The impact of dietary interventions on cardiometabolic health

Abstract

Obesity and cardiometabolic diseases are leading causes of morbidity and mortality among adults worldwide. These conditions significantly contribute to and exacerbate other major causes of illness and death, including cancer, neurodegenerative diseases, and chronic kidney disease. The growing burden of these diseases has increased the interest of modern medicine in understanding metabolic processes and health, with diet emerging as a pivotal modifiable factor, alongside physical inactivity and smoking. In this review, we discuss the pathophysiological and evolutionary foundations of metabolic processes that may link "unhealthy" nutrition to obesity and cardiometabolic diseases and review the current literature to assess the effects of various diet interventions and patterns on cardiometabolic parameters. Special emphasis is placed on summarizing the latest, albeit partially contradictory, evidence to offer balanced dietary recommendations with the ultimate aim to improve cardiometabolic health.

Fig. 1

Central illustration. General dietary recommendations for cardiometabolic health. Visual representation of common foods and the level of general consensus regarding the strength of evidence (foods in the upper part have wide consensus), as well as the general recommendations (foods on the right should be emphasized in the diet)

Fig. 2

Pathophysiological background of the clinical biomarkers (adapted from ref [20]). During excess calorie intake, de novo lipogenesis processes carbohydrates that cannot be stored as glycogen, promoting fat accumulation in the liver. Because this process is stimulated by insulin, individuals with some degree of insulin resistance (determined by genetic and lifestyle factors) accumulate liver fat more quickly due to higher insulin concentrations. Increased liver fat further exacerbates resistance to the suppression of hepatic glucose production by insulin. A small increase in plasma glucose triggers increased insulin secretion to maintain euglycemia. This resulting hyperinsulinemia further enhances the conversion of excess calories into liver fat, creating a vicious cycle. Fatty liver leads to an increased export of VLDLs into the circulation, which promotes fat delivery to all tissues, including the pancreas. Moreover, high levels of VLDL, in concert with increased CETP activity, result in the enrichment of LDL and HDL with triacylglycerols, while depleting their cholesterol content. This leads to the typical lipid triad: high triacylglycerols, low HDL cholesterol, and small LDL particles. Excess fatty acids in the pancreatic islets can impair insulin secretion in response to ingested food, leading to postprandial hyperglycemia. The hyperglycemia further increases insulin secretion, which consequently elevates hepatic lipogenesis, speeding up the liver cycle and driving the pancreas cycle. Eventually, the inhibitory effects of fatty acids and glucose on the islets reach a threshold, triggering β-cell failure and a fairly sudden onset of clinical diabetes. Adapted from ref. [21], with permission from Elsevier