Risk Factors for Chronic Diseases

Why This Matters

In epidemiology, understanding risk factors is the foundation for everything from disease surveillance to intervention design. You're being tested on your ability to classify risk factors, explain their mechanisms, and analyze how they interact to influence population health outcomes. The key concepts here include modifiable vs. non-modifiable factors, proximal vs. distal causes, biological vs. behavioral vs. social determinants, and the critical idea of causal pathways connecting exposures to outcomes.

Don't just memorize a list of risk factors—know what category each belongs to, how factors cluster together, and why some populations face higher disease burdens than others. When an exam question asks you to design an intervention or explain health disparities, you need to identify which risk factors are actionable and at what level (individual, community, policy). That's the epidemiological thinking that earns full credit.

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Behavioral Risk Factors

These are modifiable factors involving individual choices and habits. Behavioral risk factors are among the most important targets for public health intervention because they're theoretically changeable, though social context heavily influences actual behavior.

Tobacco Use

• Leading preventable cause of death—linked to lung cancer, cardiovascular disease, COPD, and at least 12 other cancer types
• Dose-response relationship demonstrates clear epidemiological evidence; more pack-years equals higher risk
• Secondhand smoke extends risk to non-users, making tobacco a population-level exposure affecting even those who don't smoke

Physical Inactivity

• Independent risk factor for cardiovascular disease, type 2 diabetes, colon cancer, and depression—even controlling for weight
• Sedentary behavior is increasingly recognized as distinct from lack of exercise; sitting for prolonged periods carries its own risks
• Prevalence rising globally due to urbanization and technology, making this a key target for built-environment interventions

Unhealthy Diet

• Dietary patterns matter more than single nutrients—high processed food intake and low fruit/vegetable consumption drive chronic disease risk
• Ultra-processed foods are associated with obesity, metabolic syndrome, and cardiovascular disease through multiple mechanisms
• Food environment shapes individual choices, connecting this behavioral factor to social determinants

Excessive Alcohol Consumption

• J-shaped or U-shaped curve describes the relationship with mortality; moderate intake may show lower risk than abstinence or heavy use, though this is debated
• Causal link established for liver cirrhosis, several cancers (breast, colorectal, esophageal), and injury-related mortality
• Binge drinking patterns carry different risks than chronic heavy use—frequency and quantity both matter epidemiologically

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Biological and Physiological Risk Factors

These factors represent measurable biological states that increase disease risk. They often serve as intermediate outcomes on the causal pathway between behavioral/social factors and disease endpoints.

Obesity

• Body mass index (BMI) ≥ 30 is the standard classification, though waist circumference and body fat distribution provide additional risk information
• Metabolic effects include insulin resistance, chronic inflammation, and hormonal changes that promote cancer and cardiovascular disease
• Both a risk factor and an outcome—obesity results from upstream factors while causing downstream diseases, illustrating complex causal chains

High Blood Pressure (Hypertension)

• "Silent killer" designation reflects that hypertension is typically asymptomatic until target organ damage occurs
• Blood pressure ≥ 130/80 mmHg (current guidelines) increases risk of stroke, heart attack, heart failure, and chronic kidney disease
• Population-attributable fraction for cardiovascular disease is enormous—hypertension control is a high-impact intervention target

High Cholesterol (Hyperlipidemia)

• LDL cholesterol drives atherosclerotic plaque formation; HDL is protective, creating the "good vs. bad cholesterol" distinction
• Modifiable through diet, exercise, and statins—one of the most successfully treated biological risk factors
• Screening guidelines make this a key example of secondary prevention in epidemiological practice

Diabetes

• Type 2 diabetes is largely driven by modifiable factors (obesity, inactivity) while Type 1 is autoimmune—important distinction for intervention design
• Complications cascade includes cardiovascular disease, nephropathy, retinopathy, and neuropathy, making diabetes a risk factor for multiple outcomes
• Prediabetes represents an opportunity for prevention, illustrating the disease continuum concept

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Non-Modifiable Risk Factors

These factors cannot be changed but are essential for identifying high-risk populations and understanding disease distribution. Non-modifiable factors help epidemiologists target screening and prevention efforts efficiently.

Genetic Predisposition

• Family history is a practical proxy for genetic risk in clinical and epidemiological settings
• Gene-environment interaction means genetic risk often requires environmental triggers—lifestyle modification can mitigate inherited susceptibility
• BRCA mutations, familial hypercholesterolemia are examples where genetic testing guides prevention strategies

Age

• Cumulative exposure model explains why chronic disease risk rises with age—more time for risk factors to cause damage
• Biological aging involves cellular senescence, immune decline, and reduced repair capacity independent of exposures
• Age-adjustment in epidemiological analyses controls for this powerful confounder when comparing populations

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Social and Environmental Determinants

These are upstream factors that shape exposure to behavioral and biological risks. Social determinants explain why disease burden is unevenly distributed across populations and are increasingly central to epidemiological analysis.

Socioeconomic Status (SES)

• Gradient relationship with health—outcomes improve at each step up the socioeconomic ladder, not just above/below a poverty threshold
• Operates through multiple pathways: access to resources, chronic stress, health behaviors, environmental exposures, and healthcare access
• Fundamental cause theory argues SES will always predict health outcomes because resources can be deployed against whatever risks emerge

Lack of Access to Healthcare

• Prevents primary, secondary, and tertiary prevention—uninsured populations miss screenings, early treatment, and chronic disease management
• Healthcare deserts in rural and low-income urban areas create geographic disparities in outcomes
• Confounded with SES but independently important—even controlling for income, access barriers worsen health

Environmental Pollutants

• Air pollution (PM2.5, ozone) is causally linked to respiratory disease, cardiovascular disease, and lung cancer with clear dose-response relationships
• Water contamination and toxic exposures (lead, arsenic, industrial chemicals) disproportionately affect disadvantaged communities
• Environmental justice framework connects pollution exposure to social determinants—vulnerable populations face higher exposures

Occupational Hazards

• Exposure-specific risks include asbestos (mesothelioma), silica (silicosis), and repetitive strain (musculoskeletal disorders)
• Healthy worker effect is a methodological consideration—employed populations are healthier than general populations, potentially masking occupational risks
• Workplace interventions demonstrate how policy-level changes can modify "individual" risk

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Psychosocial Risk Factors

These factors bridge biological and social domains, operating through stress pathways and behavioral mechanisms. Chronic stress translates social conditions into biological disease risk.

Chronic Stress

• Hypothalamic-pituitary-adrenal (HPA) axis activation leads to sustained cortisol elevation, promoting inflammation, metabolic dysfunction, and immune suppression
• Allostatic load concept captures cumulative wear-and-tear from chronic stress responses—measurable through biomarker panels
• Links upstream and downstream factors—stress mediates how social disadvantage "gets under the skin" to cause biological disease

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Quick Reference Table

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Self-Check Questions

1. Which two risk factors are best classified as intermediate outcomes on the causal pathway between behavioral factors and cardiovascular disease? Explain why they occupy this middle position.

2. Compare and contrast genetic predisposition and socioeconomic status as risk factors. How do they differ in modifiability, and what does this mean for intervention design?

3. If an FRQ asks you to explain why low-income communities have higher rates of chronic disease, which risk factors would you discuss, and how would you connect them in a causal chain?

4. Tobacco use and excessive alcohol consumption are both behavioral risk factors, but their dose-response relationships differ. Describe this difference and explain how it affects public health messaging.

5. A researcher finds that employed factory workers have lower mortality than the general population despite occupational exposures. What epidemiological concept explains this finding, and why does it matter for interpreting occupational risk data?