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B11: The Effect of Lifestyle on Non-Communicable Diseases

Higher

Causal mechanisms, correlation vs causation, and disease costs

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Key Definitions

Causal mechanism โ€” A biological explanation of HOW a risk factor directly causes a disease.
Correlation โ€” A statistical relationship where two variables change together; does not prove one causes the other.
Risk factor โ€” Any aspect of lifestyle or environment that increases the probability of developing a disease.
Confounding variable โ€” A third factor that may affect both the risk factor and the disease, making a causal link difficult to prove.

Causal Mechanisms: How Lifestyle Factors Cause Disease

How Smoking Causes Cardiovascular Disease and Lung Disease

Cardiovascular disease:
1. Chemicals in tobacco smoke damage the lining of arteries.
2. This damage promotes the buildup of fatty deposits (atheroma/cholesterol) in the artery walls.
3. Carbon monoxide in smoke binds to haemoglobin, reducing the oxygen-carrying capacity of the blood. The heart must work harder to deliver enough oxygen, increasing blood pressure.
4. Nicotine causes vasoconstriction (narrowing of blood vessels), further raising blood pressure.
5. High blood pressure increases the risk of arteries bursting or atheroma rupturing, leading to heart attack or stroke.

Lung disease (COPD and cancer):
1. Carcinogens in smoke damage DNA in lung cells, causing mutations that can lead to uncontrolled cell division (lung cancer).
2. Smoke damages cilia on the epithelial cells lining the airways, so mucus and trapped pathogens are not cleared effectively.
3. Mucus accumulates, leading to infections and chronic inflammation.
4. Toxins in smoke break down the alveoli walls, reducing the surface area for gas exchange (emphysema, a type of COPD).

How Alcohol Causes Liver Disease

Causal mechanism:
1. Alcohol is broken down by the liver into toxic products (including acetaldehyde).
2. These toxic products damage liver cells and cause inflammation.
3. Over time, chronic inflammation leads to fatty liver (fat deposits build up in liver cells).
4. This can progress to alcoholic hepatitis (inflammation and cell death).
5. Eventually, liver cells die and are replaced by fibrous scar tissue โ€” this is cirrhosis.
6. Cirrhosis permanently reduces liver function and can lead to liver failure or liver cancer.
7. The liver cannot detoxify harmful substances, regenerate properly, or produce essential proteins (e.g. albumin, clotting factors).

How Obesity Causes Type 2 Diabetes

Causal mechanism:
1. Excess body fat, particularly visceral fat (around the abdomen), causes body cells to become insulin resistant โ€” they do not respond properly to insulin.
2. Insulin normally triggers cells to take in glucose from the blood, reducing blood glucose levels.
3. When cells are insulin resistant, glucose is not absorbed efficiently, so blood glucose levels remain high.
4. The pancreas produces more insulin to try to compensate (hyperinsulinaemia).
5. Over time, the insulin-producing beta cells in the pancreas become exhausted and can no longer produce enough insulin.
6. Blood glucose levels stay permanently high โ€” this is Type 2 diabetes.
7. Long-term high blood glucose damages blood vessels, nerves, and organs (kidneys, eyes, heart).
Example 1: Interpreting Data on Smoking and Lung Cancer
A study shows that in a population where 30% of adults smoke, the lung cancer rate is 60 per 100,000. In a similar population where only 10% smoke, the lung cancer rate is 20 per 100,000. This data shows a positive correlation between smoking rate and lung cancer rate. The causal mechanism is that carcinogens in cigarette smoke directly damage DNA in lung cells, causing mutations that lead to cancer. The data supports but does not alone prove the causal link โ€” the known biological mechanism provides the proof.
Example 2: Evaluating Evidence for Obesity and Type 2 Diabetes
Data shows that countries with higher rates of obesity also have higher rates of Type 2 diabetes. However, correlation alone does not prove causation โ€” other factors could be involved (e.g. diet quality, physical activity levels, genetics). The causal mechanism (excess body fat causing insulin resistance, leading to persistently high blood glucose) provides the biological explanation for WHY obesity increases diabetes risk. Multiple large-scale studies consistently supporting the link strengthen the evidence.
Example 3: Identifying a Confounding Variable
A study finds that people who drink more coffee have a higher rate of heart disease. Before concluding that coffee causes heart disease, we must consider confounding variables. For example, coffee drinkers might also smoke more, exercise less, or have more stressful jobs. Any of these could be the actual cause of the increased heart disease risk. Without controlling for confounding variables, we cannot say coffee causes heart disease.
Example 4: How to Evaluate Evidence for Risk Factors
To evaluate whether a risk factor truly causes a disease, consider:
1. Is there a correlation? โ€” Do the data show a consistent relationship?
2. Is there a known causal mechanism? โ€” Can we explain biologically HOW the factor causes the disease?
3. Have confounding variables been controlled? โ€” Were other possible causes ruled out?
4. Has the study been replicated? โ€” Do multiple independent studies show the same result?
5. Is the sample size large enough? โ€” Larger studies give more reliable results.
6. Was it a prospective study or retrospective? โ€” Prospective (following people over time) is stronger than retrospective.

Costs of Non-Communicable Diseases

Non-communicable diseases have significant costs to individuals, the NHS, and society:

Costs to the individual:
โ€” Financial cost of treatment and medication.
โ€” Loss of income if unable to work.
โ€” Reduced quality of life and mental health impact.
โ€” Impact on family members who may need to provide care.

Costs to the NHS:
โ€” Treatment costs (medication, surgery, hospital stays, ongoing care).
โ€” NHS spends billions annually on treating smoking-related diseases, diabetes complications, and cardiovascular disease.
โ€” Resources diverted from other areas of healthcare.

Costs to society:
โ€” Lost productivity when people cannot work.
โ€” Economic cost of early deaths.
โ€” Cost of research and public health campaigns.
โ€” Increased taxes or insurance premiums to fund healthcare.
Exam tip: When evaluating data on risk factors, always mention: (1) correlation does not prove causation, (2) whether a causal mechanism is known, (3) whether confounding variables have been controlled, and (4) the size and design of the study. Show both sides of the argument before reaching a conclusion.

Practice Questions

1. Higher Explain the causal mechanism by which smoking increases the risk of cardiovascular disease.
Chemicals in tobacco smoke damage the lining of arteries, promoting the buildup of fatty deposits (atheroma). Carbon monoxide binds to haemoglobin, reducing oxygen transport so the heart must work harder. Nicotine causes vasoconstriction and raises blood pressure. Higher blood pressure increases the risk of atheroma rupture, leading to blood clots that can block coronary arteries, causing a heart attack.
2. Higher Describe the causal mechanism by which obesity leads to Type 2 diabetes.
Excess body fat causes body cells to become insulin resistant โ€” they no longer respond effectively to insulin. This means glucose is not absorbed from the blood efficiently, so blood glucose levels remain high. The pancreas produces more insulin to compensate, but over time the beta cells become exhausted and can no longer produce enough insulin. Blood glucose stays permanently high, resulting in Type 2 diabetes.
3. Higher A study finds a correlation between eating red meat and bowel cancer. Explain why this correlation alone does not prove that red meat causes bowel cancer.
A correlation only shows that two variables change together; it does not prove one causes the other. There may be confounding variables โ€” for example, people who eat more red meat might also eat less fibre, exercise less, or drink more alcohol, and any of these could be the actual cause of the increased bowel cancer risk. To prove a causal link, a biological mechanism must be identified (e.g. specific chemicals in red meat damaging DNA in bowel cells) and confounding variables must be controlled in the study.
4. Higher Describe the causal mechanism by which alcohol causes liver disease.
Alcohol is broken down in the liver into toxic products (including acetaldehyde) that damage liver cells, causing inflammation. Over time, fat builds up in liver cells (fatty liver), which progresses to alcoholic hepatitis (inflammation and cell death). Eventually, liver cells die and are replaced by fibrous scar tissue (cirrhosis), which permanently reduces liver function and can lead to liver failure or liver cancer.
5. Higher Explain two ways that non-communicable diseases create costs for society.
1) Lost productivity โ€” people who are ill may be unable to work, reducing the workforce and economic output. 2) Financial cost to the NHS โ€” treating non-communicable diseases requires expensive medication, surgery, hospital stays, and ongoing care, diverting resources from other healthcare areas.

๐Ÿ”ข Maths Skills

Mathematical Skills

Interpreting risk data: calculate relative risk from data tables. For example, if the risk of CVD in non-obese people is 8% and in obese people is 20%, the relative risk = 20 รท 8 = 2.5. This means obese people are 2.5 times more likely to develop CVD. You may also need to interpret scatter graphs showing the relationship between BMI and disease risk โ€” identify whether the relationship is positive, negative, or shows no clear pattern.

โš ๏ธ Common Misconceptions

Watch Out!

Students often think only old people get CVD. Wrong: Cardiovascular disease only affects elderly people Correct: Lifestyle risk factors (smoking, poor diet, lack of exercise) accumulate over time, so CVD can develop in younger people with unhealthy lifestyles

Students often think BMI perfectly measures health. Wrong: A high BMI always means a person is unhealthy Correct: BMI has limitations โ€” it does not distinguish between muscle mass and fat mass, so a very muscular person may have a high BMI but low body fat

โœ๏ธ 6-Mark Question

Extended Answer

6 marks: Evaluate evidence linking obesity to type 2 diabetes and CVD.

There is strong evidence linking obesity to type 2 diabetes and cardiovascular disease. Large-scale studies consistently show a positive correlation between BMI and the incidence of both conditions โ€” as obesity rates increase, rates of type 2 diabetes and CVD also increase. A causal mechanism exists for type 2 diabetes: excess body fat causes insulin resistance, meaning cells do not respond effectively to insulin, so blood glucose remains high; over time, pancreatic beta cells become exhausted, leading to permanently elevated blood glucose (type 2 diabetes). For CVD, excess body fat raises blood pressure and blood cholesterol, promoting atheroma formation in coronary arteries. However, confounding variables must be considered โ€” obese individuals may also have poor diets, lack exercise, or smoke, and any of these could independently increase disease risk. Studies that control for these variables still show obesity as an independent risk factor. BMI also has limitations as a measure, as it does not distinguish fat from muscle mass. Overall, the evidence strongly supports a causal link, but obesity is one of several interacting risk factors.

Mark scheme: 1 mark for stating the correlation between obesity and each disease; 1 mark for the causal mechanism for type 2 diabetes; 1 mark for the causal mechanism for CVD; 1 mark for discussing confounding variables; 1 mark for mentioning limitations of BMI; 1 mark for a balanced evaluation with a justified conclusion

๐Ÿ“Š AO3: Analyse & Evaluate

Analysis and Evaluation

Interpret lifestyle and disease data: a table shows that in a population of 10,000, obese individuals have a 15% rate of type 2 diabetes compared to 3% in non-obese individuals. However, obese individuals in the sample also report lower physical activity (40% meet guidelines vs 75% in non-obese) and higher smoking rates (25% vs 10%). Evaluate whether obesity alone increases diabetes risk. The data shows a correlation (5ร— higher rate in obese group), but confounding variables (exercise, smoking) are not controlled. To isolate the effect of obesity, researchers would need to compare obese and non-obese people with similar activity levels and smoking habits. The known causal mechanism (insulin resistance from excess fat) supports a direct link, but the data alone cannot prove obesity is the sole cause without controlling confounders.

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