1.7, 1.10 - Risk factors and perceived risk

Risk is a chance

Cardiovascular disease, or CVD, includes diseases of the heart and blood vessels. Coronary heart disease is one example: disease of the coronary arteries can reduce the supply of oxygenated blood to the heart muscle. Atherosclerotic plaques narrow arteries, and a thrombus, a blood clot formed inside a vessel, may obstruct blood flow. These processes explain why damage to arteries or an increased tendency to clot can raise CVD risk.

The outcome and time period matter. The risk of a first heart attack within ten years is a different quantity from the risk of any cardiovascular disease during a lifetime. A risk factor increases a chance; it does not predict which individual will experience the outcome. A person can have several risk factors and remain free of the specified disease during the period studied. Someone with fewer known risk factors can still develop it.

CVD is multifactorial: several influences contribute and may interact. For example, inherited high blood cholesterol and smoking can both contribute to arterial disease through different biological routes. The effect depends on the combination, intensity and duration of exposures. Counting two factors does not establish that the risk is exactly twice that of a person with one factor. Nor can separate percentages simply be added, because factors may affect the same biological pathway and occur together.

Evidence of an association is also different from evidence that a factor causes a particular outcome. Biological mechanisms and other evidence help establish causal links. A single person's story cannot measure the chance for a whole population.

Inherited and age-related risk

Some influences on risk cannot be changed by altering a habit, but their effects still depend on the rest of a person's circumstances.

Genetics

Inherited gene variants can affect blood cholesterol, blood pressure and other processes involved in CVD. LDL, low-density lipoprotein, is a particle that carries cholesterol in the blood. Persistently high LDL cholesterol can contribute to cholesterol accumulation in artery walls and atherosclerosis.

In the inherited condition familial hypercholesterolaemia, some gene variants reduce the removal of LDL from the blood. The resulting high LDL concentration can expose arteries to increased cholesterol from an early age, increasing the risk of coronary heart disease. This is a useful example of how a molecular difference can affect a blood measurement and then an organ's blood supply. It is not the explanation for every case of CVD. A family history may also reflect shared environments and habits, so it is not proof that every relative has inherited the same variant. MedlinePlus Genetics

Age

Risk generally increases with age. There has been more time for damaging exposures and atherosclerotic plaques to accumulate, and ageing can alter the structure and function of blood vessels. This helps explain why long-term exposure matters even when a person currently feels well. Age is not a guarantee of disease, and younger people are not immune.

Gender and sex-related patterns

Many health data sets compare groups labelled men and women, or males and females. Biological sex influences features such as hormone levels; gender-related social and behavioural patterns can also affect exposures such as smoking and activity. On average, men tend to develop coronary heart disease earlier than women. Before menopause, oestrogen is associated with some protection; after menopause, falling oestrogen levels contribute to increasing risk in women. These are population patterns, and risk also depends on the other factors. A woman with several major risk factors can have greater risk than a man with fewer factors. People of any sex can develop CVD. NHLBI risk factors, NHLBI women and heart disease

Diet, activity and blood pressure

Diet and physical activity influence CVD risk partly by changing conditions in the blood and blood vessels over time.

Diet

A dietary pattern high in saturated fats can raise LDL cholesterol, increasing the contribution of cholesterol to arterial plaque formation. High salt intake can raise blood pressure; its effects involve the regulation of salt and water and the circulation. An intake of energy that repeatedly exceeds expenditure can promote increased body fat and obesity, which can contribute to high blood pressure and other cardiovascular risk factors. These are different routes, so saying only that a diet is “unhealthy” does not explain how it affects risk. CDC risk factors

The relevant exposure is a dietary pattern, its amount and its duration. A single food is not a complete measure of a person's diet. Eating one high-fat meal does not imply an inevitable heart attack, just as eating one vegetable does not cancel years of other risk factors. Detailed energy budgets and the roles of different lipids are developed in later lessons.

Inactivity

Low physical activity can contribute to an energy imbalance and increased body fat. It can also worsen blood pressure and blood lipid profiles. Together, these effects can increase the likelihood of arterial disease. The association is not explained only by body mass: blood pressure and metabolic changes matter too. Activity is one influence among several; being active does not eliminate an inherited susceptibility or the effects of smoking. NHLBI risk factors

High blood pressure

Blood pressure is the pressure exerted by blood on vessel walls. Persistently high pressure places greater stress on the arterial wall and can contribute to endothelial dysfunction, impaired function of the cells lining the artery. Inflammation and plaque development can follow. Plaques may restrict blood supply, and plaque rupture can trigger a thrombus. In coronary arteries, reduced oxygen supply can damage heart muscle.

High blood pressure is itself a risk factor, rather than a lifestyle behaviour. Diet, activity, genetics and other influences can affect it. Arterial narrowing can also increase resistance to blood flow and contribute to raised pressure: the link between pressure and arterial disease can therefore reinforce itself. It is not a simple chain in which every person starts with exactly the same cause. NHLBI causes and prevention

Consider two adults with similar inherited susceptibility. Repeated differences in salt intake and activity could affect their blood pressure differently. Differences in saturated-fat intake could affect their LDL concentrations. These routes can contribute together to differences in CVD risk; they cannot be assigned exact personal percentages from this description alone.

Smoking and the circulation

Tobacco smoke affects the cardiovascular system through several routes, so its effect cannot be reduced to one chemical or one change.

Nicotine stimulates responses that increase heart rate and constrict blood vessels, raising blood pressure and the heart's workload. Greater pressure can add to stress on arterial walls. Other smoke constituents damage the endothelium and promote processes involved in inflammation and plaque formation. Smoking also increases the tendency of blood to form clots. If a thrombus obstructs an already narrowed coronary artery, the blood supply to heart muscle may fall sharply. CDC risk factors, CDC smoking and CVD

Carbon monoxide binds strongly to haemoglobin, forming carboxyhaemoglobin. This reduces the blood's capacity to carry oxygen. Reduced oxygen delivery is especially important when coronary blood flow is already restricted and the heart has a greater workload. Carbon monoxide's oxygen-transport effect is distinct from the mechanisms that damage arteries and increase clotting; it should not be described as directly making an atherosclerotic plaque. CDC risk factors

The mechanisms can reinforce one another. A higher heart rate increases the heart muscle's oxygen demand, while carbon monoxide reduces oxygen-carrying capacity and an obstructed artery reduces delivery. Smoking alongside high blood pressure or persistently high LDL cholesterol can therefore contribute through several interacting routes. This explains why considering only one favourable factor, such as being young or physically active, can give a misleading impression of overall risk. Exposure to second-hand tobacco smoke can also damage blood vessels and increase cardiovascular risk. CDC smoking and CVD

Expressing risk as probability

Risk becomes easier to interpret when it is expressed as the chance of a stated outcome in a defined period for a stated population.

An observed proportion can be used to estimate a probability for a relevant population. For a study in which each person can have the specified event once and is followed for the same complete period:

In an original fictional study, 24 of 600 adults have a first heart attack during a complete five-year follow-up. The observed proportion is $24/600 = 0.04$, or 4%. This is equivalent to 4 in 100. The proportion without that event is $1-0.04 = 0.96$, or 96%; it does not mean that these people have no other illness.

The calculation is dimensionless: it is a fraction of people, not a pressure or an annual rate. The five-year period remains essential in the interpretation. A 4% five-year risk is not automatically a 4% risk in each year. It also does not mean that exactly four of every subsequent group of 100 similar people must have a heart attack. Outcomes vary, and an observed proportion is an estimate rather than an exact guarantee for a new group. Comparisons require the same outcome, population context and time period.

Why perception differs from risk

The chance of disease and a person's judgement of that chance are different things.

An estimate of actual risk has uncertainty, but it can still be more informative than an impression based on a vivid story or an incomplete headline. Underestimating risk means judging the chance to be lower than the evidence suggests; overestimating means judging it to be higher.

Why risk can be underestimated

A person who feels healthy may discount long-term harm from smoking, diet or inactivity because the effects are not immediately visible. Atherosclerosis can develop over time before an obvious event. Someone may also focus on an exceptional case, such as a smoker who lived a long life, and overlook the many other outcomes. That example is possible precisely because increased risk is not certainty; it does not show that smoking leaves risk unchanged.

Optimistic bias means judging oneself less likely to experience harm than is justified. Feeling in control, being young, or focusing on one favourable habit can contribute to underestimating the combined effect of several factors. Primary research comparing reported heart-attack risk with risk estimates has found optimistic judgements in many participants; this does not imply that every person underestimates risk. Avis and colleagues

Why risk can be overestimated

A frightening heart attack in a friend or family member, or repeated dramatic reports, can make the event feel especially likely. A family history may be relevant evidence, but a vivid event alone does not establish that the same outcome is inevitable. For example, fear that one high-fat meal must produce a heart attack confuses a long-term risk factor with certainty of an immediate event. Primary research has found that knowing friends with disease can influence perceived risk as well as knowing affected relatives; it does not establish a universal response or measure everyone's actual risk. Montgomery and colleagues

The way numbers are framed

The following original fictional comparison concerns a first heart attack over the same complete ten-year period in both groups. It illustrates numerical framing and makes no claim about a particular real diet or population.

Original risk table: the same counts can be described using absolute risk or a relative comparison.

The absolute risk in Group B is 3%. The absolute difference is $3\%-2\% = 1$ percentage point, or 10 additional events per 1000 people. The relative risk is $3/2 = 1.5$: the observed proportion is one and a half times that in Group A, or 50% higher. “50% higher risk” does not mean that 50% of Group B have the event. A percentage change and a change in percentage points are different quantities.

A headline that gives only “50% higher” can sound alarming because it omits the starting risk. Conversely, saying “only 1 percentage point more” can encourage someone to dismiss a difference that represents real additional events. The same comparison can be framed to emphasise either size. Experiments have found that presenting effects as relative changes rather than absolute measures can influence decisions; a frame can change an impression without changing the underlying numerical comparison. Carling and colleagues

When reading a claim about diet or another lifestyle factor, identify the event, the people compared, the time period and the starting probability. Translate a relative claim back into absolute numbers where these are supplied. Then distinguish the numerical claim from a feeling of fear or safety. Neither a frightening story nor a reassuring label can substitute for the relevant evidence.