Simon Murphy & Paul Bennett. The Sage Handbook of Health Psychology. Editor: Stephen Sutton, Andrew Baum, Marie Johnston. Sage Publication. 2008.
This chapter focuses on the influence that a number of individual and social contexts have on health, in particular those associated with gender, ethnicity and the family, and how these may differentially affect health at different stages of the lifespan. These factors are intertwined in a complex web of causality; so much so, that an individual’s health is likely to be influenced by a variety of related factors. The aim of this chapter is to outline the biological, social and psychological factors that may interact around these social categories.
Gender and Health
An average woman’s life expectancy in the West is significantly greater than that of men of the same birth cohort. United Kingdom data for 1997, for example, from the World Health Organization (2003) showed that women live 6 years longer than men, with women likely to die at 80 and men at 74 years old. These differences are the result of a number of factors including higher rates of accidents, violence, and adverse work environments among men. A significant portion of this difference is also attributable to the earlier onset of coronary heart disease (CHD) in men than in women. In the USA, for example, nearly three-quarters of those who die of myocardial infarction before the age of 65 years are men (American Heart Association, 1995): men’s age-adjusted death rate for heart disease is twice that of women’s. Age-adjusted cancer rates are also significantly higher in men than women (Department of Health and Human Services, 1996). Despite the observed differences in mortality, men demonstrate higher self-rated health, contact medical services less frequently and experience less acute illness than women (Reddy, Fleming & Adesso, 1992). By contrast, women have been shown to have higher levels of somatic symptoms and long-standing illnesses than men (Lahelma, Martikainen, Rahkonen & Silventoinen, 1999).
It is, perhaps, cautionary to note that while this pattern of mortality is common among industrialized countries, the pattern of health advantage is often different in industrializing countries. Here, differences in the life expectancy of men and women are smaller and in some cases are reversed, with mortality linked to issues of structural disadvantage and higher rates of infant deaths. Compared with males, females in industrializing countries are more likely to experience higher rates of premature morbidity and mortality due to their more frequent experience of pregnancy, with its associated risks from shorter birth spacing and inadequate health services (Doyal, 2001), and poorer access to health care, education and nutrition (Gray, 1993).
Explanations for Health Differentials
Biological Sex Differences
Biological models suggest that gender differences in mortality can be explained by underlying physical mechanisms. From this perspective, being born female is seen as conferring a natural biological advantage in terms of longevity. Some have suggested these differences are genetically mediated through immunological differences, with females demonstrating greater resistance to infections (Davey & Halliday 1994). However, the majority of research has focused on the beneficial effect of oestrogen and sex variation in the stress response. It has been argued that oestrogen delays the onset of CHD by reducing clotting tendency and blood cholesterol levels, whilst testosterone increases platelet aggregation (McGill & Stern, 1979). This would help to explain observed increases in the prevalence of CHD in post-menopausal women (Office for National Statistics, 1996). Apparent gender differences in stress response have been found in studies of reactions to environmental stressors in laboratory settings, in which men typically evidence greater stress hormone, blood pressure, and cholesterol rises in response to stressors than do women (Matthews & Stoney 1988).
These hormonal differences have also been used to explain the higher levels of risk-taking activities in men. In an investigation of the relationship between testosterone and health-risk behaviours in men, Booth, Johnson and Granger (1999), for example, found that high levels of testosterone increased the likelihood of health-compromising behaviours such as smoking and alcohol misuse. Whether these are innate differences or the result of variation in gender roles and masculine and feminine identity is unclear. Work by Lundberg, de Chateau, Winberg and Frankenhauser (1981) and others, reviewed below, suggests that social and cultural processes may be implicated. Together, these data suggest that while biological factors may contribute to gender differences in risk for poor health, these may at least in part be driven by social factors, and have both a direct and an indirect influence on health.
The gendered roles that men and women inhabit have been shown to influence disease through environmental risk and stress processes. Research in this area has focused on the impact of paid work on men’s health and the influence of work in the home on women’s. This dichotomous approach is not without its dangers. As Oakley noted, ‘both the official statistics and the social scientists have inflated gender-specific links between men and work and women and the home—so the key processes of the jigsaw to do with women and work and men and the home are missing’ (1987: 25). Given this reservation, men have been shown to be more likely to encounter adverse employment conditions than women: although health and safety legislation has improved the working conditions of most workers, there are still environments that carry a significant risk of injury or disability. This is a risk predominantly faced by males, who account for 94 per cent of job-related fatalities (Courtenay, 2000b).
Men seem to exhibit greater stress responses than women in the face of employment demands. Nordstrom, Dwyer, Merz, Shircore and Dwyer (2001), for example, measured the degree of arterial plaque in 467 workers and its association with perceived job strain. In an age-adjusted model, plaque was greatest among men scoring in the highest quintile of work stress: no such association was found among women. Lundberg et al. (1981), however, pointed to the social organization of gender work roles as facilitating particular stress responses. In an examination of gender and employment characteristics they found that women in traditional male occupations and males engaged in traditional female occupations or tasks exhibited the same level of stress hormones as their opposite sex comparison group.
Gender differences have also been found in stress-coping behaviours, with men more likely than women to adopt health-damaging behaviours in response to job strain (Weidner, Boughal, Connor & Pieper, 1997). It has been argued that such behaviours are associated with norms of behaviour, which demonstrate masculine identity. Ames and Janes (1987), for example, found job alienation, job stress, inconsistent social controls and the evolution of a masculine drinking culture to be associated with heavy drinking amongst blue-collar workers. Similarly, Westman, Eden and Shirom (1985) reported that high numbers of work hours and lack of control and support were each positively associated with smoking intensity in men but not women.
In contrast to this, competing demands from home and paid work environments have been shown to impact strongly on women’s health. Killien, Habermann and Jarrett (2001), for example, examined employment characteristics and maternal health amongst women returning to work in the year following childbirth. The most consistent predictor of their health status was the level of interference between their work and family lives. These negative effects tend to be greater for female workers with significant responsibilities beyond the workplace. Haynes and Feinleib (1980), for example, found that working women with three or more children were more likely to develop CHD than those with no children, and argued that work strain combined with home demands heightened risk of disease. Risk is increased not only by level of demand but also by the lack of material and social resources required for coping responses. As a consequence, women from lower socioeconomic groups may be doubly disadvantaged, as they experience the greatest demands and possess the fewest resources for coping. Artazcoz, Borrell and Benach (2001), for example, found that family demands had the greatest negative impact on the health of female manual workers. For women with children under the age of 15, poor health was associated with a lack of leisure time for physical activity and with sleeping 6 or fewer hours a day. Female manual workers living with adults older than 65 years also evidenced increased likelihood of poor self-reported health status and the presence of a chronic condition.
The gendered effect of work demands is further illustrated by data from Alfredsson, Spetz and Theorell (1985), who compared the risk conferred by work strain and working overtime in a sample of 100,000 men and women. They found that working 10 hours or more overtime decreased risk for MI among men but was associated with a 30 per cent increased risk in women. It has been argued that whilst men are able to compensate for increases in work demands by decreasing home demands, the expectations associated with women’s roles mean they are unable to engage in a similar process. This hypothesis is supported by Lundberg et al. (1981) who found that female managers’ stress hormone levels remained raised following work, while those of male managers typically fell: this effect was particularly marked where the female managers had children. It seems that while men relaxed once at home, women continued their efforts in the home context.
Such findings have led authors such as Weidner et al. (1997) to examine how family members interpret competing demands from within and outside the home and how they allocate resources to deal with them. They found that gender interacted with demand so that when stress originated from within the home, husbands would increase their work in the home. When the demands originated from outside the home, however, husbands’ domestic contribution did not change and women contributed more. This has led to a view that issues of social inequality resulting from the gender roles have a more profound effect on women’s health than men’s. Denton and Walters (1999), analysing Canadian data for example, found that for women, being in a high-income category, having social support and working full-time and caring for a family were more important predictors of good health than for men. Although lifestyle factors did play a part in women’s health, with body weight and physical inactivity appearing as predictors, they played more of a part in predicting the health of men, for whom smoking and alcohol consumption emerged as important predictors.
A third factor through which gender may influence health is behaviours that demonstrate masculine and feminine identity. Many of the resources and behaviours available to demonstrate and enact masculinity are largely unhealthy. Men are more likely to smoke cigarettes, and to smoke high-nicotine and high-tar cigarettes, than women. They typically eat less healthily and drink more alcohol than women (Reddy et al., 1992). Powell-Griner, Anderson and Murphy (1997) found more men than women engaged in all but three of 14 non-gender-specific health-risk behaviours including smoking, drinking and driving, not using safety belts, and not attending health screening. Courtenay (2000a) also highlighted higher levels of unhealthy eating, substance misuse, reckless driving, risky sexual activity and violent assault amongst men.
Issues of gender identity have also been shown to influence the negotiation of behaviour through differential power relationships between males and females. Buysee and Van Oost (1997), for example, found that, although young adult women demonstrated more concern regarding safe sex and tried harder to implement safe behaviour than their male counterparts, they faced greater difficulties in behavioural negotiations as a result of gender power relations. While men could implement safe sex practices either without negotiation or by raising the issue at the moment of intercourse, women often had to start negotiating long before the actual encounter in order to be as successful. Gender identity has also been shown to influence the negotiation of health behaviours in relation to family interactions (see later discussion of family).
One of the few health-related behaviours that men engage in more than women is regular exercise (Reddy et al., 1992). This may be because a concern with physical fitness allows men to demonstrate their masculinity and physical power, whereas the discourses surrounding the medicalization of the female body, adolescent physical appearance, the menopause and the stereotypes associated with ageing help to explain lower levels of exercise activity in women (Vertinsky, 1998). Female concern with body image has been used to explain poor dietary practices and it has been argued that the association between thinness and beauty, and the fact that the body represents a realm of control where power may be exerted, may help to explain the incidence of bulimia and anorexia in adolescent females (Banks, 1992; Heaven, 1996). Women have been shown to make more social comparisons around physical appearance than men and to suffer lower self-esteem when these are negative (Freeman, 1987). The importance of body image to feminine identity is perpetuated by the mass media. Andersen and DiDomencio (1992) found women’s magazines contained 10 times the amount of coverage of weight loss compared to men’s. The narrower range of socially acceptable body shapes for females in our society is illustrated by Furnham and Radley (1989) who found 16-year-olds identifying far fewer female body shapes as attractive in comparison to male body shapes.
Gender has also been shown to be associated with particular forms of stress-coping behaviour, which develop over the lifespan. Groer, Thomas and Shoffner (1992), for example, found increases in stressful life events throughout adolescence and gender-specific changes in coping with them. Utilizing a longitudinal design, they found stressors were greater for females than males at baseline and increased more over the course of the study. Significantly, females showed an increase in passive distraction and males an increase in self-destructive and aggressive coping behaviour over time. Gender socialization may also inhibit males’ ability to deal with the negative emotions associated with stress. Robertson, Lin, Woodford, Danos and Hurst (2001), in comparing men who varied on measures of gender role stress (a measure of traditional masculinity), found no differences in physiological arousal in response to stressors, but did find variation in expressed emotions. Those high on traditional masculinity had greater difficulty in expressing emotions than those with low levels of masculinity. This may inhibit opportunities to facilitate social support and impacts directly on immune functioning (Pennebaker, 1997). Glynn, Christenfeld and Gerin (1999) suggest that there are qualitative differences in the perception of and/or type of social support offered by men and women and that these differentially influence cardiovascular responses to stress. In a laboratory study of the impact of social support during a stressful task, they found that social support provided by women in a stressful situation resulted in reductions in blood pressure and heart rate for both men and women. The social support provided by men resulted in no such changes.
Courtenay (2000b) suggested that men show their masculinity and power not only by engaging in health-risking behaviours, but also by not seeking medical help when ill. According to Courtenay, when men state, ‘I haven’t been to a doctor in years,’ refuse to take sick leave from work, insist they need little sleep or assert that their driving is better when they’ve had something to drink, these attitudes and behaviours reflect both health practices and statements of masculinity. Although Kane (1991) argues that the medicalization of women’s reproduction and their increased likelihood of seeking contraception from medical services inflate female consulting rates and their exposure to health screening, Verbrugge and Steiner (1985) suggested that men visit their doctor less frequently than do women, even after excluding reproductive health care visits. When ill, men are significantly less likely to consult a doctor than women: socially disadvantaged men are twice as likely as their female counterpart not to make a consultation (Department of Health and Human Services, 1998). Of interest is that men who score highly on feminine gender role orientation are more likely to report symptoms of illness (Klonoff & Landrine, 1992). Charmaz (1994) also noted several examples of, sometimes quite extreme, behaviours that men engage in to hide potential threats to masculine power. Examples included a wheelchair-bound diabetic man skipping lunch (and risking a coma) rather than embarrass himself by asking for help in the dining area, and a middle-aged man with CHD declining offers of easier jobs to prove he was still capable of strenuous work. Similarly, Jaffe noted the advice given to a US senator not to ‘go public’ about his prostate cancer as ‘some men might think his willingness to go public with his private struggle as a sign of weakness’ (1997:134). Men’s identities are simultaneously supported by women’s identities as carers of others (see the section on the family, below).
Issues of gender identity are also reflected in health professionals’ understandings of, and responses to, help-seeking behaviours. In some cases, studies have highlighted an awareness of the negative effects that gender identity has on help seeking. Tudiver and Talbot (1999), for example, reported that family physicians attributed low levels of help seeking in men to factors including masculine identity which prevented an admission of vulnerability and structural barriers such as lack of time and role models for male care providers. Gender identity stereotypes have also been shown to influence the level of care and treatment offered. Travis (1988), for example, found that women reporting symptoms of heart disease were less likely to receive adequate treatment than men, as a consequence of physicians viewing it as a male disease, while Bertakis et al. (2001) found that females were more likely to be diagnosed as depressed when reporting the same symptoms as males.
Hunt (2002) argued for an examination of the wider social, political and economic factors that shape and confine the roles and identities available to men and women. Examining the social context highlights influences on the development of gendered norms of behaviour. In one study to do this, Van Etten and Anthony (2001) suggested that current gender differences in the prevalence of illicit drug use result from a greater social acceptance of male drug taking and more opportunities to use illicit drugs, rather than gender differences in cognitions. Women’s substance misuse has been shown to be influenced by the politics of drug prescribing. Simoni-Watsila (2000), for example, contended that women are more at risk from prescription drug misuse than men, as they are 48 per cent more likely than men to be prescribed abusable prescription drugs by health services. Wider economic and mass media influences may also play a part in determining gender identity. It has been argued that increases in female smoking can be linked to targeted advertising campaigns by tobacco companies and the growth of positive smoking images aimed at women (Amos, Currie & Elton, 1998).
Together, these data suggest that while biological factors may contribute to some of the differentials in health status between men and women, others are societally mediated. Gender differentials in mortality and morbidity arise, to a significant degree, from the cumulative effects of different social worlds that men and women experience from the moment of their birth.
Families and Health
The influence of the family on health and health behaviours is profound. It provides the social context for our experiences of health and illness throughout the lifespan, one in which individuals influence and are reciprocally influenced by each other (Birch & Davison, 2001). It is within the family that we have the potential to be cared for, care for and support others, impart health information, develop and negotiate health behaviours, and make decisions about and undertake courses of treatment. The family constructs and responds to changes across its lifespan, influencing patterns of health and illness as it does so. Key stages in the life of the family can be identified as having differing implications for health. Whilst by no means exhaustive, we highlight a number of these, and in so doing note the importance of social context and social relationships in relation to health and illness. Factors addressed include marriage and social integration, family structure, stress and social support, and health-related behaviours within the family.
Marriage and Social Integration
Married adults tend to be psychologically and physically healthier, to have better disease survival rates, and to live longer than their unmarried counterparts (Waldron, Hughes & Brooks, 1996). Of course, causal processes may work both ways: whilst marital status influences health, health may also influence marital status, with those individuals who experience poor health being more likely to be single and socially isolated (Joung, 1997).
One explanation for the link between poor health and being single is that those who remain unmarried are more socially isolated and lack social support networks relative to their married counterparts. This not only acts as an explanation but highlights the difficulty of isolating the influence of marriage from the influence of other social ties. In the USA, longevity has been associated with a relatively high number of social ties as a consequence of marriage, as well as contacts with close friends and relatives and membership of social and religious organizations (Berkman & Syme, 1979). These relationships held even after partialling out the impact of other health-compromising behaviours such as smoking, high alcohol intake, and low levels of physical activity. Higher rates of morbidity and mortality amongst those who lack social networks have also been observed (Reynolds & Kaplan, 1990). Results from Europe support these findings. Orth-Gomer and Johnsson (1987), following a cohort of 17,400 men and women for a period of 6 years, found an increased risk of morbidity associated with social isolation. Men and women scoring in the lowest third on social network measures demonstrated a 50 per cent greater risk for CHD compared to the remaining two-thirds. In addition, Williams et al. (1992), for example, found that patients already diagnosed with CHD who were unmarried and without a close friend experienced a threefold higher risk of mortality over a 5-year period than those who were socially integrated.
The relationship between marriage/social integration and good health may be less straightforward than it first appears. The positive health outcomes associated with marriage have been shown to be greater for males than females (Waldron et al., 1996), and the study by Orth-Gomer and Johnsson (1987) found that older women who had many social contacts had higher mortality levels than those with medium-sized networks. These findings have led to speculation that the important determinant of health is the quality of social and marital relationships rather than their absolute number (Kiecolt-Glaser & Newton, 2001). Empirical support for this hypothesis was reported by Orth-Gomer and Johnsson (1987), who found that the quality of relationships (in particular the provision of guidance, practical help and a feeling of ‘belonging’) proved a stronger and more consistent predictor of mortality than the absolute number of contacts.
Marriage provides both practical and emotional support (Berkman & Glass, 2000). These twin roles seem to be particularly important in explaining observed gender differences. Men are more likely to benefit from the practical and social support offered by their partners, but to turn to health-risk behaviours in response to stressful interactions. Women on the other hand are more likely to experience depression and reduced psychological functioning as a result of poor quality relationships (Kiecolt-Glaser & Newton, 2001). Finally, social relationships may exert a normative influence, by either encouraging or discouraging health-risk behaviours such as smoking, excessive eating, and alcohol consumption (Broman, 1993). This type of influence is discussed below in relation to family health behaviours.
Biological mechanisms mediating the impact of ineffective social support systems and health appear to involve both immune and sympathetically mediated processes. Negative social interactions have been associated with elevated stress hormones (Kiecolt-Glaser et al., 1988), increased cardiovascular activity in response to stress (Uchino, Holt, Uno & Flinders, 2001), and depressed immune functioning (Kiecolt-Glaser et al., 1988), while supportive interactions are associated with the opposite effects (Seeman, 2000). The health risks associated with such responses may also be increased when trait hostility is present, particularly among males (Kiecolt-Glaser & Newton, 2001).
Research examining the physiological changes associated with divorce and separation adds to these data. Those experiencing divorce demonstrate poorer immune functioning than those who remain married (Kiecolt-Glaser et al., 1988), although outcome is influenced by gender and whether or not the individual in tiated the separation. Buehler (1987), for example, identified different processes of coping and adaptation for initiators and non-initiators. Although both groups shared similar emotional reactions, the timing of the responses differed. Initiators experienced more change and stress in the 6-12 months following divorce, whilst non-initiators reported higher levels of stress 18-24 months post-decree. In general, however, non-initiators have worse immune functioning than initiators (Kiecolt-Glaser et al., 1988). The initial separation phase appears to be more stressful for women than men, regardless of initiator status (Pledge, 1992), perhaps as a result of them facing more structural disadvantage once separated (Arber, 1991).
Family Structure, Stress, and Social Support
Explaining the relationship between family structure and health has proved particularly problematic, given recent trends towards diversity in such structures and difficulties in identifying underlying causative factors. Studies that have assessed the relationship between family structure and health status by, for example, comparing the children of single and dual parents and biological and stepparents, have typically shown that children living with single mothers or non-biological parents are at increased risk for asthma, accidental injuries, and behavioural and emotional problems, and have an increased health vulnerability (Dawson, 1991).
Interpretation of these findings is complicated by the fact that a significant percentage of single mothers are socially and economically deprived relative to their married counterparts. These findings may therefore reflect social disadvantage as much as family structure. Indeed, when McMunn, Nazroo, Marmot, Boreham and Goodman (2001) partialled out the effects of benefits receipt, housing tenure, and maternal education, the differences in psychological morbidity they found between the children of single and married mothers were no longer evident. Data such as these led Sweeting (2001) to argue that the variance in child health explained by family structure alone is extremely small and that the focus of research and any interventions should be on the nature of social interactions rather than the structure in which they occur.
Stress and Family Support
Living within a supportive family with positive interactions and clear communication has been shown to be associated with low levels of stress, high levels of stress-coping behaviour, good psychological health, active adaptation to acute and chronic illness, and high levels of adherence to treatment (Wamboldt & Wamboldt, 2000). It seems that negative family functioning represents a potential source of stress, while positive interactions have a buffering effect, reducing stress responses by enhancing emotional support and the modelling of coping behaviours amongst family members. Reflecting the reciprocity of family systems, it is also possible that at least some of these data reflect higher levels of stress and poor coping and adaptation leading to the negative family interactions. The lack of longitudinal studies to study this phenomenon makes it difficult to determine the relative influence of these differing causal pathways.
The impact of family environments on the mental and physical health of family members is most apparent during periods of adaptation to change, in particular the arrival of children, psychosocial changes associated with adolescence, and the onset of chronic illness in children. Families appear to have a ‘normative lifecycle’ (Oppenheimer, 1974), with family stressors increasing when demands exceed family resources. These ‘lifecycle squeezes’ occur first when young couples attempt to set up home together, then in middle age when supporting older children, and finally in retirement. Parenthood is itself a potential stressor, which can elicit stress-coping behaviours such as smoking and alcohol consumption, particularly in families with poor material circumstances and little social support. Graham (1985), for example, found that working class women with little time to themselves used smoking as a convenient way to relieve high levels of stress and tension by providing ‘time out’ from the demands of child care. Alcohol consumption may increase for similar reasons, particularly among men (Westman et al., 1985). Gottlieb and Green (1984) highlighted how gender differences in response to family stress differ as a consequence of time constraints and the resources available to cope with the demands of parenting. When faced with increased stress, exercise levels increased among men but not women.
For those with few material resources, increased economic demands associated with bringing up children may negatively impact on behaviour. Backett (1990), for example, found that parents faced with limited resources were neglectful of their own health, sometimes doing without adequate food in order to provide children with a good diet. Families are also required to deal with demands from outside the home environment—in particular the obligations associated with paid employment. These impact more on women than men, especially those in full-time employment and with few resources to help support multiple role demands (Arber, Gilbert & Dale, 1985). Indeed, Waldron et al. (1996), utilizing prospective panel data over a 5-year period, found that the only women to gain any health benefits from marriage were those who were not engaged in paid work outside the home. Data such as these reflect back to the issues of gender roles and identity considered above and show how gender identities interact with family roles and responsibilities to determine health and wellbeing.
Supportive and cohesive family environments, including open communication, seem to help families cope with the stresses associated with adolescence. Wenk, Hardesty, Morgan and Blair (1994), for example, in a longitudinal study, found that high levels of maternal and paternal help and involvement predicted adolescents’ wellbeing, including measures of self-esteem, life satisfaction and mental health. Similarly, Jo-Lohman and Jarvis (2000) found that high levels of family cohesion were associated with more adaptive coping strategies and greater psychological health in adolescents.
Family interactions have also been shown to influence coping with acute and chronic illness. Wamboldt and Wamboldt’s (2000) summary of the available evidence suggested that negatively expressed emotion within the family was associated with poor outcomes on measures of childhood physical and psychological problems and lower levels of adherence to treatment. More positively, Markson and Fiese (2000) found that the families of children with asthma with well-founded family routines reported lower levels of health anxiety than families without clear routines. Social support from family and friends has also been identified as a key factor in reducing the burden of coping with illness in elderly relatives (e.g., Coen, O’Boyle, Swanwick & Coakley, 1999).
This is not to say that the influence of family interactions is always straightforward. Franks, Campbell and Shields (1992) found that family criticism and high family emotional involvement were both associated with depressive symptoms in the family. By contrast, they also found that high emotional involvement was associated with greater levels of health-protective behaviours, suggesting that high emotional involvement, although impacting negatively on psychological health, can act as a form of social control encouraging individuals to conform to normative family behaviours.
Family Health Behaviours
One approach to understanding family influences on behaviour has focused on the development and communication of attitudinal and behavioural norms, which may be influenced through the communication of information, the modelling of behaviour, and fear of sanctions for non-conformity Although family norms generally control behaviour, this is not always the case, and individuals within the family may reject such norms, as a result of either personal experience or the influence of factors beyond the family. How these differences are resolved is affected by the family structure, its willingness to accept non-conformity, and its strategies for resolving conflict.
Norms may change as a result of changes in the family structure. One simple example of this is that the presence of children may trigger consideration or initiation of health behaviour change and be implicated in the negotiation of new norms. During pregnancy, approximately one-fifth of women smokers, and particularly those aged below 35 years, stop smoking, while an even greater percentage reduce their alcohol consumption to within the weekly recommended units (Waterson & Murray-Lyon, 1989). Reductions in consumption of alcohol and tobacco have also been observed for fathers, although the percentages are much lower (Waterson, Evans & Murray-Lyon, 1990). Such changes can be motivated by a desire to protect the unborn child and be confined purely to the term of pregnancy, although Hyssaelae, Rautava, Helenius and Sillanpaeae (1995) argued that the arrival of a first child can act as a cue to more sustained parental reductions in alcohol consumption and cessation of smoking. This is most likely to occur when both partners make changes, resulting in new and sustainable family norms. Parenting may lead to changes in adult behaviour: it can also lead to conflicting desires in parents and the adoption of furtive behaviour to avoid children observing health-compromising behaviours such as smoking and poor dietary habits (Backett, 1990).
Changes in parental behaviours may arise out of a desire to act as healthy role models for their children. What evidence there is suggests that they may be successful in this goal. Maguire et al. (2002), for example, found positive correlations between parents’ and adolescents’ physical activity attitudes and behaviours, although it may well be the case that both parents and children are influenced by other shared social factors. Nevertheless the family environment has been identified as a key influence on the development of food preferences, patterns of food intake, eating styles and the development of activity preferences, particularly during early and middle childhood (Birch & Davison, 2001).
The influence of parents recedes during adolescence, to be replaced by an increasing influence from peers (Beal, Auisello & Perrin, 2001). The interplay between these influences has been explored predominantly in relation to substance misuse. Beal et al. (2001), for example, found that whilst parental modelling and the monitoring and disapproval of health-risk behaviour predicted alcohol use, peer influences were associated with all measured health-risk behaviours, including tobacco and alcohol use, marijuana use and sexual activity. Other studies have focused on how families negotiate the relative influence of peer groups and the developing family throughout the lifespan (Backett & Davison, 1995). Foxcroft, Lowe and May (1994), for example, found that when parents were aware of adolescent drinking, sanctioned its sensible use, and modelled appropriate drinking, their adolescent children engaged in less alcohol misuse.
A number of studies have highlighted how gender socialization influences the modelling and reinforcement of behaviours. Of interest is that women are more influential in the development of protective behaviours in their children and partners than men. Umberson (1992), for example, found that women were more likely to adopt a nurturing and controlling role within families. This was beneficial for male health, as preventive actions were controlled and supported—support that was not reciprocated. Similarly, Rossow (1992) found that the strongest predictor of eldest child’s teeth-cleaning behaviour was mother’s cleaning behaviour. Behaviour can also be influenced and reinforced by siblings. A strong relationship between the behaviour of elder and younger siblings was explained by equity in the control and reinforcement of behaviour by parents, but also by the modelling of protective behaviour of the eldest sibling. The development of risk behaviours in children has been found to be gender dependent, mirroring their same-sex parent. A 5-year longitudinal study conducted by Wickrama, Conger, Wallace and Elder (1999) highlighted gender differences in health-risk behaviours. They found an intergenerational transmission of individual behaviours as well as the transmission of a health-risk lifestyle. However, a gender effect showed boys’ lifestyle to mirror their fathers,’ and girls’ their mothers.’ Whether this transmission occurred through social modelling or the processes discussed below, such findings highlight the need to examine the influence of gender socialization within the family and its cumulative influence across the lifespan.
It is important to recognize that whilst experiences within the family may shape normative behaviours, such experiences are interpreted within an individual’s view of the world, including their personal construction of the meaning of health and health risk. In their interviews with people from families with a high risk of CHD, for example, Emslie, Hunt and Watt (2001) found that although individual family members acknowledged that heart problems may run in the family, they differentiated family risk from personal risk by distancing themselves from family members in terms of biological type and by women identifying CHD as a male disease. In addition, individuals saw a family history as legitimizing risk behaviours as there was little they could do to avoid such inherited risk and past behaviours could not now be counteracted. Individuals also focused on CHD as a source of mortality rather than a disabling chronic condition. A common view was that CHD was a sudden and ‘quick way to go’ rather than a lingering death.
The Negotiation of Behaviour
Behavioural influence within a family is not necessarily a ‘top-down’ process. Many behaviours are negotiated within the family system and are shaped through interactions between family members. In such interactions, participants bring their own understandings and expectations of appropriate behaviours. Behaviour is then shaped by the mutual responses of the participants—a process termed ‘the negotiated order.’ Existing patterns of behaviour are therefore open to modification and change dependent upon the individuals involved and the circumstances they find themselves in. Children have been shown to influence family health behaviours by active negotiation. Mintel (1991), for example, reported that the demands made by children between the ages of 5 and 12 act as significant influences on their parents’ dietary purchases. Backett (1990) characterized this process of family interaction as one in which parents negotiate meals comprising both ‘bad’ (what the children want to eat) and ‘good’ (what they consider to be healthy) elements.
Many studies have identified the importance of gender in the negotiation of family behaviour. Backett (1990), for example, found gender differences in interactional and situational constraints on opportunities to engage in preventive behaviours. Men were more likely than women to undertake preventive actions such as exercise. These differences frequently did not correspond with desired levels of exercise. Rather, they reflected women’s negotiated role within their family, and their affording higher priority to other family commitments than their own participation in regular exercise. Similarly, Young (1999) found that, for women, health-related behaviours were frequently a result of negotiation with other family members based on time-space constraints, rather than the result of individual decision making. Gender roles have also been implicated in family dietary behaviour. Although a majority of women remain the main provider of food within the household, they may exert little control over the choice of foodstuffs. Instead, they frequently find themselves in the role of food negotiator, balancing competing family demands and conflict (Kerr & Charles, 1983). Results from Backett (1990) suggested that negotiation is related not only to gender roles but also to issues of gender identity. Differences emerged relating to the acceptability of health concepts that could be raised in the home and to opportunities to talk about health. Whilst women felt they could raise issues such as diet, exercise and positive health, men felt they could only raise issues related to specific episodes of illness or, in terms of prevention, physical fitness and sport.
This process of negotiation within the family suggests that attempts to facilitate behavioural change should address the family as an interactive system, rather than as a series of isolated individuals. An example is provided by Johnson and Nicklas (1995) whose ‘Heart Smart Family’ initiative aimed to improve the cardiovascular health of families with children identified as at high risk for CHD, rather than just targeting the children. Their programme involved a 12- to 16-week intervention which focused on increasing awareness of health issues, skills development and problem solving skills. They argued that by involving the whole family system in change, the likelihood of the adoption and maintenance of new behaviours increased. The programme appeared to actually benefit parents more than children. Parents evidenced lowered blood pressures, increased exercise levels, and decreased intake of total fat, saturated fat and sodium intake, whilst children only evidenced a reduction in blood pressure. Similarly, Burke et al. (1999) reported positive changes in a range of health behaviours, self-efficacy, and reductions in perceived barriers to health following a 16-week randomized controlled programme aimed at newly married couples. They suggested that such initiatives can usefully focus on periods in families’ lifespan when gender roles and identities are evaluated.
Ethnic Minorities and Health
In the UK, rates of premature mortality amongst people in ethnic minorities are typically higher than those of the white population. Less information is available on morbidity (Harding & Maxwell, 1997). Similarly, in the USA, blacks have higher age-adjusted mortality rates for a variety of diseases including various cancers, heart disease, liver disease, diabetes and pneumonia (Krieger et al., 1999). They are also more likely to die as a result of violence (Markides, 1983). There is also marked variation within ethnic categories. Epidemiological data from the UK (Balarajan & Raleigh, 1993; Landman & Cruickshank, 2001) shows a 36 per cent higher rate of CHD amongst males from the Indian subcontinent, with rates for those between 20 and 39 years of age being two to three times higher than for whites. In addition, there are higher levels of diabetes among Asians and a greater incidence of obesity amongst South Asians. For Afro-Caribbeans, a particularly high prevalence rate of hypertension and strokes has been observed. For the former, mortality rates four times above the national average for males and seven times greater for females have been recorded. For strokes, males demonstrated a rate of 76 per cent and females a rate of 110 per cent above the national average. In contrast, African Caribbeans and Asians have lower rates of cancer than the national average (Barker & Baker, 1990).
There are difficulties in examining the relationship between ethnicity and health. These include problems in defining and measuring ethnicity, for example whether own country of origin or parents’ country of origin should be used and whether classification should be done by an interviewer or the respondent. There is also a danger that in grouping individuals together within ethnic groups, we ignore the diversity of experience and run the risk of pathologizing minority status rather than examining the underlying processes that result in the association between ethnicity and poor health. It has even been argued that including ethnicity as a variable in health research ignores the great variation in, and explanatory power of, language, religion, migration, culture, ancestry, and forms of identity associated with ethnic categories (Nazroo, 1998). These issues should be seen as dynamic and subject to constant change and negotiation. Landman and Cruickshank (2001), for example, in examining ethnicity and dietary risk behaviour, warned against the danger of ignoring generational behavioural differences within ethnic minorities. They highlighted data suggesting that second-generation offspring of former migrants adopt the dietary patterns of their peers, increasing fat and reducing vegetable, fruit and pulse consumption.
Consequently, disentangling the various genetic, social and psychological factors that may contribute to differences in morbidity and mortality between ethnic groups has proved extremely difficult. The high incidence of mental illness among African Caribbeans living in the UK, for example, has variously been explained by theories focusing on genetics, economic deprivation, discrimination and service provision problems (Littlewood & Lipsedge, 1988), whilst in the USA, explanations have focused on interactions between restricted socioeconomic mobility, lack of social resources, poor living conditions, racism and the inter-nalization of negative cultural stereotypes (Williams & Williams, 2000). Here we focus on three levels of explanation: normative health behaviours, social disadvantage, and prejudice and discrimination.
Normative Health Behaviours
The frequency and practice of differing health-related behaviours varies across ethnic groups and gender. In the UK, smoking levels are low for women across all ethnic groups, but differ according to ethnic group for males (Waterson & Murray-Lyon, 1989). Alcohol-related morbidity is high amongst African Caribbean men and Asian males of Punjabi origin, while a high dietary fat intake is common among Asians (Clarke, Ahmed, Romaniuk, Marjot & Murray-Lyon, 1990; Fox & Shapiro, 1988). In the USA, whilst black males resemble their white counterparts, black females consume less alcohol and smoke fewer cigarettes than white females (Gottlieb & Green, 1987). These differences in risk behaviours have been used to explain some of the variation in risk for disease across the different ethnic groups.
These findings may be explained by differing cultural norms of behaviour. Gudykunst, Yoon and Nishda (1987), for example, argued that as a result of their socialization, members of non-Western cultures living in the West frequently consider health risks as a concern for other groups in society, and not their own ethnic group. As a consequence they may be less likely to engage in health-protective behaviours than those who feel personally at risk of conditions thought to be present in the majority population. Differing group norms and expectations have powerfully influenced African Americans’ responses to AIDS, which have been influenced by beliefs about their identity, gender role socialization, and attitudes to contraception and homosexuality (Pittman, Solheim & Blanchard, 1992).
Cultural norms may operate as a form of informational social influence, with information communicated and behaviour modelled via social networks. This can affect such things as perceived vulnerability, knowledge and attitudes to prevention and may explain the relationship between CHD risk behaviours and low levels of awareness of cholesterol and dietary risk factors found in South Asian and Indian populations (Lip, Luscombe, McCarry Malik & Beevers, 1996). In the UK, these subgroup-specific norms may influence behaviours such as smoking, drinking, diet and sexual activity. Best et al. (2001), for example, found white respondents to be more likely to have ever smoked and drunk alcohol and to progress to regular substance use than both black and Asian respondents, who also reported a later onset and the lowest prevalence of smoking and drinking alcohol. Similarly, Dundas, Morgan, Redfern, Lemic-Stojcevic and Wolfe (2001), in a London population, found white respondents were more likely to smoke and have an unhealthy level of alcohol consumption than their African and African Caribbean counterparts, but were less likely to be overweight. It has also been argued that ethnicity may confer different sexual norms. The most common exposure route for HIV infection among whites is through sexual intercourse between men: for blacks it is through heterosexual intercourse, whilst for Asians it is mixture of both (Nazroo, 1997; Rudat, 1994).
Karlsen, Rogers and McCarthy (1998) suggested that familial, religious and peer influences play a part in the development of normative behaviours, and again highlighted the importance of recognizing diversity within ethnic categories. In a survey of inner London schools, they found white school pupils to have the highest levels of tobacco, alcohol and drug use and the highest level of peer influence. Bangladeshis reported the lowest levels of substance use and higher levels of religious and family influence, with Africans and African Caribbeans falling between the two. Other studies have examined the relative influence of families and peers on adolescents’ health behaviours. Gittelson, Roche, Alexander and Tassler (2001) provide such an example. Results from their qualitative study suggested that gender interacts with ethnicity to influence levels of conformity to peer and parental norms. They highlighted the level of identification with peer groups and the fear of sanctions for non-conformity to parents as key influences. They found that white females perceived the most permissive parental normative messages around smoking and a high desire to conform to peer smoking behaviour, whereas African American males reported the strictest parental sanctions for smoking.
This is not to say that cultural norms act within a social vacuum. As we noted in our review of gender, it is important to examine the influence of wider social processes on the behaviour of people in ethnic minorities. The mass media may differentially target and influence ethnic groups. Gittelson et al. (1999), for example, found clear differences in patterns of cigarette brand preference between white, African and Native Americans. These patterns corresponded closely with the marketing targeted at each group by tobacco companies. Similarly, Parker, Sussman, Crippens, Elder and Scholl (1998) found that young African Americans avoided tobacco use to distinguish themselves from other ethnic groups, and Latinos used their interactions with those outside their ethnic group as a way of supporting resistance to peer pressure to smoke within their social group.
In drawing attention to cultural explanations of behaviour, there is a danger of victim blaming and stereotyping. Douglas (1995) illustrated this by reference to the UK Department of Health campaign targeted at the reduction in the prevalence of rickets conducted in the 1970s. Campaigns aimed at the white population identified the problem as one of poverty, and messages concentrated on including common foods containing vitamin D in one’s diet. The campaign aimed at Asians identified the problem as one of cultural preferences and practices, and its advice focused on changing from traditional diets to British diets. Such an approach views the measurement of ethnicity as unproblematic and neglects structural influences on health.
It could be argued that by focusing on ethnicity we neglect the confounding influence of social disadvantage and exclusion. A significant proportion of people in ethnic minorities occupy relatively low socioeconomic positions, although questions have been raised as to the suitability of traditional indicators for ethnic minority groups in such judgements (Davey Smith, 2002). As a result of this, many people in minority ethnic groups are also more likely to experience environmental stressors such as poverty, poor housing, unemployment and poor working conditions, and to have fewer resources to respond to them than the wider population (Robinson, 1984). African Caribbeans, for example, have been shown to reside in poorer residential areas, to be employed in lower-paid jobs and to experience higher levels of unemployment compared to their white counterparts (Modood et al., 1997). Measures of social disadvantage vary across ethnic groups, with those classified as Bangladeshi and Pakistani facing greatest hardship. Karlsen and Nazroo (2000) found that 80 per cent of Bangladeshi and Pakistani respondents and 40 per cent of African Caribbean and Indian respondents had household incomes below half the national average. These data compared to a 25 per cent prevalence among white respondents.
Studies examining the interaction of socioeconomic status (SES) and ethnicity suggest that social disadvantage plays a significant role in determining poor health among minority ethnic groups. Although some studies have found that including SES as a predictor diminishes the effect of ethnicity on mortality and morbidity (Bassett & Krieger, 1986; Sorlie, Backlund & Keller, 1995), a significant number have found that it negates its influence completely. In the USA, Haan and Kaplan (1985), for example, found no differences in mortality rates between blacks and whites after partialling out the influence of socioeconomic status. In general, the effect of SES within minority ethnic groups follows that of other social groups, with socially and economically advantaged groups having longer life and better health (Harding & Maxwell, 1997; Davey Smith, Wentworth, Neaton, Stamler & Stamler, 1996). There are exceptions to this rule, however. In the UK there is no gradient of CHD-related mortality for men born in the Caribbean or West or South Africa (Harding & Maxwell, 1997), implicating processes outlined elsewhere in this section. Some authors have argued that ethnic groups are doubly disadvantaged, with skin colour heightening the effect of SES on health. In the USA Klag, Whelton, Coresh, Grim and Kuller (1991), for example, found that African Americans with the lowest SES and darkest skin pigmentation exhibited the highest rates of hypertension. They argued that darker skins were associated with a greater experience of racism, a source of stress which compounds social disadvantage.
Ethnicity also interacts with socioeconomic status as a predictor of health-related behaviours. Lillie-Blanton, Anthony and Schuster (1993) found that higher levels of crack cocaine use amongst African Americans and Hispanics were no longer apparent when comparing ethnic groups that shared similar social environments such as drug availability, socioeconomic status and stress-coping behaviours. Similarly, a study examining the relationship between ethnicity and low levels of self-reported mammography screening behaviour found SES to be the underlying predictor. Women with health care access or health insurance problems were least likely to report attending screening, a consistent relationship across ethnic groups (Qureshi, Thacker, Litaker & Kippes, 2000).
Prejudice and Discrimination
As a consequence of low socioeconomic status, ethnic minorities experience greater exposure to environmental stress and problems in accessing health care (Gottlieb & Green, 1987). Experiences of discrimination and racial harassment and the demands of maintaining or shifting culture provide further environmental stress and reduced access to resources (Kessler & Neighbors, 1986). In addition, as people occupying lower socioeconomic groups have been found to have less future expectancy of quality of life and to lack feelings of self-control, ethnicity may interact with low socioeconomic status to produce a double disadvantage and increased powerlessness in blacks (Sleutjes, 1990). Gilvarry et al. (1999), for example, found that amongst patients with severe mental illness, African Caribbeans reported significantly more negative life events than their white British counterparts and other ethnic minority groups. They were also more likely to attribute negative life events to discrimination. Similarly, Karlsen and Nazroo (2000) found a strong association between perceptions and experiences of racial discrimination and poor health. Respondents reporting verbal abuse had a 50 per cent greater likelihood of reporting poor health compared to those not reporting abuse: those who reported racially motivated assault were twice as likely to assess their health as poor.
One explanation of the relatively high rates of hypertension observed in African Americans is that they are a consequence of exposure to environmental stressors, including racism (Klag et al., 1991). Experiences of racism are associated with habitually stronger emotional and physiological reaction to general stress, which in turn are thought to contribute to the long-term development of hypertension (Brosschot & Thayer, 1998). Laboratory studies seem to support this, with elevated stress responses associated with exposure to racism. Clarke (2000), for example, found that among a sample of African American women, past experiences of racism were positively associated with rises in blood pressure during a task in which participants talked about their views and feelings about animal rights.
Experiences of racism can also be seen to operate at a structural level. When ethnic minorities fall ill, they have been found to experience greater problems in access to health care and poorer quality services. In the UK, ethnic minorities have been shown to experience more difficulty in gaining access to health services such as cancer screening and antenatal care (Doyle, 1991; Narang & Murphy, 1994). These disadvantages help to explain why some ethnic groups have low contact with health services and rely less on physicians and more on their family as the primary source of health information (Grisso, Freeman, Maurin, Garcia-Espana & Berlin, 1999). When structural barriers such as lack of suitable information in an appropriate language are removed, attendance at health screening has been shown to increase (Bell, Branston, Newcombe & Barton, 1999), suggesting that low uptake of this type of health care is a consequence of structural barriers rather than lack of interest among the target group.
Even if ethnic minorities are able to access health care, research, predominantly from the USA, suggests they are likely to receive poorer quality treatments. Black people may be less likely than whites to receive curative surgery for early-stage lung, colon, or breast cancer (Brawley & Freeman, 1999), and less likely to be referred for transplantation or undergo transplantation than whites in chronic renal failure (e.g., Epstein & Ayanian, 2001). These racial and gender differences remained significant after adjustments for patients’ preferences, sociodemographic characteristics, the cause of renal failure, and the presence or absence of coexisting illness. Similarly, Mitchell, Ballard, Matchar, Whisnant and Samsa (2000) found that, even after adjusting for demographic factors, comorbidity, ability to pay, and provider characteristics, African American patients with transient ischaemic attacks were significantly less likely to receive non-invasive cerebrovascular testing, cerebral angiography, or carotid endarterectomy They were also less likely to have a specialist doctor as their attending physician. Other studies have shown that there were variations in doses of analgesics administered in emergency departments, with Hispanics and African Americans substantially undertreated for pain from fractures of long bones, and that postoperative pain was inadequately managed in non-white patients (e.g., Todd, Deaton, D’Adamo & Goe, 2000). Such inequalities provide a substantial explanation of higher mortality rates following disease diagnosis (Friedman et al., 1987; Haan & Kaplan, 1985).
We have so far considered both negative and positive influences on health clustered around gender, ethnicity, and the family. This section addresses how these and other influences develop cumulatively across the lifespan. Adopting such a perspective necessitates an assessment of the opportunities for, and constraints on, physical health, psychological well-being, and social functioning, and an examination of the biological, psychological and social contextual variation associated with developmental processes. The importance of a lifespan approach to understanding health and illness was highlighted by Townsend and Davies, who stated that ‘any satisfactory explanation (of health) must build essentially on the ideas of the cumulative dispositions and experience of the lifetime and multiple causation’ (1988: 104). Despite this, Penny, Bennett and Herbert (1994) noted that here has been surprisingly little recognition within health psychology of the contribution of lifespan psychology.
There is a substantial body of knowledge and theory informing lifespan perspectives on health, from sources as varied as Freud, Piaget, Erikson, and Havighurst. These theories often emphasize the relative importance of internal biological and cognitive changes in the early stages of development, and the increasing influence of external, social, factors on health and behaviour as the individual grows older. Together, these address the relative influence and interaction of biological, psychological and social factors at different stages within the lifespan.
Given the breadth of this chapter it is not possible to cover all the relevant literature. We therefore focus on three areas where health psychologists and others have contributed to our understanding of differences across the lifespan. The first addresses the role of biologically driven cognitive versus social factors on children’s perceptions of health and illness. The second section considers the impact of social circumstances on adult health and health behaviour in relation to life events. Finally, we consider whether differing periods within the lifespan leave an individual more vulnerable to illness and other negative events than others. In doing so we raise three key issues:
- The relative influence of individual cognitive development versus social contextual factors in the developing understandings of health and illness
- The interaction of biopsychosocial factors on health and health behaviour, focusing particularly on the moderating influence of age, ethnicity and gender
- The relative and cumulative influence of challenges to health at different stages within the lifespan.
Children’s Perceptions of Health and Illness
Many of our health-related beliefs, attitudes and behaviours originate in childhood. Identifying age-related differences in such cognitions and behaviours can facilitate more effective information giving and treatment during episodes of childhood illness, and may enhance health promotion programmes. Two major theoretical stances have been adopted in the study of children’s understandings of health and illness. The dominant approach is influenced by the work of Piaget, in which researchers such as Bibace and Walsh (1980) suggest children’s understanding of health and illness follows an invariant developmental sequence, mirroring more general and equally sequential cognitive changes. As such, these stress the importance of child rather than adult development, continuity and the influence of internal rather than external factors. This approach has been severely criticized by theorists such as Eiser (1989) who have suggested cognitions and behaviour are more driven by external influences such as children’s experiences of health and illness and knowledge acquisition. As such, the microsystem offers the opportunity for change and continues to exert an influence in adulthood.
Bibace and Walsh’s (1980) model of children’s perceptions of illness causation identified a number of age-related explanations, each associated with Piagetian cognitive developmental stages, although the age ranges identified for each type of thinking are very general and there is considerable variation in the age at which children achieve each stage of illness representation. The first stage of understanding illness occurs between the ages of 5 and 7 years, and is dominated by thoughts of magic or punishment, reflecting pre-operational thinking. Illness is seen as a result of magic or witchcraft, or as a punishment for not obeying parental instructions—a phenomenon known as immanent justice. At this time, there is also the emergence of an understanding that illnesses can be contagious, though the child may overextend this principle to assume that all illnesses are contagious. Between the ages of 8 and 10 years, the child begins to consider the mechanisms of disease. He or she can describe the experience of symptoms and explain their cause in terms of external agents or events, through contamination, and that they involve the body as a whole: ‘You catch a cold by going out in the wet weather. It stays in your body … and goes up into your chest.’ They understand a germ theory of disease causation and begin to realize that not all diseases are contagious. They are also beginning to identify internal processes, focusing on explanations describing how mechanical actions lead to changes in specific internal body parts: ‘You catch a cold from germs getting into your lungs and clogging them up. You sneeze to get the germs out.’ These beliefs correspond to the concrete-operational stage. By the age of 11 years, the child develops an abstract understanding of disease and realizes that illness can result from the failure of a specific body part, reflecting the Piagetian formal operational stage. By this time, they have a sophisticated understanding of the physiological processes underlying the disease: ‘A cold involves symptoms such as … You catch the germs that are all around us. Coughing and running nose are the side effects of the body’s fighting them off. It makes mucous to carry away dead germs.’ Around the age of 14 years, some children begin to recognize that disease may be a consequence of psychological processes.
Bibace and Walsh’s model has been challenged both methodologically and theoretically. Bird and Podmore (1990), for example, noted that there were several aspects of Bibace and Walsh’s work that questioned the validity of its findings: in particular, that it was based on children’s responses to questions about disease causality that were too short to reliably code.
Other theorists, including Eiser (1989), have argued that children’s experiences of illness have more of an influence than stage of cognitive development and that these influences continue into adulthood. Evidence favouring this hypothesis can be found in the findings of Redpath and Rogers (1984), who showed that children experiencing chronic illness had a greater understanding of disease than their healthy peers. A more detailed model of this type was developed by Carey (1985), who suggested that sophisticated explanations are dependent on increased knowledge and a developing understanding of human behaviour and biology. As we develop, our understandings of illness are not constrained at a structural level as Piaget claims; rather the beliefs are logical within our intuitive knowledge of the world. Initially children are ‘naive psychologists,’ with explanations of eating as a behavioural phenomenon (‘You eat because your mum tells you it’s ready’) and illness as a result of human action (‘You get ill because you have done something wrong’). As our understanding of underlying biological processes increases we develop as ‘naive biologists’ (‘You eat because you need the food to keep your body healthy’ and ‘You become ill because of germs’). Relatively unsophisticated explanations in both children and adults are a result of uncertainty and a lack of information, not cognitive structures. Warwick, Aggleton and Homans (1988), for example, in the early days of public information on AIDS, identified three models of causation in young adults: miasmatic (‘There’s a lot of it about’; ‘It’s everywhere. You get it from the environment you live in, the people you mix with’); serendipitous (‘Whether you fall prey to infection depends on chance or luck’); and endogenous (‘Like cancer, it’s in everyone from the start, just waiting to be brought out’). This has led to alternative explanations which suggest that children’s understandings of illness are better explained by accumulated increases in knowledge than by a qualitative shift from one cognitive stage to another.
Relatively few studies have focused on children’s understandings of health (as opposed to illness). Of these, Normandeau, Kalnins, Jutras and Hanigan’s (1998) Canadian study of children from a variety of socioeconomic groups and urban and rural locations found multidimensional explanations of health reflecting their everyday experiences. These revolved around three main dimensions frequently found in adult explanations: functionality, adherence to good ‘health habits,’ and mental health. Similarly, Goldman, Whitneysaltiel, Granger and Rodin (1991), questioning 4- and 6-year-olds, found variation in illness representations dependent on type of illness. This variation closely reflected adult representations concerning causation, identity, consequences, probable duration, and whether it was curable (e.g., Nerenz & Leventhal, 1983).
A large body of research has assessed the relationship between exposure to life events and physical health, psychological and social functioning, and health-related behaviours. These studies have adopted explanatory frameworks that focus on chronic stressors, acute stressors and stress-coping behaviours.
One of the largest sources of health variation in adults is paid employment and its associated occupational class (Arber, 1991). This brings with it a number of factors that impinge on health at this particular life stage. A particularly important factor is the stress-related risk associated with psychosocial environments such as the demands of the job, the latitude the workers have in dealing with these demands, and the support available to them (Karasek & Theorell, 1990). The relative influence of each of these variables may differ across job type and at different career stages—with increased latitude, for example, in later career stages. This importance of work as a moderator of psychological and physical health is illustrated by Hobson and Delunas (2001), who found that five of the top 10 most frequently reported stressful events in adults were related to work. Work, however, also exerts a less obvious psychological influence on health. Kingsberg (2000), for example, found that the psychological impact of ageing on sexuality and intimate relationships is strongly influenced by sense of identity, self-esteem and self-worth which in turn are derived from occupation or avocation.
Other theorists have begun to address how the context in which stressful events occur can influence the individual’s response to them. Goldberg and Comstock (1980) highlighted the importance of studying different social subgroup responses to life events, as groups, defined for example by ethnicity and gender, are exposed to varying types and levels of events and experience them in different ways (see the earlier sections on gender and health and on ethnic minorities and health).
The psychological impact of adverse life events may differ according to life stage. In a study of people with a chronic illness, for example, Sherbourne, Meredith, Rogers and Ware (1992) found that the impact of stressful life events on health-related quality of life was determined by timing of exposure. Financial events had an immediate negative effect on functioning and wellbeing that persisted over time in the middle-aged. Bereavement, on the other hand, had the most negative impact when it occurred in young adulthood, although its effect was delayed somewhat over time. The importance of the age when the life event is experienced is also suggested by Ensel, Peek, Lin and Lai (1996), who found a prolonged influence for life events on mental health. Using panel data, the influences of stressors over a 15-year period were examined. Distal stressors, some occurring up to 15 years ago, maintained a direct and significant relationship with depressive symptomatology, independent of more proximal stressors. The type of stressor associated with distress varied with age, leading the authors to conclude that the stage of life at which a stressor occurs, rather than its nature, determined its subsequent influence on psychological health.
One way of coping with adverse negative experiences may involve comparing one’s experience in a more positive light than that of others. Heckhausen and Brim (1997), for example, found that a sample of people of all ages experiencing changes in relation to health status, marriage and paid work perceived other people’s problems to be more serious than their own. This effect was particularly pronounced amongst older adults. This type of evaluation may help individuals to cognitively restructure their experience, and help them cope emotionally with the experience. Of interest is that it may be particularly important in responding to life events in older age. One explanation for the particularly adverse impact of life events that occur at an inappropriate life stage (such as the death of a parent in adolescence) is that this type of social comparison is not available to the individual. Other theorists have highlighted the importance of issues such as gender, as well as age, in understanding coping responses to life events. Men and women may draw on different resources to cope with life events such as bereavement. In a 1-year follow-up study of men and women who had lost a partner in older age, it was found that, for women, having a best female friend, higher education and perceptions of higher relative health influenced levels of coping. Men, on the other hand, were more likely to share their emotional experiences as time elapsed and to be impeded in their emotional coping by financial stress (van Baarsen & Broese van Groenou, 2001). The reliance of women on family and external social support may make them particularly vulnerable to disruption of such systems (Elliott, 2001). Related to this may be problems associated with the loss of attachment to the extended family as children are more mobile and increasingly move from the family home as they mature. In addition, Simon (1995) suggested that women may react more strongly to work and family strains than men because of the importance that these roles have for their sense of worth.
Examining health behaviours in the light of life events acknowledges that such behaviours are a response to environmental conditions. In young adulthood, life events, although not associated at that stage with biological risk factors, have been shown to have an association with lifestyle. For example, Twisk, Snel, de Vente, Kemper and van Mechlen (2000) found positive and negative life events and daily uplifts and hassles were related to increases in risk behaviours. Perreira and Sloan (2001), meanwhile, examined the influence of life events on alcohol consumption in a longitudinal study of older adults aged 51 to 61 years. They found that changes in levels of drinking over a 6-year period were associated with key life events. Whilst retirement was associated with an increase in drinking, the onset of chronic conditions and episodes of hospitalization were associated with decreases in consumption. Getting married or divorced facilitated both protective and risky drinking behaviour. These findings suggest that the influence of life events on health behaviours is not necessarily negative. Brennan, Schutte and Moos (1999), in a three-wave panel study of stressors and drinking behaviour amongst late-middle-aged and older men and women, found life stressors did not predict heavier or more frequent drinking. Contrary to expectations, alcohol consumption presages fewer negative life events, health and financial stressors for women and fewer financial stressors for men. For women, health stressors, and for men, financial stressors, predicted reduced alcohol consumption, leading the authors to suggest that there may be a benign feedback cycle where moderate alcohol consumption and life stressors reduce each other. Similarly Andersson and Stanich (1996) found that exposure to negative life events in old age resulted in positive health behaviours. When individuals experienced illness or disease, health practices such as self-care, improved dietary behaviour, increased health-protective behaviour and health information seeking were chosen as positive coping techniques.
One final issue concerns the concept of stability versus change, a central debate within lifespan health psychology. A number of theorists have argued that individuals are not indelibly shaped by their earlier experiences—that change is possible throughout the lifespan. This approach is illustrated by the research discussed above examining exposure to life events such as bereavement, marriage, retirement, chronic and acute illness. In some cases these events can be random and unexpected. Others are likely to occur at particular times in the lifespan and are associated with developmental tasks (Erikson, 1959). Here the timing of experiences is seen as crucial, with normative and ordered events having a different impact on health from those that deviate from commonly shared experiences. For childhood these are conceptualized as critical periods, a time when we are particularly responsive to the presence or absence of experience such as the development of attachments. Among adults, Neugarten (1968) has highlighted the importance of on-time and off-time events. It is suggested that experiences that conform to normative age expectations facilitate adaptation and development, whereas those that are atypical or off-time, such as widowhood early in life, have greater potential for poor health outcomes. Even so, a variety of ways of experiencing and responding to them has been identified. Stress processes, resilience and adaptation to change all play a role in determining health outcomes. Those favouring the concept of stability, however, suggest that early experiences, be they advantageous or disadvantageous, influence subsequent development. We therefore review a final group of studies which examine the cumulative health impact of experiences across the lifespan.
These studies have adopted longitudinal or retrospective designs in order to examine the association between childhood and adulthood experiences and health and illness in later life. They have tended to focus on late-middle-age and old-age populations and use measures associated with SES as predictors and physical, psychological and social measures as dependent variables. Such studies hold that ‘social organisation structures life chances so that advantages and disadvantages cluster cross-sectionally and accumulate longitudinally’ (Holland, Lee, Blane & Davey Smith, 2000: 1). In this way ongoing psychosocial conditions create pathways to health and illness that operate from the start of life, with timing and duration of exposure as critical features.
Evidence suggests that the earlier and longer the exposure to conditions of social disadvantage the more profound the effect, with individuals experiencing disadvantage as children being more likely to accumulate further disadvantage as they progress through life (Lynch et al., 1994). The relationship between early experience and subsequent physical health is demonstrated by Holland et al. (2000), who found childhood chronic illness and slow growth predicted exposure to subsequent health hazards up to early old age; as childhood height decreased, lifetime exposure to hazards increased. Power (2000) also found that long duration of low family income had a negative effect on children’s cognitive development at age 5, school achievement at age 12 and subsequent adult earnings. Overall lifetime exposure measures found that 17.6 per cent of the men with the worst circumstances exhibited poor health at age 33 compared to 4.1 per cent of those with the best circumstances. For women the figures were 19.4 per cent and 3.9 per cent respectively. Similarly, Lynch, Kaplan and Salonen (1997), in a heart disease risk factor study of 2,674 middle-aged Finnish men, found health-risk behaviours and psychosocial dispositions detrimental to health associated with poor childhood conditions and low levels of parental socioeconomic status. They suggest that dietary behaviour and physical activity are determined directly by childhood social environments via the establishment of habitual behaviours early in life. Childhood background was seen to influence smoking behaviour and alcohol consumption indirectly via education level and occupation. Those individuals born to poor parents received the least education and were subsequently engaged in low-paid work with higher job and financial insecurity and more work-related injury. Such occupations were also associated with higher levels of smoking, greater alcohol consumption, more hostility and lack of hope for the future.
It has been suggested that disadvantage across the course of one’s life impacts on psychological as well as physical and social health. Using measures of parental education and occupation and attained education and personal income in adulthood, Turrell et al. (2002) found a relationship between socioeconomic position, mobility, cumulative disadvantage across the lifespan and cognitive functioning in a sample of males. Men who remained in a low socioeconomic position scored worst on all cognitive tests, whilst men who rose from disadvantage scored better than those with limited or no upward mobility. Men who experienced downward mobility, on the other hand, had poorer scores than those who remained in their social position. Given the retrospective design of this study, however, it is unclear whether socioeconomic mobility influences cognitive functioning or vice versa.
No individual can be fully described and understood without knowledge of their gender, age, and social background. The concepts are impossible to isolate, and by doing so one inevitably simplifies reality and fails to acknowledge their often complex interaction. In outlining the individual impact of each of these categories, we have inevitably had to simplify frequently complex systems. It is important to recognize that age, gender, ethnicity, and the family are frequently used labels to identify factors that influence health. They act as signifiers—convenient labels that identify broad categories of risk for advantage and disadvantage. In this chapter, we have attempted to examine the biopsychosocial processes hidden behind these categories. In doing so we have highlighted the importance of examining individual factors within an immediate and wider social context.
For gender, we have seen that health is the outcome of both biological sex differences and the differing social worlds that men and women inhabit. In reviewing the research, it has become apparent that there is great variation in the sources of stress associated with gender roles both inside and outside the home. We have also seen that gender identity impacts greatly on the availability of repertoires of health-related behaviours and their enactment, medical help-seeking behaviour, and the provision of social support. These develop across the lifespan through the process of role socialization and the development of gender identity. It is important to recognize that these processes not only continue through the lifespan, but take place within a dynamic context that encompasses the social, political and economic, which together shape and confine the roles and identities available to men and women.
The influence of gender roles and identity and social and economic conditions can also be found in research that has examined the family. The family can act both as a buffer against sources of stress, such as periods of ill-health, and as a source of models of positive coping behaviour. This may be particularly the case for males. Families may also have a negative effect on health, through family-role-related demands and unhealthy interactions, especially for females. This highlights the need to understand how family roles and responsibilities are negotiated across the lifespan and differ according to societally determined gender-related norms and power relationships (Sweeting, 2001). It is also important to recognize that the family does not exist within a vacuum. It moderates and reflects the influence of the wider social context. By concentrating purely on internal family processes and family structure, there is a danger of ignoring issues of structural advantage and disadvantage that impact on the family, particularly at key points within its lifespan (McMunn et al., 2001).
Perhaps more than any other category, ethnicity highlights the importance of examining the underlying social processes and environmental influences associated with a seemingly ‘obvious’ single epidemiological indicator. We have seen how behavioural norms are the result of a dynamic interaction involving family, peers, and inter- and intra-group processes (Gittelson et al., 1999). As with gender and the family, focusing on the single indicator of ethnicity can obscure the multiple impacts of underlying differences in socioeconomic opportunities, social resources, and living conditions on health and behaviour (Brown, 1984). Experiences of discrimination and racial harassment and the demands of maintaining or shifting culture provide further environmental stress and reduced access to resources (Kessler & Neighbors, 1986).
While it is important to recognize that gender, ethnicity, and the family represent axes whereby advantage and disadvantage impact on the individual at any one time, it is equally important to recognize the cumulative effect of these and other influences on health across the lifespan. The nature and distribution of life events and resources differ by age, as does their impact. Events that occur out of the normal developmental pattern, for example, may exert a disproportionate impact on health in comparison to those that occur at more expected life stages. More long-term age-related factors such as social and family context and material resources also contribute to understandings of health and health-related behavioural choices. They have also been implicated in cumulative health advantage and disadvantage via their influence on individual factors, such as health beliefs and expectations, and the normative constraints on behaviour that they impose. Brofenbrenner (1989), for example, proposed a model that pointed to the influence of interacting microsystems such as the family and peers as prime influences on lifespan development. These in turn are influenced by macrosystems such as economics, politics and social status.
This model has its roots in the work of theorists such as Sameroff (1986), who attempted to develop nature/nurture arguments by positing transactional explanations of change, which focus on the constant reciprocal influence between the individual and the environment. Such an approach reflects assumptions associated with the biopsychosocial model of health and frameworks adopted by the World Health Organization (Mendoza, 1990), which identified four interacting factors that determine health. These are genetic and individual features such as cognitions, the micro-social environment such as family, peers and work, the macrosocial environment such as economics and the media, and the wider physical environment. In this way, biological changes associated with conception, pregnancy, genetic inheritance, physical growth and ageing, puberty and menstruation exert an influence on health. They do so, however, alongside and in interaction with the psychological changes associated with cognitive, moral, personality and identity development and social contextual factors, including relationships with peers, the family marriage, life events, work demands, the economic environment and social status. Only by adopting such a multilevel perspective can we hope to understand and address the health inequalities associated with gender, ethnicity and the family across the lifespan.