The social determinants of health

The framework used in this section was assembled by the Commission on Social Determinants of Health, convened by the World Health Organization in 2005 and chaired by the British epidemiologist Michael Marmot. Its final report, Closing the gap in a generation, appeared in 2008 and argued that health inequities are produced by the way societies are organised rather than by individual decisions. The framework has two layers and one direction. Structural determinants begin with the socioeconomic and political context: governance and accountability, macroeconomic policy, taxation, labour-market rules, social protection, education, urban planning, and the cultural values that make inequality appear natural. Through structural mechanisms these arrangements distribute money, power and status, and so produce each person’s social position — income, schooling, occupation, class, gender, ethnicity and place of residence. Intermediary determinants then translate position into biology, but the framework insists that both layers are socially patterned rather than neutral. The Commission deliberately placed the health system inside the intermediary layer, because user fees, distance and disrespectful treatment convert an ordinary illness into a household catastrophe. Three overarching recommendations organise the report’s action: improve the conditions of daily life, meaning the circumstances in which people are born, grow, live, work and age; tackle the inequitable distribution of power, money and resources, which are the structural drivers of those conditions; and measure and understand the problem and assess the impact of action, which means building a workforce literate in social determinants and raising public awareness. The three are meant to be read together. A clinic alone cannot close a gap that taxation, schooling and housing opened, and a policy alone cannot reach the patient who is ill today.

The three moments named in the framework were formalised by the Danish public-health researcher Finn Diderichsen with Peter Evans and Margaret Whitehead in 2001, and their purpose is analytical: they let a health service see where in the chain a difference is actually created. Differential exposure is produced mainly by the labour market, housing and geography — who is hired into the dusty job, who can afford a dry house, who must live on the flood plain. Differential vulnerability is produced by the interaction of a previous exposure with a current one: the same tubercle bacillus is far more likely to produce active disease in a person who is malnourished, HIV-positive or exhausted by shift work. This is why the classic Whitehall studies of British civil servants, begun by Michael Marmot in the late 1960s, are still taught. The men were not poor, and none of them lacked access to a doctor, yet mortality rose steadily from the highest administrative grade to the lowest, where it was roughly three times as high. Something other than poverty was at work: position itself, and the control, security and recognition that came with it. The mechanism is partly psychosocial. Robert Karasek’s demand–control model, published in 1979, showed that the combination of high demand and low control over one’s own work — job strain — predicts cardiovascular disease; Johannes Siegrist later added effort–reward imbalance, the toll of working hard for pay and recognition that never arrive. Chronic insecurity of this kind raises cortisol and blood pressure and encourages smoking and heavy drinking as coping. Differential consequences are produced after the illness, and they are the least visible in a clinic: a patient who must pay cash, lose daily wages and travel 60 kilometres absorbs far more harm from the same diagnosis than a salaried patient with insurance. Two cautions belong here. First, the gradient does not prove that inequality itself is toxic; individual income, education and occupation explain much of it, and health selection — sick people drifting downwards into lower grades — contributes a part, though it cannot account for the whole. Second, none of the three moments is a destiny. Each names a place where a service, a policy or a nurse can intervene, which is precisely why the framework was built this way.

The life-course element of the framework rests on a specific biological claim, and it is worth stating precisely. In the 1980s the British physician David Barker, working from old Hertfordshire birth and death registers, found that men who had been small at birth and at one year had the highest death rates from ischaemic heart disease decades later. Barker proposed the fetal origins hypothesis: the fetus adapts to a poor intrauterine environment, and that adaptation becomes a liability when food later becomes abundant. He and Nicholas Hales called the resulting pattern the thrifty phenotype. Follow-up of the Helsinki birth cohort extended the finding from birth weight to body length and to the mother’s own nutrition, and showed that the associations run through the whole of adult life. Three mechanisms are now used to explain it, and they are not competing. The critical-period model says that organs and regulatory systems are especially plastic during defined windows — the first thousand days, from conception to the second birthday, is the window most often named — so an insult there changes the structure of the system for good. The accumulation model says that risks add up across life: poor nutrition, infection, hard physical work and stress each add a burden, and the total predicts disease better than any single exposure. The pathway model says that an early disadvantage raises the probability of the next one, so that the effect is carried forward by a chain of events rather than stored in the body. The biology that links them is called biological embedding. Chronic stress raises cortisol and other glucocorticoids; sustained elevation disturbs blood pressure, glucose handling and immune defence, and the cumulative wear is what Bruce McEwen named allostatic load. Epigenetic modification — chemical marks on DNA that change how genes are expressed without changing their sequence — is the mechanism now studied for how early experience becomes lasting physiology. The evidence for the social side comes from the adverse childhood experiences study, published by Vincent Felitti and colleagues in 1998, which found a dose–response relationship: the more categories of abuse, neglect or household dysfunction a person reported, the higher the rate of ischaemic heart disease, depression and other adult conditions decades later. Nursing practice follows directly. Antenatal care, growth monitoring, immunisation, breastfeeding support, iron and vitamin A, and counselling on play and stimulation are not merely child-health tasks; they are the earliest possible prevention of adult hypertension, diabetes and depression, and they are the interventions with the longest reach in a nurse’s whole repertoire.