Department of Pharmacology, Devaki Amma Memorial College of Pharmacy
Atherosclerosis is a long-term inflammatory condition of the blood vessels marked by the buildup of lipids, damage to the endothelial lining, and formation of plaques, which can lead to serious cardiovascular diseases such as coronary artery disease and stroke. This review explores how dietary habits influence the progression of atherosclerosis, with particular attention to differences between males and females. Evidence from existing studies shows that unhealthy diets high in saturated fats, trans fats, and refined carbohydrates increase the risk of dyslipidaemia, oxidative stress, and inflammation, all of which accelerate plaque formation, whereas diets rich in fruits, vegetables, whole grains, and healthy fats provide protective effects by improving lipid balance, reducing oxidative damage, and supporting vascular function. Significant sex-based differences are observed, with men generally developing the disease earlier, often due to less healthy dietary and lifestyle patterns, while women tend to be protected during their reproductive years due to the beneficial effects of oestrogen, although this protection declines after menopause, increasing cardiovascular risk. Furthermore, dietary patterns such as the Mediterranean and DASH diets have been shown to reduce disease progression in both sexes. Overall, dietary habits play a crucial role in the development and progression of atherosclerosis, and incorporating sex-specific nutritional strategies may improve prevention and management of cardiovascular diseases
Atherosclerosis is a progressive and chronic inflammatory disease characterized by the accumulation of lipids, fibrous elements, and immune cells within the arterial wall. It is widely recognized as the underlying pathological process responsible for major cardiovascular diseases including coronary artery disease, myocardial infarction, and ischemic stroke. Cardiovascular diseases remain the leading cause of global mortality, accounting for millions of deaths annually. The development and progression of atherosclerosis are influenced by a complex interaction of genetic, metabolic, and environmental factors. Among these, dietary habits represent one of the most significant modifiable risk factors that can either accelerate or slow the progression of the disease [1,2].
Dietary patterns rich in saturated fats, trans fats, refined carbohydrates, and processed foods have been strongly associated with elevated levels of low density lipoprotein cholesterol and systemic inflammation, both of which contribute to atherosclerotic plaque formation. Conversely, diets abundant in fruits, vegetables, whole grains, polyunsaturated fatty acids, and antioxidants have been shown to provide protective cardiovascular effects by improving lipid metabolism and reducing oxidative stress [3,4]. In recent years, increasing attention has been directed toward the role of biological sex in influencing cardiovascular disease risk. Epidemiological studies indicate that men generally develop atherosclerosis earlier in life, whereas women tend to experience increased risk after menopause. These differences may be attributed to hormonal variations, metabolic differences, and distinct lifestyle patterns, including dietary behaviours [5]. Understanding how dietary habits differentially influence atherosclerosis progression in males and females may provide valuable insights for developing sex specific preventive and therapeutic strategies.
In addition to lipid abnormalities, chronic inflammation and endothelial dysfunction play critical roles in the initiation and progression of atherosclerosis. The vascular endothelium acts as a protective barrier that regulates vascular tone, platelet activity, and immune responses. However, exposure to unhealthy dietary components, elevated cholesterol levels, and oxidative stress can impair endothelial function and promote inflammatory signalling pathways. This environment facilitates the recruitment of immune cells and promotes lipid deposition within the arterial wall, leading to the formation of early atherosclerotic lesions [6,7].
Another important factor influencing atherosclerosis progression is oxidative stress, which results from an imbalance between the production of reactive oxygen species and the body’s antioxidant defence systems. Diets deficient in antioxidant nutrients may enhance oxidative modification of lipoproteins, thereby accelerating plaque development. In contrast, plant-based foods rich in vitamins, polyphenols, and other bioactive compounds help neutralize free radicals and reduce vascular inflammation, ultimately contributing to cardiovascular protection [8,9].
Furthermore, global changes in lifestyle and dietary behaviour have contributed significantly to the rising prevalence of cardiovascular diseases. Increased consumption of energy-dense foods, sedentary lifestyles, and obesity have collectively increased the burden of metabolic disorders such as dyslipidaemia, hypertension, and insulin resistance. These conditions are strongly associated with accelerated atherosclerosis and increased risk of cardiovascular complications [10]. Therefore, understanding the influence of diet and lifestyle on vascular health has become a major focus in cardiovascular research
OVERVIEW OF ATHEROSCLEROSIS
Atherosclerosis is a multifactorial vascular disorder characterized by the progressive accumulation of lipid rich plaques within the inner lining of arteries. These plaques gradually narrow the arterial lumen and impair normal blood flow, eventually leading to serious cardiovascular complications. The disease process typically begins with endothelial dysfunction, a condition in which the protective inner layer of blood vessels loses its normal physiological functions. Several risk factors contribute to this early vascular injury, including hyperlipidaemia, hypertension, smoking, diabetes mellitus, and oxidative stress [1,2]. When the endothelium becomes damaged, it becomes more permeable to circulating lipoproteins, particularly low-density lipoprotein (LDL) cholesterol, allowing these particles to infiltrate the arterial wall where they accumulate and undergo oxidative modification [6].
The oxidation of LDL particles represents a key event in the initiation of the atherosclerotic process. Oxidized LDL stimulates inflammatory signalling pathways within the vascular wall and promotes the recruitment of immune cells. Circulating monocytes migrate into the arterial intima and differentiate into macrophages, which actively engulf oxidized lipids. As macrophages accumulate large amounts of lipids, they transform into foam cells, giving rise to fatty streaks that represent the earliest visible lesions of atherosclerosis [3,6]. Although fatty streaks may initially be asymptomatic, their persistence can lead to the gradual development of more complex atherosclerotic plaques.
As the disease progresses, vascular smooth muscle cells migrate from the media layer of the arterial wall into the intima. These cells proliferate and synthesize extracellular matrix components such as collagen and elastin, contributing to the formation of fibrous plaques. Over time, these plaques become more structurally complex, consisting of a lipid core surrounded by a fibrous cap composed of smooth muscle cells and connective tissue [7]. The stability of these plaques is an important determinant of clinical outcomes. Plaques with thick fibrous caps tend to remain stable, whereas plaques with thin fibrous caps and large lipid cores are more vulnerable to rupture.
Plaque rupture is one of the most dangerous complications of atherosclerosis. When a vulnerable plaque ruptures, it exposes thrombogenic material to circulating blood, leading to the rapid formation of a blood clot or thrombus. This thrombus may partially or completely block blood flow through the affected artery, resulting in acute cardiovascular events such as myocardial infarction or ischemic stroke [7]. These events often occur suddenly and may be life-threatening if immediate medical intervention is not provided.
The progression of atherosclerosis is influenced by a wide range of modifiable and non-modifiable risk factors. Modifiable factors include dietary habits, physical inactivity, obesity, smoking, and metabolic disorders such as dyslipidaemia and diabetes. Non-modifiable factors include age, genetic predisposition, and biological sex. Research has demonstrated that men often develop atherosclerotic lesions earlier in life, whereas women tend to experience increased cardiovascular risk after menopause due to hormonal changes [5].
In addition to these factors, chronic inflammation plays a central role in the progression of atherosclerosis. The continuous interaction between lipid accumulation and inflammatory responses promotes further endothelial injury and plaque growth. Therefore, atherosclerosis is now widely recognized not only as a lipid storage disease but also as a chronic inflammatory condition affecting the vascular system [1,6]. Understanding these complex mechanisms is essential for developing effective preventive and therapeutic strategies aimed at reducing the burden of cardiovascular diseases worldwide.
PATHOPHYSIOLOGY OF ATHEROSCLEROSIS
The pathophysiology of Atherosclerosis is a complex and dynamic process involving interactions between lipid metabolism, endothelial dysfunction, inflammation, and oxidative stress. The disease typically begins with injury or dysfunction of the vascular endothelium, the inner cellular lining of blood vessels. This dysfunction may be caused by several risk factors such as hyperlipidemia, hypertension, smoking, diabetes mellitus, and chronic oxidative stress. When endothelial cells lose their normal protective functions, the vascular wall becomes more permeable to circulating lipoproteins, particularly low-density lipoprotein (LDL) cholesterol [1,2].
Once LDL particles penetrate the arterial intima, they undergo oxidative modification through interactions with reactive oxygen species generated by endothelial cells and inflammatory cells. The resulting oxidized LDL (ox-LDL) plays a key role in triggering the inflammatory cascade associated with atherosclerosis. Oxidized LDL stimulates endothelial cells to express adhesion molecules that facilitate the attachment of circulating monocytes to the vessel wall. These monocytes migrate into the arterial intima and differentiate into macrophages, which actively engulf ox-LDL through scavenger receptors [3,6].
The accumulation of lipid-laden macrophages leads to the formation of foam cells, which are the hallmark of early atherosclerotic lesions known as fatty streaks. These fatty streaks represent the earliest visible stage of plaque development and may appear even during adolescence in individuals with elevated cardiovascular risk. As the inflammatory process continues, macrophages release cytokines, chemokines, and growth factors that further recruit immune cells and amplify the inflammatory response within the arterial wall [3,8].
Another important event in plaque development is the migration and proliferation of vascular smooth muscle cells from the media layer of the artery into the intima. These smooth muscle cells synthesize extracellular matrix components such as collagen, elastin, and proteoglycans, which contribute to the formation of a fibrous cap over the lipid rich core of the plaque. The fibrous cap plays a protective role by stabilizing the plaque and preventing rupture. However, chronic inflammation can weaken this cap by degrading its structural components through enzymes such as matrix metalloproteinases [7,9].
As the plaque grows, the arterial lumen gradually narrows, reducing blood flow to vital organs. In advanced stages of atherosclerosis, plaques may become unstable and rupture. Plaque rupture exposes the thrombogenic lipid core to circulating blood, triggering platelet activation and the formation of a thrombus. This thrombus may partially or completely block the affected artery, leading to acute cardiovascular events such as myocardial infarction or ischemic stroke [7,10].
Overall, the progression of atherosclerosis depends on the delicate balance between lipid accumulation, inflammatory activity, and vascular repair mechanisms. Disruptions in this balance can accelerate plaque formation and increase the risk of life-threatening cardiovascular complications.
Figure 1: Pathophysiology of Atherosclerosis
ROLE OF DIETARY HABITS IN ATHEROSCLEROSIS DEVELOPMENT
Dietary habits play a crucial role in the initiation and progression of Atherosclerosis by influencing lipid metabolism, systemic inflammation, oxidative stress, and endothelial function. Unhealthy dietary patterns characterized by high consumption of saturated fats, trans fats, refined carbohydrates, and processed foods have been strongly associated with increased levels of low-density lipoprotein (LDL) cholesterol and triglycerides. Elevated LDL cholesterol promotes lipid accumulation within the arterial wall and accelerates plaque formation. In addition, excessive intake of energy-dense processed foods contributes to obesity, insulin resistance, and metabolic syndrome, all of which are major risk factors for cardiovascular disease and atherosclerotic progression [11,12].
Dietary fats play a particularly important role in regulating plasma lipid levels. Diets high in saturated fatty acids and industrial trans fats increase LDL cholesterol and may promote endothelial dysfunction and vascular inflammation. These effects contribute to the formation of lipid-rich plaques within arteries. In contrast, replacing saturated fats with unsaturated fats- particularly polyunsaturated fatty acids has been shown to improve lipid profiles and reduce cardiovascular risk. Omega-3 fatty acids, commonly found in fatty fish and certain plant sources, exhibit anti-inflammatory and anti-thrombotic properties that may help prevent plaque development [4,11].
Consumption of plant-based foods such as fruits, vegetables, whole grains, legumes, and nuts provides several protective nutrients including dietary Fiber, antioxidants, vitamins, and phytochemicals. Dietary Fiber helps lower circulating cholesterol levels by reducing intestinal cholesterol absorption and promoting bile acid excretion. Antioxidants such as vitamin C, vitamin E, and polyphenols help neutralize reactive oxygen species, thereby reducing oxidative modification of LDL particles and protecting vascular endothelial cells from damage [12,13].
Several dietary patterns have been extensively studied for their cardiovascular benefits. Among these, the Mediterranean diet is widely recognized for its protective effects against atherosclerosis and cardiovascular disease. This diet emphasizes the consumption of olive oil, whole grains, fruits, vegetables, nuts, legumes, and moderate intake of fish while limiting red meat and processed foods. Clinical studies have demonstrated that adherence to the Mediterranean diet significantly reduces the incidence of cardiovascular events and improves lipid profiles and inflammatory markers [14].
Another well-established dietary approach is the Dietary Approaches to Stop Hypertension (DASH) diet. The DASH diet promotes high intake of fruits, vegetables, low fat dairy products, whole grains, and lean proteins while reducing sodium and saturated fat intake. This dietary pattern has been shown to effectively lower blood pressure and improve overall cardiovascular health, thereby reducing the risk of atherosclerotic disease [15].
SEX DIFFERENCES IN ATHEROSCLEROSIS
Significant differences exist between males and females in the prevalence, progression, and clinical manifestation of Atherosclerosis. Epidemiological studies consistently show that men tend to develop atherosclerotic lesions earlier in life compared with women. This earlier onset is largely attributed to differences in hormonal regulation, lipid metabolism, body fat distribution, and lifestyle behaviours. In contrast, women generally experience a lower risk of cardiovascular disease during their reproductive years, largely due to the protective effects of the hormone oestrogen. As a result, the incidence of atherosclerotic cardiovascular disease in women typically increases after menopause, when oestrogen levels decline significantly [5,16].
Oestrogen plays a central role in maintaining cardiovascular health through multiple mechanisms. It favourably influences lipid metabolism by increasing levels of high-density lipoprotein (HDL) cholesterol while reducing concentrations of low-density lipoprotein (LDL) cholesterol. These lipid-modifying effects help reduce lipid accumulation within arterial walls and limit the development of atherosclerotic plaques. In addition to its effects on lipid metabolism, oestrogen enhances endothelial function by stimulating the production of nitric oxide, a molecule that promotes vasodilation and improves vascular blood flow. Oestrogen also exhibits antioxidant and anti-inflammatory properties that help reduce oxidative stress and inhibit inflammatory responses involved in plaque formation [16,17].
Despite these protective mechanisms, the cardiovascular risk profile of women changes markedly after menopause. The decline in oestrogen levels is associated with unfavourable metabolic changes, including increased LDL cholesterol, reduced HDL cholesterol, central fat accumulation, and increased insulin resistance. These metabolic alterations contribute to accelerated plaque formation and increased susceptibility to atherosclerosis in postmenopausal women. Consequently, the incidence of coronary artery disease in women rises substantially after the age of 50–60 years [17,18].
Another important factor contributing to sex differences in atherosclerosis is the variation in plaque characteristics between men and women. Studies suggest that men more commonly develop plaques with larger lipid cores and higher levels of inflammatory activity, whereas women often exhibit plaques with greater fibrous content and relatively more stable structures. However, after menopause, plaque characteristics in women may become more similar to those observed in men, increasing the likelihood of plaque rupture and cardiovascular events [18].
In addition to biological factors, lifestyle behaviours such as dietary habits, physical activity, smoking, and alcohol consumption may also differ between sexes and contribute to variations in cardiovascular risk. Understanding these sex-specific biological and behavioural differences is essential when evaluating the relationship between diet and atherosclerosis progression. Such knowledge can help guide the development of targeted dietary and preventive strategies aimed at reducing cardiovascular disease risk in both men and women.
INFLUENCE OF DIET ON ATHEROSCLEROSIS IN MALES
Dietary habits play a significant role in determining cardiovascular risk among males and may contribute to the earlier onset of Atherosclerosis observed in men compared with women. Epidemiological studies suggest that men are more likely to consume diets rich in red meat, processed foods, saturated fats, and refined carbohydrates. These dietary patterns are associated with increased levels of low-density lipoprotein (LDL) cholesterol and triglycerides, which promote lipid accumulation within the arterial wall and accelerate atherosclerotic plaque formation [11,12].
High intake of saturated fatty acids and trans fats derived from animal-based foods and processed products can adversely affect lipid metabolism. These fats increase circulating LDL cholesterol and reduce protective high-density lipoprotein (HDL) cholesterol levels, thereby contributing to endothelial dysfunction and vascular inflammation. Chronic exposure to such dietary patterns may promote oxidative stress and enhance the inflammatory processes involved in plaque development [11,19].
In addition to unhealthy fat consumption, men often demonstrate lower intake of Fiber-rich foods such as fruits, vegetables, and whole grains compared with women. Dietary Fiber plays an important role in maintaining cardiovascular health by reducing cholesterol absorption in the intestine and improving overall lipid profiles. Furthermore, fruits and vegetables provide essential micronutrients, antioxidants, and phytochemicals that help neutralize reactive oxygen species and protect vascular endothelial cells from oxidative damage. Reduced intake of these protective nutrients may therefore increase susceptibility to atherosclerotic progression in men [12,13].
Lifestyle factors commonly associated with male populations may further compound the effects of poor dietary habits. Higher prevalence of smoking, alcohol consumption, and sedentary behaviour among men can exacerbate metabolic disturbances such as dyslipidaemia, obesity, and insulin resistance. These factors collectively contribute to chronic inflammation and endothelial injury, which are key mechanisms underlying the development of atherosclerotic lesions [20].
Evidence from population studies also suggests that dietary modification can significantly reduce cardiovascular risk in men. Increasing the intake of plant-based foods, whole grains, and unsaturated fatty acids while reducing consumption of saturated fats and processed foods has been shown to improve lipid profiles and reduce markers of inflammation. Such dietary interventions may play a critical role in preventing the early development and progression of atherosclerosis among male populations [12,14].
HORMONAL AND METABOLIC FACTORS AFFECTING SEX DIFFERENCES
Hormonal and metabolic differences between males and females play a crucial role in modulating cardiovascular risk and influencing the progression of Atherosclerosis. Sex hormones, particularly oestrogen and testosterone, regulate several physiological processes including lipid metabolism, vascular function, inflammation, and glucose homeostasis. These biological differences contribute to variations in the onset, progression, and clinical manifestations of atherosclerotic cardiovascular disease between men and women [5,16].
Oestrogen has been widely recognized for its protective effects on the cardiovascular system. It enhances endothelial function by stimulating the production of nitric oxide, a vasodilator that helps maintain vascular tone and prevents platelet aggregation. Oestrogen also exhibits antioxidant properties that reduce oxidative stress within vascular tissues. Furthermore, it favourably regulates lipid metabolism by decreasing low-density lipoprotein (LDL) cholesterol levels while increasing high-density lipoprotein (HDL) cholesterol concentrations. These combined actions help reduce lipid accumulation in arterial walls and delay the development of atherosclerotic plaques [16,22].
In contrast, testosterone exerts more complex effects on cardiovascular physiology. Moderate levels of testosterone may contribute to the maintenance of muscle mass and metabolic function; however, alterations in testosterone levels have been associated with changes in lipid metabolism and cardiovascular risk. Some studies suggest that low testosterone levels in men may be linked to metabolic syndrome, obesity, and insulin resistance, whereas excessively high levels may contribute to unfavourable lipid profiles and vascular dysfunction. Therefore, the overall impact of testosterone on atherosclerosis appears to depend on hormonal balance and metabolic context [23].
Metabolic differences between males and females also play an important role in determining cardiovascular risk. One of the most notable differences is body fat distribution. Men typically accumulate a greater proportion of visceral adipose tissue, particularly in the abdominal region. Visceral fat is metabolically active and is strongly associated with insulin resistance, systemic inflammation, and increased production of pro-inflammatory cytokines. These metabolic disturbances contribute significantly to the development of atherosclerosis and other cardiovascular diseases [21,24].
In contrast, women especially during their reproductive years tend to accumulate more subcutaneous fat, particularly in the hips and thighs. Subcutaneous adipose tissue is generally considered metabolically less harmful and may even provide some protective metabolic effects. However, after menopause, women often experience a shift toward increased visceral fat accumulation, which is associated with increased cardiovascular risk and a greater likelihood of atherosclerotic plaque development [21,24].
These hormonal and metabolic differences may also influence how dietary factors affect cardiovascular health in men and women. Nutrient metabolism, lipid responses to dietary fat intake, and inflammatory responses to dietary components may vary between sexes due to hormonal regulation and body composition differences. Consequently, understanding these biological variations is important for developing sex specific dietary strategies aimed at preventing or slowing the progression of atherosclerosis [5,22].
EPIDEMIOLOGICAL EVIDENCE FROM POPULATION STUDIES
Epidemiological studies conducted across different populations have provided important insights into the relationship between dietary habits and the risk of atherosclerosis and other cardiovascular diseases. Large-scale cohort studies and population-based investigations have consistently demonstrated that dietary patterns play a critical role in determining cardiovascular health outcomes. Individuals who adhere to healthy dietary patterns characterized by high consumption of fruits, vegetables, whole grains, legumes, and unsaturated fats tend to exhibit lower incidence of atherosclerosis and reduced rates of cardiovascular events compared with those consuming diets high in saturated fats, refined carbohydrates, and processed foods [12,14].
One of the most widely studied dietary patterns in cardiovascular epidemiology is the Mediterranean diet. Evidence from large clinical and observational studies indicates that adherence to the Mediterranean diet is associated with a significant reduction in cardiovascular morbidity and mortality. The diet emphasizes the consumption of olive oil, fruits, vegetables, nuts, legumes, whole grains, and fish while limiting red meat and processed foods. Research findings from the landmark clinical trial conducted by Ramon Estruch and colleagues demonstrated that individuals following the Mediterranean diet experienced a substantially lower risk of major cardiovascular events, including myocardial infarction and stroke [14].
Another important source of epidemiological evidence comes from large international studies examining modifiable cardiovascular risk factors. The global case–control study led by Salim Yusuf identified several key lifestyle-related risk factors contributing to myocardial infarction, including unhealthy diet, obesity, smoking, and physical inactivity. These findings highlight the strong association between dietary patterns and cardiovascular disease across diverse populations and geographic regions [20].
Sex-based differences in cardiovascular disease prevalence and progression have also been well documented in epidemiological research. Studies indicate that men generally exhibit earlier onset of atherosclerotic plaque development and greater plaque burden during middle age compared with women. This difference is often attributed to hormonal and metabolic factors, as well as differences in lifestyle behaviours including dietary habits and physical activity patterns [5,17].
Further evidence from large population-based imaging studies supports these observations and provides additional insights into age-related patterns of atherosclerosis. A major ultrasound-based investigation involving 6420 individuals aged 25–84 years demonstrated that the prevalence of carotid atherosclerosis was higher in men (55.4%) compared with women (45.8%). The prevalence increased progressively with age in both sexes; however, the pattern differed, with men showing a relatively linear increase, while women exhibited a slower rise during early adulthood followed by a sharp increase after approximately 50 years of age. In older age groups (75–84 years), the prevalence became comparable, reaching 76.5% in men and 81.2% in women, indicating a convergence of risk with advancing age [25]
In addition to differences in prevalence, important variations in plaque morphology have been reported. Among individuals with detectable plaques, soft (lipid-rich) plaques were observed in approximately 40.4% of men compared to 34.5% of women. This sex difference persisted across age groups and became more pronounced with advancing age. Since soft plaques are more prone to rupture, their higher prevalence in men may partly explain the increased risk of acute cardiovascular events such as myocardial infarction and stroke, despite similar overall plaque prevalence in older populations. [25]
However, the cardiovascular risk profile of women changes significantly after menopause. The decline in oestrogen levels is associated with unfavourable lipid profile changes, increased visceral fat accumulation, and greater susceptibility to metabolic syndrome. As a result, the incidence of coronary artery disease and other cardiovascular conditions increases markedly among postmenopausal women. Epidemiological evidence therefore suggests that although women may initially experience lower cardiovascular risk during their reproductive years, this protective advantage diminishes with age [17,21].
PREVENTIVE DIETARY STRATEGIES
The prevention and management of Atherosclerosis require a comprehensive approach that integrates dietary modification, healthy lifestyle practices, and control of metabolic risk factors. Since atherosclerosis is strongly influenced by modifiable behaviours, particularly dietary habits, preventive nutritional strategies play a crucial role in reducing cardiovascular disease risk. Health organizations and cardiovascular guidelines recommend limiting the intake of saturated fats, trans fats, dietary cholesterol, and refined carbohydrates while increasing the consumption of plant-based foods, whole grains, legumes, nuts, and lean protein sources [11,12].
Reducing dietary intake of saturated and trans fats is particularly important for improving lipid profiles. These fats are known to elevate levels of low-density lipoprotein (LDL) cholesterol, which contributes to lipid deposition in arterial walls and promotes plaque formation. Replacing saturated fats with unsaturated fats such as monounsaturated and polyunsaturated fatty acids has been shown to lower LDL cholesterol levels and improve cardiovascular outcomes. Foods rich in unsaturated fats, including olive oil, nuts, seeds, and fatty fish, are therefore recommended as part of a heart healthy diet [11,19].
Among the dietary patterns that have demonstrated strong cardioprotective effects, the Mediterranean diet is one of the most extensively studied. This dietary pattern emphasizes high intake of fruits, vegetables, whole grains, legumes, nuts, and olive oil, along with moderate consumption of fish and limited intake of red meat and processed foods. Clinical trials have shown that adherence to the Mediterranean diet significantly reduces the incidence of major cardiovascular events such as myocardial infarction and stroke. The beneficial effects of this diet are attributed to its high content of antioxidants, dietary Fiber, and healthy fats that help reduce inflammation and improve lipid metabolism [14].
Another well-established preventive dietary approach is the Dietary Approaches to Stop Hypertension (DASH) diet. The DASH diet focuses on increasing the intake of fruits, vegetables, low-fat dairy products, whole grains, and lean protein while reducing sodium and saturated fat consumption. This dietary pattern has been shown to effectively lower blood pressure, improve lipid profiles, and reduce overall cardiovascular risk, making it an important strategy for preventing atherosclerosis and related cardiovascular complications [15].
In addition to dietary modifications, lifestyle interventions play an essential role in cardiovascular prevention. Maintaining a healthy body weight, engaging in regular physical activity, and avoiding tobacco use are key strategies for reducing the risk of atherosclerosis. Physical activity improves lipid metabolism, enhances endothelial function, and reduces systemic inflammation, while smoking cessation helps prevent vascular damage and oxidative stress. When combined with healthy dietary habits, these lifestyle measures can significantly reduce the incidence and progression of atherosclerotic cardiovascular disease [20].
FUTURE PERSPECTIVES
Future research on Atherosclerosis should focus on understanding the complex interactions between dietary habits, biological sex, genetic factors, and metabolic pathways that influence disease progression. Although considerable progress has been made in identifying the role of diet in cardiovascular health, many aspects of how sex-specific biological mechanisms interact with nutritional factors remain insufficiently understood. Further investigation into these mechanisms may provide deeper insights into the development of targeted preventive and therapeutic strategies for atherosclerosis [5,10].
One promising area of research involves the application of personalized nutrition approaches in cardiovascular disease prevention. Personalized nutrition aims to design dietary interventions based on individual characteristics such as genetic background, metabolic status, hormonal profiles, and lifestyle factors. Because males and females exhibit differences in hormone levels, body composition, and metabolic responses to nutrients, personalized dietary strategies may offer more effective ways to prevent or slow the progression of atherosclerosis. Advances in nutrigenomics and metabolomics may help researchers better understand how specific nutrients influence gene expression and metabolic pathways related to cardiovascular health [12,13].
Another important direction for future research is the investigation of sex-specific responses to dietary interventions. While many dietary recommendations for cardiovascular health are currently generalized, growing evidence suggests that men and women may respond differently to certain nutrients and dietary patterns. For example, hormonal regulation may influence lipid metabolism, inflammatory responses, and endothelial function, which may alter how dietary components affect cardiovascular risk in each sex. Therefore, future clinical trials and epidemiological studies should incorporate sex-specific analyses in order to develop more effective dietary guidelines [5,17].
Emerging technologies and advanced research methodologies may also contribute significantly to the understanding of atherosclerosis. Modern imaging techniques, molecular biomarkers, and systems biology approaches allow researchers to study the progression of atherosclerotic plaques with greater precision. These tools may help identify early indicators of disease development and evaluate the long-term effects of dietary interventions on vascular health [10].
Furthermore, public health strategies aimed at improving global cardiovascular health should emphasize the importance of healthy dietary patterns and lifestyle modifications. Increasing awareness of the role of nutrition in cardiovascular disease prevention, along with promoting balanced diets rich in plant-based foods and healthy fats, may help reduce the global burden of atherosclerosis. Integrating sex-specific considerations into these public health approaches may further enhance the effectiveness of prevention programs [20] .
CONCLUSION
In conclusion, dietary habits play a critical role in the development and progression of Atherosclerosis, which is one of the primary underlying causes of cardiovascular diseases worldwide. Unhealthy dietary patterns characterized by high consumption of saturated fats, trans fats, refined carbohydrates, and processed foods contribute to dyslipidaemia, oxidative stress, and chronic inflammation, all of which accelerate atherosclerotic plaque formation. In contrast, diets rich in fruits, vegetables, whole grains, legumes, nuts, and healthy unsaturated fats provide protective effects by improving lipid metabolism, reducing oxidative stress, and enhancing endothelial function
Evidence from epidemiological and clinical studies also indicates that the influence of dietary habits on cardiovascular health may vary between males and females. Biological sex differences, including variations in hormonal regulation, metabolic responses, and body fat distribution, significantly affect the progression and clinical manifestation of atherosclerosis. For instance, oestrogen provides protective cardiovascular effects in premenopausal women by improving lipid profiles and promoting vascular health, whereas the decline of oestrogen after menopause is associated with increased cardiovascular risk
Furthermore, lifestyle factors such as dietary patterns, physical activity, and smoking behaviour may differ between sexes and contribute to variations in cardiovascular risk profiles. Understanding these sex based differences is therefore essential for developing targeted prevention strategies and dietary recommendations aimed at reducing the burden of cardiovascular disease
REFERENCES
Muhammed Anas P, Syamjith P, Anson S Maroky, Differential Impact of Dietary Habits on the Progression of Atherosclerosis : A Sex Based Comparative Review, Int. J. of Pharm. Sci., 2026, Vol 4, Issue 4, 3555-3567. https://doi.org/10.5281/zenodo.19684405
10.5281/zenodo.19684405
