Medical, Socialogical and environmental issues in cardiovascular disease epidemiology, prevention and rehabilitation.
Rajeev Gupta, TS Kler, VP Gupta
Monilek Hospital and Research Centre, Jaipur; Escorts Heart Institute and Research Centre, New Delhi; and University of Rajasthan, Jaipur, India
A growing body of evidence points to significant relationship between risk of coronary heart disease (CHD) and psychosocial factors. Social determinants of health as defined by the World Health Organisation (WHO) and relevant to cardiovascular health are- social gradient, stress, early life events, social exclusion, work-related conditions, unemployment, lack of social support, addiction, food and transport. Socioeconomic status (SES) is a simple tool to measure the social gradient. Its principal measures are education, occupation, and income or a combination of these. Education has been the most frequent measure because it does not usually change (as occupation or income might) after young adulthood and information about it can be obtained easily. In developed countries there is an inverse relationship between CHD and many indicators of SES, i.e., higher SES is associated with lower CHD incidence. Similar inverse relationship is emerging in India also.

Substantial evidence has amassed linking psychological factors, e.g., depression, anxiety, personality traits, type A behaviour, hostility, social isolation, chronic and subacute life stress, and acute stress to CHD. However, little is known of mechanisms by which these factors contribute to the increased risk. Deleterious physiological effects of stress are disturbed endothelial function, endothelial injury, vasoconstriction, platelet activation, haemostatic changes, increased heart rate and blood pressure, and arrhythmogenesis. Acute and chronic stress may affect other coronary risk factors, e.g., high blood pressure, cholesterol levels, smoking, physical inactivity and overeating. Studies using psychosocial therapies to prevent CHD are promising but limited by small sample size and methodological flaws. More data are needed to clearly define the role of stress management in alleviating heart disease risk.
Psychosocial factors and individual lifestyles have significant impact on health. Unhealthy habits (smoking, sedentary lifestyles, etc.) account for 54% of known contributions to coronary heart disease (CHD). Behavioural and biological risk factor interventions can reduce morbidity, disability and death due to heart disease. However, there is a gap in understanding between scientists concerned with psychosocial risk factors (sociologists, psychologists) and biological risk factors. If prevention of CHD is to be achieved in India, these two sciences should be fully integrated because psychosocial factors are major determinants of coronary risk factors and CHD.
The concept of risk factors constitutes a major advance for developing strategies for preventing CHD. Framingham Heart Study in USA played a vital role in defining the contribution of risk factors for CHD occurrence in the general population.1 The major risk factors found important were cigarette smoking, hypertension, high serum cholesterol and various cholesterol fractions, low levels of high-density lipoprotein cholesterol, and diabetes mellitus. Factors other than those termed major risk factors also increase the likelihood of developing CHD. Among these are obesity, physical inactivity, family history of premature CHD, hypertriglyceridaemia, small dense low-density lipoprotein (LDL) particles, increased lipoprotein(a) levels, increased serum homocysteine, and abnormalities in several coagulation factors.

Insulin resistance which refers to a generalised metabolic disorder characterised by muscle abnormalities, truncal obesity and hyperinsulinaemia has emerged an important risk factor, especially among Indians. Clustering of several metabolic risk factors in a single patient has been termed the metabolic syndrome.2 This syndrome is characterised by atherogenic dyslipidaemia (borderline high LDL cholesterol, raised triglycerides, dense LDL particles, low HDL cholesterol), hypertension, insulin resistance with or without non-insulin dependent diabetes, and a procoagulant state, and could be important in our population. Psychosocial factors that include psychological factors (mental stress, personality type, etc.) and socioeconomic status are not listed in the Framingham risk factor list1 but are important.

Numerous efforts have been directed in identifying probable psychosocial and behavioural factors that may contribute to the development of CHD. The most likely candidates have been identified anecdotally for a long time and include states of high emotional arousal, poverty, disruption of social ties, adverse major life events, and "coronary-prone" personality types.5 These psychosocial factors are often lumped together under the umbrella rubric of stress, a term first utilised in a biological context by Cannon in 1914 and then elaborated and popularised by Selye in 1930's.
Table 1: Psychosocial Risk Factors
Lack of social support, social isolation
Lack of social cohesion
Coping styles
Behaviour, type A
Job strain and stress
Low-level job control
Hostility, anger and other negative emotions
Lack of religious affiliations
Among the first epidemiological observations relevant to stress and heart disease was the finding that different countries have very different rates of heart disease and that these differences cannot be completely explained by genetic differences or by traditional risk factors.6 For example, American men in the Framingham Heart Study were found to have twice the risk of developing CHD as European men having the same standard risk factors. Other studies showed a marked gradient of CHD mortality between individuals in Japan (1.8 deaths/1000), Hawaiian Japanese (3.2/1000), and Caucasians (9.8/1000) making a Caucasian US male five times as likely to die of CHD as a Japanese male living in Japan.6 Similar CHD mortality gradients were observed between South Asians living in India and Britain.7 Urban-rural differences in prevalence of CHD in India also suggest that psychosocial factors involved in urbanisation are important.8 Psychosocial factors that are important in CHD incidence are poor social support, lack of cohesion, work stress, low-level job control, hostility, type A behaviour, and negative emotions (Table 1).3,5 Depression has emerged as a major risk factor for mortality in survivors of myocardial infarction.
World Health Organisation (WHO) has identified the following social determinants of health in general and cardiovascular health in particular. These are- the social gradient, social class differences, stress, early life, social exclusion, work, unemployment, social support, addiction, food and transport. It is important to know the contribution of each of these factors on cardiovascular health. These factors are also gaining importance in developing countries as evinced by many new epidemiological studies.
Poor social and economic circumstances affect health throughout life. People further down the social ladder usually run at least twice the risk of serious illness and premature death of those near the top. Between the top and bottom, health standards show a continuous social gradient, so even junior office staff tends to suffer much more disease and earlier death than more senior staff. Most diseases and causes of death are more common lower down the social hierarchy. The social gradient in health reflects material disadvantages and the effects of insecurity, anxiety and lack of social integration. Disadvantage has many forms and may be absolute or relative. It can include: having few family assets, having a poorer education during adolescence, becoming stuck in a dead-end job or having insecure employment, living in poor housing and trying to bring up a family in difficult circumstances. These disadvantages tend to concentrate among the same people, and their effects on health are cumulative. The longer people live in stressful economic and social circumstances, the greater the physiological wear and tear they suffer, and the less likely they are to enjoy a healthy old age.
Table 2: Measures of Socioeconomic Status
Social class differences
Educational status
Employment status
Indices of social class
Measures of living conditions
Area-based measures
Life-span measures of social class
Measures of income inequality
Eminent epidemiologist, Sir Geoffrey Rose stated16 that "the primary determinants of disease are mainly economic and social, and therefore its remedies must also be economic and social". It has been common to characterise CHD as a disease of affluence. This may have been a reasonable description as CHD reached epidemic proportions in the western world and now in India. But it does not serve sufficiently to describe the present picture of CHD world-wide because17:
:: CHD is emerging as a major cause of death in developing countries.
:: CHD rates are rising in many countries of Central and Eastern Europe.
:: CHD rates are falling in the wealthy countries of Europe, North America, and Australia.
:: Within wealthy countries, CHD is now more common among the less wealthy groups.
:: The decline in CHD in the UK and the USA has occurred faster among higher socio-economic groups.
Rather than characterise CHD as a disease of affluence, it is more accurate to say that difference in CHD between and within countries can only be understood with reference to the social, cultural, and economic forces that determine them. Preston and Nelson18 reviewed mortality data from 165 countries and showed an inverse association between CHD and all-cause mortality. Countries from low CHD mortality are usually third-world developing countries with high mortality from infectious diseases. Epidemiological transition in these countries has led to a decline in infectious diseases and increase in chronic diseases predominantly CHD and cancer. Gupta et al commented on the influence of socioeconomic factors involved in epidemiological transition in causing increased CHD prevalence in India.

Conventionally, increasing CHD prevalence in Indian and other Asian countries has been attributed to changes in various metabolic coronary risk factors as a result of modernisation. However, there are many factors involved in epidemiological evolution of cardiovascular diseases in an ethnic group (acculturation, urbanisation, affluence, etc.). These result in altered intake of saturated fat, salt and tobacco. Prevalence of cardiovascular diseases initially increases with a rise in these factors, then stabilises, and finally decreases. In Indians these social and economic indices of epidemiological transition explain the increasing hypertension and CHD prevalence. Urban population, as proportion of total, has doubled in last 90 years (11% in 1901, 26% in 1991). Affluence measured by per capita net domestic product, growth of production, and human development index has also increased. Per capita consumption of total fats does not show an increase but intake of hydrogenated fats increased significantly from 1956 to 1986. In Delhi, serum cholesterol levels increased from 157±29 mg/dl in 1982 to 199±39 mg/dl in 1996. Per capita tobacco consumption per adult person per year in kg was 0.7 in 1974, 0.8 in 1990 and is projected to increase to 0.9 in the year 2000. Per capita consumption of salt increased from 10.5 g/day in 1970 to 16.8 g in 1994. Situation in other developing countries, where CHD is rapidly increasing, can be similarly explained.
Marmot has highlighted the fact that income inequalities are more closely related to life expectancy than the overall income level, or wealth, of a society. Therefore it is not only important to examine socioeconomic groups within a country but to study the social class differences in a particular society. Currently in many Western countries there are social class differences in CHD mortality. In Whitehall Study of British Civil Servants, Marmot et al reported that there was a clear inverse relation of employment grade with CHD mortality.22 Studies from USA have reported that educational level which is an important determinant of socioeconomic status is inversely associated with CHD incidence as well as mortality.23

Although social class differences in CHD incidence and mortality presently show an inverse relationship it was not always the case.17 In Britain, in 1930's when CHD was on the rise it was more common in classes I and II than in semi-skilled and unskilled clases IV and V. The change-over had occurred by the early 1960's. Subsequently as the CHD rates have started to decline, there has been a marked decline in subjects in non-manual occupations and no decline at all in manual occupations.22 The implication of the changing social class pattern of CHD is that the factors linking economic position to disease may change. This can be put together with the observation that, as economic development proceeds CHD appears to increase, and as it proceeds further it declines. It is as if CHD passes through the society in a wave, affecting first the more privileged and subsequently the less privileged, declining first in those better-off and presumably subsequently in the rest.17

Black and his colleagues24 suggested four possible types of explanations linking social class and CHD: artefact, social selection, culture/lifestyle, and material conditions. After detailed examination of the evidence, they rejected artefact as well as the possibility that social class differences are all due to selection of unhealthier people into lower grades. Black favoured a materialistic explanation, that social class differences in health are due to material conditions in life that show correlation of income levels and wealth: housing, transport, and the environment. Marmot17 also includes nutrition and smoking into lifestyle or material conditions and considers them important. Barker's studies25 suggest that it may not only be conditions acting during adult life that are important; circumstances in utero or in infancy may have a persisting effect on mortality rates throughout life.

Life contains a series of critical transitions: emotional and material changes in early childhood, the move from primary to secondary education, starting work, leaving home and starting a family, changing jobs and facing possible redundancy, and eventually retirement. Each of these changes can effect health by pushing people onto a more or less advantaged path. People who have been disadvantaged in the past are at the greatest risk in each transition. This means that welfare policies need to provide not only safety nets but also springboards to offset earlier disadvantages.

Good health involves reducing levels of education failure, the amount of job insecurity and the scale of income differences in society. We need to ensure that fewer people fall and that they fall less far. Policies for education, employment and housing affect health standards. Societies that enable all their citizens to play a full and useful role in the social, economic and cultural life of their society will be healthier than those where people face insecurity, exclusion and deprivation.
Level of education is the most widely used measure of socioeconomic status.23 Education has been the most frequent measure because it does not usually change (as occupation or income might) after young adulthood, information about education can be obtained easily, and it is unlikely that poor health in adulthood influences level of education.

Analysis of mortality in US National Health and Nutrition Examination Survey showed a strong association between educational level and risk of death. Men aged 45 to 64 years with 0 to 7 years of education had 1.96 times the risk of death than those with 12 or more years of education. Keil et al found in the Charleston (USA) Heart Study that the age -adjusted rates per 1000 for CHD mortality among men of low education was 7.1 compared with 3.5 among high educational level. Mulcahy et al in Ireland found that higher educational groups had lower levels of coronary risk factors (smoking, diastolic blood pressure, weight, and plasma cholesterol levels) and a lower level of coronary morbidity. Studies in Finland, New Zealand, Sweden, Norway and other countries have found similar relationships.23

Measures of income are important marker of SES. Income provides access to goods and services, including quality education and medical care. However, the measurement of income level is complex and not used in many epidemiological studies. Other measures of SES include occupation, employment status, composite indices of social class, measures of living conditions, area-based measures, life span measures of social class and measures of income inequality. Inverse associations between SES and all-cause mortality and CHD incidence as well as mortality has been shown in many studies from developed countries.23
CHD prevalence studies from India have conventionally reported a greater prevalence in upper and middle socio-economic classes. Padmavati did not report CHD among low-income group urban subjects in Delhi26. Sarvotham and Berry27 in Chandigarh in 1960's reported CHD prevalence in adults >30 years among high class, high-middle class, low-middle class and low class as 11.4%, 7.7%, 6.9% and 2.4 in men and 3.9%, 7.7%, 4.6% and 1.1% in women respectively. The difference in prevalence among men from the low and low-middle income groups was significant (p<0.01) and from high and low income groups was highly significant (p<0.001). Chadha et al28 studied urban subjects in Delhi in late 1980's and classified socio-economic status as high and low based on housing conditions, occupational pattern and income. The prevalence of CHD was greater in high-class as compared to low class in both men (6.1% vs. 2.0%) and women (3.0% vs. 0.8%) (p<0.01).

In rural India, Kutty et al from Kerala29 reported an inverse relationship of socioeconomic status with CHD prevalence. The prevalence was 1.7%, 2.2%, 5.3% and 7.9% respectively in social classes I (poorest) to IV (high class). Wander et al30 from rural Punjab also reported a greater CHD prevalence in skilled workers, priests, teachers and retired government service personnel (9.2%, 9.1%, 6.2%, 4.8% respectively) as compared to small time businessmen (3.4%), housewives (3.1%) and labourers (1.7%).

Gupta et al31 studied influence of educational status on prevalence of CHD and coronary risk factors in rural Rajasthan. 3148 subjects (1982 men, 1166 women) aged20 years were divided into four groups according to years of schooling. Illiteracy and low educational levels were associated with less prestigious occupations (agricultural and farm labouring) and inferior housing. The prevalence of CHD diagnosed by ECG was significantly greater among uneducated and less educated persons and showed an inverse relation with education in both sexes (Figure 1). Among uneducated and less educated there was a higher prevalence of coronary risk factors smoking and hypertension. Other measures of social class, such as exact employment status, income inequality, deprivation, and psychosocial factors (social isolation, coping styles, behaviour, job strain, and anger), which are also possible mechanisms by which social class and education influence CHD incidence, were not inquired. It was also noted that those subjects who were involved in prayers regularly had a significantly lower CHD prevalence.10

In a case control study, Pais et al reported a greater CHD prevalence among the less educated and the poor in Bangalore.32 Stein et al reported33 that poor in-utero foetal growth and low maternal weight was associated with a greater CHD incidence in adults in a retrospective study from Mysore, Karnataka. In a descriptive study Sanjivi and Gopalkrishnan reported that acute coronary events and CHD was more in poor classes in Madras.34

Thus, studies show that CHD epidemic in India has entered into advanced phase of epidemiological transition and more and more of poor and illiterate persons shall be burdened with it.35 Social and economic factors need to be improved. Literacy has a major role in preventive efforts. It has been shown that people in higher educational strata are more likely to care about health and might be following a healthier lifestyle.23 Public health systems that are geared to prevention of chronic diseases are urgently needed in India.35

There is a substantial body of evidence for a consistent relation between SES and incidence and prevalence of cardiovascular disease, secular trends in CHD mortality, survival in CHD patients, prevalence of cardiovascular risk factors, and access to high-quality care and diagnostic services. Based on this several recommendations for public education, cardiovascular research, medical care, and public policy have emerged.23 Public education should be broad based and address not only specific cardiovascular risk factors but also the societal conditions that lead to adoption and maintenance of high-risk behaviour. Promotion of products associated with increased CHD risk (tobacco, high-fat foods, hydrogenated oils, etc.) should be regulated. Preventive health-care for cardiovascular diseases among low SES subjects should receive high national priority.
Social and psychological circumstances can cause long-term stress. Continuing anxiety, insecurity, low self-esteem, social isolation and lack of control over work and home life have powerful effects on health. Such psychosocial risks accumulate during life and increase the chances of poor mental health and premature death. Long periods of anxiety and insecurity and the lack of supportive friendships are damaging in whatever area of life they arise.

How do these psychosocial factors affect physical health? In emergencies, the stress response activates a cascade of stress hormones that affect the cardiovascular and immune system. Our hormones and nervous system prepare us to deal with an immediate physical threat by raising the heart rate, diverting blood to muscle and increasing anxiety and alertness. Nevertheless, turning on the biological stress response too often and for too long is likely to carry multiple costs to health. These include depression, increased susceptibility to infection, diabetes, and a harmful pattern of cholesterol and fats blood, high blood pressure and the attendant risks of heart attack and stroke.

Human and various non-human primates studied in the wild and in captivity have similar mechanisms for dealing with psychosocial stress. Studies of primates show that subordinate animals are more likely than socially dominate animals are more likely than socially dominant animals to suffer from clogged blood vessels and other changes in their metabolism. In humans, such changes are linked to a higher risk of cardiovascular disease. The lower people are in the social hierarchy of industrialised countries, the more common these health problems become.

A medical response to the biological changes that come with stress might be to try to control them with drugs. But attention should be focused upstream, on tackling the causes of ill health. In schools, businesses and other institutions, the quality of the social environment and material security are often as important to health as the physical environment. Institutions that can give people a sense of belonging and of being valued are liked to be healthier places than those in which people feel excluded, disregarded and used. Governments should recognise that welfare programmes need to address both psychosocial and material needs: both are sources of anxiety and insecurity. In particular, governments should support families with young children, encourage community activity, combat social isolation, reduce material and financial insecurity, and promote coping skills in education and rehabilitation.
Important foundations of adult health are laid in prenatal life and early childhood. Slow growth and a lack of emotional support during this period raise the lifetime risk of poor physical health and reduce physical, cognitive and emotional functioning in adulthood. Poor social and economic circumstances present the greatest threat to a child's growth, and launch the child on a low social and educational trajectory.

Acting through poor inappropriate nourishment of the mother and through smoking, parental poverty can reduce prenatal and infant development. Slow early growth is associated with reduced cardiovascular, respiratory, kidney and pancreatic functioning in adulthood. Parents' smoking impedes the child's respiratory development; this decreases respiratory functioning and thus increases vulnerability in the adult.

Barker initially reported that in Britain babies born underweight had an increased incidence of heart attacks, diabetes and mortality as they grew up. This was hypothesised as being due to a smaller size of pancreatic cells leading to a greater prevalence of diabetes, hypertension and abnormal lipids finally leading to premature HCD and deaths. A study reported from South India has confirmed these observations and shown that low-birth weight babies had in creased incidence of short height, diabetes and CHD deaths. More studies are needed within India to confirm this hypothesis in India.

Parental poverty starts a chain of social risk. It begins in childhood with reduced readiness for and acceptance of school, goes on to poor behaviour and attainment at school, and leads to a raised risk of unemployment, perceived social marginality and to low-status, low-control jobs in adult life. This pattern of poor education and employment damages health and, ultimately, cognitive functioning in old age. New action is needed to foster health and development in early life, particularly among people in poor social economic circumstances. Policy should aim to:
:: Reduce parents' smoking;
:: Increase parents' knowledge of health understanding of children's emotional needs;
:: Introduce pre-school programmes not only to improve reading and stimulate cognitive development but also to reduce behaviour problems in childhood and promote educational attainment, occupational chances and healthy behaviour in adulthood;
:: Involve parents in such pre-school programmes to reinforce their educational effects and reduce child abuse;
:: Ensure that mothers have adequate social and economic resources; and
:: Increase opportunities for educational attainment at all ages, since education attainment at all ages, since education is associated with raised health awareness and improved self-care.
Investment in these policies would greatly benefit the health and working capacity of the future adult population.
Processes of social exclusion and the extent of relative deprivation in a social have a major impact on health and premature death. The harm to health comes not only from material deprivation but also from the social and psychological problems of living in poverty. Poverty, unemployment and homelessness have increased in many countries, including some of the richest. In some countries, as much as one quarter of the total population-and a higher proportion of children-live in relative poverty (defined by the European Union as less than half the national average income). Relative poverty, as well as absolute poverty, leads to worse health and increased risks of premature death. People who lived most of their lives in poverty suffer particular bad health.

Migrants from other countries, ethnic minority groups, guest workers and refugees are particularly vulnerable to social exclusion, and their children are likely to be at special risk. They are sometimes excluded from citizenship and often from opportunities from work and education. The racism, discrimination and hostility that they often face may harm their health.

In addition, communities are likely to marginalise and reject people who are ill, disabled or emotionally vulnerable, such as former residents of children's homes, prisons and psychiatric hospitals. Those with physical or mental health problems often have difficulty gaining an adequate education or earning a living. Disabled children are most likely to live in poverty. Stigmatising conditions such as mental illness, physical disability or disease such as AIDS makes matters worse. People living on the streets, that may suffer a combination of these problems, suffer the highest rates of premature death. Societies that pursue more egalitarian policies often have faster rates of economic growth and higher standards of health.

A variety of actions at a number of different levels is needed to tackle the health effects of social exclusion. These include the following.
1. Legislation can help protect the right of migrants and minority groups, and prevent discrimination.
2. Public health interventions should remove barriers to access to health care, social service and affordable housing.
3. Income support, adequate national minimum wages and educational and employment policies are needed to reduce social exclusion.
4. Income and wealth should be redistributed to reduce material inequalities and the scale of relative poverty; more egalitarian societies tend to have higher standards of health.
Evidence show that stress at work plays an important role in contributing to the large difference in health, sickness absence and premature death that are related to social status. Several workplace studies in Europe show that health suffers when people have little opportunity to use their skills, and low authority over decisions. Having little control over one's work is particularly strongly related to an increased risk of low back pain, sickness absence and cardiovascular disease. These risks have been found to be independent of the psychological characteristics of the people studied. In short, they seem to be related to the work environment.

Studies have also examined the role of demands at work. Some show an interaction between demands and control. Jobs with both high demand and low control carry special risks. Some evidence indicates that social support in the workplace may reduce this effect. Further, receiving inadequate rewards for the effort put into work has been found to be associated with increased cardiovascular risk. Rewards can take the forms of money, status and self-esteem. Current changes in the labour market may change the opportunity structure, and make it harder for people to get appropriate rewards.

Thus, work related factors are also important predictors of CHD. Architectural layout, excessive noise, and exposure to danger may have a significant impact on stress and health. Stressors such as unrealistic time pressures among assembly line workers, high level of responsibility for safety of others, nonsupportive superiors, and work overload have all been associated with increased incidence of myocardial infarction.

In studies in Sweden and USA, a two-dimensional model of job stress has been associated with both psychological stress and CHD risk. It has been proposed that combination of high job-strain and low job-control is a coronary risk factor. In two large surveys in USA, Health Examination Survey (1960-61) and Health and Nutrition Examination Survey (1971-75) Karasek and colleagues found increased prevalence of infarctions in high-strain occupations. A prospective Swedish study in 1461 male workers also showed that over a 6-year period job-strain predicted CHD incidence.
Policy implications of these findings are:
1. There is no trade-off between health and productivity at work. A virtuous circle can be established: improved conditions of work will lead to a healthier work force; this will lead to improved productivity, and hence to the opportunity to create a still healthier more productive workplace.
2. Appropriate involvement in decision-making is likely to benefit employees at all levels of an organisation.
3. Redesigning practices in offices and other workplaces- to enable employees to have more control, greater variety and more opportunities for development at work- benefits health.
4. Work that does not provide appropriate rewards- in terms of money, self- esteem and status- damages health.
5. To reduce the burden of musculo-skeletal disorders, workplaces must be appropriate ergonomically as well as in the organisation of work.
Unemployment puts health at risk, and the risk is higher in region where unemployment is widespread. Evidence from a number of countries shows that, even after allowing for other factors, unemployment people and their families suffer a substantially increased risk of premature death. The health effects of unemployment are linked to both its psychological consequences and financial problems, especially debt.

The effects start when people first feel their jobs are threatened, even before they actually become unemployed. This shows that anxiety about insecurity is also detrimental to health. Job insecurity has been shown to increase effects on mental health (particularly anxiety and depression), self-reported ill health, heart disease and risk factor for heart disease. Because unsatisfactory or insecure jobs can be as harmful as unemployment, merely having a job cannot protect physical or mental health. Job quality is important.

During the 1990s, changes in the economies and labour markets of industrialised countries have increased feelings of job insecurity. As job insecurity continues, it acts as a chronic stressor whose effects increase with the length of exposure; it increases sickness absence and health service use. Therefore a proper work policy should have three goals:
:: preventing unemployment and job insecurity;
:: reducing the hardship suffered by the unemployment; and
:: restoring people to secure jobs.
Government management of the economy of the economy, to reduce the highs and lows of the business cycle, can make an important contribution to job security and the reduction of unemployment. Limitations on working hours may also be beneficial, if they are pursued alongside job security and satisfaction. To equip people for the work available, high standards of education and good retraining schemes are important. For those out of work, unemployment benefits set a higher proportion of wages are likely to have a protective effect. Further, credit unions may be beneficial by reducing debts and increasing social networks.
Social support and good social relations make an important contribution to health. Social support helps give people the emotional and practical resources they need. Belonging to a social network of communication and mutual obligation makes people feel cared for, loved, esteemed and valued. This has a powerful protective effect on health. Support operates on the levels of both the individual and the society. Social isolation and exclusion are associated with increased rates of premature death and poorer chances of survival after a heart attack. People who get less emotional social support from others are more likely to experience less wellbeing, more depression, a greater risk of pregnancy complications and higher levels of disability from chronic diseases. In addition, the bad aspects of close relationships can lead to poop mental and physical health.
Access to emotional and practical social support varies by social and economic status. Poverty can contribute to social exclusion and isolation. Social cohesion, the existence of mutual trust and respect in the community and wider society, helps to protect people and their health. Societies with high levels of income inequality tend to have less social cohesion, more violent crime and higher death rates. One study of a community with high levels of social cohesion showed low rates of coronary heart disease, which increased when social cohesion in the community declined.
Experimental studies suggest that good social relations can reduce the physical response to stress. Interventions in high-risk groups have shown that providing social support improves outcome after heart attacks, longevity in people with some type of cancer and pregnancy outcome in vulnerable groups of women.

In an acculturation study, Marmot and Syme determined CHD incidence in 3809 Japanese Americans in the San Francisco bay area some of whom had adopted the American lifestyle and some of whom had maintained strong ties with the more traditional Japanese culture.9 When classified according to cultural upbringing (years spent in Japan, years spent in Japanese language school, religious environment when growing up), the group who had traditional Japanese upbringing had 2.5 times less CHD than those who had non-traditional (acculturated) upbringing. This was, independent of diet, smoking, serum triglycerides, serum cholesterol, blood pressure, body weight and serum glucose. Furthermore, when classified according to cultural upbringing and the degree of disassociation from Japanese ethnic group, friends, co-workers and employer, and religion, a 5-fold difference in CHD between the most and the least acculturated groups was seen. This difference was also not explained by genetics or by differences in traditional coronary risk factors including diet. Similar findings were present in cross-cultural studies that reported influence of social support and cohesion in Italians settled in US Roseto/Bangor Study and Alameda County Studies.5

In Alameda County Study, Berkman and Syme studied 4775 adults aged 30 to 69 years. Data were gathered to assess the presence of four types of social connections: marriage, contacts with extended family and friends, church membership, and other formal and informal group affiliations. A combined social network rating that incorporated all these four attributes showed that persons who had low scores indicating poor social support were twice as likely to die in 9 years as compared to those with high scores. In many other studies also measures of social integration predicted mortality in both men and women.

In the community, reducing income inequalities and social exclusion can lead to greater social cohesiveness and better health in the population. Improving the social environment in school, the workplace and the community in general will help people feel valued and supported in more areas of their lives and contribute to health, especially mental health. In all areas of personal and institutional life, practices should be avoided that cast other socially inferior or less valuable; they are divisive.
Drug use is both a response to a social breakdown and an important factor in worsening the resulting inequalities in health. It offers users a mirage of escape from adversity and stress, but only makes their problem worse. Alcohol dependence, illicit drug use and cigarette smoking are closely associated with markers of social and economic disadvantage. In the Russian Federation, for example, the past decade has been a time of great social upheaval. Deaths linked to alcohol use- from accidents, violence, poisoning, injury and suicide- have risen sharply. Alcohol dependence and violent death are associated in other countries including India also. Studies from Jaipur and Dehi in Northern India have reported an inverse association between social status and smoking.

The casual pathway probably runs both ways. People turn to alcohol to numb the pain of harsh economic and social conditions, and alcohol dependence leads downward social mobility. The irony is that, apart from a temporary release from reality, alcohol intensifies the factors led to its use in the first place. The same is true of tobacco. Social deprivation- as measured by any indicator: poor housing, low income, lone parenthood, unemployment or homelessness- is associated with high rates of smoking and very low rates of quitting. Smoking is a major drain on poor people's income and a huge cause of ill health and premature death. But nicotine offers no real relief from stress or improvement in mood.

Work to deal with drug problem needs not only to support and treat people who have developed addictive patterns of use but also to address the patterns of social deprivation in which the problems are rooted. Policies need to regulate availability through pricing and licensing, for instance, to inform people about less harmful forms of use, to use health education to reduce recruitment of young people and to provide effective treatment services for addicts.

None of these will succeed if the social factors that breed drug use are left unchanged. Trying to shift the whole responsibility on to the user is a clearly inadequate response. This blames the victim, rather than addressing the complexities of the social circumstances that generate drug use. Effective drug policy must therefore be supported by the broad framework of social and economic policy.
Healthy food is a political issue. A good diet and adequate food supply are central for promoting health and wellbeing. The shortage of food and lack of variety cause malnutrition and deficiency disease. Excess intake (also a form of malnutrition) contributes to cardiovascular disease, disease, diabetes, cancer, degenerative eye disease, obesity and dental caries. Food poverty exists side by side with food plenty. The important public health issue is the availability and cost of healthy, nutritious food. Access to good, affordable food makes more difference to what people eat than health education.

Industrialization brought with it the epidemiological transition from infectious to chronic disease- particularly heart disease, stroke and cancer. This was associated with a nutritional transition, when diets changed to overconsumption of energy-dense fats and sugars, producing more obesity. At the same time, obesity became more common among the poor than the rich.

World food trade is now big business. The General Agreement on Tariffs and Trade and the Common Agriculture Policy of the European Union allow global market forces to shape the food supply. International committees such as Codex Alimentarius, which determine food quality and safety standards, lack public health representatives, and food industry interests are strong.

Social and economic conditions result in a social gradient in diet quality that contributes to health inequalities. The main dietary difference between social classes is the source of nutrients. The poor substitute cheaper processed foods for fresh food. High fat intakes often occur in all social groups. People on low income, such as young families, elderly people and the unemployed, are least able to eat well. Dietary goals to prevent chronic disease emphasise eating more fresh vegetables, fruits and pulses (legumes) and more minimally processed starchy foods, but less animal fat, refined sugars and salt. More than 100 expert committees have agreed on these dietary goals.

Local, national and international government agencies, non-government organisations and the food industry should ensure that:
1. the availability of high-quality fresh food to all regardless of their circumstances;
2. democratic decision-making and accountability in all food regulation matters with participation by all stakeholders, including consumers;
3. support for sustainable agriculture and food production methods that conserve natural resources and the environment;
4. the protection of locally produced foods from the inroads of the global food trade;
5. a stronger food culture for health, fostering people's knowledge of food and nutrition, cooking skills and the social value of preparing food and eating together;
6. the availability of useful information about food, diet and health; and
7. use of scientifically based nutrient reference values and food-based dietary guidelines to facilitate the development and implementation of policies on food and nutrition.
Probably Not relevant to India but important in metropolitan cities is the issue of transportation. Healthy transport means reducing driving and encouraging more walking and cycling as seen in rural areas of India where CHD prevalence is low. Cycling, walking and the use of public transport promote health in four ways. They provide exercise, reduce fatal accidents, increase social contact and reduce fatal accidents, increase social contact and reduce air pollution.

Because mechanisation has reduced the exercise involved in jobs and house work, people need to find new ways of building exercise into their lives. This can be done by reducing the reliance on cars, increasing walking and cycling and expanding public transport. Regular exercise protects against heart disease and, by limiting obesity, reduces the onset of diabetes. It promotes a sense of wellbeing and protects older people from depression.

Reducing road traffic would reduce the toll of road deaths and serious accidents. Although accidents involving cars injure cyclists and pedestrians, those involving cyclists injure relatively few people. Well planned urban environments, which separates cyclists and pedestrians from car traffic, increase the safety of cycling and walking. More cycling and walking, plus greater use of public transport, would stimulate social interaction on the streets, where cars have insulated people from each other. Road traffic separates communities and divides one side of the street from the other. Fewer pedestrians mean that streets cease to be social spaces, so that isolated pedestrians often fear attack. Further, suburbs that depend on cars for access isolate people without cars, particularly young and old. Social isolation and lack of community interaction are strongly associated with poorer health.

Reduced road traffic means decreasing harmful pollution from exhaust. Walking and cycling make minimal use of non-renewable fuels and do not lead to global warming. They do not create disease from air pollution, make little noise and are preferable for the ecologically compact cities of the future. Bicycles, which can be manufactured locally, have a good " ecological footprint "- in contrast to cars.

Despite their health- damaging effects, journeys by car are rising rapidly in all Asian and European countries, while journeys by foot or bicycle are falling. National and local public policies must reverse these trends. Yet transport lobbies have strong vested interests. Many industries- oil, rubber, road building, car manufacturing, sales and repairs, and advertising- benefit from the use of cars. Just as the twentieth century has seen a start made on reducing addiction to tobacco, alcohol and drugs, so the twenty- first century must see a reduction in people's dependence on cars.

Roads should give precedence to cycling and walking for short journeys, especially in towns. Public transport should be improved for longer journeys, with regular and frequent connections for rural areas. Incentives need to be changed; this means, for example, reducing state subsidies for road building, increasing financial support for public transport, creating tax disincentives for the business use of cars and increasing the costs and penalties of parking. Changes in land use are also needed, such as: converting road space into green spaces, removing car parking spaces, dedicating roads to the use of pedestrians and cyclists, increasing bus and cycle lanes, and stopping the growth of low-density suburbs and out-of-town supermarkets, which increase the use of cars. Increasingly, the evidence suggests that building more roads encourages more car use, while traffic restrictions may, contrary to expectations, reduce congestion.
The notion that there is interrelationship between emotions and cardiac disease is deeply rooted in folklore, but it was only recently that a substantial body of evidence linking psychosocial factors to CHD has amassed.3 Less than half of the CHD incidence in the United States is explained by the combined effect of all traditional risk factors.1 Addition of recently identified biochemical factors (metabolic syndrome, atherogenic dyslipidaemia, coagulation abnormalities) increase this to 70-80%.2 In India too, about 20-30% of CHD prevalence is not explained by conventional coronary risk factors (smoking, sedentary lifestyle, obesity, truncal obesity, hypercholesterolaemia, and hypertension).4
A large number of psychological factors have been implicated in CHD incidence. Although the importance of psychosocial factors in the development and expression of coronary artery disease (CAD) has been debated, an extensive recent literature now establishes that psychosocial factors contribute significantly to the pathogenesis of CAD. Furthermore, by use of new technologies and animal models, elucidation of the basic pathophysiology underlying the relationship between psychosocial factors and CAD is expanding rapidly. However, because the literature relating psychosocial factors to CAD is multidisciplinary, there may be an under-appreciation of the strength of some of the epidemiological and pathophysiological observations that have been reported. Accordingly, we will review the relationship between psychosocial stress and CAD development, with emphasis on the following psychosocial factors: (1) depression, (2) anxiety, (3) personality factors and character traits (eg, hostility), (4) social isolation, and (5) chronic and subacute life stress.
Episodes of major depression are characterized by the presence of a depressed mood and markedly decreased interest in all activities, persisting for at least 2 weeks and accompanied by at least 4 of the following additional symptoms: changes in appetite, sleep disturbance, fatigue, psychomotor retardation or agitation, feelings of guilt or worthlessness, problems concentrating, and suicidal thoughts. The 1-month community-based prevalence of major depression episodes is 5%. Studies from India have reported that major depression is present in 8-10% adults.
Among CHD patients, however, the prevalence of major depression is 3-fold higher. Also, depressive symptoms that are not sufficient in magnitude to meet the criteria for major depression occur at least as commonly among cardiac patients. Recent epidemiological studies evaluating the relationship between depression and CHD among healthy and CHD populations consistently demonstrate a significant prospective relationship between the occurrence of major depression episodes and the incidence of cardiac events. Two additional findings are notable. First, the presence of depressive symptoms, in the absence of diagnosed major depression episodes, is also associated with an increased risk for cardiac events. Second, a number of studies support a gradient between the magnitude of depression and future cardiac events.

Data suggest that risk for CHD associated with depression exists along a continuum, according to the magnitude of depressive symptoms. One particular aspect of depression, the absence of hope, has received particular attention. Hopelessness has been linked to sudden death, both in observational studies and in animal models of hopelessness.

Recently, prospective epidemiological studies have also reported a relationship between symptoms of hopelessness and the development of CAD. In one study, for example, a positive answer to the question "(During the last month) have you felt so sad, discouraged, hopeless, or had so many problems that you wondered if anything was worthwhile?" more than doubled the risk of CAD. It has also been demonstrated that men experiencing hopelessness develop significantly more carotid atherosclerosis over time. A related phenomenon is "vital exhaustion." This syndrome, measured by the 37-item Maastricht questionnaire, focuses on a triad of symptoms: fatigue, irritability, and demoralised feelings. The presence of vital exhaustion has also been reported to predict future CAD and/or cardiac events in healthy and CAD populations.

Considerable evidence indicates that depression has both behavioral and direct pathophysiological effects. With respect to behavioral mechanisms, depression is associated with both unhealthy lifestyle behaviors, such as smoking, and poor patient compliance. Direct pathophysiological effects of depression involve at least 3 mechanisms. First, depression is accompanied by hypercortisolemia. Associated findings include attenuation of the adrenocorticotropin hormone response to corticotropin-releasing factor administration, nonsuppression of cortisol secretion after dexamethosone administration, and elevated corticotropin-releasing factor concentrations in the cerebrospinal fluid of depressed patients. Second, depressed individuals may develop significant impairments in platelet function, including enhanced platelet reactivity and release of platelet products such as platelet factor 4 and ß-thromboglobulin. The combination of hypercortisolemia and enhanced platelet function establishes the theoretical basis for explaining the proatherogenic effects of depression. In addition, reduced heart rate variability and impaired vagal control have been reported among depressed patients. These findings suggest that depressed patients may also be subject to enhanced arrhythmogenic potential.
Until recently, evidence linking anxiety to CAD was limited to demonstrations of elevated mortality rates among psychiatric patients with anxiety disorders. Increasing evidence now links anxiety disorders to development of cardiac events in general populations. Most notably, 3 large-scale community-based studies, including one involving 34 000 men, have now reported a significant relationship between anxiety disorders and cardiac death. Moreover, a dose-dependent relationship has been noted between anxiety levels and the occurrence of cardiac death. Anxiety has not been associated with myocardial infarction in these studies. Rather, the excess mortality appears to be confined to sudden (versus nonsudden) cardiac death. Notably, these community-based studies did not include women, even though anxiety disorders are more common among women.

Prospective positive associations between CAD and panic disorder and between CAD and "worry" (a subcategory of generalised anxiety disorder) have also been noted in 2 recent studies; however, more studies are needed to establish whether these findings are indeed valid. The epidemiological investigation of anxiety disorders among CAD patients has also been quite sparse. Because 4 small studies have each noted a relationship between anxiety and a constellation of hard and soft cardiac events among CAD patients, more large-scale epidemiological studies among CAD patients now appear to be warranted.

The association between anxiety and sudden death, but not myocardial infarction, suggests that ventricular arrhythmias may be the mechanism for cardiac death among individuals with anxiety disorders. In support of this hypothesis, it has been observed that individuals with anxiety disorders have reduced heart rate variability. Hence, there may be a pathological alteration in cardiac autonomic tone. This alteration could involve either increased sympathetic stimulation, which has been linked to the occurrence of arrhythmias and sudden death, or impaired vagal control, which has also been linked to increased cardiac mortality. With respect to the latter possibility, reduced vagal control has been linked to impaired, vagally mediated baroreflex control of the heart. Such impairment appears to be a particularly important risk factor for sudden death. Along these lines, a recent study reported reduced baroreflex cardiac control in patients with anxiety, but prospective work is needed to determine whether this is a common operative mechanism for sudden deaths among patients with anxiety syndromes.

Individuals with anxiety disorders are prone to more unhealthy lifestyle behaviors; however, the lack of correlation between anxiety syndromes and myocardial infarction (a sign of underlying atherosclerosis) suggests that, at least among initially healthy individuals, this behavioral association is not a significant pathogenic mechanism. It is conceivable, nonetheless, that this behavioral association could be of importance among CAD patients manifesting anxiety.
In addition to external social influences it has been thought for some time that inner psychological and personality factors and behavioural expressions predispose to CHD. These characteristics are collectively called as coronary-prone behaviour. The so-called type-A behaviour pattern has been subject of much research. Friedman and Rosenman observed that cardiac patients shared many behavioural characteristics. These were (i) almost obsessive attempts to achieve many poorly defined goals, (ii) love of competition, (iii) a strong need for recognition and advancement, (iv) a consistent preoccupation with time and need to get things done in a hurry, (v) intense concentration and alertness, and (vi) high levels of free-floating hostility. The standard measures for determining type-A personality are a structured interview and Jenkins Activity Survey.

As originally described in the late 1950s, the syndrome was characterized by competition, hostility, and exaggerated commitment to work. Many studies have investigated whether personality patterns or individual character traits promote the development of CAD. Other personality types have included "type D" personality, "social dominance," and a "hardy personality" construct ; these latter personality types have not been widely studied as potential risk factors for CAD. Interest in type A behavior accelerated after the Western Collaborative Group Study, which reported that type A behavior was associated with a 2-fold increased risk of CAD and 5-fold increased risk of recurrent MI over an 8.5-year follow-up. Although type A behavior continues to receive attention, a series of studies have reported no correlation between type A behavior and CAD risk. This lack of consistency has cast doubt on the potential robustness of the type A behavior as a clinical syndrome. Potential confounders have been suggested. For instance, animal model studies and some human studies suggest that social support is a potential confounding variable. Furthermore, suspecting that not all components of type A behavior are pathogenic, investigators have examined the components of this behavior pattern.

The Western Collaborative Study was the first large epidemiological study to identify causal link between type A behaviour and development of CHD. 3154 men aged 39-59 years were followed for more than 8 years. The study showed that type A men were twice as likely to develop some manifestations of CHD as non-type A men (type B). The effect of type A was independent of other coronary risk factors. Other studies showed a strong correlation of type A personality with extent of coronary atherosclerosis. However, two large studies- Multiple Risk Factor Intervention Trial (MRFIT) and Aspirin Myocardial Infarction Study (AMIS) failed to find an association between risk of reinfarction and type A behaviour.

Barefoot and other investigators therefore trimmed the original Jenkins scale and proposed a hostility-cynicism factor. This pattern of behaviour has been described as a cynical and untrusting view of humankind, the frequent experience of negative emotions when dealing with others, and the frequent expression of overt anger and aggression when faced with frustration of problems. Further sub-analysis of hostility-cynicism factor has been done. Antagonistic hostility characterised by a disagreeable and uncooperative interpersonal interaction has been shown to be a coronary risk factor in MRFIT reanalysis. A great deal of work continues in the field of type A behaviour and CHD. The relationship of type A personality with CHD incidence is not as straight-forward as previously proposed and current evidence suggests that overt expression of hostility and cynicism is a more potent predictor.

In India, Gupta et al studied lifestyle related (physical activity, smoking, diet) and social risk factors in urban and rural subjects in Rajasthan.10 Results showed that psychosocial factors that were associated with lower prevalence of CHD in these populations were joint family support, lesser number of children, literacy, religious affiliations and prayer habit. Studies also show that although excess of major coronary risk factors in urban subjects explained greater CHD4,11-13 a substantial proportion that remained unexplained may be due to psychosocial factors.

Studies have also evaluated role of type A personality in CHD in India. Verghese et al14 studied 18 cases of CHD and found that there was a strong correlation of angiographic coronary artery disease with type A behaviour (r=0.88). Chadda et al15 reported similar results in survivors of myocardial infarction. However, these studies are small case-control studies that are only suggestive. Prospective studies are needed to exactly define the role of personality characteristics and CHD in the Indian context.
Hostility, a major attribute of the type A behavior pattern, has received considerable attention as a potential "toxic" element in this personality construct. Hostility is a broad psychological construct, encompassing negative orientations toward interpersonal relationships, and includes such traits as anger, cynicism, and mistrust. Table 3 lists 10 studies assessing the relationship between hostility and CAD in healthy subjects. The results of these prognostic studies are mixed, with both positive and negative studies. However, the studies are of uneven quality. For instance, in one negative study, 57% of the individuals were lost to follow-up, whereas the follow-up of healthy individuals in another study was only 3 years. Of note, 2 large studies that used tailored scales to focus on cynical mistrust and anger have yielded positive associations with cardiac events. In the anger study, a gradient was noted between anger levels and the frequency of subsequent cardiac events. Thus, it is possible that certain components of the hostility construct are more pathogenic.

To date, there have been no large-scale epidemiological studies evaluating hostility among CAD patients. Four small epidemiological studies among CAD patients, however, have been positive, as noted in Table 3. In addition, studies have reported that CAD patients with high levels of hostility have a greater rate of restenosis after angioplasty, experience more rapid atherosclerosis progression during serial carotid ultrasonography, and manifest more ischemia during stress testing than other CAD patients.

Hostility may affect atherogenic activity by behavioral mechanisms. Hostility is associated with a higher concentration of unhealthy lifestyle behaviors, including smoking, poor diet, obesity, and alcoholism. Hostile individuals are also more likely to manifest other psychosocial factors associated with CAD, such as social isolation. An accumulating body of evidence also suggests multiple pathophysiological mechanisms by which hostility may be linked to CAD. For example, compared with nonhostile individuals, hostile subjects manifest higher heart rate and blood pressure responses to physiological stimuli, such as mental tasks, as well as higher ambulatory blood pressure levels during daily-life activity. Also, evidence suggests that hostile individuals are more likely to exhibit hypercortisolemia and high levels of circulating catecholamines, as well as diminished mononuclear leukocyte ß-adrenergic receptor function. Preliminary data suggest that hostile individuals may also manifest diminished vagal modulation of heart function and increased platelet reactivity.
Since the late 1970s, a series of prospective community-based studies have examined the influence of social factors on the development of CAD. Initial studies focused on quantitative aspects of social support, such as the presence of family affiliations, number of friends, and the extent of one's participation in group and organizational activities. This domain of measurement has been called one's "social network." Within this domain, some studies evaluated the influence of partner status (living alone, marital status, and/or marital disruption), and others have assessed aspects of "instrumental" (ie, tangible) support, such as access to guidance and practical community services.

Over time, however, the qualitative nature of one's social support system (eg, amount of perceived emotional support) has also been increasingly subject to study. A relatively small network has been found, on average, to be associated with a 2- to 3-fold increase in the incidence of CAD over time. Similarly, low levels of perceived emotional support confer an even greater increased risk for future cardiac events. Table 5 lists 11 studies evaluating the relationship between social factors and prognosis in patients with preexisting CAD. Significant prognostic relationships are present in most of these studies, and the risk ratios are substantial. For instance, Berkman et al observed a nearly 3-fold increase in subsequent cardiac events in post-MI patients reporting a low level of emotional support, and Williams et al observed a similar 3-fold increase in mortality over 5 years among CAD patients who were unmarried or had no significant confidant in their life.

In addition to the consistency and magnitude of these findings, the cause-and-effect relationship between social factors and CAD development is also supported by other evidence. First, an inverse gradient has been reported between the magnitude of social support and the incidence of CAD and/or future cardiac events. Moreover, acculturation independently influences CAD development. For instance, in one study, 3809 Japanese-Americans in California were classified according to the degree to which they retained a traditional Japanese culture. The most traditional group of Japanese-Americans had a CAD prevalence as low as that observed in Japan, whereas the group that was most acculturated had a 3- to 5-fold excess in CAD prevalence. Major CAD risk factors did not account for these differences. In another study, temporal rates of CAD development were assessed in Roseto, Pa, and an adjacent town. Initially, CAD incidence was significantly lower in Roseto, despite shared medical resources. At that time, Roseto was a cohesive and homogeneous community of 3-generation households, descendants of Italian immigrants. As the distinguishing social characteristics of the Roseto community disappeared over time, its lower incidence of CAD vanished. Finally, animal studies have also implicated social factors in the promotion of atherogenesis. For instance, Ratcliffe and Cronin described the potential importance of social disruption among animals, noting that crowding and social disruption were the apparent causal factors for a 10-fold increase in atherosclerotic lesions that occurred among birds and mammals over a 20-year period at the Philadelphia Zoo. Ratcliffe et al also studied social support experimentally by deliberately assigning swine to various social situations (alone, pairs, groups). At postmortem examination, coronary arteriosclerosis was most advanced in isolated females, intermediate in isolated males, and least advanced in animals sustained in groups. More recently, the extent of atherosclerosis was compared at autopsy among 39 cynomolgus female monkeys exposed to 2 different housing conditions: 15 monkeys housed in single cages and 24 housed in groups. The extent of atherosclerosis was 4 times greater, on average, in the females that were housed alone than in those housed in social groups. This difference occurred in the absence of significant differences in plasma lipids. In combination, these data provide strong evidence that social factors relating to grouping and isolation can promote atherogenesis.
Work-related stress is the most widely studied chronic life stress relative to CAD. Although many aspects of one's work environment relative to the development of CAD have been studied, much interest has focused on models of inherent "tension" at work. One such model has been the "job strain" model, defined by Karasek et al as jobs with high demand but low decision latitude. In one prospective study of 1928 male workers followed up for 6 years, job strain was associated with a 4-fold increase in the risk of cardiovascular system-related death. Subsequent studies have supported the relationship between job strain and CAD risk, but negative studies have also been reported.

More recently, research has begun to focus on other forms of work-related stress. For example, one model views work stress as the outcome of high work demand and low reward. This model both predicts cardiac events and has been correlated with progression of carotid atherosclerosis. Also, low job control, per se, predicts future cardiac events. Taken together, the studies regarding presence of stress at work and subsequent CAD development have been largely positive, suggesting a strong causal relationship between this form of chronic stress and development of atherosclerosis.

Because many observational studies have reported psychological prodromata in the months preceding development of acute MI, interest has also been focused on the potential pathogenicity of "subacute" life stress (defined as an accumulation of stressful life events over a duration of months). In one of the earliest attempts to quantify the relationship between subacute psychological stress and CAD, Holmes and Rahe developed a "Recent Life Change Questionnaire," with a predetermined weighting assigned to different life events, ranging from high numbers for such events as the death of a spouse, divorce, or loss of a job to low weightings for vacations and holidays. In one study, marked elevations in Recent Life Change scores were seen for most cases of MI or sudden cardiac death during the 6-month period preceding these events. Similar confirmations of increased life stress before cardiac events can be extended to specific cohorts, ranging from healthy middle-aged men to patients pre- senting with acute myocardial infarction.

Like other psychosocial factors, chronic stress appears to exert direct pathophysiological effects, including elevation of arterial blood pressure and neurohumoral arousal. Evidence of neurohumoral arousal has also been noted in situations associated with subacute stress.
Although psychosocial stresses have been reviewed here as individual entities, generally, these stresses tend to cluster together. When they do so, risk ratios for cardiac events often rise substantially. For example, in one study of post-MI patients, the presence of high levels of life stress and social isolation were each associated with an 2-fold increase in subsequent events. But when the 2 factors occurred together, the rate of subsequent events was 4-fold higher. A similar synergy between these 2 factors has also been reported among healthy individuals. Similarly, the combination of anxiety and depression compounds cardiac risk in post-MI patients, and many other examples can be found within the psychosocial literature. These data indicate that psychological factors occurring in combination substantially magnify risk associated with individual psychological factors, resulting in risk elevations that are comparable to those associated with hypercholesterolemia, hypertension, and other major risk factors for CAD. Furthermore, psychosocial factors also interact synergistically with conventional CAD risk factors to heighten the risk for cardiac events. For example, depressed patients who smoke have a substantially higher risk of cardiac events than depressed patients who do not smoke.

From a pathophysiological point of view, the increase in cardiac events associated with clustering of psychosocial stresses suggests that this clustering compounds the health-damaging effects of individual psychosocial stresses. However, because psychosocial stresses and behavioral risk factors in humans change over time and cluster together in variable fashion, it is difficult to study the potential mechanisms by which they exert their pathophysiological effects.

In contrast, adequate experimental control can be achieved in animal models, especially monkeys. In this regard, cynomolgus monkeys (Macaca fascicularis) provide a potentially relevant model for studying the interaction of multiple psychological factors in a controlled setting. Like humans, cynomolgus monkeys develop coronary atherosclerosis when fed fatty diets and manifest similarities to people in the development of coronary lesions and coronary vasodilator abnormalities. Notably, cynomolgus monkeys resemble human beings in both the organization and expression of their social behavior. For example, dominance and nurturance are sometimes considered to be the 2 major dimensions that define the content of interpersonal human behavior. Cynomolgus monkeys are characterized by well-defined social status hierarchies in which some animals (dominants) reliably defeat others (subordinates) in competitive interactions, as well as by elaborate, generation-spanning, networks of affiliation, alliance, and mutual support. Humans and monkeys also use similar facial expressions and postures to communicate an antagonistic or combative mood, and both rely extensively on visual cues to signal moods quickly and unambiguously in complex social settings. These behavioral similarities suggest that monkeys might be especially useful for modeling the human expression of anger or hostility.

In a set of investigations designed to evaluate the interaction between personality factors and a stressful social environment, 30 male monkeys were fed a moderately atherogenic diet while housed in 5-member social groups and assigned to 1 of 2 social conditions : (1) an "unstable" environment in which animals were switched among groups on a regular basis so that animals periodically had to reestablish their dominance and affiliative relationships or (2) a "stable" environment in which initial group memberships were maintained without disruption throughout a 22-month period. Repeated behavioral observations permitted identification of individuals as relatively more dominant or subordinate in their social groups. The index of coronary artery atherosclerosis in this and all other cited monkey experiments was the average lesion extent as measured in 15 cross sections of pressure-perfused coronary arteries. Five sections each were taken from the left circumflex, left anterior descending, and right coronary arteries for these determinations. At the end of this study, quantitative evaluation of the coronary arteries of these animals revealed that dominant male monkeys in an unstable environment had significantly more coronary artery atherosclerosis than the other 3 subgroups. These results were independent of variations in serum lipid concentrations and blood pressure. Thus, this animal model revealed that it was the interaction between 2 psychosocial factors that proved pathogenic in cynomolgus monkeys: the trait of "dominance," coupled with environmental stress.

Cynomolgus monkeys have also been used to study the influence of chronic psychosocial stress on coronary endothelial integrity. First, it was demonstrated that the stress model cited above induces atherosclerosis in dominant male monkeys in the absence of hypercholesteremia, albeit with smaller lesions than those noted for monkeys concomitantly fed a high-cholesterol diet. Thus, under conditions of chronic psychological stress, endothelial injury can occur even without dietary provocation. Subsequently, quantitative coronary angiography was used to demonstrate that psychosocial stress in cynomolgus monkeys can also lead to impairment of endothelial function in the presence of underlying coronary atherosclerosis. Specifically, arterial responses in nonatherosclerotic controls (which always consumed a low-cholesterol diet and were housed in stable groups) were compared with those in monkeys that consumed a high-cholesterol diet for 1 year and were subsequently assigned to 1 of 3 experimental conditions: (1) continued consumption of a high-cholesterol diet plus exposure to periodic social disruption, (2) consumption of a low-cholesterol diet plus exposure to periodic social disruption, and (3) consumption of a low-cholesterol diet and housed in stable social groups. Coronary vascular responses to acetylcholine differed across groups in a manner consistent with the exposure to psychosocial stress. Thus, chronic psychosocial stress can impair endothelium-dependent vascular responses in a manner that is not necessarily dependent on extent of underlying atherosclerosis or diet.
Having determined via psychological assessment that a patient has a high degree of life stress, social isolation, hostility and anger, or trouble expressing feelings, the physician can initiate appropriate intervention.3,5 Many of the changes physicians want for their patients might best be initiated and reinforced by recommending participation in mind-body oriented group stress reduction and relaxation programs. Individual health behaviour counselling, behaviour modification clinics targeting behaviour modification, and various support groups targeting specific social situations (isolation, bereavement) are also helpful. A physician with good communication skills and knowledge of the role of psychosocial factors in health and disease, can have a profound impact on health of his patients.

Martha Hill, president of American Heart Association, recently commented about the gap between social/ behavioural sciences and biological sciences in efforts for prevention of CHD.36 Tremendous advances have occurred in biology of CHD that have provided new insights into genetics, physiology, pathophysiology, and disease processes and clinical research. These have been supplemented by important advances in behavioural sciences, clinical outcomes and healthcare delivery systems.

However, the gap between efficacy of interventions and their effectiveness, a gap between potential and reality, intention and action, and information and behaviour illustrates the urgent need to more fully integrate the social and behavioural sciences with the biomedical sciences. Understanding of psychosocial factor in CHD genesis and perpetuation are important to bridge the gap between science and society. Preventive measures for CHD are urgently needed in India to stem its tide. Population measures that are more cost-effective than a high risk approach are recommended.16

The need to contain the epidemic as well as combat its impact and minimise the cardiovascular diseases toll in Indians is obvious and urgent.35 National strategies to meet this objective must be developed and effectively implemented. Regional and global initiatives by international agencies concerned with health care are also required. A large number of social issues that are determinants of health behaviour in Indians must be considered before embarking on such a policy. These factors are illiteracy and low educational status, breakdown of traditional family systems, improper peer influence, lack of guidance, caste system and social hierarchy, lack of media awareness, and lack of motivation to change.

Traditional lifestyles that are associated with a lower CHD prevalence in India and many Asian countries (joint family system, good education, religious habits, prayers, small families, social support) should be encouraged. Traditional dietary habits of vegetarianism, fish consumption, use of plant-based oils for cooking, high fibre predominant carbohydrate based diets, antioxidant containing fruits and vegetables; and physical exercise should be maintained.37 Meditation and other stress reducing activities should be encouraged.38 Expanded interdisciplinary health-focussed models should be used.
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