Commentary on Social Mobility and Coronary Heart Disease Risk

Adaptation to conflicts arising out of social mobility (up or down) has been explored as a CHD risk factor. An upwardly mobile individual has a moderately increased risk of CHD (but in one study protestants only), with downward mobility Catholics appeared in the mortality statistics (Wardwell, 1968). A California study found CHD risk higher among college graduates who were sons of foreign born fathers – compared.to less mobile non-graduate sons of foreign born fathers, graduate sons of native born fathers with less status inconsistency (Syme, 1966).

A nationwide USA survey of social mobility specialists (corporation employees) showed a relationship between social mobility and CHD mortality. Executives (without college education) recruited into lower occupational ranks who worked their way up showed increased CHD mortality compared to college educated executives directly recruited to management (Lehman, 1967a, b). Executives recruited from lower ranks had a higher incidence of CHD mortality than those who remained as craftsmen, and directly recruited management had a lower incidence than the occupationally mobile (Lehman, 1967a, b).

Highly mobile individuals may be at extra risk of CHD due to social and cultural factors operating to increase disease risk. Societies are networks of social relationships that include the interactions of individuals in and between various social groups (Halsey, 1972) with social mobility the movement of individuals from one position in the network to another. This movement can be upward, downward or transverse, within a system of social stratification.
The stratification system may comprise classes, strata, status groups or castes. Usually the common unit of social mobility is the family, but may extend to larger groups. The usual time-scale for individual mobility is the life-time, but larger group time-scale may encompass generations.

Selective social mobility is not a random process, either upwards or downwards, through social strata. Vertical mobility is channelled and can meet resistance in the recipient group. Selective social mobility indicates society stratified according to criteria that include selected qualities or abilities (Glass, 1954). Social mobility is not always vertical but can be horizontal (lateral, transverse) due to divorce, remarriage, occupational status change – especially when regarded as a preliminary to upward social mobility.

With social mobility the interpretation of correlations between occupation and disease must consider factors leading individuals to choose particular occupations – important with reference to those with chronic diseases. Such individuals may be unable to keep demanding jobs in higher socioeconomic strata and tend to migrate down the social scale. Disease can cause precipitation out of one social stratum and downward social mobility (Farmer, 1983).

Medically, social mobility can characterise diseases. Morbidity shows social movement – peptic ulcers show downward social movement and CHD may follow this pattern – (Susser, 1975, 1985), with the trail of morbidity and mortality relative to smoking and social class now established. Individual social mobility has clinical importance because mobility carries a burden of ‘stress’. This may account for variable distribution of morbidity and mortality within/between classes and strata. Mortality differentials linking CHD and occupation are often speculative but a correlation exists for stress, smoking and occupational stress (Russek, 1962).

Social mobility forces people into transitional situations in new social environments requiring new personal adjustments, social encounters, obligations, responsibilities. Social mobility creates ‘discontinuities’ in role and status encompassing sociocultural norms and values. These discontinuities function as ‘stresses’ that impinge on socially mobile individuals in social situations and can be compared to in-migrants experiencing `transitional neurosis` and `culture shock’. Similar to spatial migration, social migration as social mobility implies the mobile take their genetic susceptibilities and, in so doing, may alter their risks of exposure to harmful agents (e.g., stressful environments). Socially mobile individuals, like spatial migrants, may be self-selected thus suggesting caution because their morbidity/mortality risks may differ from both donor and recipient populations or strata.

Socially mobile individuals move to another relatively stable strata or population and therefore become so-called `marginal` man or woman. There arises `status incongruity` or `status inconsistency’. Status inconsistency is the paradox of high status and low income e.g., nurses and teachers. This process can be posited against the background of economic development involving industrialisation and urbanisation, where technological changes create `oscillating social strata`, that disrupts old cultures, family ties and creates fragmented impersonal communities.

Social and emotional consequences, affects arise from `transitional discontinuities`. Such discontinuities or `transition states` include changes in social status, living conditions and social environment that may have a role in `stress` reaction (McK. Rioch, 1971). Certain illnesses may accompany adaptations (or maladaptations) to social mobility incongruities, and can be seen as challenging life-events. Transition states are thus human-social environmental interactions occurring in situations such as migration, retirement etc (McK. Rioch, 1971). It must not be overlooked that “Clinical episodes of CHD can themselves cause life changes.” (Rahe, 1988).

Upward occupational transitions in socially mobile societies show overtly competitive individuals and strivers for ‘success’ (though not all become `winners`). There is often a behaviourally competitive component delineating socially mobile individuals, but not necessarily, because this view based on personality typology ascribes social ‘success’ to rigidly defined personality traits.

There are ascribed ‘extranormal steps’ in social mobility possibly functioning as risk factors for CHD – forced, premature family separations. occupational, or social migrations. CHD has been related to ‘extranormal transitions’ and ‘status incongruity’ with significant correlations between CHD and number of occupation changes (Syme, 1964, 1966). A study amongst agricultural workers in Dakots showed occupational mobility into `white collar’ jobs showed increased CHD risk. This more apparent when compared to agricultural workers who became manual ‘blue collar’ or who remained on farms – disease risk increased for upward mobility, especially in combination with spatial mobility (Wardwell, 1964).

The ‘transition component’ in social mobility may generate stress and culture conflict exposing susceptible individuals to increased CHD risk thus the “…build-up of life changes prior to coronary death was ,even seen to be significant for those persons with prior CHD histories.” (Rahe, 1988). However, successful social transitions do occur and bring with them their rewards and compensations.

Social ascent and descent occurs in time, and the relative size of UK social classes have altered over time (1921-1961). Classes I, II and III have increased in size, IV and V have decreased (perhaps reflected in the study sample?) due to technological advances and concentration of capital intensive industries, and redistribution of the population from rural to urban environments. Vertical social mobility is a significant factor in epidemiology because mobility is a continuous process that may create biological disparities between social classes (Susser, 1975). Migration tends to homogenise populations and social mobility may thus achieve the same result. Individuals may be selected for specific traits positing upward or downward social mobility – but any selected traits are usually multifactorial and will affect more than just the biology of social classes.

Coronary prone individuals have been described (the extreme example the Type A personality) as extremely competitive, striving for achievement, and chronic sense of time urgency (Friedman, 1986). The typological link between personality and CHD is very contradictory with not all Type A’s showing the typical cardiovascular neuroendocrine hyperactivity ascribed to the group. It is illogical to assume rigid personality types would  be selected for in socially mobile societies.

Classic work on Type A’s did not indulge in typology (Friedman, 1986) but described the behaviour as a ‘pattern’, stressing there was no observed correlation between occupation and type of personality. Type A qualities are not inherited (whereas detected frequencies of hypercholesterolaemia, hyperinsulinaemia, hyperlipidaemia associated with CHD, are familial). In the San Francisco Bay area (Friedman, 1986) Type A patterns were increasing with the alleged Type A behaviour ‘patterns’ only overt when individuals were upwardly mobile. The pattern may be an adopted attitude, learned behaviour, rather than a personality of fixed typology.

Some, not all, upwardly mobile individuals could appear highly competitive and extremely goal directed. Before personality typology can be correlated with CHD more research must be done to determine those variables which associate Type A’s with the disease, and dissociate others from it. Hypertension resulting from hyperactivity rather than aspects of personality may be a better, more fruitful exploration.

Typology falls when considering excessive cardiovascular reactivity may be a response to stressful life events resulting from upward social mobility. However, in such a multifactorial phenomenon as CHD, personality and behavioural traits are involved in the aetiological matrix somewhere. Selection pressures in employment and retirement in the incidence of CHD could also be involved (Cairns-Smith, 1984). Type A behaviour has been seen to develop readily in the highly active children of mothers who strive to make achievers (‘winners’ not ‘losers’) of their offspring – thus adaptation to modern urban life expectations encourages Type A behaviour (Nixon, 1978), and therefore it could be that competitive, goal directed behaviour in some upwardly mobile individuals may violate homeostasis. The effect could be that in a challenging environment an upwardly mobile individual would increase his/her risk for CHD and set in motion events that would precipitate a downward social spiral.

References to follow.

Originally published as Appendix 181 of my MPhil (CNAA) thesis entitled ‘Population Variation for Risk Factors in Ischaemic Heart Disease’. Oxford Polytechnic and Oxford Brookes University, September 1992.

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