control and cardiometabolic risk factors.
• Plausible mechanisms include post-meal glycemic spikes, oxidative stress, endothelial dysfunction, and repeated insulin responses that can promote harmful inflammatory and metabolic processes.
• The evidence is predominantly observational: it suggests associations but cannot, by itself, demonstrate definitive cause-and-effect relationships. Context, quantity, frequency, and overall diet quality influence the risk.

Abstract: what does science say?

The topic concerns the quality of carbohydrates evaluated with indices such as the glycemic index (GI) and glycemic load (GL) and their association with cardiovascular events and mortality. Large-scale population studies have found that high GI/GL diets are associated with a higher risk of heart attack, stroke, and death compared to low GI/GL diets, even in people without known cardiovascular disease. Controlled research in diabetic patients shows that low GI dietary patterns can improve glycemic control and some cardiometabolic risk factors. Possible biological mechanisms include post-meal glycemic spikes, increased insulin, oxidative stress, and endothelial dysfunction. However, most associations come from observational studies: dietary measurements, cultural habits, and lifestyle factors necessitate cautious interpretation and comparison with experimental evidence.

What the main studies show

A large international analysis conducted on a broad multi-continental sample found that, comparing consumption quintiles, a diet with a high glycemic index was associated with a significant increase in the composite risk of major cardiovascular events and death compared to a diet with a low glycemic index [1]. European studies on pan-continental cohorts have reported similar results for the correlation between GI/GL and coronary risk, with some differences for weight groups and carbohydrate sources [2]. Meta-analyses of prospective cohorts show variable relationships between GI/GL and mortality or chronic diseases, confirming associations but also heterogeneity among studies [3].

To contextualize: in people with diabetes, reviews of randomized trials indicate that low GI or GL dietary patterns produce modest but consistent improvements in glycemia, lipids, and some inflammatory indicators, which makes a positive effect on long-term risk plausible if these modifications are maintained [4]. Experimental research and mechanistic studies support the potential biological pathways that would link glycemic spikes and post-meal lipid profiles to vascular damage [5].

Plausible biological mechanisms

Epidemiological observations find plausibility in several biological mechanisms linked to the response to the intake of poor-quality carbohydrates. After meals rich in rapidly digestible carbohydrates, glycemic spikes and a marked insulin response can be observed: these repeated events alter lipid metabolism, increase oxidative stress, and promote inflammatory responses at the vascular level. Over time, these processes favor atherosclerosis and endothelial dysfunction, both central factors in cardiovascular risk [7][5]. Furthermore, a highly insulinemic diet or one associated with chronic hyperinsulinemia is considered plausibly linked to cell growth processes that can influence the progression of some cancers; however, the direct link between diet-GI and cancer incidence remains complex and not definitively proven [9][3].

Post-meal glycemia, oxidative stress, and endothelial function

Glycemic spikes after meals have been associated with an increase in biomarkers of oxidative stress and acute worsening of endothelial function; interventions that attenuate the post-meal glycemic response show functional improvements in several clinical studies, suggesting a plausible chain between high GI foods, vascular damage, and the risk of cardiovascular events [7][8].

Hyperinsulinemia, cell growth, and cancer risk

Insulin has anabolic effects and proliferative signals that, if chronically elevated (hyperinsulinemia), can contribute to microenvironments favorable to cell growth. Reviews and meta-analyses indicate an association between elevated insulinemic dietary patterns and worse prognosis or mortality in some oncological contexts, but the strength and specificity of the association vary by cancer type and clinical situation [9][3].

Foods, carbohydrate quality, and dietary context

The concept of glycemic index classifies foods based on their average effect on post-meal glucose; the glycemic load also integrates the quantity consumed. Foods such as refined flour products, white bread, white rice, sweets, and sugary drinks tend to have higher GI/GL than whole grains, legumes, whole fruits, and many vegetables. However, the glycemic response to a food is influenced by the meal context (fiber, fats, and proteins present), processing, ripeness, and portion size.

Traditional dietary styles recognized as healthy — for example, patterns rich in fiber, legumes, fish, fruit, and olive oil — tend to have a more favorable overall glycemic impact compared to diets high in refined carbohydrates, even when the total carbohydrate quantity is similar [2][5]. For this reason, the label "carbohydrates" alone does not summarize the quality or associated risk: the source, form, and frequency of use are determining factors.

What it means in practice

For the general public, the evidence suggests that prioritizing quality carbohydrates and moderating the intake of rapidly digestible carbohydrates can be part of a dietary strategy aimed at cardiometabolic health. This translates into concrete choices such as preferring whole grains and legumes, choosing whole fruit instead of juices, limiting sweets and sugary drinks, and increasing the presence of fiber, vegetables, and healthy protein sources in meals. Such choices tend to reduce post-meal glycemic spikes and improve the post-meal lipid profile, elements associated with reduced risk in the medium term [5][4].

It is important to emphasize that no foods are "forbidden" for everyone: consumption frequency, portions, and individual clinical picture (for example, presence of diabetes or obesity) matter. The most robust approach at the population level remains to improve the overall quality of the diet by reducing ultra-processed foods and those rich in added sugars, and increasing foods high in fiber and nutrients.

Key takeaways

• There is large-scale observational evidence linking high GI/GL diets to a higher risk of cardiovascular events and mortality [1][2].
• Controlled interventions in diabetic patients show modest clinical benefits when low GI/GL dietary patterns are used [4].
• Probable mechanisms include post-meal glycemic spikes, oxidative stress, endothelial dysfunction, and chronic hyperinsulinemia [7][9].
• The overall quality of the diet and the cultural and socioeconomic context strongly influence the risk; simply measuring carbohydrate grams is not enough [5].

Limitations of the evidence

Most published associations derive from observational studies; these can identify correlations but do not prove causality. Errors in dietary measurement (food frequency questionnaires), variations between populations, residual lifestyle biases, and unmeasured confounders can influence the results. The definition and estimation of GI/GL also vary between food databases and countries, introducing methodological heterogeneity [3][2].

Randomized controlled trials provide more robust evidence on intermediate outcomes (glycemia, lipids, inflammation), but they have rarely been conducted with long-term clinical endpoints. Consequently, observations must be interpreted with caution: consistent and biologically plausible signals exist, but further long-term studies with more precise measures are needed to establish clear causal relationships and to define more targeted interventions.

Editorial conclusion

Available evidence indicates that the quality of carbohydrates — measured with tools such as the glycemic index and glycemic load — is correlated with differences in cardiometabolic risk and mortality at the population level. The associations are biologically plausible and supported by some trials on intermediate outcomes, but methodological limitations and confounding factors remain. For the general public, the most prudent and sustainable approach is to choose carbohydrate sources rich in fiber and nutrients, limit refined carbohydrates and added sugars, and consider one's personal clinical picture before adopting significant dietary changes.

Final editorial note

This text is an update of a previous article. The update is based on the latest available reviews and studies published in peer-reviewed journals. The content is for informational purposes only and does not replace clinical advice.

SCIENTIFIC RESEARCH

1. [1] Jenkins DJA, Dehghan M, Mente A, et al. Glycemic Index, Glycemic Load, and Cardiovascular Disease and Mortality. N Engl J Med. 2021;384:1312-1322. https://doi.org/10.1056/NEJMoa2007123
2. [2] Sieri S, et al. Glycemic index, glycemic load, and risk of coronary heart disease: a pan‑European cohort study. Am J Clin Nutr. 2020. https://doi.org/10.1093/ajcn/nqaa157
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8. [8] Miglitol improves postprandial endothelial dysfunction in patients with acute coronary syndrome and new‑onset postprandial hyperglycemia. Cardiovasc Diabetol. 2013;12:92. https://doi.org/10.1186/1475-2840-12-92
9. [9] Review: Insulin and cancer: mechanistic links and clinical associations. Biochem J. 2022; (review). https://doi.org/10.1042/BCJ20210134