“Your heart health is closely connected to your metabolic health! High blood sugar, insulin resistance, and chronic inflammation can damage your blood vessels and increase your risk of heart problems. Understanding these factors is an important step toward protecting your heart and improving your overall health.”

The core proposition is mainstream cardiology, not a fringe position. The American Heart Association formalized it in a 2023 presidential advisory: the advisory identifies the strong connections among cardiovascular disease, kidney disease, Type 2 diabetes and obesity, suggests redefining CVD risk, prevention and management, and defines cardiovascular-kidney-metabolic (CKM) syndrome for the first time. The AHA describes CKM syndrome as a health disorder made up of heart disease, kidney disease, diabetes and obesity, leading to poor health outcomes, and the advisory notes a high prevalence of poor cardiovascular-kidney-metabolic health in the population and provides guidance on definition, staging, prediction paradigms and holistic care. On magnitude of association: a systematic review and meta-analysis found metabolic syndrome associated with an increased risk of cardiovascular disease (RR 2.35, 95% CI 2.02 to 2.73) and CVD mortality (RR 2.40, 95% CI 1.87 to 3.08). A separate meta-analysis of longitudinal studies found a relative risk of cardiovascular events and death of 1.78 (95% CI 1.58 to 2.00). Risk is elevated even below the diabetes threshold: a BMJ review found that in the general population, prediabetes was associated with a 13% increased risk of all cause mortality and a 15% increased risk of cardiovascular disease over roughly 10 years of follow-up. On insulin resistance specifically: a review concludes that cross-sectional and prospective studies, meta-analyses, and systematic reviews provide evidence that insulin resistance by itself is a cardiovascular risk factor in the general population and in patients with diabetes, with estimations of insulin resistance consistently associated with elevated cardiovascular event rates independently of other risk factors and diabetes status. On the vascular damage mechanism: a 2025 review describes hyperglycemia-driven processes that collectively promote excessive oxidative damage, endothelial dysfunction, inflammation, and adverse cardiac remodeling, accelerating cardiovascular damage. Another review states there is strong evidence that endothelial dysfunction precedes and fosters atherosclerotic damage, predisposing to cardiovascular events, and that in type 2 diabetes hyperglycemia plays a central role. On inflammation, the evidence goes beyond association to a randomized causal test: the CANTOS trial showed that canakinumab 150 mg was superior to placebo at preventing adverse cardiac events, with patients randomized to canakinumab who achieved on-treatment hsCRP below 2 mg/L showing a reduction in major adverse cardiac events (HR 0.75, 95% CI 0.66 to 0.85), compared with no benefit among those with on-treatment hsCRP at or above 2 mg/L. The result was described as supporting the hypothesis of atherothrombosis due to inflammation, and it was achieved in patients with prior myocardial infarction and evidence of ongoing subclinical inflammation.