Gene expression networks regulated by human personality.

Genome-wide association studies of human personality have been carried out, but transcription of the whole genome has not been studied in relation to personality in humans. We collected genome-wide expression profiles of adults to characterize the regulation of expression and function in genes related to human personality. We devised an innovative multi-omic approach to network analysis to identify the key control elements and interactions in multi-modular networks. We identified sets of transcribed genes that were co-expressed in specific brain regions with genes known to be associated with personality. Then we identified the minimum networks for the co-localized genes using bioinformatic resources. Subjects were 459 adults from the Young Finns Study who completed the Temperament and Character Inventory and provided peripheral blood for genomic and transcriptomic analysis. We identified an extrinsic network of 45 regulatory genes from seed genes in brain regions involved in self-regulation of emotional reactivity to extracellular stimuli (e.g., self-regulation of anxiety) and an intrinsic network of 43 regulatory genes from seed genes in brain regions involved in self-regulation of interpretations of meaning (e.g., production of concepts and language). We discovered that interactions between the two networks were coordinated by a control hub of 3 miRNAs and 3 protein-coding genes shared by both. Interactions of the control hub with proteins and ncRNAs identified more than 100 genes that overlap directly with known personality-related genes and more than another 4000 genes that interact indirectly. We conclude that the six-gene hub is the crux of an integrative network that orchestrates information-transfer throughout a multi-modular system of over 4000 genes enriched in liquid-liquid-phase-separation (LLPS)-related RNAs, diverse transcription factors, and hominid-specific miRNAs and lncRNAs. Gene expression networks associated with human personality regulate neuronal plasticity, epigenesis, and adaptive functioning by the interactions of salience and meaning in self-awareness.

Polygenic risk for schizophrenia predicting social trajectories in a general population sample.

BACKGROUND: We investigated (a) whether polygenic risk for schizophrenia predicts different trajectories of social development among those who have not developed psychoses and (b) whether possible associations are PRSSCZ-specific or evident also for any polygenic risk for mental disorders, e.g. for major depression. METHODS: Participants came from the population-based Young Finns Study (n = 2377). We calculated a polygenic risk score for schizophrenia (PRSSCZ) and for major depression (PRSDEP). Diagnoses of psychotic disorders were derived from the hospital care register. Social development from adolescence to middle age was measured by (a) perceived social support from friends, family, and a close other, (b) perceived sociability, and (c) family structure (partnership status, number of children, age of first-time parenthood). RESULTS: Among those without manifest psychoses, high PRSSCZ predicted lower experienced support from friends (B = -0.04, p = 0.009-0.035) and family (B = -0.04, p = 0.009-0.035) especially after early adulthood, and also lower perceived sociability (B = -0.05, p = 0.010-0.026). PRSSCZ was not related to family structure. PRSDEP did not predict any domain of social development. CONCLUSIONS: Individuals at high PRSSCZ (not converted to psychosis) seem to experience a lower preference to be with others over being alone. Individuals with high (v. low) PRSSCZ seem to have a similar family structure in terms of partnership status or number of children but, nevertheless, they experience less support from their family. Among those not converted to psychosis in a typical age period, high PRSSCZ may predict a 'later risk phase' and reduced functional resilience when approaching middle age.

Magical thinking in individuals with high polygenic risk for schizophrenia but no non-affective psychoses-a general population study.

A strong genetic background for psychoses is well-established. Most individuals with a high genetic risk for schizophrenia, however, do not develop the disorder. We investigated whether individuals, who have a high genetic risk for schizophrenia but no non-affective psychotic disorders, are predisposed to develop milder forms of deviant thinking in terms of magical thinking. Participants came from the population-based Young Finns Study (n = 1292). The polygenic risk score for schizophrenia (PRS) was calculated on the basis of the most recent genome-wide association study (GWAS). Psychiatric diagnoses over the lifespan were collected up to 2017 from the registry of hospital care. Magical thinking was evaluated with the Spiritual Acceptance Scale (e.g., beliefs in telepathy, miracles, mystical events, or sixth sense) of the Temperament and Character Inventory in 1997, 2001, and 2012 (participants were 20-50-year-olds). We found that, among those who did not develop non-affective psychotic disorders, high PRS predicted higher magical thinking in adulthood (p = 0.001). Further, PRS predicted different developmental courses: a low PRS predicted a steady decrease in magical thinking from age 20 to 50 years, while in individuals with high PRS the decrease in magical thinking ceased in middle age so that their level of magical thinking remained higher than expected for that age. These findings remained when controlling for sex, childhood family environment, and adulthood socioeconomic factors. In conclusion, if high PRS does not lead to a non-affective psychotic disorder, it predicts milder forms of deviant thinking such as elevated magical thinking in adulthood, especially in middle age. The finding enhances our understanding of different outcomes of high genetic psychosis risk.

Three genetic-environmental networks for human personality.

Phylogenetic, developmental, and brain-imaging studies suggest that human personality is the integrated expression of three major systems of learning and memory that regulate (1) associative conditioning, (2) intentionality, and (3) self-awareness. We have uncovered largely disjoint sets of genes regulating these dissociable learning processes in different clusters of people with (1) unregulated temperament profiles (i.e., associatively conditioned habits and emotional reactivity), (2) organized character profiles (i.e., intentional self-control of emotional conflicts and goals), and (3) creative character profiles (i.e., self-aware appraisal of values and theories), respectively. However, little is known about how these temperament and character components of personality are jointly organized and develop in an integrated manner. In three large independent genome-wide association studies from Finland, Germany, and Korea, we used a data-driven machine learning method to uncover joint phenotypic networks of temperament and character and also the genetic networks with which they are associated. We found three clusters of similar numbers of people with distinct combinations of temperament and character profiles. Their associated genetic and environmental networks were largely disjoint, and differentially related to distinct forms of learning and memory. Of the 972 genes that mapped to the three phenotypic networks, 72% were unique to a single network. The findings in the Finnish discovery sample were blindly and independently replicated in samples of Germans and Koreans. We conclude that temperament and character are integrated within three disjoint networks that regulate healthy longevity and dissociable systems of learning and memory by nearly disjoint sets of genetic and environmental influences.

Bidirectional pathways between psychosocial risk factors and paranoid ideation in a general nonclinical population.

We investigated (a) whether psychosocial factors (experienced stress, anticipatory worry, social detachment, sleeping disturbances, alcohol use) predict the course of paranoid ideation between the ages of 24 to 50 years and (b) whether the predictive relationships are more likely to proceed from the psychosocial factors to paranoid ideation, or vice versa. The participants (N = 1534-1553) came from the population-based Young Finns study. Paranoid ideation and psychosocial factors were assessed by reliable self-report questionnaires in 2001, 2007, and 2011/2012. The data were analyzed using growth curve and structural equation models. High experienced stress, anticipatory worry, social detachment, frequent sleeping disturbances, and frequent alcohol use predicted more paranoid ideation. More risk factors predicted increasing paranoid ideation. There were bidirectional predictive relationships of paranoid ideation with experienced stress, anticipatory worry, social detachment, and sleeping disturbances. The link between alcohol use and paranoid ideation was only correlative. In conclusion, paranoid ideation increases by reciprocal interactions with stress, worry, social detachment, and sleeping disturbances. The findings support the threat-anticipation model of paranoid ideation, providing important implications for treatment of paranoia.

Uncovering the complex genetics of human temperament.

Experimental studies of learning suggest that human temperament may depend on the molecular mechanisms for associative conditioning, which are highly conserved in animals. The main genetic pathways for associative conditioning are known in experimental animals, but have not been identified in prior genome-wide association studies (GWAS) of human temperament. We used a data-driven machine learning method for GWAS to uncover the complex genotypic-phenotypic networks and environmental interactions related to human temperament. In a discovery sample of 2149 healthy Finns, we identified sets of single-nucleotide polymorphisms (SNPs) that cluster within particular individuals (i.e., SNP sets) regardless of phenotype. Second, we identified 3 clusters of people with distinct temperament profiles measured by the Temperament and Character Inventory regardless of genotype. Third, we found 51 SNP sets that identified 736 gene loci and were significantly associated with temperament. The identified genes were enriched in pathways activated by associative conditioning in animals, including the ERK, PI3K, and PKC pathways. 74% of the identified genes were unique to a specific temperament profile. Environmental influences measured in childhood and adulthood had small but significant effects. We confirmed the replicability of the 51 Finnish SNP sets in healthy Korean (90%) and German samples (89%), as well as their associations with temperament. The identified SNPs explained nearly all the heritability expected in each sample (37-53%) despite variable cultures and environments. We conclude that human temperament is strongly influenced by more than 700 genes that modulate associative conditioning by molecular processes for synaptic plasticity and long-term memory.

Uncovering the complex genetics of human character.

Human personality is 30-60% heritable according to twin and adoption studies. Hundreds of genetic variants are expected to influence its complex development, but few have been identified. We used a machine learning method for genome-wide association studies (GWAS) to uncover complex genotypic-phenotypic networks and environmental interactions. The Temperament and Character Inventory (TCI) measured the self-regulatory components of personality critical for health (i.e., the character traits of self-directedness, cooperativeness, and self-transcendence). In a discovery sample of 2149 healthy Finns, we identified sets of single-nucleotide polymorphisms (SNPs) that cluster within particular individuals (i.e., SNP sets) regardless of phenotype. Second, we identified five clusters of people with distinct profiles of character traits regardless of genotype. Third, we found 42 SNP sets that identified 727 gene loci and were significantly associated with one or more of the character profiles. Each character profile was related to different SNP sets with distinct molecular processes and neuronal functions. Environmental influences measured in childhood and adulthood had small but significant effects. We confirmed the replicability of 95% of the 42 SNP sets in healthy Korean and German samples, as well as their associations with character. The identified SNPs explained nearly all the heritability expected for character in each sample (50 to 58%). We conclude that self-regulatory personality traits are strongly influenced by organized interactions among more than 700 genes despite variable cultures and environments. These gene sets modulate specific molecular processes in brain for intentional goal-setting, self-reflection, empathy, and episodic learning and memory.

Risky emotional family environment in childhood and depression-related cytokines in adulthood: The protective role of compassion.

BACKGROUND: Previously, compassion has been found to protect against depressive symptoms, while emotional adversities in childhood are suggested to increase inflammatory responses. The current study investigated (a) whether emotional family environment in childhood predicts levels of such cytokines in adulthood that are previously found to be elevated in depression (interleukin [IL]-2, IL-6, IL-1b, monocyte chemoattractant protein-1, interferon-gamma [IFN-γ], and tumor necrosis factor alpha [TNF-α]) and (b) whether these associations are modified by compassion in adulthood. METHODS: The participants (N = 1,198-1,523) came from the prospective population-based Young Finns data. Emotional family environment and parental socioeconomic factors were evaluated in 1980; participants' compassion in 2001; and participants' cytokine levels and adulthood covariates in 2007. RESULTS: Risky emotional family environment in childhood predicted higher levels of IL-2, IL-6, IFN-γ, and TNF-α in adulthood. Additionally, there were significant interaction effects between compassion and emotional risk in childhood, when predicting IL-2, IL-6, and TNF-α. Specifically, individuals who grew up in a risky emotional family environment had on average higher levels of IL-2, IL-6, and TNF-α in adulthood when combined with low compassion. CONCLUSIONS: In individuals coming from risky emotional family environments, high compassion for others may protect against elevated levels of cytokines previously linked with depression.

Genetic differential susceptibility to the parent-child relationship quality and the life span development of compassion.

The development of compassion for others might be influenced by the social experiences made during childhood and has a genetic component. No research has yet investigated whether the parent-child relationship quality interacts with genetic variation in the oxytocin and dopamine systems in predicting compassion over the life span. In the prospective Young Finns Study (N = 2099, 43.9% men), we examined the interaction between mother-reported emotional warmth and intolerance toward their child assessed in 1980 (age of participants, 3-18 years) and two established genetic risk scores for oxytocin levels and dopamine signaling activity. Dispositional compassion for others was measured with the Temperament and Character Inventory 1997, 2001, and 2012 (age of participants, 20-50 years). We found a gene-environment interaction (p = .031) that remained marginally significant after adjustment for multiple testing. In line with the differential susceptibility hypothesis, only participants who carry alleles associated with low dopamine signaling activity had higher levels of compassion when growing up with emotionally warm parents, whereas they had lower levels of compassion when their parents were emotionally cold. Children's genetic variability in the dopamine system might result in plasticity to early environmental influences that have a long-lasting effect on the development of compassion. However, our findings need replication.

The Contribution of Neighborhood Socioeconomic Disadvantage to Depressive Symptoms Over the Course of Adult Life: A 32-Year Prospective Cohort Study.

The association between socioeconomic disadvantage and increased risk of depressive symptoms in adulthood is well established. We tested 1) the contribution of early exposure to neighborhood socioeconomic disadvantage to later depressive symptoms throughout life, 2) the persistence of the potential association between early exposure and depressive symptoms, and 3) the contributions of other known risk factors to the association. Data were collected from the Young Finns Study, a prospective, population-based 32-year follow-up study that included participants aged 3-18 years at baseline in 1980. Participants were followed up with repeated measurements of depressive symptoms between 1992 and 2012 (n = 2,788) and linked to national grid data on neighborhood disadvantage via residential addresses. We examined the associations in mixed models separately for the 5-, 10-, 15-, and 20-year follow-ups. Living in a disadvantaged neighborhood during childhood and adolescence was associated with a higher level of depressive symptoms in adulthood during all follow-up periods (ß = 0.07, P = 0.001) than living in a nondisadvantaged area. Individual adulthood socioeconomic status mediated the associations. These findings suggest that living in a socioeconomically disadvantaged area during childhood and adolescence has a long-lasting negative association with mental health irrespective of family-related risks, partially due to socioeconomic adversity later in life.

Does Compassion Predict Blood Pressure and Hypertension? The Modifying Role of Familial Risk for Hypertension.

BACKGROUND: This study investigated (i) whether compassion is associated with blood pressure or hypertension in adulthood and (ii) whether familial risk for hypertension modifies these associations. METHOD: The participants (N = 1112-1293) came from the prospective Young Finns Study. Parental hypertension was assessed in 1983-2007; participants' blood pressure in 2001, 2007, and 2011; hypertension in 2007 and 2011 (participants were aged 30-49 years in 2007-2011); and compassion in 2001. RESULTS: High compassion predicted lower levels of diastolic and systolic blood pressure in adulthood. Additionally, high compassion was related to lower risk for hypertension in adulthood among individuals with no familial risk for hypertension (independently of age, sex, participants' and their parents' socioeconomic factors, and participants' health behaviors). Compassion was not related to hypertension in adulthood among individuals with familial risk for hypertension. CONCLUSION: High compassion predicts lower diastolic and systolic blood pressure in adulthood. Moreover, high compassion may protect against hypertension among individuals without familial risk for hypertension. As our sample consisted of comparatively young participants, our findings provide novel implications for especially early-onset hypertension.

Breastfeeding and offspring's compassion and empathy in adulthood: A study with an over 30-year follow-up.

This study investigated whether breastfeeding predicts offspring's dispositional compassion and empathy from early adulthood to middle age. The parents of the participants (N = 1,394) of the Young Finns study answered questions about breastfeeding in 1983, and the participants' compassion and empathy were evaluated in 1997-2012 (participants were aged 20-50 years). Breastfeeding did not predict the course of compassion or empathy in adulthood at the age of 20-50 years. The associations remained non-significant, when adjusted for age, gender, socioeconomic factors, and a wide range of characteristics of the family environment (including mother's gestational age; premature birth; birth weight; number of other children at home; parental mental disorder; parental relationship status; parental postnatal smoking; parental postnatal alcohol use; parenting behavior; and child's externalizing behavior). In conclusion, breastfeeding seems not to predict offspring's compassion or empathy in adulthood. The findings may present a hopeful perspective for children growing up with non-breastfeeding caregivers.

The role of oxytocinergic genes in the intergenerational transmission of parent-child relationship qualities.

Parenting qualities are known to transmit across generations, but less is known about genetic processes that may modify how strongly parenting quality carries across generations. We examined in prospective data whether oxytocinergic genes of offspring moderate the intergenerational transmission of warm and accepting parent-child relationship qualities. The sample comprised 1167 Finnish parents (G2, 62% female) and their mothers (G1). At the study baseline, G1 mothers (Mage = 38) reported parent-child relationship qualities towards G2 children (age range 3-18). After 28-34 years, G2 offspring reported parent-child relationship qualities towards their own children using the same questionnaire. A cumulative genetic score was computed for G2 by summing up previously identified four alleles associated with non-optimal parenting or social impairments across OXTR (rs1042778, rs2254298, rs53576) and CD38 (rs3796863) genes. Results indicated no interaction effects of G2 cumulative genetic score on the transmission of parent-child relationship qualities. Among single polymorphisms in OXTR, the interaction effects of rs53576 and rs1042778 were found. G1 maternal emotional warmth was associated with higher G2 emotional warmth among G2 participants with the OXTR rs53576 AA/AG genotype, but not among those with the GG genotype. G1 maternal acceptance was associated with higher G2 acceptance among those G2 participants with the OXTR rs1042778 GG/GT genotype, but not among those with the TT genotype. Oxytocinergic genes may influence sensitivity to quality of parent-child relationship, although this needs replication in future studies.

Gene-environment correlations in parental emotional warmth and intolerance: genome-wide analysis over two generations of the Young Finns Study.

BACKGROUND: Genomic analysis of the child might offer new potential to illuminate human parenting. We examined whether offspring (G2) genome-wide genotype variation (SNPs) is associated with their mother's (G1) emotional warmth and intolerance, indicating a gene-environment correlation. If this association is stronger than between G2's genes and their emotional warmth and intolerance toward their own children, then this would indicate the presence of an evocative gene-environment correlation. To further understand how G1 mother's parenting has been evoked by genetically influenced characteristics of the child (G2), we examined whether child (G2) temperament partially accounted for the association between offspring genes and parental responses. METHODS: Participants were from the Young Finns Study. G1 mothers (N = 2,349; mean age 39 years) self-reported the emotional warmth and intolerance toward G2 in 1980 when the participants were from 3 to 18 years old. G2 participants answered the same parenting scales in 2007/2012 (N = 1,378; mean age = 38 years in 2007; 59% female) when their children were on average 11 years old. Offspring temperament traits were self-reported in 1992 (G2 age range 15-30 years). Estimation of the phenotypic variance explained by the SNPs of G2 was done by genome-wide complex trait analysis with restricted maximum likelihood (GCTA-GREML). RESULTS: Results showed that the SNPs of a child (G2) explained 22.6% of the phenotypic variance of maternal intolerance (G1; p-value = .039). G2 temperament trait negative emotionality explained only 2.4% points of this association. G2 genes did not explain G1 emotional warmth or G2's own emotional warmth and intolerance. However, further analyses of a combined measure of both G1 parenting scales found genetic effects. Parent or child gender did not moderate the observed associations. CONCLUSIONS: Presented genome-wide evidence is pointing to the important role a child plays in affecting and shaping his/her family environment, though the underlying mechanisms remain unclear.

Is It Good To Be Good? Dispositional Compassion and Health Behaviors.

BACKGROUND: Despite the documented importance of dispositional compassions for a range of health-related outcomes, its role in predicting health behaviors remains unclear. PURPOSE: This study examined the associations between dispositional compassion and three domains of health behavior, including physical activity, alcohol use, and smoking. METHODS: The participants (N = 1,279-1,913) were from the Finnish population-based Young Finns study. We collected self-reports of compassion in 1997 and 2011 and health behaviors in 2001, 2007, and 2011. In addition, an objective pedometer measure of physical activity was collected in 2011. Linear and logistic regression models were fitted to estimate the cross-sectional and longitudinal associations between compassion and the health behavior outcomes. RESULTS: In a cross-sectional analysis, compassion was associated with having never smoked and a reduced likelihood of at-risk alcohol use and binge drinking. There was no robust association between compassion and physical activity. In longitudinal analyses over a 14-year period, the associations remained for at-risk alcohol use and binge drinking. CONCLUSIONS: Dispositional compassion may have a protective effect against unhealthy behaviors, especially excessive alcohol consumption.

Personality traits and perceptions of organisational justice.

This study examined the association between five-factor model personality traits and perceptions of organisational justice. The sample for the study comprised 903 participants (35-50 years old; 523 women) studied in 2007 and 2012. Measures used were the Neuroticism, Extraversion, Openness, Five-Factor Inventory questionnaire and the short organisational justice measure. The results showed that high neuroticism was associated with low distributive, procedural and interactional justice. Furthermore, high agreeableness was associated with high procedural and interactional justice and high openness with high distributive justice. This study suggests that neuroticism, agreeableness and openness are involved in perceptions of organisational justice and that personality should be considered in research and in practices at the workplace.

Neuroticism Associates with Cerebral in Vivo Serotonin Transporter Binding Differently in Males and Females.

Background: Neuroticism is a major risk factor for affective disorders. This personality trait has been hypothesized to associate with synaptic availability of the serotonin transporter, which critically controls serotonergic tone in the brain. However, earlier studies linking neuroticism and serotonin transporter have failed to produce converging findings. Because sex affects both the serotonergic system and the risk that neuroticism poses to the individual, sex may modify the association between neuroticism and serotonin transporter, but this question has not been investigated by previous studies. Methods: Here, we combined data from 4 different positron emission tomography imaging centers to address whether neuroticism is related to serotonin transporter binding in vivo. The data set included serotonin transporter binding potential values from the thalamus and striatum and personality scores from 91 healthy males and 56 healthy females. We specifically tested if the association between neuroticism and serotonin transporter is different in females and males. Results: We found that neuroticism and thalamic serotonin transporter binding potentials were associated in both males and females, but with opposite directionality. Higher neuroticism associated with higher serotonin transporter binding potential in males (standardized beta 0.292, P=.008), whereas in females, higher neuroticism associated with lower serotonin transporter binding potential (standardized beta -0.288, P=.014). Conclusions: The finding is in agreement with recent studies showing that the serotonergic system is involved in affective disorders differently in males and females and suggests that contribution of thalamic serotonin transporter to the risk of affective disorders depends on sex.

Accumulation of Depressive Symptoms and Carotid Intima-Media Thickness: the Cardiovascular Risk in Young Finns Study.

BACKGROUND: The association between depressive symptoms and subclinical atherosclerosis has been inconsistent. PURPOSE: We sought to replicate our previous study, which demonstrated a positive relation between depressive symptoms and subclinical atherosclerosis assessed with carotid intima-media thickness (IMT) in men, using a newer measurement of carotid IMT and a cumulative loading of depressive symptoms over three follow-ups. METHODS: The sample comprised 996 adults (352 men) aged 30 to 45 years in 2007 from a prospective population-based Finnish sample. The participants completed a modified version of Beck Depression Inventory in 1992, 1997, and 2001. Carotid IMT was assessed with ultrasound in 2001 and 2007. Cardiovascular risk factors (i.e., body mass index, systolic blood pressure, low-density lipoprotein cholesterol, and smoking) were measured in childhood (1980) and in adulthood (2007). RESULTS: We found no association between the accumulative depression index and carotid IMT before or after controlling for the traditional risk factors (all p values ≥0.67). Depressive symptoms did not predict IMT progression over two time points and the highest level of carotid wall thickening. Imputed and non-imputed data sets provided similar results. Results remained the same when men and women were analyzed separately. Additional analyses revealed no significant interactions between depressive symptoms and cardiovascular risk factors (i.e., body mass index and systolic blood pressure) on carotid IMT (all p values >0.15). CONCLUSIONS: The findings of this population-based study did not indicate any direct association between depressive symptoms and carotid IMT in asymptomatic, young adults.

Psychosocial environment in childhood and body mass index growth over 32years.

The psychosocial environment and especially various psychosocial risks in childhood have been shown to predict later negative health behavior and health problems. In this study, we examined whether various psychosocial factor domains in childhood and adolescence: socioeconomic status, the emotional family environment (parental nurturance, life-satisfaction), parental lifestyle, life-events, the child's self-regulatory behavior and the child's social adaptation were associated with body mass index (BMI) trajectories individually by domain and as a cumulative score across domains. The participants were a nationally representative sample of 2016 men and women from the Young Finns study aged 3-18years at study entry in 1980. Their BMI was measured at six study phases from 1980 to 2012. Their parents reported all the factors related to their psychosocial environment in 1980. The participants responded to questions on adulthood socioeconomic status in 2007. The accumulation of psychosocial factors in childhood was the main exposure variable. The findings from repeated measures multilevel modeling showed that parental lifestyle and life-events and the more positive cumulative psychosocial factors score were associated with a slower increase in BMI during follow-up (regression coefficient range from -0.06 to -0.50). In conclusion, the psychosocial environment in childhood and adolescence, particularly parental lifestyle and lack of stressful life-events, are associated with a lower increase of BMI.

The Association Between Social Support, Body Mass Index and Increased Risk of Prediabetes: the Cardiovascular Risk in Young Finns Study.

PURPOSE: The psychosocial determinants of prediabetes are poorly understood. The aims of our study were (1) to analyse the association between perceived social support in young adulthood and fasting glucose levels and prediabetes in mid-adulthood in a cohort of healthy Finns, (2) to explore whether body mass index (BMI), inflammation or depression mediate this relationship, (3) and to examine the association between social support trajectory groups and fasting glucose. METHOD: A prospective design was used with an analytic sample of 1250 participants aged 3-18 years at baseline (1980) and aged 12-39 years when social support was measured. Fasting glucose and prediabetes were assessed 32 years after baseline. Linear and logistic regression was used to examine the association between social support and the outcome measures. A bootstrapping technique was used to examine mediation effects. RESULTS: Social support was associated with future glucose levels in women after adjusting for childhood socioeconomic status (SES) and youth depression (ß = -0.136, p = 0.001) and also predicted prediabetes in women after adjusting for childhood SES (ß = 1.31, 95 % CI 1.02 to 1.69, p = 0.031). Both associations were attenuated after adjusting for BMI in mid-adulthood. BMI was found to mediate the relationship between social support and prediabetes in women (ß for indirect effect ß = 0.09, SE = 0.03, CI = 0.03 to 0.16). CONCLUSION: Low perceived social support in young adulthood is associated with high fasting glucose and prediabetes in mid-adulthood in women but not men. The association between social support and prediabetes in women can be partly explained by BMI.