Original report

Rethinking disease: Where do we go from here?

Adolescent mental health is becoming a critical concern. Mental illness rates are rising and many psychological disorders first present symptoms during teenage years. Studies consistently show associations between the built environment and mental health, including internalising mental health disorders in adults, but the evidence for adolescents is less robust and few studies attempt to isolate causality. This review examines the relationship between the urban public realm and adolescent mental health and wellbeing. Our search yielded 24 studies for inclusion. We undertook qualitative synthesis of 20 cross-sectional studies and conducted a separate quality analysis of four longitudinal studies. Greenspace and neighbourhood quality are associated with adolescent mental health and wellbeing although this may be due more to residual confounding, selection effects and same-source bias than evidence for a causal effect. Furthermore, the few longitudinal studies that seek to test causality remain prone to these biases. Overall, we find little evidence of an effect of the urban public realm on adolescent mental health and wellbeing, which, we argue, reflects the difficulty of researching complex pathways between environments and health and highlights a challenge to the field. To address this challenge, we propose a research agenda that prioritises more and better data drawn from diverse study designs, and more and better theories developed from diverse epistemologies.

Previous work from our lab demonstrated that social environment influences the progression of atherosclerosis in genetically hyperlipidemic rabbits. The purpose of the current study was to examine behavioral and physiological responses associated with these distinct chronic social conditions. Normolipidemic rabbits were exposed to one of three social environments for 4 hours/day over 20 weeks: 1) an Unstable Group in which animals were paired weekly with a different unfamiliar rabbit, 2) a Stable Group in which rabbits were paired with the same littermate for the entire study, and 3) an Individually Caged Group in which animals were socially isolated. It was found that the Unstable Group, characterized by increased agonistic behavior and relatively less affiliative behavior, exhibited physiological responses indicative of chronic stress (increased urinary norepinephrine, plasma cortisol, splenic weight, and decreased visceral fat and body weight compared to the other groups). These animals also had increased acute plasma oxytocin responses relative to the other groups 10 minutes into the social pairing. In contrast, the Stable Group exhibited more affiliative behavior and less stressful physiological and tissue responses. The Individually Caged Group had elevated urinary norepinephrine relative to the Stable Group, and they exhibited higher heart rates at the end of the study compared to the other groups, suggesting that this social environment is also associated with chronic sympathetic arousal. It was concluded that distinct social contexts lead to different patterns of behavioral and physiological responses, and these responses are relevant to the pathophysiology of atherosclerosis and cardiovascular disease.

Variability in the health of human populations is greater in economically vulnerable areas. We tested whether this variability reflects and can be explained by: (1) underlying vulnerabilities and capacities of populations and/or (2) differences in the distribution of individual socioeconomic status between populations. Health outcomes were rates of mortality from 12 causes (cardiovascular disease, malignant neoplasms, accidents, chronic lower respiratory disease, cerebrovascular disease, pneumonia and influenza, diseases of the nervous system, suicide, chronic liver disease and cirrhosis, diabetes, homicide, HIV/AIDS) for 59 New York City neighborhoods in 2000. Negative binomial regression models were fit with a measure of socioeconomic vulnerability, median income, predicting each mortality rate. Overdispersion of each model was used to assess whether variability in mortality rates increased with increasing neighborhood socioeconomic vulnerability. To assess the two hypotheses, we examined changes in the variability of mortality rates (as indicated by changes in overdispersion of the models) for outcomes with significant non-constant variability after accounting for (1) vulnerabilities and capacities (social control, quality of local schools, unemployment, low education), and (2) the distribution of individual socioeconomic status (low income, poverty, socioeconomic distribution, high income). Some variability in all mortality rates was explained by accounting for a range of potential vulnerabilities and capacities, supporting the first explanation. However, variability in some causes of mortality was also explained in part by accounting for the distribution of individual resources, supporting the second explanation. The results are consistent with a theory of underlying socioeconomic vulnerabilities of human populations. In areas with lower levels of income, other characteristics of those neighborhoods exacerbate or temper the economic vulnerability, leading to more or less healthy conditions. Understanding the vulnerabilities and capacities that characterize populations may help us better understand the production of population health, and may inform efforts aimed at improving population health.

To further disentangle multimorbidity and its relation with psychosocial characteristics, by categorizing combinations of diseases within a patient as general or disease-related susceptibility, based on the presence or absence of a pathophysiological communality of diseases.

A cohort of 3,460 patients that previously took part in a study on multimorbidity was followed up for a period of 2 years. Context: the Registration Network Family Practices, which is a continuous and computerized database in Dutch general practice that covered over 60,000 patients at the time of the study.

During 2-year follow-up 91.6% did not show susceptibility, 4.2% showed general susceptibility, 1.4% disease-related susceptibility, 0.8% both general and disease-related susceptibility, and 1.9% patients could not be classified. None of the studied characteristics was significantly related to the occurrence of disease-related susceptibility. A decreased risk for general disease susceptibility related to an internal health locus of control, an active and palliative coping style, and the occurrence of positive life events.

The distinction between general susceptibility and disease-related susceptibility is feasible and seems useful. Further development of this methodology is needed, as is confirmation of these results in a larger study population.