The idea of a ‘social ladder’ may be metaphorical, but actual and perceived societal ranking have real consequences for the health of an individual (Adler et al., 2000). How social structure influences health and disease is overwhelmingly studied in high-income countries, where coronary heart disease (CHD for short) is the leading cause of death (Institute for Health Metrics and Evaluation, 2019).
In these societies, the relationship between an individual’s social position and their CHD risk is astonishingly consistent, with disadvantaged populations being more likely to suffer from the disease and to die from it (Schultz et al., 2018). Despite the clarity of this evidence, the public health workforce has not yet reached a unified consensus on why these inequalities occur, and what can be done to reduce them (Marmot, 2004).
Lifestyle factors such as diet, sedentarism or smoking, and their ensuing effects like hypertension, only partially account for the excess burden of CHD in disadvantaged groups (Schultz et al., 2018). Yet primary prevention efforts appear to focus on these health behaviours over other factors linked to social inequality. In fact, targeting lifestyle alone is likely to exacerbate inequalities in post-industrial societies (Marmot, 2004).
Investigating inequalities in populations that have not adopted Western diets and activity levels – a challenging undertaking given the proliferation of this lifestyle worldwide – could be a way to confront the underlying assumption that behavioural differences are responsible for the observed inequality in CHD (Kopp, 2019). Now, in eLife, Adrian Jaeggi (University of Zurich and Emory University), Aaron Blackwell (Washington State University) and co-workers based in the United States, France and Germany report the most comprehensive study on social structure and health in a pre-industrial society in the Bolivian Amazon known as the Tsimane (Jaeggi et al., 2021).
This population relies on subsistence farming supplemented by hunter-gatherer practices, resulting in an extremely physically active life and a diet that is rich in fibres and micronutrients. In turn, they have remarkably modest rates of obesity and hypertension, and the lowest prevalence of biological markers for poor artery health ever recorded around the world (Pontzer et al., 2018). Thus, any putative relationship between social position and heart health is unlikely to be the result of differences in health behaviour.
Overall, Jaeggi et al. discovered consistent links between wealth-related circumstances and blood pressure in the Tsimane: the poorer the individual, the higher their blood pressure. In people over the age of 15, the pressure on artery walls during and between heartbeats was lower in those with higher household wealth, that is, those with more common household assets: this can include traditional goods made from local organic materials, industrially produced items acquired through trade or purchase, and livestock. The researchers also investigated the association between wealth inequality and overall health in several geographically separated communities – defined as clusters of households connected through kin networks that produce or consume food together. They found that communities with greater inequality between rich and poor members had higher blood pressure.
Most Tsimane have normal blood pressure. This means that associations between wealth and individual blood pressure within communities, or between wealth inequality and overall blood pressure across communities both capture variations below a clinically significant level (Jaeggi et al., 2021; Pontzer et al., 2018). However, these findings are not inconsequential: in post-industrial societies, small reductions in blood pressure in the overall population have proved effective in lowering CHD incidence (Cook et al., 1995).
If no members of the Tsimane population live an unhealthy lifestyle, and if they all have little to no access to healthcare, then what drives higher blood pressure in poorer adults and in more unequal communities? Psychosocial mechanisms and pathways to poor health may provide an answer, drawing on how feelings which result from inequality, domination, or subordination may directly alter biological processes (Bartley, 2017). Social hierarchies, maintained by societal arrangements of power, lead to disadvantaged populations being disproportionally exposed to psychosocial stressors such as lack of community support, low control and autonomy, and an imbalance between effort and reward. In turn, psychosocial stress can have a severe impact on the body, triggering a sustained fight or flight response and altering the hormone system that controls biological reactions to stress (Bartley, 2017; Jaeggi et al., 2021).
Jaeggi et al. therefore tested how psychosocial factors related to unequal wealth and wealth distribution may have influenced feelings and interactions among the Tsimane (e.g., depression, social conflicts), or altered their body chemistry (e.g., the level of the stress hormone cortisol in urine). The analyses highlighted a weak connection between these factors and increased levels of blood pressure in individuals who possess less wealth or are from more unequal communities. However, this link may only be weakly supported by the analyses because the markers used could have insufficiently measured psychosocial stress. It may therefore be worth also examining whether a pathway can be identified when looking at C-reactive protein, an inflammatory biomarker for blood pressure which is relatively elevated in the Tsimane population (Pontzer et al., 2018). Yet, detecting these small effects in such a healthy society requires a large sample size, and psychosocial markers were only collected in a subset of participants with blood pressure data: thus, it is more likely that the analyses were underpowered.
The Tsimane face growing exposure to psychosocial stress as contact with ethnic majority groups increase, and their economy becomes more integrated. These developments urge researchers to explore individual-level and macro-level mechanisms for health inequality in the Tsimane, and remind us, once again, to look beyond lifestyle when tackling public health problems.
BookHealth Inequality: An Introduction to Concepts, Theories and MethodsCambridge Polity Press.
Implications of small reductions in diastolic blood pressure for primary preventionArchives of Internal Medicine 155:701–709.https://doi.org/10.1001/archinte.1995.00430070053006
WebsiteGBD compareAccessed June 8, 2021.
How western diet and lifestyle drive the pandemic of obesity and civilization diseasesDiabetes, Metabolic Syndrome and Obesity: Targets and Therapy 12:2221–2236.https://doi.org/10.2147/DMSO.S216791
The association between cardiovascular disease (CVD) and selected psychiatric disorders has frequently been suggested while the potential role of familial factors and comorbidities in such association has rarely been investigated.
We identified 869,056 patients newly diagnosed with CVD from 1987 to 2016 in Sweden with no history of psychiatric disorders, and 910,178 full siblings of these patients as well as 10 individually age- and sex-matched unrelated population controls (N = 8,690,560). Adjusting for multiple comorbid conditions, we used flexible parametric models and Cox models to estimate the association of CVD with risk of all subsequent psychiatric disorders, comparing rates of first incident psychiatric disorder among CVD patients with rates among unaffected full siblings and population controls.
The median age at diagnosis was 60 years for patients with CVD and 59.2% were male. During up to 30 years of follow-up, the crude incidence rates of psychiatric disorder were 7.1, 4.6, and 4.0 per 1000 person-years for patients with CVD, their siblings and population controls. In the sibling comparison, we observed an increased risk of psychiatric disorder during the first year after CVD diagnosis (hazard ratio [HR], 2.74; 95% confidence interval [CI], 2.62–2.87) and thereafter (1.45; 95% CI, 1.42–1.48). Increased risks were observed for all types of psychiatric disorders and among all diagnoses of CVD. We observed similar associations in the population comparison. CVD patients who developed a comorbid psychiatric disorder during the first year after diagnosis were at elevated risk of subsequent CVD death compared to patients without such comorbidity (HR, 1.55; 95% CI, 1.44–1.67).
Patients diagnosed with CVD are at an elevated risk for subsequent psychiatric disorders independent of shared familial factors and comorbid conditions. Comorbid psychiatric disorders in patients with CVD are associated with higher risk of cardiovascular mortality suggesting that surveillance and treatment of psychiatric comorbidities should be considered as an integral part of clinical management of newly diagnosed CVD patients.
This work was supported by the EU Horizon 2020 Research and Innovation Action Grant (CoMorMent, grant no. 847776 to UV, PFS, and FF), Grant of Excellence, Icelandic Research Fund (grant no. 163362-051 to UV), ERC Consolidator Grant (StressGene, grant no. 726413 to UV), Swedish Research Council (grant no. D0886501 to PFS), and US NIMH R01 MH123724 (to PFS).
Background: Over a life-course, human adaptive immunity to antigenically mutable pathogens exhibits competitive and facilitative interactions. We hypothesize that such interactions may lead to cyclic dynamics in immune responses over a lifetime.
Methods: To investigate the cyclic behavior, we analyzed hemagglutination inhibition titers against 21 historical influenza A(H3N2) strains spanning 47 years from a cohort in Guangzhou, China and applied Fourier spectrum analysis. To investigate possible biological mechanisms, we simulated individual antibody profiles encompassing known feedbacks and interactions due to generally recognized immunological mechanisms.
Results: We demonstrated a long-term periodicity (about 24 years) in individual antibody responses. The reported cycles were robust to analytic and sampling approaches. Simulations suggested that individual-level cross-reaction between antigenically similar strains likely explain the reported cycle. We showed that the reported cycles are predictable at both individual and birth-cohort level and that cohorts show a diversity of phases of these cycles. Phase of cycle was associated with the risk of seroconversion to circulating strains, after accounting for age and pre-existing titers of the circulating strains.
Conclusions: Our findings reveal the existence of long-term periodicities in individual antibody responses to A(H3N2). We hypothesize that these cycles are driven by pre-existing antibody responses blunting responses to antigenically similar pathogens (by preventing infection and/or robust antibody responses upon infection), leading to reductions in antigen specific responses over time until individual's increasing risk leads to an infection with an antigenically distant enough virus to generate a robust immune response. These findings could help disentangle cohort-effects from individual-level exposure histories, improve our understanding of observed heterogeneous antibody responses to immunizations, and inform targeted vaccine strategy.
Funding: This study was supported by grants from the NIH R56AG048075 (D.A.T.C., J.L.), NIH R01AI114703 (D.A.T.C., B.Y.), the Wellcome Trust 200861/Z/16/Z (S.R.) and 200187/Z/15/Z (S.R.). This work was also supported by research grants from Guangdong Government HZQB-KCZYZ-2021014 and 2019B121205009 (Y.G. and H.Z.). D.A.T.C., J.M.R. and S.R. acknowledge support from the National Institutes of Health Fogarty Institute (R01TW0008246). J.M.R. acknowledges support from the Medical Research Council (MR/S004793/1) and the Engineering and Physical Sciences Research Council (EP/N014499/1). The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.