Olli T Raitakari

Turku University Hospital, Turku, Varsinais-Suomi, Finland

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Publications (682)4673.17 Total impact

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    ABSTRACT: Both fetal growth restriction and prematurity have been associated with elevated blood pressure (BP). However, their combined effects on adult BP are unclear. Our analyses were based on 1756 participants in the population-based Cardiovascular Risk in Young Finns Study who had information on birth weight and gestational age, together with longitudinal data on cardiovascular risk markers from age 3-18 years in 1980 to age 34-49 years in 2011. Three groups were defined by birth data: those born at term (term); those born preterm (<37 weeks) with an appropriate birth weight (>-1 SD z score according to national sex and gestational week-stratified data) for gestational age (preterm appropriate birth weight for gestational age); and those born preterm with low birth weight (≤-1 SD z score) for gestational age [preterm small birth weight for gestational age (SGA)]. There were no differences between the three groups in BP at baseline, but at the 31-year follow-up (mean age 41 years), mean SBP in the preterm SGA group was 7.2 mmHg (95% confidence interval = 2.3-12.1 mmHg, P = 0.004) higher than the preterm appropriate birth weight for gestational age group and 7.3 mmHg (95% confidence interval = 5.2-9.4 mmHg, P < 0.0001) higher than the term group, adjusted for age and sex. In addition, preterm SGA individuals had a higher prevalence of adult hypertension compared with those born at term (36.9 vs. 25.4%; age, sex, and risk factors adjusted P = 0.006). These longitudinal data suggest that elevated BP levels associated with prematurity are more likely to be present in those with fetal growth restriction.
    Journal of Hypertension 08/2015; 33(8). DOI:10.1097/HJH.0000000000000612 · 4.22 Impact Factor
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    ABSTRACT: Reference panels from the 1000 Genomes (1000G) Project Consortium provide near complete coverage of common and low-frequency genetic variation with minor allele frequency ≥0.5% across European ancestry populations. Within the European Network for Genetic and Genomic Epidemiology (ENGAGE) Consortium, we have undertaken the first large-scale meta-analysis of genome-wide association studies (GWAS), supplemented by 1000G imputation, for four quantitative glycaemic and obesity-related traits, in up to 87,048 individuals of European ancestry. We identified two loci for body mass index (BMI) at genome-wide significance, and two for fasting glucose (FG), none of which has been previously reported in larger meta-analysis efforts to combine GWAS of European ancestry. Through conditional analysis, we also detected multiple distinct signals of association mapping to established loci for waist-hip ratio adjusted for BMI (RSPO3) and FG (GCK and G6PC2). The index variant for one association signal at the G6PC2 locus is a low-frequency coding allele, H177Y, which has recently been demonstrated to have a functional role in glucose regulation. Fine-mapping analyses revealed that the non-coding variants most likely to drive association signals at established and novel loci were enriched for overlap with enhancer elements, which for FG mapped to promoter and transcription factor binding sites in pancreatic islets, in particular. Our study demonstrates that 1000G imputation and genetic fine-mapping of common and low-frequency variant association signals at GWAS loci, integrated with genomic annotation in relevant tissues, can provide insight into the functional and regulatory mechanisms through which their effects on glycaemic and obesity-related traits are mediated.
    PLoS Genetics 07/2015; 11(7):e1005230. DOI:10.1371/journal.pgen.1005230 · 8.17 Impact Factor
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    ABSTRACT: Individual differences in aggressive behavior emerge in early childhood and predict persisting behavioral problems and disorders. Studies of antisocial and severe aggression in adulthood indicate substantial underlying biology. However, little attention has been given to genome-wide approaches of aggressive behavior in children. We analyzed data from nine population-based studies and assessed aggressive behavior using well-validated parent-reported questionnaires. This is the largest sample exploring children's aggressive behavior to date (N = 18,988), with measures in two developmental stages (N = 15,668 early childhood and N = 16,311 middle childhood/early adolescence). First, we estimated the additive genetic variance of children's aggressive behavior based on genome-wide SNP information, using genome-wide complex trait analysis (GCTA). Second, genetic associations within each study were assessed using a quasi-Poisson regression approach, capturing the highly right-skewed distribution of aggressive behavior. Third, we performed meta-analyses of genome-wide associations for both the total age-mixed sample and the two developmental stages. Finally, we performed a gene-based test using the summary statistics of the total sample. GCTA quantified variance tagged by common SNPs (10-54%). The meta-analysis of the total sample identified one region in chromosome 2 (2p12) at near genome-wide significance (top SNP rs11126630, P = 5.30 × 10(-8) ). The separate meta-analyses of the two developmental stages revealed suggestive evidence of association at the same locus. The gene-based analysis indicated association of variation within AVPR1A with aggressive behavior. We conclude that common variants at 2p12 show suggestive evidence for association with childhood aggression. Replication of these initial findings is needed, and further studies should clarify its biological meaning. © 2015 Wiley Periodicals, Inc. © 2015 Wiley Periodicals, Inc.
    American Journal of Medical Genetics Part B Neuropsychiatric Genetics 06/2015; DOI:10.1002/ajmg.b.32333 · 3.27 Impact Factor
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    ABSTRACT: Environmental risks in childhood have been shown to predict later depressive symptoms. In this study, we examined whether various environmental risk domains in childhood and adolescence, socioeconomic, psychoemotional, parental lifestyle and life-events, predict depressive symptom trajectories in adulthood individually by domain and as a cumulative risk score across domains. Participants were a nationally representative sample of 1289 men and 1585 women from the Young Finns study, aged 3-18 years at study entry in 1980. They responded to questions on depressive symptoms (modified version of the Beck Depression Inventory) at four study phases from 1997 to 2012. Findings from longitudinal repeated multilevel modelling showed that all clusters of risk within domain and the cumulative risk score were associated with later depressive symptoms (regression coefficient range from 0.07 to 0.34). Socioeconomic risk, psychoemotional risk and the cumulative risk score predicted later depressive symptoms after adjustment for the effects of adulthood risk. No interaction with time was observed. Our findings suggest that environment risks in childhood and adolescence, particularly in the socioeconomic and psychoemotional domains, are associated with a higher risk, but not an increased progression, of depressive symptoms in adulthood. Published by the BMJ Publishing Group Limited. For permission to use (where not already granted under a licence) please go to http://group.bmj.com/group/rights-licensing/permissions.
    Journal of epidemiology and community health 06/2015; DOI:10.1136/jech-2014-205352 · 3.29 Impact Factor
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    ABSTRACT: Background/Objectives Adenovirus-36 (Adv-36) infection is associated with exaggerated adipogenesis in cell culture, and the development of obesity in animal models and humans, but a causal relationship remains unproven. Our objective was to determine whether serological evidence of Adv-36 infection in childhood and/or adulthood is associated with adult obesity.Subjects/Methods Paired plasma concentrations of Adv-36 antibodies were measured by a novel enzyme-linked immunosorbent assay in a subgroup (n=449) of the Cardiovascular Risk in Young Finns Study in childhood (mean age 11.9 years) and adulthood (mean age 41.3 years). The study group included i) individuals who had maintained normal-weight status ii) those who became obese adults from a normal weight status in childhood, and iii) those that were overweight/obese as a child and obese as an adult.ResultsMean (SD) time between baseline and follow-up was 29.4 (3.2) years (range 21-31 years). 24.4% of individuals who were normal weight throughout life were seropositive for Adv-36 during child and/or adulthood, compared with 32.3% of those who became obese adults (P=0.11). Those who became obese in adulthood were more likely to be Adv-36 seropositive as adults compared to those who maintained normal weight (21.3% vs. 11.6%, P=0.02). This difference was mediated by a decline in Adv-36 seropositivity between child and adulthood in those maintaining normal weight. No differences were observed in Body Mass Index across the life-course, nor in waist circumference in adult life, between those who were Adv-36 seronegative or seropositive at any age.Conclusions Individuals who gained weight across the life-course were more likely to be Adv-36 seropositive in adult life than those who did not gain weight. However, analysis of change in weight status in relation to Adv-36 positivity did not support a causal role for Adv-36 in the development of obesity.International Journal of Obesity accepted article preview online, 09 June 2015. doi:10.1038/ijo.2015.108.
    International journal of obesity (2005) 06/2015; DOI:10.1038/ijo.2015.108 · 5.39 Impact Factor
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    ABSTRACT: The causal role of circulating sex hormone-binding globulin (SHBG) for type 2 diabetes is controversial. Information on the relations between SHBG and new biomarkers of cardiometabolic risk is scarce. We applied quantitative nuclear magnetic resonance metabolomics in three Finnish population-based cohorts to comprehensively profile circulating lipids and metabolites and study their associations with SHBG. Mendelian randomization was used to examine potential causality of SHBG on the metabolic measures and insulin resistance. Prospective associations and causal effect estimates of SHBG on type 2 diabetes were assessed via meta-analysis including summary statistics from the DIAGRAM consortium. In cross-sectional analysis in 6475 young adults (mean age 31, 57% men), higher SHBG was linked with a more favourable cardiometabolic risk profile, including associations with lipoprotein subclasses, fatty acid composition, amino acids, ketone bodies and inflammation-linked glycoproteins. Prospective analysis of 1377 young adults with 6-year follow-up indicated that SHBG is also associated with future insulin resistance. Mendelian randomization suggested only minor, if any, causal effects of SHBG on lipid and metabolite measures and insulin resistance(n = 10 895).Causal effect estimates on type 2 diabetes for 41 439 cases and 103 870 controls indicated a causative protective role of SHBG (OR = 0.83 per 1-SD, 95% CI: 0.76, 0.91); however, effects were considerably weaker than observed in meta-analysis of prospective studies [hazard ratio (HR) = 0.47 per 1-SD, 95% CI: 0.41, 0.53]. Circulating SHBG is strongly associated with systemic metabolism and predictive for insulin resistance and diabetes. The weaker causal estimates suggest that the observational associations are partly confounded rather than conferred directly via circulating SHBG. © The Author 2015; all rights reserved. Published by Oxford University Press on behalf of the International Epidemiological Association.
    International Journal of Epidemiology 06/2015; DOI:10.1093/ije/dyv093 · 9.20 Impact Factor
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    ABSTRACT: Paraoxonase-1 (PON1) is suggested to have a role in the antioxidant activity of high-density lipoprotein (HDL). PON1 activity levels are strongly genetically determined by the rs662 polymorphism (PON1 Q192R). To clarify the role of PON1 in lipoprotein oxidation at the population level, we examined the relations between PON1 activity, the rs662 polymorphism and oxidized lipoprotein lipids in young adults. A population-based cross-sectional study of 1895 Finnish adults ages 24-39 years (872 males and 1023 females). PON1 activity was determined with paraoxon as the substrate. Analysis of oxidized lipids in isolated HDL (oxHDLlipids) and low-density lipoprotein (oxLDLlipids) was based on the determination of conjugated dienes. Oxidized LDL was also measured with a method based on antibodies against oxidized Apo-B (oxLDLprot). Serum lipids and apolipoproteins were measured. Genotyping was performed with the Illumina Bead Chip (Human 670 K). In multivariable models, PON1 activity associated inversely with oxLDLlipids (p = 0.0001, semi-partial R(2) = 0.09%), but it was not associated with oxHDLlipids (p = 0.93). There was a borderline significant association between PON1 activity and oxLDLprot (p = 0.08). PON1 rs662 polymorphism was strongly associated with PON1 activity (P-value<0.0001), but not with oxidized lipoprotein lipids and oxLDLprot. Higher PON1 activity is associated with decreased oxLDLlipids levels, but not with oxHDLlipids in a population of young Finnish adults. These findings support the suggestion that PON1 activity may have a role in the oxidation of LDL lipids. There is a strong association between PON1 rs662 polymorphism and PON1 activity, but PON1 rs662 polymorphism is not associated with oxidized lipoprotein lipids and oxLDLprot. Copyright © 2015 Elsevier Ireland Ltd. All rights reserved.
    Atherosclerosis 06/2015; 241(2). DOI:10.1016/j.atherosclerosis.2015.06.004 · 3.97 Impact Factor
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    ABSTRACT: Neuroticism is a pervasive risk factor for psychiatric conditions. It genetically overlaps with major depressive disorder (MDD) and is therefore an important phenotype for psychiatric genetics. The Genetics of Personality Consortium has created a resource for genome-wide association analyses of personality traits in more than 63 000 participants (including MDD cases). To identify genetic variants associated with neuroticism by performing a meta-analysis of genome-wide association results based on 1000 Genomes imputation; to evaluate whether common genetic variants as assessed by single-nucleotide polymorphisms (SNPs) explain variation in neuroticism by estimating SNP-based heritability; and to examine whether SNPs that predict neuroticism also predict MDD. Genome-wide association meta-analysis of 30 cohorts with genome-wide genotype, personality, and MDD data from the Genetics of Personality Consortium. The study included 63 661 participants from 29 discovery cohorts and 9786 participants from a replication cohort. Participants came from Europe, the United States, or Australia. Analyses were conducted between 2012 and 2014. Neuroticism scores harmonized across all 29 discovery cohorts by item response theory analysis, and clinical MDD case-control status in 2 of the cohorts. A genome-wide significant SNP was found on 3p14 in MAGI1 (rs35855737; P = 9.26 × 10-9 in the discovery meta-analysis). This association was not replicated (P = .32), but the SNP was still genome-wide significant in the meta-analysis of all 30 cohorts (P = 2.38 × 10-8). Common genetic variants explain 15% of the variance in neuroticism. Polygenic scores based on the meta-analysis of neuroticism in 27 cohorts significantly predicted neuroticism (1.09 × 10-12 < P < .05) and MDD (4.02 × 10-9 < P < .05) in the 2 other cohorts. This study identifies a novel locus for neuroticism. The variant is located in a known gene that has been associated with bipolar disorder and schizophrenia in previous studies. In addition, the study shows that neuroticism is influenced by many genetic variants of small effect that are either common or tagged by common variants. These genetic variants also influence MDD. Future studies should confirm the role of the MAGI1 locus for neuroticism and further investigate the association of MAGI1 and the polygenic association to a range of other psychiatric disorders that are phenotypically correlated with neuroticism.
    JAMA Psychiatry 05/2015; DOI:10.1001/jamapsychiatry.2015.0554 · 12.01 Impact Factor
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    ABSTRACT: Obesity is highly heritable. Genetic variants showing robust associations with obesity traits have been identified through genome-wide association studies. We investigated whether a composite score representing healthy diet modifies associations of these variants with obesity traits. 32 BMI- and 14 waist-hip ratio (WHR)-associated SNPs were genotyped and genetic risk scores (GRS) calculated in 18 cohorts of European ancestry (n=68,317). Diet score was calculated based on self-reported intakes of whole grains, fish, fruits, vegetables, nuts/seeds (favorable) and red/processed meats, sweets, sugar-sweetened beverages, fried potatoes (unfavorable). Multi-variable adjusted, linear regression within each cohort, followed by inverse variance-weighted fixed-effects meta-analysis was used to characterize: a) associations of each GRS with BMI and BMI-adjusted WHR; b) diet score modification of genetic associations with BMI and BMI-adjusted WHR. Nominally significant interactions (P=0.006-0.04) were observed between the diet score and WHR-GRS (but not BMI-GRS), two WHR loci (GRB14 rs10195252; LYPLAL1 rs4846567), and two BMI loci (LRRN6C rs10968576; MTIF3 rs4771122), for the respective BMI-adjusted WHR or BMI outcomes. Although the magnitudes of these select interactions were small, our data indicated that associations between genetic predisposition and obesity traits were stronger with a healthier diet. Our findings generate interesting hypotheses; however, experimental and functional studies are needed to determine their clinical relevance. © The Author 2015. Published by Oxford University Press.
    Human Molecular Genetics 05/2015; DOI:10.1093/hmg/ddv186 · 6.68 Impact Factor
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    ABSTRACT: We examined the independent association between dispositional optimism compared to dispositional pessimism and ideal cardiovascular health (defined by the American Heart Association). A prospective design with a study sample of 1113 participants aged 24-39 years from the longitudinal Young Finns Study. Ideal cardiovascular health (comprised of seven ideal cardiovascular health metrics) was measured in 2001. The ideal cardiovascular health metrics were reassessed in 2007. Low pessimism rather than high optimism was a better predictor of ideal cardiovascular health in 2007. When examining the association between optimism and pessimism and the seven ideal cardiovascular health metrics in 2007 (BMI, diet, physical activity, smoking status, blood pressure, total cholesterol and plasma glucose), low pessimism predicted non-smoking status, ideal physical activity and eating a healthy diet, while high optimism was associated with eating a healthy diet. Our findings suggest that low pessimism rather than high optimism is associated with ideal cardiovascular health, especially with health behaviours such as not smoking, being physically active and eating a healthy diet. Socio-economic status was the potential mediating or confounding factor. Future studies should examine the differential meaning of the optimism/pessimism concepts to further clarify their relation to health outcomes.
    Psychology & Health 05/2015; DOI:10.1080/08870446.2015.1041394 · 1.95 Impact Factor
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    ABSTRACT: Using a genome-wide screen of 9.6 million genetic variants achieved through 1000 Genomes Project imputation in 62,166 samples, we identify association to lipid traits in 93 loci, including 79 previously identified loci with new lead SNPs and 10 new loci, 15 loci with a low-frequency lead SNP and 10 loci with a missense lead SNP, and 2 loci with an accumulation of rare variants. In six loci, SNPs with established function in lipid genetics (CELSR2, GCKR, LIPC and APOE) or candidate missense mutations with predicted damaging function (CD300LG and TM6SF2) explained the locus associations. The low-frequency variants increased the proportion of variance explained, particularly for low-density lipoprotein cholesterol and total cholesterol. Altogether, our results highlight the impact of low-frequency variants in complex traits and show that imputation offers a cost-effective alternative to resequencing.
    Nature Genetics 05/2015; DOI:10.1038/ng.3300 · 29.65 Impact Factor
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    ABSTRACT: Objective: To examine the bidirectional relationship between job strain and cynicism. Methods: The study sample was obtained from the Young Finns study and comprised 757 participants (399 women, 53%). The bidirectional association between cynicism and job strain over a 6-year-follow-up was examined with a cross-lagged structural equation model, controlling for a number of demographic variables. Results: High job strain (β = 0.08; P = 0.007) was associated with higher baseline-adjusted cynicism 6 years later. Nevertheless, cynicism was not associated with baseline-adjusted job strain. The additional analysis showed that cynicism mediated 21.5% of the relationship between job strain and depression. Conclusions: Perceptions of having a highly strenuous job may elicit mistrustful and cynical attitudes in employees, which in turn may lead to mental health problems.
    Journal of Occupational and Environmental Medicine 05/2015; 57(5):479-484. DOI:10.1097/JOM.0000000000000430 · 1.80 Impact Factor
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    ABSTRACT: To investigate whether an infancy-onset, low saturated fat-oriented dietary intervention influences serum adiponectin concentration in adolescents, and to study the association of adiponectin with subclinical markers of vascular health, and cardio-metabolic risk factors. The longitudinal, randomized Special Turku Coronary Risk Factor Intervention Project aimed to modify child's dietary fat quality replacing saturated fat with unsaturated fat. Serum adiponectin (n = 521) along with weight, height, high-density lipoprotein cholesterol, C-reactive protein (CRP), triglycerides, and insulin were measured at age 15 years. Adiposity was assessed using body mass index, waist circumference, and abdominal fat thickness measured with ultrasound. Metabolic syndrome was defined according to International Diabetes Foundation criteria. Vascular ultrasound measures including carotid intima-media thickness (IMT) were assessed. Adiponectin concentrations were similar in the intervention and control groups (P = .16). Adiponectin associated with carotid IMT (r = -0.13, P = .005), high-density lipoprotein cholesterol (r = 0.18, P < .0001), triglycerides (r = -0.16, P = .0004), CRP (r = -0.10, P = .02), insulin (r = -0.14, P = .002), and adiposity (r = -0.18-0.24, P ≤ .0001). When adjusted for adiposity indices, the association with carotid IMT was only marginally diluted (P = .03-.06), but the associations with insulin and CRP became nonsignificant. Adolescents with adiponectin ≤median had 4-fold risk of metabolic syndrome than peers with adiponectin >median (CI 1.8-10.2, P = .0001). In healthy adolescents, low serum adiponectin is related with carotid IMT and metabolic syndrome. We found no evidence that repeated low saturated fat-oriented dietary counseling would influence serum adiponectin in adolescence. Registered with ClinicalTrials.gov: NCT00223600. Copyright © 2015 Elsevier Inc. All rights reserved.
    The Journal of pediatrics 05/2015; DOI:10.1016/j.jpeds.2015.04.044 · 3.74 Impact Factor
  • Neurology 05/2015; DOI:10.1212/WNL.0000000000001606 · 8.30 Impact Factor
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    ABSTRACT: While many associations between neighborhood characteristics and individual well-being have been reported, there is a lack of longitudinal studies that could provide evidence for or against causal interpretations of neighborhood effects. This study examined whether neighborhood urbanicity and socioeconomic status were associated with within-individual variation in depression, mistrust and social support when individuals were living in different neighborhoods with different levels of urbanicity and socioeconomic status. Participants were from the Young Finns prospective cohort study (N = 3074) with five repeated measurement times in 1992, 1997, 2001, 2007, and 2011. Neighborhood urbanicity and socioeconomic status were measured at the level of municipalities and zip-code areas. Within-individual variation over time was examined with multilevel regression, which adjusted the models for all stable individual differences that might confound associations between neighborhood characteristics and individual well-being. Social support from friends was higher in urban areas and in areas with higher socioeconomic status, whereas social support from the family was higher in rural areas. These associations were observed also in the within-individual analyses, and they were partly accounted for by employment and socioeconomic status of the participants. There were no associations between neighborhood characteristics and depression or mistrust. These findings suggest that people receive less support from their families and more support from their friends when living in urban compared to rural regions of Finland. These differences are partly explained by people's changing socioeconomic and employment statuses. Copyright © 2015. Published by Elsevier Ltd.
    Social Science [?] Medicine 05/2015; 136-137C:10-16. DOI:10.1016/j.socscimed.2015.04.034 · 2.56 Impact Factor
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    ABSTRACT: AimThis study examined whether there was an association between a repeated dietary and lifestyle intervention that began in infancy and participants’ psychological wellbeing at the age of 20.Methods We examined the psychological wellbeing of 457 young adults participating in the Special Turku Coronary Risk Factor Intervention Project (STRIP), a randomised controlled trial conducted in Finland between 1989 and 2011. We assessed potential differences in psychological wellbeing between the intervention and control groups by examining participants’ satisfaction with life, how they rated their health, their experiences of stress and the consequences of any stress and symptoms of depression at the age of 20. We also assessed socio-economic status during childhood as a potential confounding factor.ResultsWe found no association between the long-term dietary and lifestyle intervention and participants’ psychological wellbeing in adulthood. Adjusting for sex and childhood socio-economic status did not affect the results and socio-economic status did not moderate the association between the intervention and psychological wellbeing.Conclusion Our findings showed no association between intensive dietary and lifestyle counselling that was initiated in infancy with psychological wellbeing in adulthood and the initiative did not appear to pose any psychological risks.This article is protected by copyright. All rights reserved.
    Acta Paediatrica 05/2015; DOI:10.1111/apa.13036 · 1.84 Impact Factor
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    ABSTRACT: The melanocortin 1 receptor (MC1-R) is expressed by vascular endothelial cells and shown to enhance nitric oxide (NO) availability and vasodilator function on pharmacological stimulation. However, the physiological role of MC1-R in the endothelium and its contribution to vascular homeostasis remain unresolved. We investigated whether a lack of functional MC1-R signaling carries a phenotype with predisposition to vascular abnormalities. Recessive yellow mice (MC1R(e/e)), deficient in MC1-R signaling, and their wild-type littermates were studied for morphology and functional characteristics of the aorta. MC1R(e/e) mice showed increased collagen deposition and arterial stiffness accompanied by an elevation in pulse pressure. Contractile capacity and NO-dependent vasodilatation were impaired in the aorta of MC1R(e/e) mice supported by findings of decreased NO availability. These mice also displayed elevated levels of systemic and local cytokines. Exposing the mice to high-sodium diet or acute endotoxemia revealed increased susceptibility to inflammation-driven vascular dysfunction. Finally, we investigated whether a similar phenotype can be found in healthy human subjects carrying variant MC1-R alleles known to attenuate receptor function. In a longitudinal analysis of 2001 subjects with genotype and ultrasound data (The Cardiovascular Risk in Young Finns Study), weak MC1-R function was associated with lower flow-mediated dilatation response of the brachial artery and increased carotid artery stiffness. The present study demonstrates that deficiency in MC1-R signaling is associated with increased arterial stiffness and impairment in endothelium-dependent vasodilatation, suggesting a physiological role for MC1-R in the regulation of arterial tone. © 2015 American Heart Association, Inc.
    Arteriosclerosis Thrombosis and Vascular Biology 04/2015; DOI:10.1161/ATVBAHA.114.305064 · 5.53 Impact Factor
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    ABSTRACT: We studied prevalence of hypovitaminosis D, its determinants, and whether achievement of recommended dietary vitamin D intake (10 μg/d) is associated with absence of hypovitaminosis D in adults. The study is part of the Cardiovascular Risk in Young Finns Study. We collected serum samples of 25-hydroxyvitamin D as part of the 27-year follow-up (994 men and 1,210 women aged 30-45 years). Hypovitaminosis was defined as vitamin D concentration ≤ 50 nmol/L. Hypovitaminosis D was found in 38% of men and 34% of women. Dietary vitamin D intake (OR 0.90, 95% CI 0.86-0.93), use of vitamin-mineral supplements (0.66, 0.51-0.85), sunny holiday (0.55, 0.41-0.75), and oral contraceptive use in women (0.45, 0.27-0.75) were independently associated with reduced odds of hypovitaminosis. Increase in body mass index (1.06, 1.03-1.09), being a smoker (1.36, 0.97-1.92), investigation month (December versus other) (1.35, 1.12-1.61), and risk alleles in genotypes rs12785878 (1.31, 1.00-1.70) and rs2282679 (2.08, 1.66-2.60) increased odds of hypovitaminosis. Hypovitaminosis D was common also when recommended dietary intake was obtained (men 29%, women 24%). Several factors were associated with hypovitaminosis D. The condition was common even when recommended vitamin D intake was reported. The results support the importance of vitamin D fortification and nutrient supplement use.
    Annals of Medicine 04/2015; 47(3):1-10. DOI:10.3109/07853890.2015.1020860 · 4.73 Impact Factor
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    ABSTRACT: We investigated associations of pre-clinical coronary heart disease (CHD), adolescence and adulthood CHD risk factors, and epicardial fat volume (EFV), which is thought to influence CHD pathology. EFV and coronary calcium scores were quantified using computed tomography imaging for 557 subjects from the Cardiovascular Risk in Young Finns Study in 2007. CHD risk marker levels were assessed repeatedly from 1980 to 2007. Carotid intima-media thickness (cIMT), carotid distensibility, and brachial flow-mediated dilatation were measured by vascular ultrasound in 2007. Increased EFV was cross-sectionally associated with male sex, increased waist circumference, body-mass index (BMI), cIMT, metabolic syndrome prevalence, levels of apolipoprotein B, total cholesterol, low-density lipoprotein cholesterol, triglycerides, C-reactive protein, blood pressure, insulin, and fasting glucose, as well as ever smoking, alcoholic intake, and lower high-density lipoprotein cholesterol (HDL-C), carotid distensibility and physical activity in adulthood. In BMI-adjusted analyses, only apolipoprotein B, ever smoking, alcohol intake and metabolic syndrome prevalence were independently associated with EFV. In adolescence, skinfold thickness, BMI, and insulin levels were higher and HDL-C lower with increasing EFV. Subjects in the lowest vs. highest quarter of EFV had consistently lower BMI across the early life-course. Associations of CHD risk markers with EFV were attenuated after multivariable adjustment. We found no evidence of increased EFV being independently associated with pre-clinical atherosclerosis. EFV was most strongly associated with BMI and waist circumference. Subjects with higher EFV had consistently higher BMI from age 12 suggesting that life-long exposure to higher BMI influences the development of EFV. Published on behalf of the European Society of Cardiology. All rights reserved. © The Author 2015. For permissions please email: journals.permissions@oup.com.
    04/2015; DOI:10.1093/ehjci/jev085
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    ABSTRACT: This article examines the impact of relative age at school entry on school performance, educational attainment and labour market outcomes later in life. We find that the advantages of maturity at school entry are short-lived with relative age having no impact on the years of formal education, adulthood earnings or employment. Our findings are consistent with the view that assumes modest maturity effects in countries where formal education begins late and there are no ability-differentiated learning groups at initial grades.
    Applied Economics Letters 04/2015; DOI:10.1080/13504851.2015.1031864 · 0.23 Impact Factor

Publication Stats

20k Citations
4,673.17 Total Impact Points

Institutions

  • 1997–2015
    • Turku University Hospital
      • • Department of Clinical Physiology and Nuclear Medicine
      • • Turku PET Centre
      Turku, Varsinais-Suomi, Finland
  • 1994–2015
    • University of Turku
      • • Research Centre of Applied and Preventive Cardiovascular Medicine
      • • Department of Clinical Neurophysiology
      • • Turku PET Centre
      Turku, Province of Western Finland, Finland
  • 2012–2014
    • Tampere University Hospital (TAUH)
      Tammerfors, Pirkanmaa, Finland
    • Ludwig-Maximilians-University of Munich
      • Department of Internal Medicine I
      München, Bavaria, Germany
    • National Institute for Health and Welfare, Finland
      Helsinki, Uusimaa, Finland
    • University of Massachusetts Boston
      Boston, Massachusetts, United States
  • 2013
    • Uppsala University
      Uppsala, Uppsala, Sweden
    • University of Wuerzburg
      • Department of Biochemistry
      Würzburg, Bavaria, Germany
  • 2011–2013
    • University of Tasmania
      • Menzies Research Institute
      Hobart, Tasmania, Australia
  • 2007–2012
    • University of Tampere
      • • Medical School
      • • Department of Clinical Physiology
      • • Department of Clinical Chemistry
      Tampere, Western Finland, Finland
  • 2002–2012
    • University of Oulu
      • Institute of Clinical Medicine
      Oulu, Oulu, Finland
  • 1994–2012
    • University of Helsinki
      • • Institute for Molecular Medicine Finland (FIMM)
      • • Institute of Behavioural Sciences
      • • Department of Psychology
      • • Department of Oral Medicine
      • • Department of Nutrition
      Helsinki, Province of Southern Finland, Finland
  • 2008
    • Turku centre for biotechnology, finland
      Turku, Varsinais-Suomi, Finland
    • Kuopio University Hospital
      Kuopio, Eastern Finland Province, Finland
    • University of Leicester
      • Department of Cardiovascular Sciences
      Leicester, ENG, United Kingdom
  • 2007–2008
    • University College London
      • Department of Epidemiology and Public Health
      London, ENG, United Kingdom
  • 2006
    • University of Kuopio
      • Department of Obstetrics and Gynecology
      Kuopio, Eastern Finland Province, Finland
  • 2002–2005
    • Turku PET Centre
      Turku, Province of Western Finland, Finland
  • 1999–2003
    • Royal Prince Alfred Hospital
      • Department of Medical Oncology
      Camperdown, New South Wales, Australia
  • 2001
    • University of Jyväskylä
      Jyväskylä, Province of Western Finland, Finland