Mapping the ripple effects: how social inequalities shape multimorbidity in an aging society

This thesis examines how socioeconomic inequalities shape the development of multimorbidity, defined as the coexistence of two or more chronic conditions, in aging populations. Although rising life expectancy has led more people to live longer with chronic disease, increases in healthy life years have not kept pace, creating a growing burden of disability, healthcare use, and diminished quality of life. Multimorbidity is heterogeneous, involving clusters of physical and mental disorders, and challenges healthcare systems still designed around single-disease care. Its definition and operationalization vary widely, complicating epidemiologic estimates and comparative research. The thesis focuses on the role of socioeconomic position (SEP) as a fundamental determinant of multimorbidity. Lower SEP is associated with earlier onset, faster accumulation of chronic conditions, greater functional decline, and higher mortality. Mechanisms include behavioural factors (e.g., smoking, obesity, and physical inactivity), psychosocial stress, limited access to resources, environmental exposures, and social disadvantage accumulated across the life course. Biological pathways such as chronic inflammation and epigenetic aging illustrate how social adversity becomes physiologically embedded. Using two large population-based cohorts, the thesis investigates how SEP influences different transitions from single conditions to multimorbidity. It focuses on major noncommunicable diseases (NCDs): cardiovascular disease, type 2 diabetes (T2D), cancer, chronic obstructive pulmonary disease (COPD), and depression. Results consistently show that individuals with lower education, used as a proxy for SEP, have higher risks of developing initial disease and progressing to multimorbidity, although patterns differ by sex. Lifestyle factors only partially explain these inequalities. Formal mediation analysis demonstrates that unhealthy behaviours partly contribute to, the SEP gradient, particularly in men. To explore additional mechanisms, the thesis evaluates associations between SEP and 23 biomarkers related to inflammation, metabolic dysregulation, and physiological stress, and constructs an allostatic load (AL) indicator. Lower SEP in women was linked to more adverse biomarker profiles, supporting biological embedding of disadvantage. Overall, the thesis concludes that multimorbidity is shaped by complex, multilevel social processes. It recommends integrated, patient-centred care models, policies addressing upstream determinants, and broader preventive strategies targeting shared risk factors. Public health efforts should prioritize socially disadvantaged groups to reduce multimorbidity burden in aging societies. additional mechanisms, the thesis evaluates associations between SEP and 23 biomarkers related to inflammation, metabolic dysregulation, and physiological stress, and constructs an allostatic load (AL) indicator. Lower SEP in women was linked to more adverse biomarker profiles, supporting biological embedding of disadvantage. Overall, the thesis concludes that multimorbidity is shaped by complex, multilevel social processes. It recommends integrated, patient-centred care models, policies addressing upstream determinants, and broader preventive strategies targeting shared risk factors. Public health efforts should prioritize socially disadvantaged groups to reduce multimorbidity burden in aging societies.