OBJECTIVES: Body fat, measured with body mass index (BMI), and obesity are associated with depressive symptoms. Among younger adults there is stronger evidence of obesity leading to depressive symptoms than of depressive symptoms leading to obesity, but the temporal relationship is unknown among older adults. This study utilized dual-change-score models (DCSMs) to determine the directional relationship between body mass and depressive symptoms among older adults.

METHOD: Participants (n=1743) from the Swedish Twin Registry (baseline age range 50-96 years) completed at least one assessment of BMI (nurse measurement of height and weight) and the Center for Epidemiologic Studies-Depression scale (CESD). More than half the sample completed three or more assessments, scheduled at intervals of 2-4 years. DCSMs modeled the relationship of BMI and CESD across age, both independently and as part of bivariate relationships.

RESULTS: Depressive symptoms contributed to subsequent changes in BMI after age 70, while BMI contributed to subsequent changes in depressive symptoms after age 82. Thus, there is a reciprocal relationship that may change with age. The effect was more pronounced for women.

DISCUSSION: The association of BMI and depressive symptoms is bi-directional among older adults, and it appears to be affected by both age and sex.

The Interplay of Genes and Environment across Multiple Studies (IGEMS) is a consortium of 18 twin studies from 5 different countries (Sweden, Denmark, Finland, United States, and Australia) established to explore the nature of gene-environment (GE) interplay in functioning across the adult lifespan. Fifteen of the studies are longitudinal, with follow-up as long as 59 years after baseline. The combined data from over 76,000 participants aged 14-103 at intake (including over 10,000 monozygotic and over 17,000 dizygotic twin pairs) support two primary research emphases: (1) investigation of models of GE interplay of early life adversity, and social factors at micro and macro environmental levels and with diverse outcomes, including mortality, physical functioning and psychological functioning; and (2) improved understanding of risk and protective factors for dementia by incorporating unmeasured and measured genetic factors with a wide range of exposures measured in young adulthood, midlife and later life.

BACKGROUND: Despite advances in life expectancy, low socioeconomic status is associated with a shorter lifespan. This study was conducted to investigate socioeconomic differences in mortality by comparing preventable with non-preventable causes of death in 39 506 participants from the Swedish Twin Registry born before 1935.

METHODS: Childhood social class, own education, own social class and social mobility were used as separate indicators of socioeconomic status. These data were linked to the Swedish Cause of Death Register. Cause of death was categorized as preventable or non-preventable mortality according to indicators presented in the Avoidable Mortality in the European Union (AMIEHS) atlas. Using Cox proportional hazard models, we tested the association between the socioeconomic measures and all-cause mortality, preventable mortality and non-preventable mortality. Additional co-twin control analyses indicated whether the associations reflected genetic confounding.

RESULTS: The social gradient for mortality was most prominent for the adult socioeconomic measures. There was a social gradient in both preventable mortality and non-preventable mortality, but with an indication of a moderately stronger effect in preventable causes of death. In analyses of social mobility, those who experienced life-time low socioeconomic status (SES) or downward social mobility had an increased mortality risk compared with those with life-time high SES and upward social mobility. Adjustments for genetic confounding did not change the observed associations for education, social class or social mobility and mortality. In the co-twin control analyses of reared-apart twins, the association between childhood social class and mortality weakened, indicating possible genetic influences on this association.

CONCLUSIONS: Our results indicate that there is an association between low adult socioeconomic status and increased mortality independent of genetic endowment. Thus, we do not find support for indirect social selection as the basis for mortality inequalities in Sweden.