Depression and cognition are associated, but the role of depressive symptoms in lifestyle interventions to prevent dementia needs further study. We investigated the intervention effect on depressive symptoms and their associations with cognition in the Finnish Geriatric Intervention Study to Prevent Cognitive Impairment and Disability (FINGER; NCT01041989), a two-year multidomain lifestyle trial. One thousand two-hundred and sixty individuals (60-77 years) at risk for dementia were randomised into a multidomain intervention (diet, exercise, cognitive training, and vascular/metabolic risk monitoring) or control group (regular health advice). Depressive symptoms (Zung scale) and cognition (modified Neuropsychological Test Battery) were evaluated at baseline, 12, and 24 months. One thousand one-hundred and twenty-five participants had baseline Zung data. Mean Zung score decreased 0.73 (SD 5.6) points in the intervention and 0.36 (5.6) points in the control group, with nonsignificant between-group difference (group x time coefficient -0.006, 95% CI -0.019 to 0.007). Overall, higher baseline Zung score was associated with less improvement in global cognition (-0.140, p = 0.005) and memory (-0.231, p = 0.005). Participants with clinically significant baseline depressive symptoms (Zung >= 40 points) had less intervention benefit to executive functioning (group x time x Zung -0.096, 95% CI -0.163 to -0.028). Change in Zung score was not associated with change in cognition. Clinically significant depressive symptoms warrant more attention when designing dementia-prevention interventions.

Objectives The aims of this study were to investigate whether baseline leisure-time physical activity (LTPA) is associated with future recovery from depression among patients with a depression diagnosis and whether baseline LTPA is associated with total physical activity after five years of follow-up. Methods A total of 258 patients aged >= 35 years with clinically confirmed depression at baseline participated. The study was conducted between 2008 and 2016 in municipalities within the Central Finland Hospital District. Depressive symptoms (DS) were determined with the Beck Depression Inventory (BDI) with a cutoff score >= 10, and depression diagnoses were confirmed by the Mini-International Neuropsychiatric Interview (MINI). Blood pressure and anthropometric parameters were measured and blood samples for glucose and lipid determinations were drawn at baseline. LTPA, physical activity, and other social and clinical factors were captured by standard self-administered questionnaires at baseline and the five-year follow-up point. Results Of the 258 patients, 76 (29%) had DS at follow-up. Adjusted odds ratio (OR) for future DS was 1.43 (confidence interval [CI] 0.69-2.95) for participants with moderate LTPA and 0.92 (CI 0.42-2.00) for participants with high LTPA, compared with low LTPA at baseline. Higher baseline LTPA levels were associated with higher total physical activity in the future (beta=0.14 [95% CI: 0.02-0.26] for linearity = 0.024). Conclusion Baseline LTPA did not affect the five-year prognosis of depression among depressed patients in a Finnish adult population. Because the baseline LTPA level predicted the future total physical activity, it could be included as a part of the overall health management and treatment of depression in clinical practices.

Studies on the intergenerational transmission of depressive symptoms form a long research tradition. Numerous studies have indicated that children of depressed mothers face an up to 3-fold risk of exhibiting depressive symptoms later in life compared with those children whose mother has not had depressive symptoms. Later studies have observed that paternal depressive symptoms pose an almost equal risk factor particularly for boys. After having established the association between parental and offspring depressive symptoms, research has focused on exploring the mechanisms underlying the transmission of risk. These are also the principal point of interest in the present thesis that gives particular weight to the role of gender, socioeconomic circumstances (parental education and household income) and timing of exposure, belonging to often-hypothesized but seldom-examined shapers of the transmission of risk. Besides these, the study sheds light on the significance of gender of which previous research has produced mixed results. The interpretation of the results leans on the conceptual framework of life course epidemiology, which understands the development of a disease or a disorder as the outcome of biological, psychosocial, and environmental processes that entangle with each other throughout the life course. The study utilized the register-based EKSY014 data set that contains a 20% random sample of all Finnish households with at least one child aged 0-14 years at the end of 2000. Information on the purchases of prescription medicines and visits to inpatient and outpatient care were used as proxy for the incidence of depressive symptoms. Cox proportional hazards regression model, which belongs to the field of survival analysis, was used to compare the event rates between the groups of interest. Exposure to depression of biological parents was measured when persons were 9-14 years old, and the follow-up of an individual’s own depressive symptoms started on the first day of the year the person turned 15 and ended on the last day of the year the person turned 20. Altogether, the principal study population included more than 130,000 persons born between 1986 and 1996. A smaller sub-sample was used to study the effects of an early-life exposure at age 0-5 years and recurrent parental depressive symptoms. According to the analysis, exposure to maternal depressive symptoms at age 9-14 years poses an equally large 2-fold risk for boys and girls. Paternal depressive symptoms put boys at an equal risk as maternal depressive symptoms, but for girls, they pose a smaller 1.5-fold risk. Among those persons who are living with their biological parents, controlling for the effects of socioeconomic factors weakens the association only little and no differences are seen in the risk of intergenerational transmission across the groups of socioeconomic status. Exposure to both maternal depressive symptoms and paternal depressive symptoms poses a bigger risk than a single exposure among both girls and boys. The analysis conducted with the smaller sub-sample implies that an exposure at age 9-14 years poses a bigger risk than an exposure at age 0-5 years. Recurrent exposure to maternal depressive symptoms appears to be a particularly severe risk factor. The results of the study support the life course epidemiological processes of accumulation of risk and chains of risk: Exposure to depressive symptoms in both parents and the long-term chaining of parental depressive symptoms put the person at the greatest risk. Parental depressive symptoms and socioeconomic status appear as largely independent risk factors of adolescent depressive symptoms; thus, those adolescents having a low socioeconomic status and a history of parental depressive symptoms face a particularly elevated risk of exhibiting depressive symptoms. The preliminary analysis did not give support to the assumed sensitive period in the first years of life, but the question should be examined further with a larger sample. Overall, the results advocate a more holistic approach to the prevention of adolescent depressive symptoms, beginning from the identification of familial risk and leading to actions that target all members of the family.

Objective Depression and high blood pressure are becoming more common problems, but their relation remains unclear. This master's thesis studied the relation between depression and high blood pressure in the longitudinal Young Finns Study over a follow-up of four years. The aim was to examine whether 1) baseline depressive symptoms predict blood pressure over the follow-up, 2) the relation between depression and blood pressure differs among men and women, 3) health choices affect the relation, and 4) there is a relation between the duration of depression and blood pressure. Methods The participants (N=909) were about 42 years old, and 61 % of them were women. Their blood pressure and BDI-II depression scores were measured in 2007 ja 2011. Three-step regression analysis was used to predict the systolic and diastolic blood pressure based on the baseline depression score. The first model was controlled for age, gender and baseline blood pressure, the second model also for education and income, and the third model additionally for health choices. The average blood pressures of non-depressed, once depressed and twice depressed participants were compared in analysis of variance. The group comparisons were additionally controlled for age, gender and baseline blood pressure in analysis of covariance. Results and conclusions Baseline depressive symptoms did not predict blood pressure. Among women, a positive relation between depression and blood pressure was found in the first model, but not in the more controlled models. The relation between depression and blood pressure was partly explained by health choices; higher body mass index predicted higher blood pressure. Controlling for age, gender and baseline blood pressure, the duration of depression was connected to higher blood pressure; the diastolic blood pressure was higher, when the participant was depressed both in the beginning and end of the follow-up.

Psychological and social factors are known to influence blood pressure (BP) and risk of hypertension and associated cardiovascular diseases. To identify novel BP loci, we carried out genome-wide association meta-analyses of systolic, diastolic, pulse, and mean arterial BP, taking into account the interaction effects of genetic variants with three psychosocial factors: depressive symptoms, anxiety symptoms, and social support. Analyses were performed using a two-stage design in a sample of up to 128,894 adults from five ancestry groups. In the combined meta-analyses of stages 1 and 2, we identified 59 loci (p value < 5e−8), including nine novel BP loci. The novel associations were observed mostly with pulse pressure, with fewer observed with mean arterial pressure. Five novel loci were identified in African ancestry, and all but one showed patterns of interaction with at least one psychosocial factor. Functional annotation of the novel loci supports a major role for genes implicated in the immune response (PLCL2), synaptic function and neurotransmission (LIN7A and PFIA2), as well as genes previously implicated in neuropsychiatric or stress-related disorders (FSTL5 and CHODL). These findings underscore the importance of considering psychological and social factors in gene discovery for BP, especially in non-European populations.

Several studies have associated religiosity with better mental health, but these studies have only partially addressed the problem of confounding. The present study pooled data from multiple cohort studies with siblings to examine whether associations between religiosity and mental health are confounded by familial factors (i.e., shared family background and siblings' shared genetics). Data were collected between 1982 and 2017. Mental health was assessed with self-reported psychological distress (including depressive symptoms) and psychological well-being. Religious attendance was associated with lower psychological distress (standard-deviation difference between weekly vs. never attendance, B = -0.14, confidence interval (CI): -0.19, -0.09; n = 24,598 pairs), and this was attenuated by almost half in the sibling analysis (B = -0.08, CI: = -0.13, -0.04). Religious attendance was also related to higher well-being (B = 0.29, CI: = 0.14, 0.45; n = 3,728 pairs), and this estimate remained unchanged in sibling analysis. Results were similar for religiousness. The findings suggest that previous longitudinal studies may have overestimated the association between religiosity and psychological distress, as the sibling estimate was only one-third of the previously reported meta-analytical association (standardized correlation -0.03 vs. -0.08).

Aim: This randomised control trial (RCT) study examined the effectiveness of a mentalisation-based perinatal group intervention, Nurture and Play (NaP), in improving mother–infant interaction quality and maternal reflective functioning and in decreasing depressive symptoms. Background: Few preventive prenatal interventions have been developed for primary health care settings for mothers with depressive symptoms. Furthermore, previous prenatal intervention studies have only concentrated on reducing depressive symptoms and have not directly addressed enhancing optimal parenting qualities. Methods: The participants were 45 pregnant women with depressive symptoms. Women in the randomly assigned intervention group (n = 24) participated in the manualised, short-term NaP intervention group from pregnancy until the baby’s age of seven months, whereas control group women received treatment as usual (TAU). Maternal emotional availability (EA), reflective functioning (RF) and depressive symptoms were measured before the intervention and at the infants’ 12 months of age, and changes were evaluated using repeated measure analyses of variances (ANOVAs). Findings: The results showed that the intervention group displayed higher maternal sensitivity and RF and more reduction in depressive symptoms than the control group when babies were 12 months old. These findings provide preliminary support for the effectiveness of the NaP intervention.