We examine the childhood antecedents of somatic, social and psychological functioning over the lifespan. Our goals are: 1) to extend knowledge on the pathways connecting early-life stressors and early-life environments with later-life outcomes, 2) to extend knowledge on the factors explaining inter-generational transmission of social and health-risks, and 3) to examine how transmission of risks can be reduced by early-life preventions and interventions. We mainly use data from prospective cohort studies following individuals over several decades.  We have shown that stressors in childhood confer risk for midlife cardio-metabolic outcomes including diabetes, obesity, and atherosclerotic calcification, as well as mental health outcomes including depressive symptoms and sleep problems. We will proceed by examining the mechanisms underlying these associations and we will test whether behavioural interventions are effective in reducing the outcomes induced by early-life adversities.  In the near future, we will examine how psychosocial risks transmit over generations using a unique prospective dataset gathered during 40 years and over three generations (the Young Finns Offspring Study).

Here we focus on three streams of research: a) poor social relations / loneliness as health risks, b) socioeconomic origins of lifespan health and c) work-life stressors producing health and disease. We have shown that loneliness, social isolation and poor quality social relations are risksfor excess mortality,  cardiovascular heart disease, and cognitive decline. An other major line of research relates to socioeconomic factors predicting lifespan health and on the pathways that may explain such relations. Here we are interested in elucidating the inter-relations between psychiatric disorder and the development of socioeconomic status and social relations over the lifespan. We are also interested if accumulation of socioeconomic adversities and poor social relations over the lifespan produces permanent changes in a person’s physiological system. The changes may include for instance inflammatory activation or premature epigenetic aging (DNA methylation). We will test these hypotheses in our future work, extending knowledge on the mechanisms whereby socioeconomic and psychosocial exposures are associated with human health and wellbeing. We have also shown that negative psychosocial characteristics at the workplace, such as low level of organizational justice, lack of job control, confer risky outcomes for mental and somatic health. In the future, we will examine new mechanisms connecting work-place stressors with health outcomes, including inflammatory pathways and epigenetic pathways. Elucidating such mechanisms will enhance knowledge on how to prevent work-related health problems and how to enhance wellbeing at work

Here we leverage on new statistical approaches to examine how psychosocial factors and lifestyle factors are related each other and to mental and somatic outcomes. The network approach is a new statistical method where we can examine if some symptoms (e.g., symptoms of depressive disorder) are more central than other in producing health-related outcomes. This approach also allows examining how various symptoms evolve over time and how they may trigger other symptoms over development. Such knowledge allows combining different theoretical approaches with each other, thereby advancing the integration of research across disciplines. We will also apply accumulation models, mover-stayer models and latent profile analyses. Applying these methodologies allows us to examine how accumulation of adversity affects health and wellbeing, why people adopt healthy vs. unhealthy lifestyles, and how exposures cluster with each other, thereby enhancing knowledge on the development on mental and somatic health.