Commentary: Social capital, social epidemiology and disease aetiology.

Abstract

The role of social capital in the production of health has developed over recent years into a major academic concern, and is now beginning to feed through into policy discussions concerning the determinants of population health. Social capital has, of course, had greater resonance in fields such as development economics than it has so far had in health, but the confluence of these two threads is now marked. This is made clear by the work of the leading popularizer of social capital—Robert Putnam—who in his seminal 1993 book Making Democracy Work 1 explicitly states that health should not be considered an outcome of social capital, saying that: we must be careful not to give governments credit (or blame) for matters beyond their control. In the language of policy analysis, we want to measure ‘outputs’ rather than ‘outcomes’—health care rather than mortality rates … Health depends on factors like diet and lifestyle that are beyond the control of any democratic government. 1 Only 7 years later he had dramatically reversed his opinion and decided that: Of all the domains in which I have traced the consequences of social capital, in none is the importance of social connectedness so well established as in the case of health and well-being’. 2 The explosion of interest in social capital has not, as yet, led to greater clarity in the conceptualization of exactly what the term social capital refers to and how the supposed connections with health are generated and maintained. 3,4 We therefore welcome Simon Szreter and Michael Woolcock’s 5 clear and persuasive formulation and think that it will—rightly—become a touchstone for ongoing debates regarding social capital in the health field. Other commentators in this issue of the International Journal of Epidemiology 6‐10 have raised a variety of important points and we will not duplicate these here. Instead we would like to elaborate some specific aspects of the epidemiological interpretation of the historical evidence. This leads to more general considerations of how to interpret social influences on population health. In the central section of their article Szreter and Woolcock discuss mortality crises in 19th century Britain and date improvements in mortality to the 1870s and 1880s, as Simon Szreter has done previously. 11 They develop one specific case, that of Birmingham and the role of Joseph Chamberlain in preaching the ‘civic gospel’ of gas and water socialism over this period. In particular they consider that Chamberlain’s activities were central to the development of linking and bridging social capital which protected civil society in Birmingham from the usual nepotism and corruption that sank other British cities in the central decades of the 19th century. Without Chamberlain’s activities the rapid urbanization that translated itself into Simon Szreter’s four Ds—disruption, deprivation disease and death 12 —would have continued to bear its consequences. We will argue that consideration of age-specific mortality trends during the second half of 19th century shows that the social capital mechanism suggested by Szreter and Woolcock as being crucial, is an incomplete explanation. We will also address the same specific historical case raised by Szreter and Woolcock and illustrate the negative externalities—in this case international—that can result from the deployment of particular forms of social capital. Our main point is to highlight the need to consider specific, biologically plausible and wellsupported aetiological mechanisms when attempting to map aspects of the social environment onto health outcomes. 13