BMC Public Health 2008, 8:126 http://www.biomedcentral.com/1471-2458/8/126 Results: 700 subjects were recruited. The response (active participants per 100 invitation letters) in the least deprived group was 35.1% and in the most deprived group was 20.3%. Lowest response was seen in young males (least deprived 22.4% and most deprived 14.1%). Conclusion: This cross-sectional study recruited the planned sample of subjects from least deprived and most deprived areas within Glasgow. As evident in other studies response differed between the most and least deprived areas. This study brought together researchers/academics from diverse disciplines to build a more sophisticated understanding of the determinants of health inequalities than can be achieved through unidisciplinary approaches. Future analyses will enable an understanding of the relationships between the different types of measure, and of the pathways that link poverty, biology, behaviour and psychology and lead to health inequalities. Background Heart disease, diabetes, some cancers, rheumatoid arthri- tis and mental illness are examples of the burden of ill- health that is carried disproportionately by deprived com- munities[1]. Not only is the prevalence and incidence of disease higher in areas of deprivation but also the nature of the problem appears to be qualitatively different, and treatment less successful[2]. This inequality in disease risk can partially be explained by the higher prevalence of clas- sical risk factors in deprived areas, but this explanation fails to account for the totality of the variations [3-5]. There are social gradients in a range of biological and psy- chosocial variables which indicate that living in a deprived environment may increase the propensity to develop chronic disease, through as yet unknown mecha- nisms[6,7]. A potential underlying cause of increased prevalence of disease is chronic inflammation. This has been observed to be more common in deprived than affluent populations, [8-12] linked to coronary heart dis- ease[13,14], increased risk of type 2 diabetes[15,16] and other disorders[17], as well as cognitive dysfunction and altered psychological profile [18-21]. Atherosclerosis is now understood to be an inflammatory disorder with key components of the innate immune system being inti- mately involved in the initiation and progression of plaques on the artery wall, and in triggering an acute cor- onary event such as myocardial infarction[14]. The aetiol- ogy of diabetes appears also to involve activation of innate immunity with high levels of inflammatory biomarkers such as C reactive protein being associated with increased risk of developing the disorder[15]. Because of the aetio- logical links, some suggest that coronary heart disease and type 2 diabetes arise from a 'common soil'[22]. The cause of increased activation of the innate immune system in individuals from deprived populations is not clear. It may be linked to poor living and working condi- tions such as exposure to pathogens, or to increased levels of obesity. There is abundant evidence linking the accu- mulation of abdominal fat to raised levels of inflamma- tory cytokines in the plasma[23,24]. Further it is noteworthy that the relationship between body fat and inflammation is present even in children[25] suggesting that propensity to some adult chronic diseases may begin early in life. Abdominal obesity is believed to be a major precipitating factor in the development of insulin resist- ance and ultimately in the development of type diabe- tes[26]. For this reason the present 'epidemic' of obesity in many countries around the world is a significant concern for public health authorities and healthcare providers. Chronic inflammation, central obesity and insulin resist- ance have been associated in population surveys and in experimental studies with impaired cognitive function and with an altered (negative) mental outlook. Depres- sion appears to be more frequent in overweight individu- als[27,28] and type 2 diabetes is recognised increasingly as a risk factor for accelerated cognitive decline in the eld- erly[29,30]. Prospective studies have shown inflamma- tory markers to predict cognitive decline in initially- healthy elderly subjects over follow-ups of between one and ten years[19,30], and that those of lower socio-eco- nomic status and poorer educational attainment are more vulnerable to such inflammation-related decline[31]. Recently investigators have reported that a further feature of central obesity/metabolic syndrome is an altered men- tal state associated with depression and "loss of con- trol"[31,32]. It has also been recognised that depression is commonly found in subjects with CHD and is an impor- tant factor to overcome as part of recovery from a myocar- dial infarction [33-35]. These aetiological links need further exploration as poten- tial explanations of the burden of physical and mental ill health in deprived communities. From a public health perspective it is important to establish if those who need to take on board messages advocating lifestyle change (weight loss, physical activity) are in a position affectively and intellectually to receive them. Equally, certain person- ality and other individual difference factors modify responses to stress and challenge, conferring both vulner- ability and protection, and must be accounted for as mod- erating variables. Page 2 of 11 (page number not for citation purposes)