Understanding the Arteriometabolic Module in Chronic Disease Prevention
Chronic diseases such as cardiovascular disease, type 2 diabetes, and atherosclerosis represent leading causes of morbidity and mortality worldwide. Emerging research into the Arteriometabolic Module reveals the dynamic interplay between arterial and metabolic health in disease prevention. This article examines the scientific mechanisms, lifestyle interventions, and systemic approaches that the module encapsulates, providing a comprehensive framework for reducing chronic disease risk.
Defining the Arteriometabolic Module: A Holistic Approach to Cardiometabolic Health
What characterizes a chronic disease of the arterial system such as atherosclerosis?
Atherosclerosis is a long-term inflammatory condition affecting the arterial walls. It involves the buildup of lipid-rich plaques, primarily composed of oxidized LDL cholesterol, which can narrow arteries and restrict blood flow. The disease process starts with fatty streaks that gradually develop into fibrous, complex plaques. These plaques are vulnerable to rupture, which can lead to blood clots, occluding arteries and causing heart attacks or strokes.
Risk factors for atherosclerosis are diverse and include high cholesterol levels, high blood pressure, smoking, diabetes, obesity, and genetic tendencies. The progression of this disease underscores its intertwined nature with metabolic disturbances, highlighting the importance of a comprehensive approach that considers both arterial and metabolic health.
What is the Arteriometabolic Module?
The Arteriometabolic Module is an integrated framework aimed at preventing and managing chronic diseases such as atherosclerosis by addressing both vascular (arterial) health and metabolic function. This model recognizes that arterial disease seldom occurs in isolation; instead, it often shares common pathways with metabolic disorders like diabetes, hypertension, and dyslipidemia.
By combining these elements, the module advocates for early detection strategies—such as biomarkers, imaging, and risk calculators—and personalized interventions. These interventions include lifestyle modifications, targeted medications, and community-based programs aimed at improving overall cardiovascular health.
How does the module integrate arterial and metabolic risk factors?
Integration is achieved through a comprehensive risk assessment, which considers traditional factors like blood pressure, lipid profiles, blood glucose levels, and new insights from metabolomics and microvascular health. It promotes a combined monitoring approach that can identify individuals at high risk before clinical symptoms appear.
Prevention strategies focus on controlling blood pressure, cholesterol, blood sugar, and inflammatory markers simultaneously. Lifestyle interventions such as diet, physical activity, and stress management are tailored to modulate metabolic pathways (e.g., reducing inflammation and improving mitochondrial function) and arterial resilience.
What early detection and management strategies are involved?
Early detection involves advanced biomarkers and imaging techniques to assess arterial health and metabolic status accurately. Risk calculators, like PREVENT™, help clinicians estimate long-term risks and prioritize interventions.
Management strategies emphasize lifestyle interventions—adopting plant-based or Mediterranean diets, increasing physical activity, and reducing sedentary behavior. Medications targeting specific pathways, such as statins or anti-inflammatory agents, are also integral.
Collaborative care models that include primary care, cardiology, endocrinology, and community resources are crucial. Such coordinated approaches aim to slow disease progression, promote vascular repair, and address underlying metabolic disturbances, ultimately reducing the burden of chronic arterial and metabolic diseases.
The Interplay Between Metabolic Diseases and Cardiovascular Risk
How do metabolic diseases increase the risk of developing cardiovascular disease?
Metabolic diseases significantly elevate the risk of cardiovascular conditions primarily through a network of interrelated metabolic abnormalities. Central to this is metabolic syndrome, characterized by a cluster of risk factors including abdominal obesity, insulin resistance, and dyslipidemia.
These factors collectively contribute to vascular damage by promoting endothelial dysfunction—the impairment of blood vessel lining—which facilitates the development of atherosclerotic plaques. Elevated blood pressure and blood glucose levels further intensify inflammation and oxidative stress within blood vessels, accelerating plaque buildup.
Research indicates that metabolites like citrate and succinate serve as modulators of inflammation, influencing plaque stability. Metabolic reprogramming in immune cells such as macrophages and T cells, driven by increased glycolysis and altered amino acid metabolism, fuels chronic inflammation in plaques.
Sedentary lifestyles and chronic stress conditions exacerbate these risks by promoting increased visceral fat accumulation and dysregulated metabolic pathways. These lifestyle-related factors not only worsen insulin resistance but also contribute to a pro-inflammatory state that predisposes individuals to heart attacks, strokes, and other cardiovascular events.
In summary, metabolic syndrome's interconnected disturbances—obesity, insulin resistance, dyslipidemia, and hypertension—create a conducive environment for arterial damage and disease progression. Early detection and targeted lifestyle modifications can mitigate these risks, highlighting the importance of integrated metabolic and cardiovascular health management.
Metabolic Factors | Effect on Cardiovascular Risk | Underlying Mechanism |
---|---|---|
Abdominal Obesity | Increased risk | Promotes inflammation and endothelial dysfunction |
Insulin Resistance | Elevated risk | Facilitates a pro-inflammatory environment |
Dyslipidemia | Accelerates plaque formation | Leads to high LDL and low HDL cholesterol levels |
Elevated Blood Pressure | Damages blood vessel walls | Causes mechanical stress and promotes atherosclerosis |
High Blood Glucose | Promotes vascular damage | Glycation end-products and inflammation |
By addressing these metabolic imbalances through lifestyle and pharmacological interventions, it is possible to reduce the burden of cardiovascular disease associated with metabolic disorders.
Chronic Diseases Linked to Metabolic Syndrome
What chronic diseases are associated with metabolic syndrome?
Metabolic syndrome is a cluster of conditions that together increase the risk for various chronic diseases. These include major illnesses such as heart disease, stroke, and type 2 diabetes. People with metabolic syndrome often experience associated complications like high blood pressure (hypertension) and abnormal cholesterol levels (dyslipidemia). Additionally, research indicates a strong link between metabolic syndrome and neurodegenerative conditions like dementia, including Alzheimer's disease.
The central feature of metabolic syndrome is excess fat around the abdomen, known as central adiposity. This helps fuel processes like inflammation and insulin resistance, which drive the progression of various diseases. The interconnected nature of these conditions underscores how managing metabolic syndrome is critical to preventing a wide array of health problems.
How does metabolic syndrome influence cardiovascular health?
Metabolic syndrome significantly impacts cardiovascular health by promoting the buildup of plaques in arteries (atherosclerosis), which can lead to heart attacks and strokes. Elevated blood sugar levels and high triglycerides, along with increased blood pressure, create a hostile environment for blood vessels.
Studies show that individuals with metabolic syndrome have a higher likelihood of heart failure and peripheral artery disease. Proper management, including lifestyle interventions and medications, can reduce these risks and improve cardiovascular outcomes.
Impact on diabetes and cognitive functions
Type 2 diabetes is closely tied to metabolic syndrome due to insulin resistance. The persistent high blood sugar damages blood vessels and nerves, leading to complications such as kidney disease, vision loss, and nerve problems.
Recent evidence also links metabolic syndrome with increased risk of cognitive decline and dementia. Chronic inflammation and vascular damage contribute to neurodegenerative changes, making early detection and thorough management vital.
Check the comprehensive table below for an overview of diseases, underlying factors, and possible interventions.
Disease Type | Key Features | Underlying Factors | Potential Interventions |
---|---|---|---|
Cardiovascular Disease | Atherosclerosis, heart attack, stroke | Dyslipidemia, hypertension, obesity | Lifestyle changes, medications, metabolic control |
Type 2 Diabetes | Insulin resistance, hyperglycemia | Obesity, sedentary lifestyle | Diet, physical activity, glucose monitoring |
Dementia & Cognitive Decline | Memory loss, vascular damage | Chronic inflammation, vascular issues | Cognitive exercises, inflammation control, lifestyle management |
Addressing metabolic syndrome early through lifestyle modifications—such as diet, exercise, and weight management—can prevent or delay these chronic conditions. Emerging therapies targeting metabolic pathways show promise in reducing the burden of related diseases, highlighting the importance of integrated prevention strategies.
Immunometabolism: Linking Immune Function and Metabolic Regulation in Atherosclerosis
What is immunometabolism and why is it important?
Immunometabolism is an emerging field that explores how immune cells reprogram their metabolic pathways to support their functions during health and disease. It reveals that metabolites—once thought to be only fuels—also act as signaling molecules influencing immune responses.
This knowledge is particularly important in conditions like atherosclerosis, a chronic inflammatory disease of the arteries. Understanding how immune cell metabolism affects disease progression opens new avenues for targeted therapies that could prevent or slow cardiovascular disease.
How do immune cells utilize metabolic pathways?
Immune cells, especially macrophages and T cells, undergo significant metabolic changes when they become activated. For instance, in inflamed or unstable atherosclerotic plaques, these cells tend to increase glycolysis—the breakdown of glucose for quick energy. This shift supports their inflammatory functions but also promotes plaque growth and instability.
Conversely, higher levels of oxidative phosphorylation (OXPHOS) and fatty acid oxidation are associated with anti-inflammatory states. Promoting these pathways might help reduce inflammation and limit plaque development.
How do these metabolic pathways influence plaque development?
In atherosclerosis, immune cells within plaques show increased glucose uptake and glycolytic activity, especially in areas of active inflammation. This metabolic reprogramming fuels the inflammatory response, contributing to lipid accumulation, cell death, and plaque instability.
Interventions targeting these metabolic shifts—such as inhibiting glycolysis or enhancing fatty acid oxidation—are potential strategies to stabilize plaques and prevent cardiovascular events.
What role do metabolites and enzymes play?
Metabolites like citrate and succinate, and enzymes such as ACOD1 (which produces itaconate), are active participants in immune regulation. For example, itaconate has anti-inflammatory properties and can protect against atherosclerosis.
Additionally, gut microbiome-derived metabolites like trimethylamine N-oxide (TMAO) influence immune responses and are linked to increased cardiovascular risk, highlighting the complex interplay between metabolism, microbes, and inflammation.
Can targeting immunometabolism improve cardiovascular health?
Yes. Clinical trials using anti-inflammatory drugs such as IL-1β antibodies and colchicine have demonstrated improvements in cardiovascular outcomes, further confirming that immune system modulation affects disease.
Future therapies may involve metabolic reprogramming of immune cells—either by activating protective pathways like fatty acid oxidation or suppressing harmful glycolytic activity—to stabilize plaques and reduce cardiovascular events.
Pathway | Effect on Inflammation | Potential Impact on Atherosclerosis | Key Metabolites/Enzymes |
---|---|---|---|
Glycolysis | Promotes inflammation | Accelerates plaque growth | Glucose, lactate, HIF-1α |
Oxidative Phosphorylation | Anti-inflammatory | May limit plaque progression | NADH, FADH2, mitochondrial enzymes |
Fatty Acid Oxidation | Reduces inflammation | Helps stabilize plaques | Carnitine, CPT1 enzyme |
Metabolites (e.g., succinate, citrate) | Regulate immune response | Influence inflammation status | Succinate, citrate, itaconate |
Understanding and manipulating these metabolic pathways could be transformative in cardiovascular disease management, potentially leading to innovative treatments that address the root cause of inflammation in atherosclerosis.
Metabolic Reprogramming of Immune Cells and Its Impact on Vascular Inflammation
How do glycolysis and oxidative phosphorylation in macrophages and T cells influence atherosclerosis?
Immune cells, particularly macrophages and T lymphocytes, play a central role in the development of atherosclerosis. Their metabolic activity—especially how they produce energy—significantly affects their behavior within plaques.
In inflamed or unstable plaques, immune cells tend to increase glucose uptake, favoring glycolysis—the breakdown of glucose into lactate even when oxygen is abundant. This metabolic shift supports rapid energy needs and promotes an inflammatory phenotype. Conversely, high levels of oxidative phosphorylation (OXPHOS) and fatty acid oxidation (FAO), processes that generate energy in the presence of oxygen, are associated with more regulated, anti-inflammatory immune states.
How do metabolic shifts influence immune cell phenotype?
The balance between glycolysis and OXPHOS determines immune cell activation, polarization, and function. Macrophages, for example, can shift between pro-inflammatory (M1-like) and anti-inflammatory (M2-like) states depending on their metabolic pathways.
Pro-inflammatory macrophages predominantly rely on glycolysis, producing inflammatory mediators such as cytokines and reactive oxygen species. On the other hand, macrophages engaging in OXPHOS and fatty acid oxidation tend to promote tissue repair and stabilization of plaques.
T cells also undergo metabolic reprogramming: effector T cells (Teffs) depend on glycolysis, fueling rapid proliferation and cytokine production. Regulatory T cells (Tregs), which help control inflammation, primarily utilize OXPHOS, supporting their suppressive functions.
What is the effect of these metabolic processes on plaque stability and inflammation?
Metabolites generated during these processes, such as citrate and succinate, influence inflammation at the molecular level. Increased glycolysis correlates with heightened inflammatory responses and lipid accumulation in plaques, promoting instability and a higher risk of rupture.
Interestingly, promoting metabolic pathways like OXPHOS and fatty acid oxidation appears to reduce inflammation and may slow or prevent plaque progression. Interventions targeting key enzymes in these pathways—such as inhibiting glycolysis—could modulate immune cell behavior.
Furthermore, enzymes like ACOD1, which produces itaconate, have protective roles by dampening inflammation. Understanding these metabolic shifts offers promising strategies for therapies aimed at stabilizing plaques and reducing cardiovascular events.
In sum, the metabolic state of immune cells within arterial plaques determines their phenotype and activity, directly impacting the inflammation process that underlies atherosclerosis progression.
Metabolites as Modulators of Vascular Health and Disease
What roles do citrate, succinate, and itaconate play in atherosclerosis?
Metabolites such as citrate and succinate, generated in the TCA cycle, serve more than just energy sources. Citrate contributes to lipid synthesis and can influence inflammatory responses within plaques. Succinate, on the other hand, accumulates in hypoxic conditions common in inflamed plaques, promoting inflammation by stabilizing hypoxia-inducible factors (HIFs). Itaconate, produced by the enzyme ACOD1, has emerged as a protective agent, modulating inflammation and oxidative stress.
How does lipid signaling and microbiota-derived metabolites influence vascular inflammation?
Lipids function as signaling molecules that can either promote or inhibit inflammation within the vessel walls. Certain lipids derived from the gut microbiota, such as trimethylamine N-oxide (TMAO), are linked with increased atherosclerosis risk. Conversely, short-chain fatty acids (SCFAs) produced by beneficial gut bacteria can exert anti-inflammatory effects, helping to stabilize plaques and improve overall vascular health.
What is the therapeutic potential of targeting metabolic enzymes like ACOD1?
Targeting enzymes involved in immune cell metabolism offers new avenues for therapy. For instance, ACOD1, which catalyzes the production of itaconate, has anti-inflammatory properties that can reduce vascular inflammation. Modulating ACOD1 activity or supplementing itaconate could help limit plaque progression and promote plaque stability, representing promising targets for cardiovascular disease treatment.
Metabolite/Enzyme | Function | Impact on Atherosclerosis | Potential Therapeutic Approach |
---|---|---|---|
Citrate | Lipid synthesis, inflammation modulation | Promotes lipid accumulation if dysregulated | Modulate citrate pathway, inhibit excess accumulation |
Succinate | Stabilizes HIFs, promotes inflammation | Increases inflammation under hypoxia | Block succinate signaling, stabilize metabolic balance |
Itaconate (via ACOD1) | Anti-inflammatory, oxidative stress reduction | Limits inflammation, supports plaque stability | Enhance ACOD1 activity, supplement itaconate |
Immunometabolism continues to uncover the complex interplay between metabolism and vascular inflammation. By understanding and modulating these metabolic pathways, new strategies may emerge to prevent or treat atherosclerosis.
Targeting Immunometabolism for Cardiovascular Disease Therapeutics
What strategies can be used to alter immune cell metabolism in atherosclerosis?
Therapeutic approaches aim to modify immune cell metabolism by targeting pathways like glycolysis and fatty acid oxidation that influence inflammation within plaques. Increasing oxidative phosphorylation (OXPHOS) and fatty acid oxidation in immune cells such as macrophages and T cells appears to decrease inflammation and potentially slow disease progression.
Interventions include inhibiting glycolysis, which is often upregulated in inflamed immune cells, and modulating specific metabolic enzymes involved in energy generation and lipid synthesis. These tactics aim to shift immune cells from a pro-inflammatory to a more reparative state, thereby stabilizing plaques and reducing the risk of acute events.
How are anti-inflammatory agents being used in clinical trials?
Clinical trials have demonstrated the potential benefits of immune modulation in cardiovascular disease.
For example, anti-IL-1β antibodies like canakinumab have been shown to reduce recurrent cardiovascular events in high-risk patients. Colchicine, an anti-inflammatory drug, is also being tested for its capacity to reduce vascular inflammation and plaque instability.
These therapies highlight that controlling immune cell activity through metabolic pathways can influence disease outcomes, supporting the concept of immunometabolism as a therapeutic target.
What is the potential of metabolic enzyme inhibitors?
Targeting specific enzymes involved in immune cell metabolic reprogramming offers promising therapeutic avenues. For instance, inhibitors of glycolytic enzymes could reduce excessive immune cell activation, while compounds that enhance fatty acid oxidation might promote anti-inflammatory phenotypes.
A notable enzyme is ACOD1, which produces itaconate. This metabolite possesses anti-inflammatory effects and offers protection against atherosclerosis. Drugs designed to modulate the activity of such enzymes could fine-tune immune responses, promoting plaque stability and preventing disease progression.
Overall, the development of metabolic enzyme inhibitors represents a frontier in cardiovascular immunotherapy, aiming to reprogram immune cells and mitigate vascular inflammation.
Lifestyle 180 Program: Integrative Lifestyle Intervention for Cardiometabolic Health
How do lifestyle factors contribute to the development and prevention of chronic and noncommunicable diseases?
Lifestyle choices such as diet, physical activity, sleep, and avoidance of tobacco critically influence the risk of developing chronic and noncommunicable diseases. Unhealthy diets rich in red meats, sugars, and saturated fats, combined with sedentary behaviors, increase the likelihood of conditions like hypertension, obesity, type 2 diabetes, and systemic inflammation. These factors promote metabolic disturbances and vascular damage, leading to diseases such as atherosclerosis.
Conversely, implementing a balanced diet, engaging in regular physical activity, managing stress, and ensuring good sleep quality serve as powerful strategies for prevention. These behaviors help improve metabolic health, reduce inflammation, and maintain healthy weight and blood pressure levels. Evidence shows that comprehensive lifestyle modifications can not only prevent disease onset but also stabilize or reverse existing disease progression.
The Lifestyle 180 program exemplifies an effective approach by combining these elements into an integrative intervention. Participants typically experience significant improvements in biometric measures such as weight, waist circumference, blood pressure, and resting heart rate. Laboratory outcomes like fasting glucose, triglycerides, LDL cholesterol, and inflammatory markers also show meaningful reductions. Such improvements contribute to lowering the prevalence of metabolic syndrome, which decreased from 54% to 37% among participants over six months.
Moreover, many participants reduce their medication reliance, with some able to avoid or decrease treatments for diabetes, hyperlipidemia, and hypertension. These results demonstrate that lifestyle modifications influenced by programs like Lifestyle 180 are powerful tools for both primary and secondary prevention of cardiometabolic diseases.
Components: nutrition, exercise, stress management
The program emphasizes a holistic approach, integrating personalized nutrition plans—such as plant-based and Mediterranean diets—alongside tailored physical activity routines that include aerobic exercises, resistance training, and high-intensity interval training (HIIT). Stress management techniques, including mindfulness and relaxation practices, are incorporated to address psychological factors affecting health.
This multi-dimensional strategy fosters sustainable health behaviors, reduces disease risk factors, and promotes overall cardiovascular resilience.
Observed biometric and laboratory improvements
Within just six weeks of engagement, participants showed a notable decrease in weight, waist circumference, blood pressure, and resting heart rate. Laboratory markers including fasting blood glucose, triglycerides, LDL cholesterol, hemoglobin A1c, insulin levels, and C-reactive protein also improved early in the program. These effects were largely sustained at the six-month mark, highlighting the durability of lifestyle interventions.
Health improvements at the biometric and biochemical levels translated into a tangible reduction in health risks. The number of individuals meeting criteria for metabolic syndrome fell significantly, and many achieved normal levels in previously abnormal measures.
Effect on metabolic syndrome prevalence and medication use
A substantial outcome of the Lifestyle 180 program was the reduction in metabolic syndrome prevalence by approximately 17%, representing a meaningful decrease in overall cardiovascular risk. Additionally, medication adjustments were common, with some participants reducing or eliminating pharmacologic therapies for diabetes, lipid disorders, and hypertension.
This demonstrates the potential for lifestyle interventions to not only improve individual health metrics but also reduce healthcare costs and medication side effects. Early results suggest that sustained lifestyle changes can facilitate long-term disease control and enhance quality of life.
More insights on lifestyle interventions improving cardiometabolic outcomes
Research consistently supports that structured lifestyle programs lead to measurable improvements in cardiovascular and metabolic health. These benefits include better glycemic control, decreased blood pressure, improved lipid profiles, and reduced systemic inflammation. Multifaceted programs that incorporate dietary guidance, increasing physical activity, and stress reduction outperform isolated interventions.
The success of programs like Lifestyle 180 underscores the importance of personalized, comprehensive lifestyle modification frameworks as cornerstones of chronic disease prevention and management.
Social Determinants and Environmental Networks Influencing Chronic Disease
How do macroenvironment and social factors influence chronic disease development?
The macroenvironment, including social and cultural factors, plays a foundational role in shaping health outcomes. These broad influences impact individual behaviors, access to resources, and community norms. For instance, socioeconomic status, education, and cultural beliefs can affect diet, physical activity, and healthcare utilization. Disparities driven by these factors often lead to increased risk of chronic conditions such as cardiovascular disease and diabetes.
Further, social determinants like food insecurity and community safety influence lifestyle choices. Limited access to healthy foods or safe places for exercise may lead to poor health behaviors, fostering metabolic and arterial risks that contribute to disease progression.
Understanding these external influences emphasizes the importance of multisector strategies, integrating policy changes and community programs, to modify environments conducive to healthier lifestyles.
How do immune, neuroendocrine, and microbiome factors interact in disease processes?
The immune, neuroendocrine, and microbiome systems form a complex network that influences chronic disease development. These systems communicate through signaling molecules like hormones, cytokines, and microbial metabolites, which modulate immune responses and metabolic pathways.
For example, stress activates the neuroendocrine system, releasing cortisol and other mediators that can suppress or alter immune function, promoting low-grade inflammation—a hallmark of many chronic diseases. Simultaneously, the microbiome produces metabolites such as short-chain fatty acids that help regulate inflammation and immune cell activity.
Disruptions in these interactions, caused by environmental factors, poor diet, or microbiome imbalance, can lead to persistent inflammation, tissue damage, and disease progression, especially within vascular and metabolic tissues.
How does interstitial cell behavior affect chronic inflammation?
Interstitial cells, including macrophages and fibroblasts, are central to maintaining tissue health or driving disease. Their behavior is influenced by external signals from the environment and internal metabolic cues.
In the context of unhealthy lifestyles, these cells often shift phenotypes toward pro-inflammatory states. Macrophages can become activated, secreting cytokines that perpetuate inflammation within blood vessels, leading to plaque formation and instability in atherosclerosis.
Similarly, fibroblast activation contributes to fibrosis and tissue stiffening, impairing organ function. This dysregulation creates a cycle of low-grade inflammation, microvascular damage, and tissue remodeling.
Targeting interstitial cell phenotypes and functions offers promising avenues to prevent or reverse chronic disease processes by restoring tissue homeostasis and reducing inflammation.
Chronic Low-Grade Inflammation: The Stalled Healing Process in Disease Progression
Role of macrophages and fibroblast dysregulation
Chronic low-grade inflammation (SCI) often starts when interstitial cells like macrophages and fibroblasts become dysregulated. Normally, these cells help repair tissues and maintain healthy balance. However, when they behave abnormally, it leads to a persistent inflammatory state.
In particular, macrophages can shift between different phenotypes, such as pro-inflammatory (M1) or anti-inflammatory (M2). Dysregulated macrophages tend to stay in a pro-inflammatory state, releasing cytokines that promote tissue damage and contribute to plaque growth in arteries.
Fibroblasts, which are essential for tissue repair and extracellular matrix production, can also become overactive. This results in fibrosis, a thickening and stiffening of tissues that impairs normal function. This imbalance perpetuates a cycle of ongoing inflammation that stalls healing rather than resolving it.
Fibrosis and microvascular damage
When dysregulated fibroblasts produce excess extracellular matrix, fibrosis occurs. This scar-like tissue disrupts the normal architecture of blood vessels and organs, impairing blood flow and promoting microvascular damage.
Microvascular damage is critical in atherosclerosis, as it contributes to unstable plaques and tissue ischemia. The persistent inflammation damages the small vessels, reducing oxygen and nutrient delivery. This damage further sustains inflammation, creating a vicious cycle that can escalate to more severe cardiovascular and metabolic diseases.
Salutogenic approaches to restore health
Addressing this stalled healing process involves salutogenic, or health-promoting, strategies. These focus on restoring the balance of immune and interstitial cell functions.
Lifestyle modifications like nutritious diets, regular physical activity, and stress reduction can reduce systemic inflammation. Pharmacologic interventions targeting inflammatory pathways and specific enzymes involved in macrophage and fibroblast activation are also being explored.
The goal is to shift the inflammatory response from a chronic, harmful state to a healthy, resolving one. Supporting the body's natural healing capacity can prevent the progression of diseases like atherosclerosis and diabetes, ultimately leading to better health outcomes.
Personalized Therapeutic Lifestyle Changes in Cardiometabolic Risk Reduction
Impact on waist circumference, blood pressure, glucose control
Implementing personalized lifestyle changes can significantly improve various cardiovascular risk factors. Participants often see reductions in waist circumference, which is a critical marker of metabolic health. Additionally, targeted interventions can lead to lower blood pressure levels and better control of fasting blood glucose and insulin levels. These improvements collectively diminish the risk of developing or worsening conditions like hypertension, diabetes, and dyslipidemia.
Reversion of abnormal findings
Studies demonstrate that a substantial portion of individuals can reverse abnormal health markers through tailored lifestyle modifications. In a notable 2021 study, up to half of the participants who initially presented with conditions like high blood pressure, elevated blood glucose, or high cholesterol experienced normalization of these parameters within six months. Some individuals achieved even more remarkable results, losing over 5% or 10% of their initial body weight, further enhancing their cardiovascular health.
Importance of early detection and lifestyle modification
Early identification of metabolic and arterial risk factors is crucial. Detecting these issues beforehand allows clinicians to initiate personalized lifestyle interventions promptly, which can slow or even halt the progression of cardiovascular disease. Modifications such as adopting a Mediterranean or plant-based diet, increasing physical activity, and improving sleep patterns have proven effective in stabilizing or reducing disease risk.
By focusing on early intervention, not only can disease progression be slowed, but many individuals can return to healthier states without the need for medications. The approach emphasizes the importance of customizing lifestyle changes to each individual's unique health profile, facilitating better adherence and more substantial health benefits.
Dietary Patterns and Their Effects on Cardiometabolic Health
Benefits of Mediterranean and Plant-Based Diets
Consuming diets rich in plant-based foods and the Mediterranean style has been consistently linked to lower risks of cardiovascular disease and improved overall metabolic health. These diets emphasize fruits, vegetables, whole grains, nuts, and healthy fats like olive oil, which together help reduce inflammation and oxidative stress. Meta-analyses show that high adherence to a Mediterranean diet can lower all-cause mortality by 23% and cardiovascular-related deaths by 27%. Such eating patterns support healthy lipid profiles, blood pressure, and glucose levels, contributing to the stabilization of atherosclerotic plaques.
Anti-inflammatory Herbs and Spices
Certain herbs and spices, including cinnamon, turmeric, ginger, cumin, and saffron, possess anti-inflammatory properties. These foods contain bioactive compounds that can modulate immune responses and reduce chronic low-grade inflammation — a driver of atherosclerosis and metabolic syndrome. Incorporating these spices into daily meals can enhance diet quality and offer additional vascular protection, making them valuable components of a heart-healthy lifestyle.
Risks of Pro-Inflammatory Diets
Conversely, diets characterized by high intakes of red meat, refined grains, sugars, and saturated fats are associated with increased inflammation and enhanced lipid accumulation within plaques. Such pro-inflammatory diets contribute to endothelial dysfunction and promote immune cell activation in plaques, accelerating disease progression. Avoiding overly processed foods and reducing red and processed meat consumption are recommended to lower cardiovascular risk.
Dietary Pattern | Health Impact | Notable Components | Additional Insights |
---|---|---|---|
Mediterranean | Reduces CVD and mortality | Olive oil, vegetables, fish | Enhances lipid profiles and reduces inflammation |
Plant-Based | Lowers inflammation and CVD risk | Fruits, legumes, nuts | Supports metabolic health and weight control |
Pro-Inflammatory | Increases CVD risk | Red meats, refined carbs | Promotes endothelial damage and plaque instability |
Physical Activity and Sedentary Behavior: Dual Influences on Cardiovascular Risk
What are the recommended physical activity guidelines?
Health authorities, including the American Heart Association, recommend at least 150 minutes of moderate-intensity aerobic activity each week, complemented by resistance training and flexibility exercises. These guidelines aim to improve cardiovascular health, control weight, and reduce the risk of chronic diseases. Short bouts of activity—like brisk walking—are effective and accessible options.
How does high-intensity interval training (HIIT) compare to moderate exercise?
Recent studies suggest that HIIT can be more effective than moderate continuous exercise for improving cardiorespiratory fitness and lowering blood pressure, especially in hypertensive individuals. HIIT involves short bursts of intense activity followed by recovery periods, which increases the efficiency of workouts and can lead to more significant metabolic improvements.
What strategies can help reduce sedentary time?
Reducing sitting time is crucial for cardiovascular health. Simple strategies include taking short breaks every 30 minutes, incorporating standing meetings, using sit-stand desks, and walking or stretching during work hours. Regular movement breaks decrease the adverse effects of prolonged inactivity and promote overall metabolic health.
Strategy | Description | Additional Benefits |
---|---|---|
Movement breaks | Interrupt sitting every 30 mins with light activity | Reduces risk of cardiovascular disease and metabolic syndrome |
Standing desks | Alternate between sitting and standing at work | Enhances posture, increases calorie expenditure |
Walking meetings | Conduct meetings on the move | Boosts creativity, improves circulation |
Active commutes | Walk or cycle instead of driving | Combines exercise with transport, reduces stress |
Incorporating these practices into daily routines can significantly enhance cardiovascular outcomes. Personalizing activity levels and reducing sedentary behavior are vital steps toward healthier lives.
Sleep Quality, Circadian Rhythms, and Cardiometabolic Health
What are the effects of sleep duration extremes?
Both insufficient and excessive sleep are linked to increased health risks. Sleeping less than six hours or more than eight hours per night has been associated with heightened risks of developing metabolic syndrome, obesity, and high blood pressure. These conditions are significant contributors to cardiovascular disease.
Research indicates that short sleep duration can lead to elevated cortisol levels, insulin resistance, and increased appetite, all of which promote weight gain and metabolic disturbances. Conversely, long sleep durations may reflect underlying health problems or sleep disorders, which can exacerbate inflammation and impair cardiovascular function.
How does insomnia and circadian disruption affect heart health?
Insomnia, along with irregular sleep schedules such as those caused by daylight saving time changes, can increase the risk of acute myocardial infarction. Disrupted circadian rhythms alter sympathetic nervous system activity and hormone release, contributing to increased blood pressure and heart rate variability.
Circadian misalignment has been shown to impair lipid metabolism and promote vascular inflammation, fostering the development and progression of atherosclerosis. Such disturbances can also interfere with restorative sleep processes crucial for vascular health.
What are current recommendations for cardiovascular prevention?
Healthcare providers emphasize improving sleep hygiene, maintaining regular sleep-wake schedules, and avoiding sleep deprivation or excessive sleep as part of a comprehensive cardiovascular prevention strategy. Ensuring at least 7 hours of quality sleep per night can reduce inflammatory markers and metabolic dysregulation.
Additionally, addressing sleep disorders like sleep apnea through appropriate intervention can significantly lower cardiovascular risk. Lifestyle modifications, including stress management and limiting stimulant use before bedtime, further support better sleep and overall vascular health.
Incorporating sleep assessments into routine care and educating patients about the importance of sleep can help mitigate the adverse effects of abnormal sleep patterns, ultimately contributing to healthier cardiovascular outcomes.
Integrative Frameworks for Clinicians: Implementing Lifestyle and Systemic Interventions
How can clinicians effectively assess diet, exercise, and sleep in practice?
Clinicians play a vital role in screening and assessing patients' lifestyle behaviors that influence cardiovascular health. Practical tools include patient questionnaires such as the Household Food Security Survey Module or the 2-item Hunger Vital Sign to identify food and nutrition insecurity. For physical activity, clinicians can employ standardized assessments like the International Physical Activity Questionnaire (IPAQ) or simply inquire about weekly activity levels, duration, and intensity.
Sleep evaluation involves asking about sleep duration, quality, and disturbances. Recognizing sleep patterns like short sleep (<6 hours) or long sleep (>8 hours) can flag increased risk for metabolic syndrome and hypertension. Incorporating these assessments into routine visits helps tailor personalized lifestyle interventions.
How is decision-making facilitated through algorithms?
Decision-support algorithms are increasingly instrumental in guiding clinicians through complex management of cardiovascular risk factors. These tools synthesize patient data—such as blood pressure, cholesterol levels, and metabolic markers—into personalized risk estimates with calculators like PREVENT™ equations.
Using algorithm-guided assessments ensures evidence-based, consistent decision-making. They assist in selecting appropriate interventions, whether pharmaceutical or lifestyle modifications, and enable ongoing monitoring of risk reduction over time.
What are the roles of multidisciplinary care models?
Multidisciplinary approaches, exemplified by the ProtecT-2-D trial’s Cardio-Metabolic Clinic (CMC), integrate various healthcare professionals—including cardiologists, endocrinologists, nutritionists, and behavioral therapists—to deliver comprehensive prevention strategies. This team-based model allows for tailored management plans involving dietary counseling, physical activity prescriptions, medication adjustments, and behavioral support.
Such collaborative care enhances patient engagement, improves adherence, and addresses multiple risk factors simultaneously, creating a systemic effort to slow or prevent cardiovascular disease.
Overview of the integrated approach
Component | Description | Impact on Cardiovascular Prevention |
---|---|---|
Lifestyle assessment | Screening diet, activity, sleep | Identifies areas for intervention |
Decision algorithms | Personalized risk scores | Guides targeted treatment |
Multidisciplinary care | Teams of specialists | Ensures comprehensive management |
Implementing these frameworks in clinical practice bridges individual lifestyle behaviors and systemic healthcare strategies, fostering effective prevention of atherosclerosis and cardiovascular disease.
Microbiome and Metabolome Alterations as Early Biomarkers of Ischemic Heart Disease
How do gut microbiota changes precede clinical disease?
Recent research has uncovered that alterations in the gut microbiome and metabolome can be detected well before the onset of ischemic heart disease (IHD). These changes often occur in individuals with dysmetabolism, which generally comes before noticeable clinical symptoms. The microbiome shifts occur long before traditional risk markers like cholesterol levels or blood pressure suggest disease, making these microbial and metabolic signatures promising early warning signs.
In particular, these early signatures involve disruptions in microbial pathways responsible for producing metabolites that influence inflammation and lipid metabolism. Because the microbiome is dynamic and modifiable, detecting these changes provides a window for early intervention that could delay or prevent disease progression.
What are the key microbial species and metabolites involved?
Several specific microbial species and metabolites have been linked to IHD. Notably, intermediates of the trimethylamine N-oxide (TMAO) pathway – a metabolite associated with increased cardiovascular risk – are often elevated in at-risk individuals. Elevated levels of inflammatory lipids and reduced beneficial compounds like ergothioneine and alpha-tocopherol have also been observed.
In addition, low gut bacterial cell density correlates with IHD, suggesting compromised microbiome health may play a role in disease development. Pathways involving short-chain fatty acids (SCFAs)—which generally have anti-inflammatory properties—and aromatic amino acids are also affected in those with early signs of IHD.
Is it possible to modify microbiome features with treatments like statins?
Yes, some treatments such as statins, widely used to lower cholesterol, may also help restore healthy microbiome features. Evidence suggests that statins can influence microbial composition and reduce harmful microbiome-related metabolites like TMAO. Additionally, dietary interventions aimed at increasing fiber intake, or use of probiotics and prebiotics, have the potential to modulate these microbial signatures.
Overall, the identification of specific microbiome and metabolome signatures opens new avenues for early diagnosis and personalized interventions in cardiovascular disease prevention. By targeting these microbial pathways, clinicians might better manage or even preempt the development of IHD.
The ProtecT-2-D Trial and Multidisciplinary Cardio-Metabolic Clinics
Trial objectives and design
The ProtecT-2-D trial is a large-scale study that aims to determine whether a specialized and collaborative approach can reduce cardiovascular complications in patients with type 2 diabetes (T2D). The trial compares a multidisciplinary Cardio-Metabolic Clinic (CMC) model, which uses an algorithm-based decision-making process, with standard care. The primary goal is to see if this integrated method can lower the risk of cardiovascular death, heart attacks, strokes, or hospitalizations for heart failure over five years by 15%. The study involves a comprehensive evaluation of each patient’s health and personal risk factors, ensuring tailored interventions.
Comprehensive assessment and algorithm-guided treatment
Within the CMC, patients undergo detailed assessments that examine both arterial and metabolic health factors. An evidence-based decision-making algorithm guides clinicians in managing conditions such as dyslipidemia, hypertension, and diabetes. This systematic approach ensures each patient receives personalized treatment plans. The team includes nurses, medical students, and specialists like cardiologists, endocrinologists, nephrologists, and hepatologists, providing a holistic care experience.
The management strategy involves addressing lifestyle behaviors—such as diet, exercise, and smoking cessation—and optimizing medication use based on current guidelines. Regular monitoring through disease registries and electronic health records helps track progress and adjust treatments as necessary. Training healthcare providers in evidence-based practices enhances the quality and consistency of care.
Expected impact on cardiovascular outcomes in T2D
The collaborative approach in the CMC is expected to significantly improve cardiovascular health outcomes by early detection and precise management of risk factors. Previous studies like STENO-2 and RAMP support the notion that multifaceted and personalized care reduces cardiovascular events and mortality. The simulation of the ProtecT-2-D study hypothesizes a 15% reduction in these adverse outcomes compared to standard care.
By integrating lifestyle modification programs with medical management, the trial fosters better patient engagement and adherence, ultimately leading to fewer hospitalizations and improved quality of life for individuals with T2D. If successful, this model could reshape standard practices, emphasizing preventive and personalized strategies to combat the rising burden of cardiovascular disease associated with diabetes.
The Chronic Care Model: Systematic Redesign for Chronic Disease Management
Components of CCM
The Chronic Care Model (CCM) is a comprehensive framework designed to improve the management of chronic illnesses such as diabetes and cardiovascular disease. It includes six essential components: health care organization, self-management support, decision support, delivery system design, clinical information systems, and community resources and policies. Together, these elements foster a proactive, patient-centered approach that promotes better health outcomes.
Health care organization sets the foundation, emphasizing leadership and policy support for quality care. Self-management support empowers patients with education and tools to manage their conditions daily. Decision support ensures clinicians have access to evidence-based guidelines. Delivery system design reorganizes health services to be more efficient, while clinical information systems enable tracking and monitoring patient progress. Lastly, community resources link patients to external services, broadening their support network.
Evidence Supporting Diabetes Management Improvements
Research indicates that implementing the CCM in primary care settings significantly enhances diabetes outcomes. Notably, studies have demonstrated reductions in Hemoglobin A1c levels by at least 1% over 12 months, reflecting better blood sugar control. Patients also experience improvements in psychosocial well-being and self-management capabilities. These benefits point to the model's effectiveness in creating a sustainable system for managing complex, long-term conditions.
Role of Disease Registries and Self-Management Support
Disease registries and electronic medical records are key tools within the CCM that facilitate detailed tracking of laboratory results and clinical data. They enable care teams to identify gaps in care, set personalized goals, and monitor progress over time. Self-management education (DSME) programs complement these systems by providing patients with knowledge and skills to adhere to treatment plans, manage symptoms, and make healthy lifestyle choices. Together, these strategies foster a collaborative environment that supports continuous improvement in health outcomes for individuals with chronic diseases.
PREVENT Equations: Personalized Risk Estimation for Cardiovascular Disease
Development and validation
The PREVENT™ equations are innovative tools designed to estimate an individual's 10-year and 30-year risk of developing total cardiovascular disease (CVD), including conditions such as atherosclerotic cardiovascular disease and heart failure. Developed by the American Heart Association (AHA) in 2023, these equations were created using data drawn from over 6.5 million U.S. adults across extensive datasets. Their development involved rigorous statistical modeling to ensure accuracy and applicability across diverse populations.
Integration of metabolic, kidney, and social factors
What sets the PREVENT equations apart is their comprehensive approach. They incorporate a variety of clinical measures including traditional cardiovascular risk factors like blood pressure, cholesterol levels, and age, but also extend further by integrating markers of kidney health, such as urine albumin-creatinine ratio. Additionally, they consider metabolic parameters like hemoglobin A1c, which reflects blood sugar control.
Beyond biological factors, these tools incorporate social determinants of health through a social deprivation index. This inclusion acknowledges that social and economic factors significantly influence disease risk and can impact the effectiveness of prevention strategies. The ability to personalize risk estimates based on such a broad spectrum of variables makes the PREVENT equations especially valuable.
Clinical application in prevention strategies
Clinicians can utilize the PREVENT equations to inform personalized preventive measures. They are particularly useful in adults aged 30 to 79 years who have no prior history of CVD, providing critical insights that guide decision-making around managing hypertension, cholesterol levels, and other risk factors.
The equations generate options for individual risk assessment and can help tailor interventions such as lifestyle modifications, medication management, and ongoing monitoring. For example, a higher risk score might prompt earlier pharmacological intervention or more intensive lifestyle counseling.
Incorporating these tools into routine practice supports the move toward precision medicine—delivering targeted, effective strategies to prevent cardiovascular events before they occur. The 2025 AHA/ACC guidelines recommend using the outcome-specific risk estimates from PREVENT, especially for adults with borderline risk profiles, like those with Stage 1 hypertension.
By focusing on early detection and personalized prevention, the PREVENT equations serve as a cornerstone in reducing the incidence and burden of cardiovascular disease, ultimately improving patient outcomes on an individual and population level.
Addressing Chronic Systemic Inflammation: A Central Target in Disease Prevention
What are the sources and factors promoting systemic inflammation?
Chronic systemic inflammation (SCI) is driven by various external and internal factors that create a persistent inflammatory state throughout the body. Common sources include infections, physical inactivity, poor diet, environmental toxicants, and psychological stress. These factors activate immune responses and disrupt normal cellular functions, leading to a low-grade, ongoing inflammatory process.
Environmental toxicants like industrial pollutants and chemicals can further exacerbate inflammation by stimulating immune pathways. Conversely, lifestyle behaviors such as lack of physical activity and unhealthy diets rich in saturated fats, refined grains, and sugars also promote SCI. Psychological stress triggers inflammatory responses via hormonal pathways, such as increased cortisol and adrenaline levels.
How do systemic inflammation and associated factors connect to multiple chronic diseases?
This persistent inflammation is a common underlying mechanism in various diseases including cardiovascular disease, diabetes, cancer, chronic kidney disease, and neurodegenerative disorders. It contributes to endothelial dysfunction, insulin resistance, and tissue damage, accelerating disease progression.
Inflammation involving immune cells like macrophages and fibroblasts promotes fibrosis and microvascular damage, compounding health risks. Additionally, factors such as unhealthy diets and inactivity not only promote SCI but also influence lifestyle-related diseases directly. The interconnectedness of these influences underscores the importance of addressing SCI comprehensively.
What are potential strategies for early intervention?
Early detection and proactive management of SC can prevent or delay the onset of many chronic conditions. Strategies include lifestyle modifications such as adopting anti-inflammatory diets—e.g., plant-based, Mediterranean, or spices like turmeric and cinnamon—and increasing physical activity levels.
In clinical settings, interventions involve screening for markers of inflammation like C-reactive protein (CRP) and addressing modifiable environmental and behavioral factors. Workplace wellness programs and community-based efforts can foster healthier behaviors and environments, reducing exposure to inflammatory triggers.
Moreover, emerging therapies targeting inflammation pathways—like precision medicine approaches involving immune modulation or enzyme inhibition—show promise. Addressing underlying causes of SC at early stages can restore immune homeostasis and reduce disease burden.
Factors Promoting SCI | Impact on Health | Intervention Strategies |
---|---|---|
Infections | Trigger immune response | Vaccination, infection control |
Poor diet | Promotes inflammation | Nutrition counseling, dietary changes |
Physical inactivity | Leads to metabolic imbalance | Exercise programs, physical activity promotion |
Toxic environmental exposures | Increase toxic load | Environmental regulation, detoxification support |
Psychological stress | Elevates inflammatory cytokines | Stress management, mental health support |
Tackling systemic inflammation through these approaches offers a promising path to lowering the incidence of chronic diseases and improving overall health outcomes.
Workplace Wellness Programs: Preventing Cardiovascular Disease through Environmental Change
Components promoting healthy behaviors
Workplace wellness programs incorporate various strategies to foster healthier lifestyles among employees. These include health risk assessments, screenings for blood pressure, cholesterol, and blood glucose, as well as providing education on nutrition and physical activity. Creating supportive environments, such as dedicated spaces for exercise and healthy eating, encourages regular engagement in health-promoting activities.
Additionally, initiatives like smoking cessation support, stress management workshops, and weight management programs are central. Providing resources for early detection of health issues and ongoing disease management helps employees stay healthier and reduces long-term risks.
Targeting risk factors like smoking, obesity, hypertension
Addressing major risk factors for cardiovascular disease is a core element of workplace wellness strategies. Interventions target smoking cessation through counseling and nicotine replacement, helping reduce tobacco-related cardiovascular risks. Obesity management involves promoting physical activity and healthy eating, often through on-site fitness facilities or subsidized healthy meals.
Hypertension control is supported by regular blood pressure monitoring and education about lifestyle modifications such as stress reduction, diet, and exercise. Programs also focus on managing dyslipidemia and reducing sedentary behavior, which collectively diminish the likelihood of developing severe cardiovascular conditions.
Policy and regulatory supports to enhance effectiveness
Successful health programs are reinforced by supportive policies and regulations. Employers are encouraged to implement environmental changes, like creating safe walking paths and offering healthy food choices.
Regulatory efforts include adherence to safety and health standards, offering incentives for healthy behaviors, and integrating health promotion into organizational culture. These policies help sustain employee engagement, ensure consistency, and ultimately improve health outcomes.
Through comprehensive environmental modifications, targeted risk factor management, and supportive policies, workplace wellness programs serve as a pivotal platform to prevent cardiovascular disease and improve public health.
Component | Description | Benefit |
---|---|---|
Health assessments | Regular screenings and evaluations | Early detection and intervention |
Behavioral support | Smoking cessation, stress management | Reduced risk factors |
Physical environment | Exercise spaces, healthy food access | Encourages active lifestyles |
Policy support | Regulations, incentives | Sustained engagement and culture change |
Food and Nutrition Security: Addressing Disparities to Prevent Cardiometabolic Disease
What are food and nutrition insecurity?
Food insecurity refers to limited or uncertain access to enough nutritionally adequate and safe foods, which hampers individuals' ability to maintain a healthy diet. Nutrition insecurity is a related concept, emphasizing consistent access to nutritious foods that support overall health and disease prevention. Both issues disproportionately affect vulnerable populations, leading to health disparities. Accurate measurement tools are essential to identify at-risk groups and monitor trends.
How are populations screened for risk?
Healthcare providers use screening tools like the Household Food Security Survey Module (HFSSM) and the Hunger Vital Sign, a simple two-item questionnaire, to identify individuals experiencing food insecurity. For nutrition insecurity, newer tools such as the 2-item Nutrition Security Screener and the 4-item GusNIP tool have been developed. These assessments help clinicians and community programs pinpoint needs early, enabling targeted interventions.
What interventions exist to improve access and diet quality?
Efforts to combat food and nutrition insecurity include federal programs like SNAP (Supplemental Nutrition Assistance Program), school meal initiatives, and special programs for older adults. Healthcare-based approaches, such as medically tailored meals and produce prescriptions, also provide direct support. These strategies aim to enhance diet quality, reduce material deprivation, and lower risks of cardiometabolic diseases by ensuring consistent access to wholesome foods and promoting healthier eating habits.
Integrating Science, Lifestyle, and Systems for Chronic Disease Prevention
The Arteriometabolic Module exemplifies a multifaceted approach combining immunometabolic science, personalized lifestyle modification, and systemic healthcare strategies to prevent chronic diseases, particularly cardiovascular conditions and metabolic disorders. Understanding the intricate communication between immune and metabolic pathways opens new therapeutic avenues, while comprehensive lifestyle programs demonstrate measurable improvements in health outcomes. The synergy of early detection, multidisciplinary care, and addressing social determinants forms the cornerstone of effective chronic disease prevention. By embracing these integrated models, clinicians and public health practitioners can significantly reduce the burden of chronic diseases and enhance quality of life for at-risk populations.
References
- Metabolism in atherosclerotic plaques - PubMed Central
- Immunometabolism in atherosclerosis: a new understanding of an ...
- Mitigating preventable chronic disease: Progress report of the ...
- A Sedentary and Unhealthy Lifestyle Fuels Chronic Disease ...
- Lifestyle Interventions to Modify Cardiovascular Disease Risk
- Microbiome and metabolome features of the cardiometabolic ...
- [PDF] A Systematic Review - Preventing Chronic Disease
- ProtecT-2-D trial protocol: cardiovascular protection in patients with ...