Plant-Based Nutrition: Exploring Health Benefits for Atherosclerosis, Chronic Diseases, and Metabolic Syndrome—A Comprehensive Review

The review addresses whether and how plant-based diets (PBDs) can prevent and/or mitigate atherosclerosis, chronic non-communicable diseases (NCDs), and metabolic syndrome (MetS). It frames concerns about potential micronutrient deficiencies in plant-forward eating while contrasting them with extensive evidence of benefits for type 2 diabetes, hypertension, dyslipidemia, atherosclerosis, and cancer. The authors distinguish between veganism (ethical focus, not necessarily health-oriented) and a healthful PBD emphasizing whole, minimally processed plant foods (legumes, whole grains, fruits, vegetables, nuts, seeds), noting that diet quality is pivotal. MetS is defined by central obesity, dyslipidemia, hypertension, and impaired fasting glucose, with elevated cardiovascular and all-cause mortality risks. The review’s purpose is to synthesize mechanistic and clinical evidence on plant-derived macronutrients, micronutrients, and bioactive compounds in modulating key pathways—lipids, inflammation, oxidative stress, gut microbiota, and vascular function—to inform prevention and treatment strategies for atherosclerosis, NCDs, and MetS.

The narrative review compiles mechanistic, preclinical, and human evidence across several domains: (1) Atherosclerosis: pathophysiology centers on LDL infiltration/oxidation, ApoB particles, inflammatory signaling (TLR/NF-κB, IL-1β, IL-6, TNF-α), and endothelial dysfunction. Diets low in saturated fat and higher in mono-/polyunsaturated fats, nuts, and extra-virgin olive oil reduce LDL-C, inflammation, and atherosclerotic progression; fiber and antioxidants mitigate oxidative stress and foam cell formation. (2) Trimethylamine N-oxide (TMAO) and microbiota: animal-origin nutrients (choline, L-carnitine) can raise TMAO via gut microbial metabolism, though causality is debated and context-dependent; microbiota composition differs with plant-based vs. omnivorous diets. SCFAs from fiber improve gut barrier (tight junctions, MUC-2), lower endotoxemia, and may reduce TMAO and inflammation. (3) Endothelial function: high salt and saturated fat impair flow-mediated dilation (FMD); plant foods rich in nitrates (leafy greens, beets), flavanols (cocoa), nuts, and soy improve FMD and vascular biomarkers. (4) Fermented plant foods/bioactives: kimchi components, whole grains (including fermented products), red yeast rice (monacolin K), β-glucans (oat/barley), berries, proanthocyanidins, mulberry polyphenols, coffee chlorogenic acids, and probiotics exert lipid-lowering, anti-inflammatory, antioxidant, and anti-atherogenic effects. (5) Chronic diseases: higher adherence to healthful PBDs is linked with lower risk of type 2 diabetes, hypertension, and dyslipidemia; benefits are mediated by improved insulin sensitivity (AMPK/PPAR pathways), reduced ectopic fat, enhanced endothelial function, favorable lipid profiles, and gut microbiome modulation. Evidence also notes heterogeneity in TMAO responses and HDL-C changes. (6) Metabolic syndrome: plant bioactives and higher fiber/potassium intakes reduce insulin resistance, blood pressure, triglycerides, visceral adiposity, and waist circumference; unhealthy PBDs (refined grains, sugars, ultra-processed foods) can negate benefits.

This is a comprehensive narrative review synthesizing mechanistic, preclinical, and human observational and interventional studies on plant-based diets, atherosclerosis, chronic diseases, and metabolic syndrome. The article organizes evidence thematically (atherosclerosis pathways, dietary fats, microbiota/TMAO, endothelial function, SCFAs, fermented foods/bioactive compounds, and specific NCD/MetS components). Explicit database search strategies, inclusion/exclusion criteria, and formal quality assessments are not detailed.

- Healthful plant-based diets are associated with lower risks and improved markers across atherosclerosis, NCDs, and MetS; diet quality is critical (healthy vs. unhealthy PBDs show opposite associations). - Lipids and atherosclerosis: Replacing saturated fat with MUFAs/PUFAs lowers LDL-C and improves LDL/HDL ratios; nuts and extra-virgin olive oil reduce inflammation and atherogenesis. Meta-analysis indicates exchanging 1% energy from carbs to MUFAs/PUFAs raises HDL and lowers TG with attenuated LDL/TC increases. Walnuts and other nuts associate with 13–23% lower CVD/CHD risk; walnut-rich diets reduce aortic plaque in animals (~55%). β-glucans (oat/barley) at ~3 g/day reduce total, LDL, and non-HDL cholesterol. - Endothelial function: High salt and saturated fat impair FMD; walnuts, hazelnuts, soy nuts, high-flavanol cocoa (~5 days), and nitrate-rich beetroot juice (~6 weeks) improve FMD and vascular biomarkers. Leafy vegetable nitrate intake inversely associates with carotid IMT and ischemic events in older women. - Microbiota/SCFAs/TMAO: Plant-rich diets foster microbiota diversity and SCFA production (butyrate, propionate, acetate), strengthening gut barrier (tight junctions, MUC-2), lowering endotoxemia and inflammatory signaling (NF-κB). Vegetarians/vegans show reduced capacity to produce TMAO from carnitine challenges vs. omnivores; however, TMAO responses to healthy diets can be inconsistent across trials. - Bioactive compounds: Polyphenols (berries, coffee chlorogenic acids, mulberry, proanthocyanidins), isoflavones (genistein/daidzein), phytosterols, and saponins exert antioxidative, anti-inflammatory, lipid-lowering, and insulin-sensitizing effects; red yeast rice (low-dose monacolin K) lowers LDL-C and blood pressure. - Diabetes/insulin resistance: Healthful PBDs associate with reduced incidence of type 2 diabetes; mechanisms include improved insulin sensitivity (AMPK activation, GLUT4 translocation), reduced β-cell stress, and microbiome modulation. Anthocyanidins show dose-response risk reductions (~5% lower T2D risk per 7.5 mg/day). Trials with blueberries, strawberries/cranberries improve insulin sensitivity in insulin-resistant adults. - Hypertension: Higher phytochemical-rich foods and healthy PBD adherence associate with lower incident hypertension (e.g., top quintile healthy PBD ~35% lower incidence); anthocyanins improve arterial stiffness and central SBP; potassium intake and sodium reduction are key (renal “potassium switch,” endothelial/vascular effects). - Dyslipidemia: Healthful PBD adherence links to lower incident dyslipidemia (per SD increase in healthy PDI ~16% lower risk); fiber, phytosterols/stanols, and unsaturated fats are central. Quinoa intakes in trials lowered TG substantially (up to ~36% in specific protocols). Walnut interventions show TG improvements, particularly in men and those with comorbidities. - HDL-C nuance: PBDs can lower HDL-C alongside greater LDL-C and TC reductions, improving TC/HDL and LDL/HDL ratios, which better predict risk than HDL-C alone. Very high HDL-C may not be uniformly protective; HDL functionality and subspecies (e.g., Apo-CIII content) matter. - Diet quality matters: Unhealthy PBDs (refined grains, sweets, sugary beverages, ultra-processed foods) associate with higher MetS and dyslipidemia risk; healthy PBDs with whole foods, fiber, and bioactives confer benefits.

The synthesis indicates that healthful plant-based dietary patterns address key mechanistic drivers of atherosclerosis and cardio-metabolic disease: lowering LDL-C/ApoB-mediated atherogenesis, attenuating oxidative stress and inflammatory signaling, improving endothelial function and nitric oxide bioavailability, and beneficially shaping the gut microbiome with SCFA production and enhanced gut barrier integrity. These mechanisms translate into improved clinical biomarkers (lipids, blood pressure, insulin sensitivity) and reduced incidence of type 2 diabetes, hypertension, and dyslipidemia in cohort studies. However, heterogeneity in outcomes (e.g., TMAO responses, HDL-C changes, sex-specific effects) underscores the importance of dietary quality and individual context (microbiota composition, comorbidities). Emphasizing minimally processed plant foods rich in fiber, potassium, nitrates, and polyphenols, and moderating saturated fat, sodium, and ultra-processed foods, appears central to realizing benefits. Where lipid lowering is prioritized, plant bioactives (β-glucans, phytosterols) and specific foods (nuts, whole grains) are effective adjuncts. The findings support PBDs as viable strategies for both prevention and management of atherosclerosis and MetS components, with professional guidance to ensure nutritional adequacy.

A healthful plant-based diet—centered on whole, minimally processed plant foods and rich in fiber, unsaturated fats, potassium, and diverse bioactive compounds—can beneficially modify lipid profiles, reduce inflammation and oxidative stress, improve endothelial function and insulin sensitivity, and promote a favorable gut microbiome. Collectively, these effects help prevent and mitigate atherosclerosis, chronic non-communicable diseases, and metabolic syndrome. Optimizing diet quality and leveraging fermented and bioactive-rich plant foods enhance these benefits. With appropriate professional guidance to ensure micronutrient adequacy (e.g., vitamin B12, vitamin D, calcium, iron, omega-3), PBDs are suitable across the lifespan. Future research should standardize PBD definitions, delineate the role of diet quality, clarify causal pathways (e.g., TMAO), evaluate HDL functionality versus concentration, and test targeted bioactive/food-based interventions in diverse populations.

- As a narrative review, explicit search strategies, inclusion/exclusion criteria, and study quality assessments are not provided, limiting reproducibility and potential selection bias. - Considerable heterogeneity exists in definitions of “plant-based” and diet quality across studies, complicating comparisons and causal inference. - Many findings rely on observational data subject to confounding and reverse causality; some mechanistic insights stem from animal/cell studies with limited direct generalizability to humans. - Mixed evidence on TMAO modulation by healthy diets and on HDL-C changes highlights individual variability (e.g., microbiome composition, comorbid conditions) and measurement timing. - Short intervention durations in several trials limit assessment of long-term clinical outcomes.