Lifestyle factors and cardiometabolic risk

Abstract

Cardiometabolic risk encompasses the interconnected conditions of cardiovascular diseases (CVDs), type 2 diabetes (T2D), and other metabolic diseases, which are leading global health challenges. The American Heart Association (AHA) has introduced “Life’s Essential 8” (LE8), a framework emphasizing eight key lifestyle and health factors, including diet, physical activity, smoking, sleep health, body weight, blood glucose, blood lipids, and blood pressure to optimize cardiovascular health and reduce the burden of cardiometabolic risk. This review examined the associations between individual and combined lifestyle factors and the development and progression of cardiometabolic risk, using CVD and T2D as representative conditions. Evidence highlighted that adherence to healthy lifestyle behaviors, such as maintaining a balanced diet, engaging in physical activity, avoiding smoking, and achieving a healthy weight, significantly reduced the risks of CVD, T2D, and hypertension. Studies showed that adherence to 3–4 healthy lifestyle factors lowers the risk of transition from baseline to diabetes, complications, and mortality. Despite the proven benefits, barriers such as limited access to healthy food and safe environments for physical activity hinder widespread adoption. Addressing these challenges requires innovative public health interventions and personalized strategies targeting high-risk populations. This review underscored the importance of promoting and adhering to LE8 principles to reduce the global burden of cardiometabolic risk and improve overall health outcomes.

Introduction

Cardiovascular diseases (CVDs) and type 2 diabetes (T2D) are two of the major global health challenges, accounting for a substantial proportion of morbidity and mortality worldwide. These cardiovascular and metabolic disorders often coexist, forming a complex web of interrelated conditions known as cardiometabolic risk.^[1,2] In response to this growing burden, the American Heart Association (AHA) introduced a novel framework for cardiovascular health in 2010, marking a paradigm shift from a disease-centered approach to one emphasizing holistic health promotion and preservation across the lifespan.^[3] This initiative led to the development of Life’s Simple 7 (LS7), a widely adopted metric assessing seven key health domains: Smoking status, diet, physical activity, body mass index (BMI), blood pressure, cholesterol levels, and fasting glucose. Over time, extensive research has both validated LS7’s utility and revealed limitations in its original design, prompting further refinements in cardiovascular health assessment.^[4] This metric was updated in 2022 to the Life’s Essential 8 (LE8), incorporating a new domain of sleep and refining the previous seven domains.^[4,5] The LE8 metrics have been widely adopted worldwide in cardiovascular health assessment,^[6,7] recommended by multiple guidelines^[8,9] and reports,^[10] with robust epidemiological studies consistently demonstrating significant associations between LE8 scores and CVD.^{[11,12,13,14,15,16,17]}

To gain a comprehensive understanding of cardiometabolic risk, it is crucial to examine various lifestyle factors that contribute to its development. These factors—including diet and nutrition, physical activity and sedentary behavior, obesity and weight management, smoking, sleep, alcohol, coffee and tea consumption, and social determinants of health—are integral to our overall health and are modifiable through targeted interventions. Given that cardiometabolic risk encompasses a wide range of conditions (e.g., metabolic syndrome, insulin resistance, dyslipidemia, hypertension, chronic kidney disease [CKD], and inflammation), this review focuses on using CVD and T2D as representatives of cardiometabolic risk. Table 1 summarizes shared lifestyle factors for CVD and T2D, while Table 2 presents findings from selected epidemiological studies on these factors.

Table 1.

Summary of shared lifestyle factors for cardiovascular disease and type 2 diabetes.

Lifestyle factors	Increased risk of CVD and T2D	Decreased risk of CVD and T2D
Diet	Unhealthy diet (A)	MedDiet (A), DASH diet (A), Plant-based diet (A), CHH diet (B) and Spicy diet (B)
Physical activity	Inactive lifestyle (A) or sedentary behavior (B)	Active lifestyle (A)
Body weight	Overweight and obesity (A)	Normal weight (A)
Smoking	Current smoking, or passive smoking (B)	Quitting smoking or never smoking (B)
Sleep	Short or long sleep duration (B), irregular sleep duration and timing (B), or circadian rhythm disruption (B)	High-quality sleep (B)
Alcohol	Heavy drinking (B), or Chinese liquor (baijiu) (B)	Light drinking (B)
Coffee		Moderate coffee consumption (B)
Tea		Green tea consumption (B)

The content in parentheses represents the level of evidence. Level A: Evidence is from multiple randomized controlled clinical trials or meta-analyses composed of randomized controlled clinical trials; Level B: Evidence is from a single randomized clinical trial or multiple large-scale non-randomized controlled studies; Level C: Evidence is from expert consensus and/or small-scale studies, retrospective studies, or registry studies. CVD: Cardiovascular disease; CHH diet: Chinese Heart-Healthy diet; DASH diet: Dietary approaches to stop hypertension diet; MedDiet: Mediterranean diet: T2D: Type 2 diabetes.

Table 2.

Findings from selected epidemiological studies of shared lifestyle factors for cardiovascular disease and type 2 diabetes.

Risk factors	Cardiovascular disease			Type 2 diabetes incidence
	Measure	Relative risk	Type and Refs.	Measure	Relative risk	Type and Refs.
Diet	MedDiet	CHD incidence (RR 0.73, 95% CI 0.62–0.86) Stroke incidence (RR 0.80, 95% CI 0.71–0.90) CVD mortality (RR 0.79, 95% CI 0.77–0.82) CHD mortality (RR 0.83, 95% CI 0.75–0.92) Stroke mortality (RR 0.87, 95% CI 0.80–0.96)	Prospective studies[21]	MedDiet	RR 0.87, 95% CI 0.82–0.93	Prospective studies[24]
		CVD incidence (RR 0.62, 95% CI 0.50–0.78) MI incidence (RR 0.65, 95% CI 0.49–0.88)	RCTs[21]		RR 0.60, 95% CI 0.43–0.85 for olive oil RR 0.82, 95% CI 0.61–1.10 for mixed nuts HbA1c (MD −0.47%, 95% CI −0.56 to −0.38%) in T2D patients	RCTs[25,26]
	DASH diet	CVD incidence (RR 0.80, 95% CI 0.76–0.85) CHD incidence (RR 0.79, 95% CI 0.71–0.88) Stroke incidence (RR 0.81, 95% CI 0.72–0.92)	Prospective studies[27]	DASH diet	RR 0.81, 95% CI 0.72–0.92	Prospective studies[24]
		Systolic blood pressure (MD −5.2 mmHg, 95% CI −7.0 to −3.4 mmHg) Diastolic blood pressure (MD −2.60 mmHg, 95% CI −3.50 to −1.70 mmHg) Total cholesterol (MD −0.20 mmol/L, 95% CI −0.31 to −0.10 mmol/L) LDL cholesterol (MD −0.10 mmol/L, 95% CI −0.20 to −0.01 mmol/L) HbA1c (MD −0.53%, 95% CI −0.62 to −0.43%) Body weight (MD −1.42 kg, 95% CI −2.03 to −0.82 kg)	RCTs[27]		HbA1c (MD −0.53%, 95% CI −0.62 to −0.43%), insulin (MD −0.15 µU/mL, 95% CI −0.22 to −0.08 µU/mL).	RCTs[27]
	Plant-based diet	CVD incidence (RR 0.85, 95% CI 0.79–0.92) CHD incidence (RR 0.79, 95% CI 0.71–0.88) as vegetarians compared to non-vegetarians CHD incidence (RR 0.82, 95% CI 0.68–1.00) as vegans compared to non-vegetarians	Prospective studies[29]	Plant-based diet	RR 0.77, 95% CI 0.71–0.84	Prospective studies[33]
		Total cholesterol (MD −0.36 mmol/L, 95% CI −0.55 to −0.17 mmol/L) LDL cholesterol (MD −0.34 mmol/L, 95% CI −0.57 to −0.11 mmol/L), HDL cholesterol (MD −0.10 mmol/L, 95% CI −0.14 to −0.06 mmol/L) Non-HDL cholesterol (MD −0.30 mmol/L, 95% CI −0.50 to −0.10 mmol/L) Systolic blood pressure (MD −2.66 mmHg, 95% CI −3.76 to −1.55 mmHg)Diastolic blood pressure (MD −1.69 mmHg, 95% CI −2.97 to −0.41 mmHg) Body weight (MD −2.02 kg, 95% CI −2.80 to −1.23 kg)	RCTs[31,32]		HbA1c (MD −0.40%, 95% CI −0.59 to −0.21%) BMI (MD −0.96 kg/m2, 95% CI −1.58 to −0.34 kg/m2) in patients with diabetes	RCTs[32]
	CHH diet	Systolic blood pressure (MD −10 mmHg, 95% CI −12.1 to −7.9 mmHg) Diastolic blood pressure (MD −3.8 mmHg, 95% CI −5.0 to −2.5 mmHg)	RCT[36]
	Spicy diet	CVD mortality (HR 0.83, 95% CI 0.74–0.95)	Prospective cohort studies[39]
Physical Activity	Moderate-intensity 150 min/week	CVD incidence (RR 0.83, 95% CI 0.77–0.89) CVD mortality (RR 0.77, 95% CI 0.71–0.84)	Prospective studies[49]	High vs. low physical activity	RR 0.75, 95% CI 0.71–0.79	Prospective studies[53,54]
Sedentary behavior		All-cause mortality (HR 1.24, 95% CI 1.09–1.41) CVD mortality (HR 1.18, 95% CI 1.11–1.26) CVD incidence (HR 1.14, 95% CI 1.00–1.73)	Prospective studies[58]	Sedentary behavior	HR 1.91, 95% CI 1.64–2.22	Prospective studies[58]
Obesity	Each 5 kg/m2 increase in BMI	Hypertension incidence (RR 1.49, 95% CI 1.40–1.60) Heart failure incidence (RR 1.41, 95% CI 1.32–1.50) Stroke incidence (RR 1.07, 95% CI 1.02–1.12) CHD incidence (HR 1.15, 95% CI 1.12–1.20) CVD mortality (HR 1.49, 95% CI 1.45–1.53) All-cause mortality (HR 1.31, 95% CI 1.29–1.33)	Prospective studies[59]	Each 5 kg/m2 increase in BMI	RR 1.72, 95% CI 1.65–1.81	Prospective studies[61]
Smoking	Current smoking	CVD incidence (HR 1.63, 95% CI 1.56–1.71) CVD mortality (HR 2.75, 95% CI 2.37–3.19)	Prospective study[69]	Current smoking	RR 1.37, 95% CI 1.33–1.42	Prospective studies[76]
	Quitting smoking within 5 years	CVD incidence (HR 0.61, 95% CI 0.49–0.76)	Prospective studies[72]	Quitting smoking	RR 1.14, 95% CI 1.10–1.18
	Passive smoking	CVD incidence (RR 1.28, 95% CI 1.09–1.50) CVD mortality (HR 1.12, 95% CI 1.06–1.20)	Meta-analysis[73]	Passive smoking	RR 1.22, 95% CI 1.10–1.35
Sleep	Short sleep duration (<7 h/night)	CHD (RR 1.48, 95% CI 1.22–1.80) Stroke (RR 1.15, 95% CI 1.00–1.31)	Prospective studies[80]	Sleep <7 h/night	RR 1.09, 95% CI 1.04–1.15 compared with sleep 7–8 h/night	Prospective studies[82]
	Long sleep duration (≥9 h/night)	CHD (RR 1.38, 95% CI 1.15–1.66) Stroke (RR 1.38, 95% CI 1.15–1.66) CVD (RR 1.41, 95% CI 1.19–1.68)	Prospective studies[80]	Sleep ≥9 h/night	RR 1.14, 95% CI 1.03–1.26 compared with sleep 7–8 h/night	Prospective studies[82]
	Standard deviation of sleep duration	Positive association for CVD incidence	Prospective studies[81]	Sleep <7 h/night	An average increase in HbA1c at 0.23% (95% CI 0.10–0.36%) in patients with T2D compared with sleep 7–8 h/night	Prospective studies[83]
				Sleep ≥9 h/night	An average increase in HbA1c at 0.13% (95% CI 0.02–0.25%) in patients with T2D compared with sleep 7–8 h/night	Prospective studies[83]
				Poor sleep quality	An average increase in HbA1c at 0.35% (95% CI 0.12–0.58)	Prospective studies[83]
Alcohol consumption	Low drinking (up to two drinks or 1.30–24.9 g per day)	CHD mortality (RR 0.80, 95% CI 0.69–0.93)	Prospective study[86]	Up to 16 g of pure alcohol per day	RR 0.69, 95% CI 0.64–0.74 among women	Prospective studies[90]
	One standard deviation increase in alcohol intake	Hypertension incidence (RR 1.3, 95% CI 1.2–1.4) CHD incidence (RR 1.4, 95% CI 1.1–1.8)	Prospective study[87]	Above 49 g of pure alcohol per day	RR 0.82, 95% CI 0.68–0.99 among women
Coffee consumption	3–4 cups/day vs. none	All-cause mortality (RR 0.83, 95% CI 0.79–0.88) CVD mortality (RR 0.81, 95% CI 0.72–0.90) CVD incidence (RR 0.85, 95% CI 0.80–0.90)	Prospective studies and RCTs[92]	Each 1 cup/day increase	RR 0.91, 95% CI 0.89–0.94 for caffeinated coffee consumption RR 0.94, 95% CI 0.91–0.98 for decaffeinated coffee consumption	Prospective studies[93]
Green tea consumption	Compared with nondrinkers	Stroke incidence RR 0.96 (95% CI 0.94–0.99) for tea drinking occasionally RR 0.94 (95% CI 0.90–0.98) for tea drinking weekly RR 0.92 (95% CI 0.89–0.95) for tea drinking daily	Prospective studies[95]	–	–

–: Not available; BMI: Body mass index; CHD: Coronary heart disease; CI: Confidence interval; CHH diet: Chinese Heart-Healthy diet; CVD: Cardiovascular disease; DASH diet: Dietary approaches to stop hypertension diet; HbA1c: Hemoglobin A1c; HDL cholesterol: High-density lipoprotein cholesterol; HR: Hazard ratio; LDL cholesterol: Low-density lipoprotein cholesterol; MedDiet: Mediterranean diet; MD: Mean difference; MI: Myocardial infarction; RCT: Randomized controlled trial; Refs.: References; RR: Relative risk. T2D: Type 2 diabetes.

Diet and Nutrition

Diet is closely linked to cardiometabolic risk, and it plays a crucial role in preventing and managing CVD and T2D. Nutrients such as unsaturated fats, complex carbohydrates, high-quality proteins, and dietary fiber have been shown to reduce risks associated with hypertension, T2D, and CVD. When considering the association between food groups and incident T2D, prospective epidemiological studies show some variability, likely due to the diverse dietary patterns consumed globally. Generally, plant-based foods are linked to a lower risk of T2D compared to meat-based diets, while low-energy-dense foods tend to offer more protection than high-energy-dense foods. Fermented dairy products may offer more benefits than non-fermented ones, and nuts may help protect against T2D. Conversely, refined grains and sugary beverages increase the risk of obesity and T2D.

The emphasis on individual nutrients in preventing chronic diseases has shifted, with greater attention now placed on overall dietary patterns. Recent dietary guidelines from the U.S. government no longer focus on specific limits for carbohydrates, fats, and proteins, but instead advocate for the consumption of specific food types and patterns.^[18]

Mediterranean diet

The Mediterranean diet (MedDiet), characterized by high consumption of olive oil, fruits, vegetables, and legumes, has gained recognition for its cardioprotective effects. Many studies used a MedDiet score to evaluate adherence, such as the MedDiet Score (MDS), introduced by Trichopoulou et al^[19] in 1995. The MDS includes nine components, assigning one point for intakes of “healthy foods” that exceed the sex-specific median (including vegetables, fruits/nuts, legumes, fish/seafood, cereals, and the ratio of monounsaturated to saturated fats), one point for intakes of meat and dairy products that fall below the median, and one point for moderate intake of alcoholic beverages.^[19] Another commonly used dietary assessment is the alternate Mediterranean diet (aMED).^[20] This pattern adjusts nine food groups of the MDS, assigning one point for intakes of “healthy foods” that exceed the sex-specific median (including vegetables, fruits, nuts, legumes, whole grains, and monounsaturated to saturated fat ratio), one point for intakes of red/processed meat that fall below the median, and one point for moderate intake of alcoholic beverages.^[20]

MedDiet and CVD

Adherence to the MedDiet is widely recognized for its cardioprotective benefits, supported by both prospective cohort studies and randomized controlled trials (RCTs). A systematic review and meta-analysis of 38 cohort studies found that the highest (vs. lowest) categories of MedDiet adherence significantly reduced the risk of incident coronary heart disease (CHD) (relative risk [RR]: 0.73, 95% confidence interval [CI] 0.62–0.86), stroke (RR: 0.80, 95% CI: 0.71–0.90), and myocardial infarction (MI) cases (RR: 0.73, 95% CI: 0.61–0.88), as well as CVD mortality (RR: 0.79, 95% CI: 0.77–0.82), CHD mortality (RR: 0.83, 95% CI 0.75–0.92), and stroke mortality (RR: 0.87, 95% CI: 0.80–0.96).^[21]

The landmark Primary Prevention of Cardiovascular Disease with a Mediterranean Diet (PREDIMED) trial in Spain is the largest intervention study focusing on the MedDiet’s impact on primary cardiovascular prevention in high-risk individuals. This study showed that participants following the MedDiet supplemented with olive oil or mixed nuts had a lower incidence of major adverse cardiovascular events compared to those on a low-fat diet (hazard ratio [HR]: 0.69, 95% CI: 0.53–0.91 for olive oil; HR: 0.72, 95% CI: 0.54–0.95 for mixed nuts).^[22] Furthermore, a systematic review and meta-analysis of three RCTs revealed that the MedDiet effectively reduced the incidences of total CVD (RR: 0.62, 95% CI: 0.50–0.78) and MI (RR: 0.65, 95% CI: 0.49–0.88).^[21]

MedDiet and T2D

Evidence from prospective cohort studies and clinical trials consistently shows that adherence to the MedDiet is inversely associated with the risk of developing T2D. A meta-analysis of one RCT and eight prospective studies found that greater adherence to the MedDiet was associated with a 19% reduction in the risk of T2D (RR: 0.81, 95% CI: 0.73–0.90).^[23] Another meta-analysis of 48 studies confirmed this relationship, reporting a 13% reduction in T2D risk by following the MedDiet (RR: 0.87, 95% CI: 0.82–0.93).^[24]

An inverse association in observational cohort studies was confirmed by a subgroup analysis of the PREDIMED trial, in which the MedDiet resulted in a 40% reduction in T2D risk with olive oil (RR: 0.60, 95% CI: 0.43–0.85) and an 18% reduction with mixed nuts (RR: 0.82, 95% CI: 0.61–1.10).^[25] Notably, this beneficial effect was mainly attributed to the overall composition of the dietary pattern and not to caloric restriction, physical activity, or weight loss.^[25] Some recent meta-analyses also show that the MedDiet improves glycemic control in patients with T2D and prediabetes, with significant reductions in glycated hemoglobin A1c (HbA1c) levels (mean difference [MD]: −0.47%, 95% CI: −0.56 to −0.38%) compared to control diets.^[26]

Dietary approaches to stop hypertension diet

The dietary approaches to stop hypertension (DASH) diet is specifically designed to help reduce blood pressure and improve overall cardiovascular health. It emphasizes limiting intake of saturated fats, red meat, sweets, and sodium, while encouraging the consumption of vegetables, fruits, fat-free or low-fat dairy products, whole grains, nuts, and legumes, with moderate amounts of fish, poultry, and healthy fats.

DASH diet and CVD

The DASH diet has been proven effective in managing hypertension and reducing CVD risk. A meta-analysis of 15 prospective cohort studies involving over 942,000 participants indicated that adherence to the DASH dietary pattern reduced the risk of incident CVD (RR: 0.80, 95% CI: 0.76–0.85), CHD (RR: 0.79, 95% CI: 0.71–0.88), and stroke (RR: 0.81, 95% CI: 0.72–0.92).^[27]

In addition, some RCTs also showed that the DASH diet decreased systolic blood pressure (MD: −5.2 mmHg, 95% CI: −7.0 to −3.4 mmHg), diastolic blood pressure (MD: −2.6 mmHg, 95% CI: −3.50 to −1.70 mmHg), total cholesterol (MD: −0.20 mmol/L, 95% CI: −0.31 to −0.10 mmol/L), low-density lipoprotein (LDL) cholesterol (MD: −0.10 mmol/L, 95% CI: −0.20 to −0.01 mmol/L), HbA1c (MD: −0.53%, 95% CI: −0.62 to −0.43%), and body weight (MD: −1.42 kg, 95% CI: −2.03 to −0.82 kg).^[27]

DASH diet and T2D

The DASH diet has also shown promise in reducing the incidence of T2D. A meta-analysis of prospective studies found a 20% reduction in T2D risk among adherents to the DASH diet,^[28] and the effect was similar to the MedDiet. A subsequent meta-analysis, which included 48 articles and 16 cohorts, confirmed that adherence to the DASH diet was associated with a reduction in T2D risk (RR: 0.81, 95% CI: 0.72–0.92).^[24] In addition, clinical trials confirmed that the DASH diet improved HbA1c levels (MD: −0.53%, 95% CI: −0.62 to −0.43%) and reduced insulin levels (MD: −0.15 µU/mL, 95% CI: −0.22 to −0.08 µU/mL).^[27]

Plant-based diet

There is no precise definition of a plant-based diet, and it generally refers to a diet that emphasizes foods derived from plants, including fruits, vegetables, whole grains, legumes, nuts, and seeds. While a vegan diet excludes all animal products, a plant-based diet may also include moderate amounts of dairy, eggs, or fish, such as vegetarian diets (which may contain eggs and dairy) and semi-vegetarian diets (like pescatarian or macrobiotic, which include small amounts of meat or fish). The advantage of such a broad definition is its wider applicability, as recommendations of moderate dietary changes, such as gradual reductions in animal food intake, may be easier to adopt and adhere to than more extreme recommendations such as complete exclusion of animal foods. Studies have shown that plant-based diets can be effective for managing both CVD and T2D, even when they include a small amount of animal products.

Plant-based diet and CVD

A pooled analysis of 13 cohort studies, involving 844,175 participants (with 115,392 cases of CVD, 30,377 cases of CHD, and 14,419 cases of stroke), found that vegetarians had a reduced risk of CVD (RR: 0.85, 95% CI: 0.79–0.92) and CHD (RR: 0.79, 95% CI: 0.71–0.88).^[29] Vegans also showed a reduced risk of CHD (RR: 0.82, 95% CI: 0.68–1.00) compared to non-vegetarians.^[29] However, the results for stroke risk were not statistically significant.^[29] In many of these studies, the inverse associations were stronger among younger participants who had a longer duration of adherence to a vegetarian diet, and among men compared to women.^[30]

Given the likely long induction periods of CVD, particularly regarding their dietary causes, plant-based diets have not been studied in RCTs that focus on hard cardiovascular endpoints. However, several RCTs have investigated the effects of vegetarian diets on intermediate risk factors for CVD. A meta-analysis by Wang et al^[31] found that vegetarian diets significantly reduced lipid levels, including total cholesterol (RR: −0.36 mmol/L, 95% CI: −0.55 to −0.17 mmol/L), LDL cholesterol (RR: −0.34 mmol/L, 95% CI: −0.57 to −0.11 mmol/L), high-density lipoprotein (HDL) cholesterol (RR: −0.10 mmol/L, 95% CI: −0.14 to −0.06 mmol/L), and non-HDL (RR: −0.30 mmol/L, 95% CI: −0.50 to −0.10 mmol/L) cholesterol compared to various omnivorous diets. Other meta-analyses have shown that vegetarian diets lowered blood pressure (RR: −2.66 mmHg, 95% CI: −3.76 to −1.55 mmHg for systolic blood pressure; RR: −1.69 mmHg, 95% CI: −2.97 to −0.41 mmHg for diastolic blood pressure),^[32] and promoted weight loss (−2.02 kg, 95% CI −2.80 to −1.23 kg) more effectively than omnivorous diets.

Collectively, the positive effects of plant-based diets on established cardiovascular risk factors from RCTs, along with their inverse associations with hard endpoints observed in prospective cohort studies, strongly support the adoption of healthy plant-based diets for CVD prevention.^[30]

Plant-based diet and T2D

Adherence to a plant-based diet has been linked to a reduced risk of developing T2D, regardless of the positive association of meat consumption with its development. A meta-analysis of nine prospective studies involving 307,099 participants with 23,544 cases of incident T2D revealed that higher adherence to a plant-based diet reduced the incidence of T2D (RR: 0.77, 95% CI: 0.71–0.84).^[33] This association was strengthened when healthy plant-based foods, such as fruits, vegetables, whole grains, legumes, and nuts, were included in the definition of plant-based patterns (RR: 0.70, 95% CI: 0.62–0.79).^[33]

Clinical trials have also shown that vegetarian diets could lead to better glycemic control in patients with diabetes. Based on seven RCTs, consumption of vegetarian diets was associated with a significant reduction in HbA1c (MD: −0.40%, 95% CI: −0.59 to −0.21%) and BMI (MD: −0.96 kg/m², 95% CI: −1.58 to −0.34 kg/m²) (moderate certainty evidence).^[34]

Healthy diets in China and cardiometabolic risk

Notably, there are significant variations in lifestyle patterns between Eastern and Western populations. More than one-fifth of the world’s population consumes Chinese cuisine regularly, and China has unique dietary patterns that play a significant role in the prevention and management of cardiometabolic risk factors.

The Chinese Heart-Healthy Diet (CHH) and spicy diets are recommended as Chinese dietary patterns for the treatment of hypertension in the latest “Chinese Guidelines for the Prevention and Treatment of Hypertension (2024 Revised Edition)”.^[35] The CHH diet is the first healthy diet based on Chinese food culture (such as high sodium intake and low whole grain, fruit and vegetable intake). It encompasses recipe versions of four major Chinese cuisines: Shandong cuisine, Huaiyang cuisine, Cantonese cuisine, and Sichuan cuisine. Each version consists of non-repetitive breakfast, lunch, and dinner recipes, with the main courses and side dishes varying continuously for two weeks. By adjusting ingredients and cooking methods, it finalizes “two decreases and five increases”, as detailed below: A reduction in sodium intake from nearly 6 g/day to 3 g/day, a reduction in saturated fat; and increases in the intake of protein, whole grains, potassium, dietary fiber, calcium, and magnesium. A multicenter RCT showed that compared with regular diets, CHH diet reduced systolic blood pressure by an average of 10 mmHg (95% CI: −12.1 to −7.9 mmHg), and diastolic blood pressure by an average of 3.8 mmHg (95% CI: −5.0 to −2.5 mmHg).^[36] CHH diet is effective, palatable, and cost-effective in reducing blood pressure in Chinese adults with high blood pressure, with a clinically significant effect applicable across major Chinese cuisine cultures.^[36] The above study also suggested that the effect achieved by the CHH diet, if sustainable, would lead to a 20% reduction in major CVD, 28% reduction in heart failure, and 13% reduction in all-cause death.^[36]

Spicy diets were also proven to effectively reduce the risk of death among patients with CVDs, tumors, and other conditions. According to the China Kadoorie Biobank (CKB) study, individuals who frequently consume spicy foods have a significantly lower risk of developing hypertension compared to those who never consume spicy foods, with a 12% lower risk of hypertension among women and a 28% lower risk of hypertension among non-drinkers.^[37] The CKB study also supports an inverse association between spicy food consumption and vascular disease in the Chinese population. Specifically, participants consuming spicy food 1–2 days/week, 3–5 days/week, and 6–7 days/week showed a significantly lower risk of overall vascular disease compared to those consuming spicy food less than once a week.^[38] A systematic meta-analysis confirms that there is a significant correlation between regular consumption of spicy foods and a reduced risk of death from major diseases such as CVD (HR: 0.83, 95% CI: 0.74–0.95) and cancers (HR: 0.78, 95% CI: 0.56–1.09).^[39] In-depth research indicates that capsaicin, a key nutrient in spicy foods like chili peppers, can promote hypoxic-inducible factor-1 alpha (Hif-1α) deacetylation and degradation by upregulating Sirtuin 6. It inhibits osteogenic transdifferentiation and prevents arterial calcification, induces vasodilation, and regulates blood pressure, thus underpinning the role of spicy diets in preventing cardiovascular and metabolic diseases.^[40]

Medicine and food homology, a core concept in traditional Chinese medicine (TCM), posits that food and medicine share the same origin and have similar functions in preventing and treating various diseases.^[41] For thousands of years, this concept has been an important part of TCM and has been officially recognized through the list of substances that are both food and medicine, published by China’s National Health Commission (NHC).^[42,43] A TCM dietary therapy diet containing lily, Ganoderma lucidum polysaccharides, and whole-grain cereals was found to lessen hyperglycemia, reduce obesity, and increase beneficial microbiota in the human intestinal system.^[26] Ginger has anti-inflammatory and anti-nausea properties, which can reduce the risk of CVD by lowering inflammation in the body and improving blood circulation.^[44] Garlic is believed to have a wide range of health benefits. It contains components such as allicin, which have anti-inflammatory and antioxidant effects to help lower blood pressure and cholesterol levels, thereby reducing the risk of heart disease and stroke.^[45] Goji berries are considered a “superfood” due to their high antioxidant content and they have various health benefits. For instance, they may help regulate blood sugar levels and improve insulin sensitivity, making them beneficial for people with diabetes when included in their diet.^[46] American ginseng is a well-known adaptogenic herb that enhances physical energy and overall vitality. It also helps lower blood sugar levels and improve metabolic function in patients with diabetes.^[41] As interests in natural and holistic health approaches grow, TCM is being practiced in many countries, and numerous TCM-inspired dietary and herbal products have been developed. However, there is still insufficient evidence on the role of food–medicine homology substances in promoting health and preventing diseases. More research is needed to fully understand the mechanisms behind medicine–food homology and to verify the efficacy and safety of these substances.

Cooking methods are closely intertwined with health, with scientific approaches aimed at minimizing the loss of nutrients in food ingredients. Chinese cuisine, characterized by its emphasis on speed and precision, uses techniques like stir-frying, steaming, and boiling, which not only maintain the freshness and flavor of ingredients but also help preserve vital nutrients.^[47] For instance, to safeguard the vitamins and other beneficial components in our diet, it is prudent to eschew complex cooking processes such as prolonged and repetitive stewing or frying. In addition, the rational use of condiments, with a conscious reduction in salt, sugar, and edible oil, further enhances the nutritional value of meals. Given the profound impact that cooking methods have on our well-being, it is clear that adopting healthy cooking practices is an inevitable and essential trend in the realm of scientific diets for the future.

Physical Activity and Sedentary Behavior

Physical activity is defined as any skeletal muscle movement that requires energy expenditure, including exercise, leisure time activity, as well as usual occupational and/or domestic activity.^[48]

Physical activity and CVD

Increased physical activity is significantly associated with a reduced risk of CVD. A meta-analysis of 33 prospective cohort studies found that increasing physical activity from inactivity to the recommended 150 min of moderate-intensity physical activity per week led to a significant reduction in both CVD incidence (RR: 0.83, 95% CI: 0.77–0.89) and CVD mortality (RR: 0.77, 95% CI: 0.71–0.84).^[49] Another comprehensive review of nine prospective cohort studies including more than 33,000 patients with CHD revealed that CVD mortality was significantly reduced among those who were physically active (HR: 0.49, 95% CI: 0.39–0.62) or transitioned from inactivity to activity (HR: 0.63, 95% CI: 0.51–0.78) compared to those who remained inactive.^[50] Notably, those with high physical activity levels exhibited even lower CVD mortality, with no clear threshold beyond which lifespan is compromised.^[51] Furthermore, the CKB study has confirmed a strong inverse association between total physical activity and the risk of all-cause and cause-specific mortality: Compared to participants in the lowest quintile, those in the highest quintile of total physical activity had a 31% lower risk of all-cause mortality (HR: 0.69, 95% CI: 0.67–0.71) and a 32% lower risk of CVD mortality (HR: 0.68, 95% CI: 0.64–0.71).^[52]

Physical activity involves several components: Frequency, duration, and intensity, all of which contribute to the total volume of exercise. A minimum physical activity level of 500 MET-min/week (equivalent to 150 min of moderate-intensity or 75 min of vigorous-intensity activity, or an equivalent combination) is generally recommended for individuals with preexisting CVD. To maximize the benefits while minimizing potential risks, physical activity and exercise regimens should be personalized, taking into account the factors such as the individual’s baseline physical activity habits, cardiovascular health status, and the nature of their cardiovascular conditions.

Physical activity and T2D

Epidemiological studies indicate that individuals who engage in high levels of physical activity have a reduced relative risk of T2D by approximately 30% compared to those with low activity levels (RR: 35%, 95% CI: 29–39%,^[53] or RR: 26%, 95% CI: 20–31%^[54]). This protective effect is seen across all forms of physical activity, including leisure-time exercise, occupational activities, and resistance training.^[53]

Controlled trials have further demonstrated the beneficial effects of exercise on insulin sensitivity and glycemic control. For instance, both low-volume high-intensity interval training and continuous moderate-intensity exercise led to similar improvements in 24-h glycemic control (−6 ± 5%) in overweight and obese adults.^[55] Short and intermittent bouts of post-meal walking have been shown to effectively control postprandial hyperglycemia in older adults,^[56] while reallocating 30 min of sedentary time to moderate-to-vigorous physical activity was linked to a 15% improvement in insulin sensitivity, as measured by the homeostasis model assessment (HOMA) index.^[57]

Sedentary behavior

Sedentary behavior, such as prolonged sitting and excessive television watching, is strongly associated with increased risks of all-cause mortality (HR: 1.24, 95% CI: 1.09–1.41), CVD mortality (HR: 1.18, 95% CI: 1.11–1.26), CVD incidence (HR: 1.14, 95% CI: 1.00–1.73), cancer mortality (HR: 1.17, 95% CI: 1.11–1.24), cancer incidence (HR: 1.13, 95% CI: 1.05–1.21), and T2D incidence (HR: 1.91, 95% CI: 1.64–2.22) in one meta-analysis.^[58]

Obesity and Weight Management

Obesity is a well-established major risk factor for both CVD and T2D. It not only directly contributes to these conditions but also exacerbates other related cardiovascular risk factors such as hypertension, hyperlipidemia, and insulin resistance. The evidence supporting the detrimental role of obesity in the development of CVD and T2D comes from both observational studies and interventional trials.

Obesity and CVD

A large body of observational research has consistently demonstrated a strong association between obesity and various cardiovascular outcomes. An umbrella review of 501 cohort studies, involving over 30 million participants, found that each 5 kg/m² increase in BMI was linked to a higher risk of multiple cardiovascular events.^[59] For example, each 5 kg/m² increase in BMI resulted in: a 49% higher risk of hypertension (RR: 1.49, 95% CI: 1.40–1.60), a 41% higher risk of heart failure (RR: 1.41, 95% CI: 1.32–1.50), a 15% higher risk of CHD (HR: 1.15, 95% CI: 1.12–1.20), and a 7% higher risk of stroke (HR: 1.07, 95% CI: 1.02–1.12).^[59] Besides, the findings highlight that obesity is not only a risk factor for CVD events but also contributes to its severity and mortality. Each 5 kg/m² increase in BMI was linked to higher risks of CVD (HR: 1.49, 95% CI: 1.45–1.53) and all-cause mortality (HR: 1.31, 95% CI: 1.29–1.33 among never smokers, and HR: 1.05, 95% CI: 1.02–1.07 for the overall population).^[59]

Obesity and T2D

Individuals with obesity are at a significantly higher risk of developing T2D throughout their lifetime. A meta-analysis of 18 prospective cohort studies found that individuals with obesity (BMI of ≥30 kg/m²) had a sevenfold higher risk of developing T2D compared to those with normal weight.^[60] More recently, a dose response meta-analysis involving 216 cohort studies and 2.3 million individuals with T2D out of 26 million participants revealed that each 5 kg/m² increase in BMI was associated with a higher risk of developing T2D (RR: 1.72, 95% CI: 1.65–1.81),^[61] and there was a strong positive linear relationship between BMI and the risk of T2D.^[61]

Interventional studies have highlighted the critical role of weight management in preventing T2D. Key trials such as the Chinese Da Qing Diabetes Prevention Study,^[62] the Diabetes Prevention Study,^[63] and the Diabetes Prevention Program^[64] have demonstrated that lifestyle interventions targeting moderate weight loss can significantly reduce the risk of T2D among participants with impaired glucose tolerance. Participants who underwent lifestyle modifications, including dietary changes and increased physical activity, experienced a >50% reduction in T2D incidence after 3–4 years. Notably, even modest weight loss of around 5% in obese individuals resulted in improved metabolic outcomes, especially by reducing visceral fat, which is a key target for diabetes prevention. However, longer-term follow-up from these trials revealed that their long-term efficacy was diminished largely due to weight regain over time.^[65,66,67] In contrast, bariatric surgery has shown potential for sustaining weight loss and long-term protection against T2D, suggesting that sustained weight management is crucial for preventing the onset of T2D.^[68]

Smoking

Smoking is a leading cause of preventable disease and death, with profound negative effects on both cardiovascular and metabolic health. The combustion of tobacco releases thousands of harmful chemicals that damage the heart and blood vessels, increasing the risk of CVD and T2D. A wealth of scientific evidence consistently underscores the strong association between smoking and an elevated risk of these chronic conditions. Consequently, preventing the initiation of smoking and promoting smoking cessation remain as critical public health priorities.

Smoking and CVD

Tobacco smoking is one of the leading causes of CVD morbidity and mortality. A large-scale study involving 188,157 participants found that current smoking significantly increased the risk of any CVD (HR: 1.63, 95% CI: 1.56–1.71) and total CVD mortality (HR: 2.75, 95% CI: 2.37–3.19).^[69] A meta-analysis of 141 cohort studies revealed that even smoking as few as one cigarette per day can significantly increase the risk of CAD and stroke.^[70] In men, smoking one cigarette per day was associated with increased risks of CAD (RR: 1.48, 95% CI: 1.30–1.69) and stroke (RR: 1.25, 95% CI: 1.13–1.38); in women, the risks were similarly elevated: 57% for CAD (RR: 1.57, 95% CI: 1.29–1.91) and 31% for stroke (RR: 1.31, 95% CI: 1.13–1.52).^[70] These findings were further supported by a meta-analysis of 29 published Mendelian randomization studies, which strengthened a causal relationship between smoking and CVD by showing that genetic liability to smoking (either smoking initiation or lifetime smoking) was associated with an increased risk of 13 circulatory system diseases.^[71]

In addition, a retrospective analysis of 8770 heavy smokers (≥20 pack-years) found that quitting smoking within five years led to a 39% reduction in the risk of incident CVD compared to those who continued smoking (HR: 0.61, 95% CI: 0.49–0.76).^[72] This highlights the significant health benefits of smoking cessation, even for individuals with a long history of smoking.

The impact of passive smoking on CVD has also garnered increasing attention. A meta-analysis of case–control studies showed that exposure to second-hand smoke raised the risk of CVD incidence by 28% (RR: 1.28, 95% CI: 1.09–1.50), with the highest risk found among individuals exposed at home and work.^[73] Cohort studies also indicated that passive smoking was associated with a 12% increased risk of CVD mortality (HR: 1.12, 95% CI: 1.06–1.20), particularly among those exposed in multiple settings (home, work, and public places).^[73]

E-cigarettes, marketed as safer alternatives to traditional smoking primarily due to their limited ingredients and the absence of combustion, have been promoted as tools for smoking cessation. However, meta-analyses of observational studies suggested that e-cigarette use was not reliably associated with smoking cessation.^[74] Moreover, growing evidence indicates that e-cigarette emissions, which contain nicotine, oxidants, aldehydes, particulates, and flavorants, may have harmful effects on cardiovascular health. The cardiovascular effects observed in humans are consistent with the known risks of nicotine.^[75] Given the insufficient evidence on the long-term effects, caution is warranted, and further research is needed to fully understand the cardiovascular risks associated with e-cigarette use.

Smoking and T2D

The relationship between smoking and the development of T2D is well-documented. A meta-analysis of 88 prospective studies involving nearly six million participants found that current smokers had a 37% higher risk of developing T2D compared to non-smokers (RR: 1.37, 95% CI: 1.33–1.42); former smokers had a 14% increased risk (RR: 1.14, 95% CI: 1.10–1.18), while those exposed to passive smoke had a 22% higher risk (RR: 1.22, 95% CI: 1.10–1.35).^[76] Another meta-analysis of 25 prospective cohort studies highlighted a dose–response relationship, showing that the risk of T2D increased with the amount of smoking.^[77] Compared to non-smokers, the risk of T2D was higher among smokers of all patterns: Heavy smokers (RR: 1.61, 95% CI: 1.43–1.80), lighter smokers (RR: 1.29, 95% CI: 1.13–1.48), and former smokers (RR: 1.23, 95% CI: 1.14–1.33).^[77]

Sleep

Sleep is a cornerstone of overall health, and chronic sleep deprivation or poor sleep quality is associated with an increased risk of CVD and T2D. Factors such as exposure to noise or light during the night can disrupt sleep, contributing to negative health outcomes.^[78] Shift work or reduced sleep duration due to long working hours or leisure activities also has similar detrimental effects on health.^[79] Strategies for improving sleep hygiene include establishing regular sleep schedules, creating a conducive sleep environment, and avoiding stimulants close to bedtime.

Sleep and CVD

A meta-analysis of prospective studies demonstrated that both short sleep duration and long sleep duration were associated with an increased risk of developing or dying of CHD (RR: 1.48, 95% CI: 1.22–1.80 for <7 h/night; RR: 1.38, 95% CI: 1.15–1.66 for ≥9 h/night) and stroke (RR: 1.15, 95% CI: 1.00–1.31 for <7 h/night; RR 1.38, 95% CI 1.15–1.66 for ≥9 h/night).^[80] This meta-analysis identified that long duration of sleep was also associated with a greater risk of total CVD (RR: 1.41, 95% CI: 1.19–1.68); however, the association between short sleep duration and total CVD was not significant (RR: 1.03, 95% CI: 0.93–1.15).^[80]

A prospective cohort study of 1992 participants suggested that irregular sleep duration and timing may be novel risk factors for CVD, independent of traditional CVD risk factors and sleep quantity and/or quality.^[81] The results showed that the adjusted HRs (95% CIs) for CVD across categories of sleep duration standard deviation (SD) were 1.00 (reference) for ≤60 min, 1.09 (0.62–1.92) for 61 to 90 min, 1.59 (0.91–2.76) for 91 to 120 min, and 2.14 (1.24–3.68) for >120 min (P_trend = 0.002).^[81] Similarly, compared with participants with a sleep timing SD ≤30 min, the HRs (95% CIs) for CVD were 1.16 (0.64–2.13) for 31 to 60 min, 1.52 (0.81–2.88) for 61 to 90 min, and 2.11 (1.13–3.91) for >90 min (P_trend = 0.002).^[81]

Sleep and T2D

The associations between nighttime sleep duration and T2D in adults have been well-documented. A recent meta-analysis of 10 studies, involving 482,502 participants and 18,443 incident cases of T2D, found a U-shaped dose–response relationship.^[82] The lowest risk for T2D was observed in individuals with 7–8 h of sleep per night. However, those who slept less than 7 h per night had a 9% increased risk (RR: 1.09, 95% CI: 1.04–1.15) for each hour of sleep lost, while those who slept longer than 8 h had a 14% increased risk (RR: 1.14, 95% CI: 1.03–1.26) for each additional hour of sleep.^[82]

Recent epidemiological studies have also indicated an association between sleep disturbances and glycemic control in patients with T2D. A systematic review and meta-analysis revealed a U-shaped relationship between sleep duration and HbA1c levels.^[83] Both short and long sleep durations were linked to higher HbA1c levels compared to normal sleep duration: Short sleep was associated with an increase in HbA1c by an average of 0.23% (95% CI: 0.10–0.36%), and long sleep with an increase in HbA1c by an average of 0.13% (95% CI: 0.02–0.25%).^[83] In addition, poor sleep quality was found to be associated with a significant rise in HbA1c levels (MD: 0.35%, 95% CI: 0.12–0.58%).^[83] These findings suggest that both the quantity and quality of sleep play important roles in the metabolic regulation of patients with T2D.

Daytime napping has been proposed as a potential risk factor for diabetes or metabolic syndrome; however, the association between daytime napping and health outcomes remains controversial. An umbrella review found that most meta-analyses found weak or suggestive evidence linking daytime napping with diabetes, metabolic syndrome, CVD, and mortality. This review also indicated that long daytime naps (≥1 h/day) were associated with higher odds of several CVD risk factors, CVD, and mortality, while no significant associations were found between short daytime naps (less than 30 min/day) and these outcomes.^[84]

Alcohol Consumption

The relationship between alcohol consumption and cardiometabolic risk is complex, varying by a variety of factors, including the amount and frequency of alcohol consumption, drinking patterns, and individual differences. Observational studies provide valuable insights into this relationship, although the findings are sometimes inconsistent due to confounding factors.

Alcohol consumption and CVD

The relationship between alcohol consumption and CVD risk remains inconsistent. It has been proposed that there is a J- or U-shaped epidemiological association between alcohol consumption and CVD. This implies that moderate consumption of alcohol, especially red wine, may have beneficial effects on cardiovascular health, but excessive alcohol consumption significantly increases the risk of CVD. The protective effect of red wine on cardiovascular health is mainly due to its low alcohol concentration and its rich antioxidant content, such as polyphenols (e.g., resveratrol), which have antioxidant and anti-inflammatory effects, and are able to improve vascular endothelial function and reduce platelet aggregation.^[85] Some research suggests that light to moderate alcohol intake (up to two drinks or 1.30–24.99 g per day) may be associated with a reduced CHD mortality (RR: 0.80, 95% CI: 0.69–0.93).^[86] However, high-quality studies adjusting for baseline cardiovascular health often fail to show significant protective effects.^[86] Moreover, the UK Biobank study involving over 370,000 participants found that the potential benefits of modest alcohol consumption attenuated after adjusting for other favorable lifestyle factors.^[87] This study also demonstrated that alcohol consumption at any level was associated with an increased cardiovascular risk, with a 1-SD increase in genetically predicted alcohol consumption associated with a 1.3-fold higher risk of hypertension (RR: 1.3, 95% CI: 1.2–1.4) and a 1.4-fold higher risk of CHD (RR: 1.4, 95% CI: 1.1–1.8).^[87] In non-linear Mendelian randomization analyses, light alcohol intake was associated with minimal increases in cardiovascular risk, whereas heavier consumption was associated with exponential increases in risk of both clinical and subclinical CVD.^[87]

On the other hand, Chinese liquor (baijiu) may have more negative impacts on the cardiovascular system, mainly due to its high alcohol concentration and complex metabolites. Baijiu usually has a high alcohol content, which may lead to faster alcohol metabolism and more acetaldehyde accumulation, thus increasing the risk of stroke. In China, people mainly consume baijiu. Data from more than 500,000 Chinese in the CKB study show that alcohol consumption is associated with an increased risk of 61 diseases in Chinese men.^[88] A further analysis has confirmed the adverse effects of alcohol consumption on the Chinese population.^[89] After a Mendelian randomization analysis, the J-shaped or U-shaped curve related to alcohol consumption disappeared and was replaced by a positively correlated linear relationship curve.^[89] After comparing with the data of women in the cohort, researchers found that the excess death risk caused by alcohol consumption is not due to genes but rather the alcohol itself.^[89]

Overall, the observational evidence suggests that light alcohol consumption, particularly red wine, may have a marginally protective effect on CVD risk; however, heavy drinking including daily drinking and heavy episodic drinking is unequivocally harmful.

Alcohol consumption and T2D

Epidemiological studies suggest a dose-dependent relationship between alcohol consumption and the risk of developing T2D. A meta-analysis involving over 2.5 million participants found a J-shaped relationship among women, with a 31% risk reduction (RR: 0.69, 95% CI: 0.64–0.74) for daily intake of up to 16 g of pure alcohol, while a smaller 18% risk reduction (RR: 0.82, 95% CI: 0.68–0.99) for daily intake of above 49 g of pure alcohol.^[90] However, no statistically significant relationship was identified among men or in normal-weight or underweight women.^[90]

Coffee Consumption

Moderate coffee consumption has been associated with lower risks of several chronic diseases. A narrative review of literature found that coffee may help prevent inflammatory and oxidative stress-related diseases, including obesity, metabolic syndrome, and T2D, and it is also linked to reduced all-cause mortality.^[91] An umbrella review, based on 201 meta-analyses of observational research and 17 meta-analyses of interventional research, confirmed a non-linear association between coffee consumption and some outcomes. The most significant relative risk reductions were observed with a consumption of 3–4 cups per day, showing a reduction in all-cause mortality (RR: 0.83, 95% CI: 0.79–0.88), CVD mortality (RR: 0.81, 95% CI: 0.72–0.90), and CVD incidence (RR: 0.85, 95% CI: 0.80–0.90).^[92] Further evidence from a systematic review demonstrated a dose–response association between coffee consumption and T2D. The relative risks (RRs [95% CIs]) for diabetes were 0.92 (0.90–0.94), 0.85 (0.82–0.88), 0.79 (0.75–0.83), 0.75 (0.71–0.80), 0.71 (0.65–0.76), and 0.67 (0.61–0.74) for 1–6 cups/day, respectively.^[93] Both caffeinated and decaffeinated coffee were associated with a reduced risk of diabetes, with the RR for a 1-cup/day increase being 0.91 (95% CI 0.89–0.94) for caffeinated coffee and 0.94 (95% CI 0.91–0.98) for decaffeinated coffee.^[63]

Although some studies have suggested adverse effects of high coffee consumption, such as low birth weight, preterm birth, and pregnancy loss, these findings were largely mitigated when controlling for smoking, except for during pregnancy. Overall, coffee consumption is more frequently associated with health benefits than harms. A daily intake of up to 400 mg of caffeine (equivalent to 1–4 cups) is generally considered safe.^[91]

Tea Consumption

Some prospective studies indicate that regular tea consumption, particularly green tea, may help reduce the risk of stroke, likely due to its high antioxidant content. This protective effect is thought to arise from improvements in lipid profiles, blood pressure reduction, and the prevention of atherosclerosis. A large cohort study in China, where green tea is the predominant type of tea consumed, found a dose–response inverse relationship between tea consumption and stroke risk (P_trend <0.001). The HRs and 95% CIs for stroke risk were as follows: 0.96 (0.94–0.99) for occasional tea drinkers, 0.94 (0.90–0.98) for weekly drinkers, and 0.92 (0.89–0.95) for daily drinkers, compared to non-consumers.^[94]

A recent meta-analysis of five studies, which included 645,393 participants and 11,421 stroke cases, revealed a non-linear association between green tea consumption and stroke risk. The RRs for stroke at various levels of green tea consumption were as follows: 0.91 (95% CI: 0.89–0.94) for 150 mL/day, 0.84 (95% CI: 0.80–0.89) for 300 mL/day, 0.79 (95% CI: 0.74–0.84) for 500 mL/day, 0.77 (95% CI: 0.72–0.82) for 900 mL/day, and 0.84 (95% CI: 0.77–0.91) for 1500 mL/day.^[95] Gender differences in stroke risk have been observed, with stronger protective effects noted in men, possibly due to higher tea consumption and differences in lifestyle factors, such as smoking and alcohol use.^[94] Notably, while green tea was significantly associated with a reduced risk of stroke, this was not the case for non-green teas such as black or oolong tea.^[94]

Biological Mechanisms Linking Lifestyle Factors to Cardiometabolic Risk

The biological mechanisms linking lifestyle factors to cardiometabolic risk have been extensively and thoroughly investigated. For instance, the MedDiet is characterized by its bioactive components, which can exert cardioprotective effects via multiple pathways. Each component of the MedDiet is potentially involved in processes related to cardiometabolic homeostasis, and many components share common physiological and pathological pathways. The most significant adaptations include protection against oxidative stress, inflammation, and platelet aggregation; optimization of lipid metabolism; and improvement of endothelial function.^[96,97] Furthermore, other adaptive effects include the production of metabolites mediated by the gut microbiota that influence metabolic health.^[96,97]

The cardioprotective effect of regular exercise is achieved through multi-level physiological mechanisms. In terms of the core mechanisms, exercise comprehensively improves cardiorespiratory fitness by synergistically increasing cardiac output, improving vascular endothelial function, and enhancing skeletal muscle adaptation.^[98] In addition to the regulation of traditional risk factors (such as reducing blood pressure, optimizing lipid profiles, and improving blood glucose control), regular exercise can optimize cardiovascular health through various non-traditional mechanisms, including antiatherogenic effects in the vasculature, improving autonomic balance (thereby reducing the risk of malignant arrhythmias), and inducing cardioprotection against ischemia-reperfusion injury.^[99] At the same time, exercise can promote a healthy anti-inflammatory milieu (largely through the release of muscle-derived myokines), stimulate myocardial regeneration, and alleviate age-related loss of muscle mass and strength, which is a frequently overlooked non-traditional CVD risk factor.^[99] It is worth noting that the benefits of exercise can also be achieved by promoting a healthy gut microbiota.^[99] These diverse mechanisms collectively reveal the complex and crucial role of exercise in maintaining cardiovascular health, providing a more comprehensive theoretical basis for the prevention and intervention of CVDs.

In addition to diet and exercise, the mechanistic relationships between other lifestyle factors and cardiometabolic risk have also drawn significant attention. For instance, nicotine alters vasoreactivity through endothelium-dependent and/or endothelium-independent mechanisms, leading to clinical manifestations in both cigarette smokers and e-cigarette users. In addition, nicotine induces vascular remodeling through its effects on proliferation, migration, and matrix production of both vascular endothelial and vascular smooth muscle cells.^[100] Excessive alcohol consumption can lead to organ damage. Its mechanism involves the direct toxic effects of ethanol and its metabolites (such as acetaldehyde and fatty acid ethyl esters), as well as the oxidative stress reactions triggered thereby.^[101] Circadian rhythm disruption not only inhibits melatonin secretion and impairs fat oxidation,^[102] increasing the risk of metabolic disorders, but also causes an imbalance between leptin and ghrelin, stimulating appetite and leading to weight gain. Furthermore, it interferes with insulin signaling, resulting in insulin resistance,^[103] while also exacerbating oxidative stress and triggering chronic inflammation.^[104]

Adherence to Healthy Lifestyle Factors and Cardiometabolic Risk

We have discussed previously in this review the associations between individual components of lifestyles and cardiometabolic risk. Many studies showed that adherence to a combination of healthy lifestyle factors may have a synergistic effect on reducing the risk of cardiometabolic diseases. Healthy lifestyles include a combination of never smoking, vigorous physical activities, normal weight, being in a healthy dietary pattern, and/or moderate alcohol consumption. Evidence suggests that the more of these behaviors were adhered to, the greater the protective effect against cardiometabolic diseases such as CVD,^{[105,106,107,108]} heart failure,^[109] and T2D,^[110] and these associations are gradually becoming inverse. Selected key findings on combined lifestyle factors for CVD and T2D, derived from important epidemiological studies, are presented in Table 3. Patel et al^[111] concluded that compared to those with ≤1 healthy lifestyle factors, the risk of death among patients with T2D was reduced by 42% with two factors, 41% with three, and 44% with four or more factors. One recent systematic review and meta-analysis synthesized evidence on the associations between lifestyle scores/indices and metabolic syndrome from 19 cross-sectional and cohort studies. It was found that participants with the healthiest lifestyles had a 43% lower risk of metabolic syndrome compared to those with the least-healthy lifestyles.^[112] Another cohort study explored the association between MTNR1B gene variants (rs10830963 and rs1387153) and stroke, along with the potential mitigating effects of a healthy lifestyle. These genetic–lifestyle interactions highlighted the role of a healthy lifestyle in reducing genetic predisposition to ischemic stroke (IS).^[113] Using data from the UK Biobank, researchers also found that adherence to 3–4 healthy lifestyle factors was associated with lower risks of transitioning from baseline to diabetes (HR: 0.966), diabetes to complications (HR: 0.869), baseline to death (HR: 0.528), and diabetes to death (HR: 0.765), compared to adherence to 0–1 healthy lifestyle factors.^[110] In a prospective nested case–control study based on the Swedish Twin Registry, investigators found that among patients with T2D, adherence to an intermediate lifestyle reduced heart disease risk by 32%, and a favorable lifestyle reduced it by 56%, compared to an unfavorable lifestyle.^[114] Based on all the evidence, in 2022, the AHA introduced LE8 as a comprehensive framework to optimize cardiovascular health and reduce the risk of CHD and stroke. This framework emphasizes eight key lifestyle and health factors: Diet, physical activity, nicotine exposure, sleep health, body weight, blood glucose, blood lipids, and blood pressure. Together, these factors serve as measurable and modifiable components that individuals can address to enhance overall heart and vascular health. The AHA highlights the importance of these factors not only for preventing CVDs but also for promoting long-term well-being. By adopting and maintaining these essential practices, individuals can significantly lower their risk of chronic illnesses and improve their quality of life. LE8 offers a practical, evidence-based approach to achieving ideal cardiovascular health in diverse populations.^[4] Since then, a lot of studies have focused on the association between LE8 and cardiometabolic health.^{[7,115,116,117]} A prospective community-based study utilizing the LE8 framework found that greater adherence to LE8 metrics is associated with a lower risk of heart failure incidence and post-HF mortality.^[118]

Table 3.

Findings from selected important epidemiological studies of combined lifestyle factors for cardiovascular disease and type 2 diabetes.

Outcomes	Measure	Ref group	Relative risk	Type and Refs.
Coronary heart disease	Healthy lifestyle score 1–6	Healthy lifestyle scores ≥5	HR: 1.61 (95% CI 1.51–1.72) for those scored 2–4 HR: 2.24 (95% CI 2.09–2.40) for those scored ≤1	Retrospective study[106]
	Overall lifestyle score 0–5	Lifestyle score 0–1	HR: 0.80 (95% CI 0.75–0.86) for those scored 2–3 HR: 0.75 (95% CI 0.70–0.81) for those scored 4–5	Retrospective study[107]
Heart failure	Number of healthy lifestyle factors	0	Men: HR: 0.68 (95% CI 0.54–0.86) for scored 1 HR: 0.44 (95% CI 0.35–0.57) for scored 2 HR: 0.33 (95% CI 0.24–0.45) for scored 3 HR: 0.30 (95% CI 0.16–0.54) for scored 4 Women: HR: 0.53 (95% CI 0.33–0.85) for scored 1 HR: 0.42 (95% CI 0.27–0.67) for scored 2 HR: 0.24 (95% CI 0.14–0.40) for scored 3 HR: 0.19 (95% CI 0.09–0.40) for scored 4	Retrospective study[109]
Stroke	Number of healthy lifestyle factors	0–1	HR: 0.66 (95% CI 0.58–0.76) for scored 2 HR: 0.57 (95% CI 0.50–0.66) for scored 3 HR: 0.51 (95% CI 0.42–0.61) for scored 4 HR: 0.33 (95% CI 0.23–0.50) for scored 5	Prospective study[105]
Type 2 diabetes	Low-risk lifestyle factors 0–6	0	HR: 0.65 (95% CI 0.60–0.70) for 1 HR: 0.35 (95% CI 0.33–0.38) for 2 HR: 0.22 (95% CI 0.20–0.24) for 3 HR: 0.16 (95% CI 0.14–0.19) for 4 HR: 0.17 (95% CI 0.09–0.35) for ≥5	Retrospective study[132]
	Healthy life score 0–4	0–1	HR: 0.981 (95% CI 0.951–1.011) for 2 HR: 0.966 (95% CI 0.935–0.998) for 3–4	Retrospective study[110]

CI: Confidence interval; HR: Hazard ratio; Refs.: References.

Digital health interventions (DHIs) are playing a crucial and irreplaceable role in the field of diagnosis, monitoring, and management of chronic cardiovascular conditions. The technological scope covered by DHIs is extremely extensive, ranging from electronic health record systems to wearable devices and further extending to remote consultation software. In 2018, the World Health Organization (WHO) introduced the Classification of Digital Health Interventions, systematically categorizing DHIs into 28 distinct classes to establish a standardized framework for comparative evaluation.^[119] A meta-analysis further summarizes DHI technologies into three core types: Smartphone-based application tracking tools represented by the MyFitnessPal app and WeChat mini-programs, as well as wearable devices such as smartwatches; email and short message service communication systems; and website and web portal platforms.^[120] The research results indicated that in multiple important dimensions such as nicotine dependence cessation, blood pressure regulation, blood glucose level management, exercise capacity improvement, and weight control, DHIs have demonstrated remarkable effects comparable to traditional control methods.^[120]

Telemedicine, as an important component of the WHO’s classification of DHIs, has had a direct and profound impact on the model of clinical medical service provision. With the help of this technology, efficient remote consultations between patients and clinicians can be realized, while also supporting case management, real-time remote monitoring of health data, and accurate transmission of data to healthcare providers. A targeted meta-analysis pointed out that telemedicine platforms integrated with artificial intelligence-driven analysis functions have shown unique and great potential in primary and secondary prevention of CVDs.^[96] Relevant research results clearly show that for patients with heart failure, the comprehensive intervention model combining remote monitoring and remote consultation can effectively reduce the risk of cardiovascular-related mortality (RR: 0.83, 95% CI: 0.70–0.99, P = 0.036) and the risk of hospitalization due to CVDs (RR: 0.71, 95% CI: 0.58–0.87, P = 0.0002), although this conclusion is mainly derived from studies with short-term follow-ups.^[121]

Despite the numerous remarkable achievements that DHIs have already made, in practical applications, their effectiveness is still controversial in some areas. On one hand, the length of the follow-up period significantly affects the evaluation results of the intervention’s effectiveness; on the other hand, there is still no consensus on the research conclusions regarding the improvement of lipid profiles, and only 36% of the studies have confirmed a significant decrease in LDL levels.^[120] These current situations fully demonstrate that it is imperative to formulate unified and standardized implementation protocols, and in-depth research on the long-term prognosis of CVDs is also urgently needed. In addition, the promotion and application of digital technologies also face severe challenges such as uneven digital literacy and unequal access opportunities, which urgently need to be addressed through the collaborative efforts of multiple parties.

Adherence to healthy lifestyle factors plays a crucial role in the prevention and management of cardiometabolic diseases. Public health interventions that promote healthy dietary patterns, encourage physical activity, support smoking cessation, and address weight management are essential for mitigating the burden of these diseases. Future research should focus on understanding the interactions between lifestyle factors, genetic predispositions, and socio-economic determinants to design targeted interventions.

Challenges and Future Directions

Despite the well-established benefits of lifestyle modifications, significant barriers to change remain. These barriers include individual-level factors such as lack of motivation and knowledge, and broader societal challenges such as limited access to healthy food and safe spaces for physical activity. To address these challenges, innovative approaches to lifestyle interventions are needed. These approaches should leverage technology and community-based programs to engage and support individuals in making sustainable lifestyle changes.

Meanwhile, cardiovascular and metabolic disorders often coexist with CKD, forming a complex web of interrelated conditions. In response to the recent advances in cardiometabolic therapies and a deeper understanding of shared risk factors and underlying mechanisms, the AHA has introduced the concept of cardio–kidney–metabolic (CKM) syndrome.^[122] This systemic disorder originates from adipose tissue dysfunction, driving pathological processes such as insulin resistance, chronic inflammation, and oxidative stress. These collectively contribute to multi-organ damage and elevated risks of adverse cardiovascular events.^[122,123] Epidemiological data reveal that nearly 90% of U.S. adults meet criteria for CKM syndrome (Stage 1 or higher), with 15% progressing to advanced stages.^[124] Although lifestyle modifications are emphasized in AHA guidelines for delaying disease progression,^[122] there are critical gaps in knowledge related to optimal strategies for lifestyle modification and weight loss.^[125] Recent evidence highlights that improving cardiovascular health metrics, especially using the LE8 framework, significantly mitigates risks in renal insufficiency populations. Studies show ideal cardiovascular health metrics are associated with a 25% reduction in CVD mortality risk per metric increment.^[126] Future research should focus on developing targeted interventions for high-risk CKM populations and evaluating their effectiveness.

Currently, research on CKM syndrome focuses on three major frontier trends and has achieved significant progress. First, in the field of gut microbiome regulation, it has been found that gut microbiota derived metabolites such as trimethylamine-N-oxide (TMAO) not only accelerate the progression of CKM by promoting atherosclerosis but also exacerbate the condition by activating the NOD-like receptor family pyrin domain containing 3 inflammasome.^[127] Given the detrimental effects of certain gut microbiota-derived metabolites, diet modulation and probiotics use have emerged as potentially effective therapeutic strategies. However, existing studies have yielded inconsistent findings, and the true efficacy of these interventions and their impact on related health outcomes remain incompletely understood.^[128] Second, the integration of artificial intelligence (AI) and multi-omics technologies has brought a revolutionary opportunity for precise disease prediction, patient stratification, and the realization of precision medicine. Machine learning (ML) algorithms, in particular, have significantly accelerated analytical procedures and surpassed traditional risk prediction models in cardiovascular studies.^[129] However, translating ML-based omics research into routine clinical practice confronts numerous challenges, such as difficulties in multi-data collection and standardization, dilemmas in multi-modal data integration, ethical considerations, data security risks, inherent flaws in AI models, and limitations in model generalizability.^[129] Despite these challenges, the joint application of ML and omics in CVD research holds promising prospects. Third, high genetic risk and an unhealthy lifestyle exhibit an additive interaction in the risk of early-onset CVD. This indicates that for young people with high genetic risk, actively practicing a healthy lifestyle can lead to more significant preventive effects.^[130] This gene–lifestyle interaction has opened up a new path for precision medicine in CVD, and polygenic risk scores (PRS) have provided crucial guidance for precision medicine practice. For example, among participants with a high PRS, adopting a favorable lifestyle was associated with a nearly 50% lower relative risk of coronary artery disease compared to those with an unfavorable lifestyle.^[131] However, current challenges include generalizability across different racial populations, unclear biological mechanisms, and ethical controversies surrounding gene-oriented interventions. Future research should build a cross-disciplinary platform to integrate multi-omics data, dynamic biomarker monitoring, and real-time wearable device data streams. This integration will create a comprehensive solution for molecular mechanism exploration, precise clinical diagnosis, and effective management.

Conclusion

The complex interplay between lifestyle factors and cardiometabolic risk underscores the need for a holistic approach to prevention and management. By addressing the multifaceted risks associated with hypertension, T2D, and CVD, we can strengthen public health and protect individuals and communities from the devastating effects of these interconnected diseases. As research, policy, and practice continue to evolve, it is crucial to integrate efforts to promote health and reduce the global burden of cardiometabolic risk.

Funding

This study is supported by the grants from the National Institute of Diabetes and Digestive and Kidney Diseases (No. R01DK132011), the National Institute of General Medical Sciences of the National Institutes of Health (No. U54GM104940), and Natural Science Foundation of Tianjin, China (No. 23JCYBJC00960).

Conflicts of interest

None.