Do cocoa flavanols influence heart and fatty liver risk factors?

A new review explores how cocoa flavanols may influence cardiovascular and hepatic risk pathways, while highlighting the limitations of current clinical evidence.

Review: Beyond Taste: The Impact of Chocolate on Cardiovascular and Steatotic Liver Disease Risk Factors. Image Credit: Pixel-Shot / Shutterstock

In a recent review published in the journal Nutrients, a group of authors evaluated the impact of cocoa-rich dark chocolate on cardiovascular disease and metabolic dysfunction-associated steatotic liver disease risk factors.

Background

Cardiovascular disease has been the leading cause of death worldwide, while metabolic dysfunction-associated steatotic liver disease affects more than 30% of adults globally.

Common risk factors such as oxidative stress, chronic inflammation, dyslipidemia, obesity, insulin resistance, and hypertension impact both diseases. These common risk factors are associated with increased risk of heart attacks, strokes, and progression of fatty liver disease, rather than the proven effects of chocolate consumption itself, and increased health care costs.

Although many medications are at the forefront of treatment, including the recent approval of resmetirom for selected noncirrhotic MASH patients, while most MASLD management still relies heavily on lifestyle approaches, many people are looking for low-cost dietary means that may accompany “standard” treatment. 

Dark chocolate with high cocoa content has been proposed as a functional dietary component rather than a primary therapy. The strong antioxidant and anti-inflammatory properties of the bioactive compounds in cocoa-rich dark chocolate warrant further research to determine whether they confer cardiometabolic protection.

Composition and Biological Potential of Dark Chocolate

Dark chocolate, derived from Theobroma cacao, is rich in bioactive compounds, including flavanols such as epicatechin, catechin, and procyanidins. It also contains phenolic acids, flavonols, phytosterols, and methylxanthines, including theobromine and caffeine. These substances have antioxidant, anti-inflammatory, vasodilatory, and metabolic properties.

Polyphenols in dark chocolate neutralize reactive oxygen species and reduce oxidative stress, a central mechanism underlying atherosclerosis and liver injury. By negatively affecting the activation of nuclear factor kappa B (NF-κB) and decreasing pro-inflammatory cytokines such as tumor necrosis factor-alpha (TNF-α) and interleukin (IL-6), they regulate inflammatory pathways. They also boost the bioavailability of nitric oxide (NO), which leads to greater vascular dilation and improved endothelial function.

Treatments such as fermentation, roasting, and conching influence flavanol concentration. Dark chocolate is more biologically active than milk or white chocolate when the cocoa content is 70% or higher.

Effects on Oxidative Stress and Inflammation

Oxidative stress occurs when reactive oxygen species overwhelm antioxidant defenses, damaging lipids, proteins, and deoxyribonucleic acid (DNA). Endothelial dysfunction, insulin resistance, and liver fat accumulation may result from this imbalance. Increased activity of antioxidant enzymes has been observed following dark chocolate intake, including glutathione peroxidase, catalase, and superoxide dismutase.

Flavanols also inhibit inflammatory mediators, including TNF-α, IL-1β, and IL-6. Cocoa compounds suppress inflammatory signaling pathways by inhibiting cyclooxygenase-2, lipoxygenase, and mitogen-activated protein kinase signaling. These molecular actions are relevant because chronic low-grade inflammation is linked to obesity, fatty liver, hypertension, and cardiovascular disease.

For individuals at metabolic risk, even modest reductions in oxidative and inflammatory burden may slow disease progression, based primarily on biomarker evidence rather than on demonstrated reductions in clinical outcomes.

Impact on Lipid Profile and Glycemic Regulation

Metabolic impairment encompasses abnormal lipid levels and reduced glucose metabolism. Clinical trials suggest that moderate amounts of dark chocolate may reduce low-density lipoprotein cholesterol and triglyceride levels and raise high-density lipoprotein cholesterol levels. This may be partly due to reduced low-density lipoprotein oxidation and increased endothelial production of NO.

Evidence on glycemic control is mixed. Some studies report modest reductions in postprandial glucose and improvements in insulin sensitivity, potentially mediated by glucagon-like peptide-1 modulation and gut microbiota interactions, although these mechanisms remain preliminary and not fully established clinically. Effects appear dose-dependent and vary according to cocoa concentration.

Excess chocolate consumption increases calorie, sugar, and fat intake, potentially offsetting any metabolic benefit.

Effects on Blood Pressure and Endothelial Function

Hypertension significantly increases cardiovascular risk. Flavanols in cocoa stimulate NO production and suppress angiotensin-converting enzyme activity, both of which are important for improving vasodilation and lowering blood pressure. Randomized crossover trials have demonstrated improvements in flow-mediated dilation following dark chocolate consumption.

Improved endothelial function reduces arterial stiffness and enhances vascular reactivity. Some studies report reduced levels of N-terminal pro B-type natriuretic peptide in patients with heart failure. However, findings are inconsistent in individuals with advanced heart disease or those taking multiple medications.

These findings suggest that dark chocolate may confer greater benefits in early-stage cardiometabolic dysfunction than in established chronic disease and should not be interpreted as evidence of reduced cardiovascular events.

Relevance to Metabolically Dysfunctional-Associated Steatotic Liver Disease

Metabolic dysfunction-associated steatotic liver disease is characterized by hepatic fat accumulation, inflammation, and oxidative injury. Small randomized trials report that dark chocolate reduces markers of oxidative stress, endotoxemia, nicotinamide adenine dinucleotide phosphate oxidase 2 activity, and hepatocyte apoptosis in patients with non-alcoholic steatohepatitis.

These intermediate improvements suggest potential protective effects along the gut-liver-heart axis, but current evidence remains insufficient to support chocolate as a therapeutic or preventive strategy for MASLD or fibrosis progression. Most studies are short-term and involve small samples, limiting conclusions about fibrosis progression or long-term liver outcomes.

Clinical Evidence and Limitations

Although multiple trials show improvements in surrogate biomarkers, flow-mediated dilation, platelet reactivity, and lipid parameters, most studies are short (2-12 weeks), involve small cohorts, and employ heterogeneous flavanol doses. Chocolate’s identifiable sensory properties complicate placebo-controlled blinding and may introduce expectancy effects.

Additional limitations include restricted study populations, incomplete dietary control, which may introduce potential confounding, and possible attenuation of effects among patients receiving multiple cardiometabolic medications.

Benefits appear stronger in primary prevention settings than in medicated populations with advanced cardiovascular disease or type 2 diabetes mellitus. No large-scale, long-term randomized controlled trials have confirmed reductions in hard clinical endpoints such as myocardial infarction or liver fibrosis progression.

Conclusions

The evidence indicates that moderate consumption of cocoa-rich dark chocolate may beneficially influence oxidative stress, inflammation, lipid metabolism, endothelial function, and selected markers of metabolic dysfunction-associated steatotic liver disease.

These effects are relevant for potential cardiometabolic risk modulation rather than established disease treatment and are derived mainly from short-term studies assessing surrogate biomarkers rather than definitive clinical endpoints. 

Large, long-duration randomized controlled studies using standardized flavanol formulations are required before definitive clinical recommendations can be made. Dark chocolate may be incorporated into an otherwise healthy dietary pattern, but should not be considered a substitute therapy.