Olli T Raitakari

University of Turku, Turku, Province of Western Finland, Finland

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Publications (629)4099.3 Total impact

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    ABSTRACT: Background Temperament characteristics have been suggested to be associated with mental health outcomes, especially depression, but the direction of the association is unknown. In this study, we tested whether temperament characteristics, as defined by the Buss–Plomin adulthood emotionality–activity–sociability (EAS) temperament model, predict depressive symptoms or whether depressive symptoms predict changes in temperament characteristics. Methods Participants comprised a population-based sample of 719 men and 1020 women from the Young Finns study aged 20–35 years at baseline in 1997 and who responded to repeated surveys of temperament and depressive symptoms in four study phases from 1997 to 2012. The associations were tested using linear regression models, repeated cross-lagged structural equation models, parallel latent growth curve models and two-dimensional continuous-time state space model (Exact Discrete Model). Results Both low sociability (β=−0.12, p<0.001) and high negative emotionality (β=0.34, p<0.001) predicted subsequent increased depressive symptoms, whereas earlier depressive symptoms predicted increased negative emotionality (β=0.50, p<0.001), but not low sociability. Limitations The depressive symptoms scale applied may not be used for measuring clinically recognized depression. Conclusions Our findings suggest that the direction of the association is from low sociability to depressive symptoms rather than the reverse, but the association between negative emotionality and depressive symptoms seems to be reciprocal.
    Journal of Affective Disorders 01/2015; 170:203–212. · 3.30 Impact Factor
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    ABSTRACT: Genome-wide association studies (GWASs) have identified multiple loci associated with cross-sectional eGFR, but a systematic genetic analysis of kidney function decline over time is missing. Here we conducted a GWAS meta-analysis among 63,558 participants of European descent, initially from 16 cohorts with serial kidney function measurements within the CKDGen Consortium, followed by independent replication among additional participants from 13 cohorts. In stage 1 GWAS meta-analysis, single-nucleotide polymorphisms (SNPs) at MEOX2, GALNT11, IL1RAP, NPPA, HPCAL1, and CDH23 showed the strongest associations for at least one trait, in addition to the known UMOD locus, which showed genome-wide significance with an annual change in eGFR. In stage 2 meta-analysis, the significant association at UMOD was replicated. Associations at GALNT11 with Rapid Decline (annual eGFR decline of 3 ml/min per 1.73 m(2) or more), and CDH23 with eGFR change among those with CKD showed significant suggestive evidence of replication. Combined stage 1 and 2 meta-analyses showed significance for UMOD, GALNT11, and CDH23. Morpholino knockdowns of galnt11 and cdh23 in zebrafish embryos each had signs of severe edema 72 h after gentamicin treatment compared with controls, but no gross morphological renal abnormalities before gentamicin administration. Thus, our results suggest a role in the deterioration of kidney function for the loci GALNT11 and CDH23, and show that the UMOD locus is significantly associated with kidney function decline.Kidney International advance online publication, 10 December 2014; doi:10.1038/ki.2014.361.
    Kidney international. 12/2014;
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    ABSTRACT: Usual sleep duration is a heritable trait correlated with psychiatric morbidity, cardiometabolic disease and mortality, although little is known about the genetic variants influencing this trait. A genome-wide association study (GWAS) of usual sleep duration was conducted using 18 population-based cohorts totaling 47 180 individuals of European ancestry. Genome-wide significant association was identified at two loci. The strongest is located on chromosome 2, in an intergenic region 35- to 80-kb upstream from the thyroid-specific transcription factor PAX8 (lowest P=1.1 × 10(-9)). This finding was replicated in an African-American sample of 4771 individuals (lowest P=9.3 × 10(-4)). The strongest combined association was at rs1823125 (P=1.5 × 10(-10), minor allele frequency 0.26 in the discovery sample, 0.12 in the replication sample), with each copy of the minor allele associated with a sleep duration 3.1 min longer per night. The alleles associated with longer sleep duration were associated in previous GWAS with a more favorable metabolic profile and a lower risk of attention deficit hyperactivity disorder. Understanding the mechanisms underlying these associations may help elucidate biological mechanisms influencing sleep duration and its association with psychiatric, metabolic and cardiovascular disease.Molecular Psychiatry advance online publication, 2 December 2014; doi:10.1038/mp.2014.133.
    Molecular Psychiatry 12/2014; · 15.15 Impact Factor
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    ABSTRACT: Elevated serum low-density lipoprotein (LDL) cholesterol is a predictor of cardiovascular disease events, and the quality of dietary fat is known to influence serum concentrations of LDL cholesterol in children. Interindividual differences in response to diet exist, but the underlying genetic factors remain largely unknown. We aimed to identify genetic variants that modify the variation in serum lipid response to dietary fat quality. We used data from 2 longitudinal Finnish cohorts designed to study risk factors for cardiovascular diseases. Large-scale genotyping was performed with Metabochip in a long-term randomized controlled dietary intervention trial, the Special Turku Coronary Risk Factor Intervention Project (STRIP), for discovery of genetic polymorphisms. The observational Cardiovascular Risk in Young Finns Study (YFS) with genome-wide genetic data was used as a replication sample for the initial findings. Dietary records were used to calculate the ratio of unsaturated to saturated fats. Interaction models and multiple follow-ups were used in the analysis. In the STRIP cohort, a variant within the PARK2 locus, rs9364628, showed moderate interaction with dietary fat quality and a consistent direction of effect in both scans on serum LDL-cholesterol concentration in children aged 5 and 7 y (P < 0.0084 and P < 0.0057, respectively). In the YFS cohort, we were unable to replicate the initial discovery signal, but rs12207186 within the PARK2 locus and dietary lipid quality had a stronger interaction effect on serum LDL-cholesterol concentration (P < 9.44 × 10(-5)) than did rs9364628 in children aged 6 y. This genotyping study involving 2 cohorts of healthy Finnish children indicates a possible interaction between PARK2 variants and dietary fat quality on serum LDL-cholesterol concentration. This trial was registered at clinicaltrials.gov as NCT00223600. © 2014 American Society for Nutrition.
    American Journal of Clinical Nutrition 12/2014; 100(6):1569-77. · 6.50 Impact Factor
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    ABSTRACT: Increased adiposity is linked with higher risk for cardiometabolic diseases. We aimed to determine to what extent elevated body mass index (BMI) within the normal weight range has causal effects on the detailed systemic metabolite profile in early adulthood. We used Mendelian randomization to estimate causal effects of BMI on 82 metabolic measures in 12,664 adolescents and young adults from four population-based cohorts in Finland (mean age 26 y, range 16-39 y; 51% women; mean ± standard deviation BMI 24±4 kg/m2). Circulating metabolites were quantified by high-throughput nuclear magnetic resonance metabolomics and biochemical assays. In cross-sectional analyses, elevated BMI was adversely associated with cardiometabolic risk markers throughout the systemic metabolite profile, including lipoprotein subclasses, fatty acid composition, amino acids, inflammatory markers, and various hormones (p<0.0005 for 68 measures). Metabolite associations with BMI were generally stronger for men than for women (median 136%, interquartile range 125%-183%). A gene score for predisposition to elevated BMI, composed of 32 established genetic correlates, was used as the instrument to assess causality. Causal effects of elevated BMI closely matched observational estimates (correspondence 87%±3%; R2 = 0.89), suggesting causative influences of adiposity on the levels of numerous metabolites (p<0.0005 for 24 measures), including lipoprotein lipid subclasses and particle size, branched-chain and aromatic amino acids, and inflammation-related glycoprotein acetyls. Causal analyses of certain metabolites and potential sex differences warrant stronger statistical power. Metabolite changes associated with change in BMI during 6 y of follow-up were examined for 1,488 individuals. Change in BMI was accompanied by widespread metabolite changes, which had an association pattern similar to that of the cross-sectional observations, yet with greater metabolic effects (correspondence 160%±2%; R2 = 0.92). Mendelian randomization indicates causal adverse effects of increased adiposity with multiple cardiometabolic risk markers across the metabolite profile in adolescents and young adults within the non-obese weight range. Consistent with the causal influences of adiposity, weight changes were paralleled by extensive metabolic changes, suggesting a broadly modifiable systemic metabolite profile in early adulthood. Please see later in the article for the Editors' Summary.
    PLoS Medicine 12/2014; 11(12):e1001765. · 15.25 Impact Factor
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    ABSTRACT: The QT interval, an electrocardiographic measure reflecting myocardial repolarization, is a heritable trait. QT prolongation is a risk factor for ventricular arrhythmias and sudden cardiac death (SCD) and could indicate the presence of the potentially lethal mendelian long-QT syndrome (LQTS). Using a genome-wide association and replication study in up to 100,000 individuals, we identified 35 common variant loci associated with QT interval that collectively explain ∼8-10% of QT-interval variation and highlight the importance of calcium regulation in myocardial repolarization. Rare variant analysis of 6 new QT interval-associated loci in 298 unrelated probands with LQTS identified coding variants not found in controls but of uncertain causality and therefore requiring validation. Several newly identified loci encode proteins that physically interact with other recognized repolarization proteins. Our integration of common variant association, expression and orthogonal protein-protein interaction screens provides new insights into cardiac electrophysiology and identifies new candidate genes for ventricular arrhythmias, LQTS and SCD.
    Nature Genetics 12/2014; · 35.21 Impact Factor
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    ABSTRACT: To identify genetic variants associated with refractive astigmatism in the general population, meta-analyses of genome-wide association studies were performed for: White Europeans aged at least 25 years (20 cohorts, N = 31,968); Asian subjects aged at least 25 years (7 cohorts, N = 9,295); White Europeans aged <25 years (4 cohorts, N = 5,640); and all independent individuals from the above three samples combined with a sample of Chinese subjects aged <25 years (N = 45,931). Participants were classified as cases with refractive astigmatism if the average cylinder power in their two eyes was at least 1.00 diopter and as controls otherwise. Genome-wide association analysis was carried out for each cohort separately using logistic regression. Meta-analysis was conducted using a fixed effects model. In the older European group the most strongly associated marker was downstream of the neurexin-1 (NRXN1) gene (rs1401327, P = 3.92E-8). No other region reached genome-wide significance, and association signals were lower for the younger European group and Asian group. In the meta-analysis of all cohorts, no marker reached genome-wide significance: The most strongly associated regions were, NRXN1 (rs1401327, P = 2.93E-07), TOX (rs7823467, P = 3.47E-07) and LINC00340 (rs12212674, P = 1.49E-06). For 34 markers identified in prior GWAS for spherical equivalent refractive error, the beta coefficients for genotype versus spherical equivalent, and genotype versus refractive astigmatism, were highly correlated (r = -0.59, P = 2.10E-04). This work revealed no consistent or strong genetic signals for refractive astigmatism; however, the TOX gene region previously identified in GWAS for spherical equivalent refractive error was the second most strongly associated region. Analysis of additional markers provided evidence supporting widespread genetic co-susceptibility for spherical and astigmatic refractive errors.
    Hum Genet. 11/2014;
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    ABSTRACT: Genetic variation in bitter taste receptors, such as hTAS2R38, may affect food preferences and intake. The aim of the present study was to investigate the association between bitter taste receptor haplotypes and the consumption of vegetables, fruits, berries and sweet foods among an adult Finnish population. A cross-sectional design utilizing data from the Cardiovascular Risk in Young Finns cohort from 2007, which consisted of 1,903 men and women who were 30-45 years of age from five different regions in Finland, was employed. DNA was extracted from blood samples, and hTAS2R38 polymorphisms were determined based on three SNPs (rs713598, rs1726866 and rs10246939). Food consumption was assessed with a validated food frequency questionnaire. The prevalence of the bitter taste-sensitive (PAV/PAV) haplotype was 11.3 % and that of the insensitive (AVI/AVI) haplotype was 39.5 % among this Finnish population. PAV homozygotic women consumed fewer vegetables than did the AVI homozygotic women, 269 g/day (SD 131) versus 301 g/day (SD 187), respectively, p = 0.03 (multivariate ANOVA). Furthermore, the intake of sweet foods was higher among the PAV homozygotes of both genders. Fruit and berry consumption did not differ significantly between the haplotypes in either gender. Individuals perceive foods differently, and this may influence their patterns of food consumption. This study showed that the hTAS2R38 taste receptor gene variation was associated with vegetable and sweet food consumption among adults in a Finnish population.
    Genes & Nutrition 11/2014; 9(6):433. · 3.33 Impact Factor
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    ABSTRACT: In adults, arterial distensibility decreases with age and relates to changes in cardiac left ventricular mass. Longitudinal data on changes in arterial distensibility from childhood to adulthood are lacking. Our aim was to study the effect of age and sex, and low-saturated fat dietary counseling on arterial distensibility from childhood to early adulthood. In addition, we assessed the association of arterial distensibility with left ventricular mass. Distensibility of the abdominal aorta and common carotid artery was measured repeatedly at ages 11, 13, 15, 17, and 19 years (n=395-472) in an atherosclerosis prevention trial (Special Turku Coronary Risk Factor Intervention Project [STRIP]). Aortic and carotid distensibility decreased with age (both P<0.0001). In boys, distensibility values were generally lower (P<0.0001) and showed steeper decrease by age (age and sex interaction: both P<0.01). The low-saturated fat dietary counseling given in STRIP was not significantly associated with arterial distensibility. Left ventricular mass increased with age (P<0.0001), and it was greater in boys (P<0.0001). In conclusion, a marked age-related decrease in vascular distensibility was found already at this young age, and this decrease was more pronounced in boys than girls. The longitudinal progression of aortic and carotid distensibility was related with changes in left ventricular mass.
    Hypertension 10/2014; · 6.87 Impact Factor
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    ABSTRACT: Background and aims. Fatty liver may have different determinants in normal-weight and in obese individuals. We measured factors associated with fatty liver in 863 normal-weight (BMI < 25) and 1135 overweight/obese (BMI ≥ 25) young and middle-aged adults (45% male, age 34-49 years) in the population-based Cardiovascular Risk in Young Finns Study. Methods and results. The prevalence of fatty liver detected with ultrasound was 29% in overweight/obese and 5% in normal-weight participants. In overweight/obese, the independent correlates were waist circumference (odds ratio for 1 standard deviation increase = 3.78), alanine transaminase (2.11), BMI (2.00), male sex (1.74), triglycerides (1.44), systolic blood pressure (1.31), fasting insulin (1.23), and physical activity (0.76). In normal weight, the independent correlates included alanine transaminase (3.05), smoking (2.56), systolic blood pressure (1.54), and alcohol intake (1.41). In normal-weight participants, the associations with fatty liver were stronger for alcohol intake and smoking, and weaker for triglycerides, than in overweight/obese participants (P for interaction < 0.05). Conclusion. Prevalence of fatty liver was 29% in overweight/obese and 5% in normal-weight adults. Differences in factors associated with fatty liver were seen between these two groups: alcohol intake and smoking were more strongly and triglycerides more weakly associated in normal-weight than in overweight/obese participants.
    Journal of Hepatology 10/2014; · 9.86 Impact Factor
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    ABSTRACT: Coffee, a major dietary source of caffeine, is among the most widely consumed beverages in the world and has received considerable attention regarding health risks and benefits. We conducted a genome-wide (GW) meta-analysis of predominately regular-type coffee consumption (cups per day) among up to 91 462 coffee consumers of European ancestry with top single-nucleotide polymorphisms (SNPs) followed-up in ~30 062 and 7964 coffee consumers of European and African-American ancestry, respectively. Studies from both stages were combined in a trans-ethnic meta-analysis. Confirmed loci were examined for putative functional and biological relevance. Eight loci, including six novel loci, met GW significance (log10Bayes factor (BF)>5.64) with per-allele effect sizes of 0.03-0.14 cups per day. Six are located in or near genes potentially involved in pharmacokinetics (ABCG2, AHR, POR and CYP1A2) and pharmacodynamics (BDNF and SLC6A4) of caffeine. Two map to GCKR and MLXIPL genes related to metabolic traits but lacking known roles in coffee consumption. Enhancer and promoter histone marks populate the regions of many confirmed loci and several potential regulatory SNPs are highly correlated with the lead SNP of each. SNP alleles near GCKR, MLXIPL, BDNF and CYP1A2 that were associated with higher coffee consumption have previously been associated with smoking initiation, higher adiposity and fasting insulin and glucose but lower blood pressure and favorable lipid, inflammatory and liver enzyme profiles (P<5 × 10(-8)).Our genetic findings among European and African-American adults reinforce the role of caffeine in mediating habitual coffee consumption and may point to molecular mechanisms underlying inter-individual variability in pharmacological and health effects of coffee.Molecular Psychiatry advance online publication, 7 October 2014; doi:10.1038/mp.2014.107.
    Molecular Psychiatry 10/2014; · 15.15 Impact Factor
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    ABSTRACT: Using genome-wide data from 253,288 individuals, we identified 697 variants at genome-wide significance that together explained one-fifth of the heritability for adult height. By testing different numbers of variants in independent studies, we show that the most strongly associated approximately 2,000, approximately 3,700 and approximately 9,500 SNPs explained approximately 21%, approximately 24% and approximately 29% of phenotypic variance. Furthermore, all common variants together captured 60% of heritability. The 697 variants clustered in 423 loci were enriched for genes, pathways and tissue types known to be involved in growth and together implicated genes and pathways not highlighted in earlier efforts, such as signaling by fibroblast growth factors, WNT/beta-catenin and chondroitin sulfate-related genes. We identified several genes and pathways not previously connected with human skeletal growth, including mTOR, osteoglycin and binding of hyaluronic acid. Our results indicate a genetic architecture for human height that is characterized by a very large but finite number (thousands) of causal variants.
    Nature Genetics 10/2014; · 35.21 Impact Factor
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    ABSTRACT: Common genetic variants have been identified for adult height, but not much is known about the genetics of skeletal growth in early life. To identify common genetic variants that influence fetal skeletal growth, we meta-analyzed 22 genome-wide association studies (Stage 1; N=28,459). We identified 7 independent top SNPs (P<1x10(-6)) for birth length, of which 3 were novel and 4 were in or near loci known to be associated with adult height (LCORL, PTCH1, GPR126 and HMGA2). The 3 novel SNPs were followed-up in 9 replication studies (Stage 2; N=11,995), with rs905938 in DC-STAMP domain containing 2 (DCST2) genome-wide significantly associated with birth length in a joint analysis (Stages 1+2; ß=0.046, S.E.=0.008, P=2.46x10(-8), explained variance=0.05%). Rs905938 was also associated with infant length (N=28,228; P=5.54x10(-4)) and adult height (N=127,513; P=1.45x10(-5)). DCST2 is a DC-STAMP-like protein family member and DC-STAMP is an osteoclast cell-fusion regulator. Polygenic scores based on 180 SNPs previously associated with human adult stature explained 0.13% of variance in birth length. The same SNPs explained 2.95% of the variance of infant length. Of the 180 known adult height loci, 11 were genome-wide significantly associated with infant length (SF3B4, LCORL, SPAG17, C6orf173, PTCH1, GDF5, ZNFX1, HHIP, ACAN, HLA locus and HMGA2). This study highlights that common variation in DCST2 influences variation in early growth and adult height.
    Human Molecular Genetics 10/2014; · 7.69 Impact Factor
  • Jari E Kaikkonen, Vera Mikkilä, Olli T Raitakari
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    ABSTRACT: Accumulating evidence indicates that childhood nutrition plays a role in the adulthood cardiovascular health. A lifelong tracking of dietary habits, following a long-term exposure to unhealthy dietary patterns or independent effects, is a potential effect-mediating mechanism. Dietary patterns have been studied by data-driven and hypothesis-based approaches. Typically, either data-driven healthy or prudent childhood dietary patterns have been characterized and found to be associated with lower adulthood cardiovascular disease (CVD) risk in the published cohort studies. With regard to the individual food groups or food quality indices, intakes particularly of vegetables and fruits (or fiber indicating plant food intake) and polyunsaturated fatty acids have shown protective effects. The evidence which could confirm the long-term healthiness of a hypothesis-based Mediterranean diet is limited, requiring further investigation. Overall, the recent literature strengthens the view that a healthy childhood diet is associated with lowered adulthood CVD risk.
    Current Atherosclerosis Reports 10/2014; 16(10):443. · 2.92 Impact Factor
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    ABSTRACT: Objective. Limited data are available regarding the relationship of thyrotropin (TSH) and arterial pulse wave velocity (PWV) at population level. Therefore, we conducted the present study to determine whether TSH is related to PWV assessed in young adulthood. Methods. The study population consisted of 1598 Finnish white young adults (aged 30-45 years, 47.4% males) who had TSH, traditional cardiovascular risk factors, and PWV measured in 2007. PWV measurements were performed using a whole-body impedance cardiography device. Results. In bivariate association analyses, TSH level was significantly associated with body mass index (BMI), smoking, diastolic blood pressure, triglyceride and insulin levels (p < 0.001). In multivariable regression model, TSH (β = 0.055, p = 0.015) was associated with PWV when adjusted with age (β = 0.295, p < 0.001) and sex (β = 0.345, p < 0.001). The association of TSH with PWV was however diluted to non-significant after further adjustment with traditional risk factors (β = 0.027, p = 0.218 for TSH). Conclusion. Serum TSH was associated with PWV on population level when adjusted with age and sex. This association was diluted when cardiovascular risk factors were added in the model, suggesting that the association of thyroid hormone on arterial stiffening is not independent of changes in the traditional risk factor levels.
    Scandinavian journal of clinical and laboratory investigation. 09/2014;
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    ABSTRACT: There has been intensive debate whether migraine with aura (MA) and migraine without aura (MO) should be considered distinct subtypes or part of the same disease spectrum. There is also discussion to what extent migraine cases collected in specialised headache clinics differ from cases from population cohorts, and how female cases differ from male cases with respect to their migraine. To assess the genetic overlap between these migraine subgroups, we examined genome-wide association (GWA) results from analysis of 23,285 migraine cases and 95,425 population-matched controls.
    Cephalalgia 09/2014; · 3.49 Impact Factor
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    ABSTRACT: Objective: The current study examines associations between five factor personality traits and average sleep duration, sleep deficiency, and sleep problems. Method: The participants were from two population-based samples from Australia (n = 1,104, age range 31-41) and Finland (n = 1,623, age range 30-45). Self-reports of sleep behavior, sleep problems (Jenkin's scale), and five factor model personality traits (NEO-FFI) were collected. Associations between personality traits and sleep were analyzed with linear regressions. Results: The results showed that higher extraversion, agreeableness, and conscientiousness were, in general, associated with better sleep, whereas higher neuroticism was associated with sleeping less well. Openness was not associated with sleep. Most of the associations were replicable between the samples from the two countries, but personality traits explained only small part of the variance in sleep behavior. Conclusions: Increasing the knowledge on personality and sleep may benefit more personalized treatment of sleep disorders and help in personnel selection to jobs in which it is critical to stay alert. However, longitudinal research is needed to confirm the current findings. (PsycINFO Database Record (c) 2014 APA, all rights reserved).
    Health psychology : official journal of the Division of Health Psychology, American Psychological Association. 08/2014;
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    ABSTRACT: FTO is the strongest known genetic susceptibility locus for obesity. Experimental studies in animals suggest the potential roles of FTO in regulating food intake. The interactive relation among FTO variants, dietary intake, and body mass index (BMI) are complex and results from previous often small-scale studies in humans are highly inconsistent. We performed large-scale analyses based on data from 177,330 adults (154,439 whites, 5,776 African Americans, and 17,115 Asians) from 40 studies to examine: 1) the association between the FTO-rs9939609 variant (or a proxy SNP) and total energy and macronutrient intake; and 2) the interaction between the FTO variant and dietary intake on BMI. The minor allele (A-allele) of the FTO-rs9939609 variant was associated with higher BMI in whites (effect per allele =0.34 [0.31, 0.37] kg/m(2), P=1.9×10(-105)), and all participants (0.30 [0.30, 0.35] kg/m(2), P=3.6×10(-107)). The BMI-increasing allele of the FTO variant showed a significant association with higher dietary protein intake (effect per allele =0.08[0.06, 0.10]%, P=2.4×10(-16)), and relative weak associations with lower total energy intake (-6.4[-10.1, -2.6] kcal/day, P=0.001) and lower dietary carbohydrate intake (-0.07 [-0.11, -0.02]%, P=0.004). The associations with protein (P=7.5×10(-9)) and total energy (P =0.002) were attenuated but remained significant after adjustment for BMI. We did not find significant interactions between the FTO variant and dietary intake of total energy, protein, carbohydrate, or fat on BMI. Our findings suggest a positive association between the BMI-increasing allele of FTO variant and higher dietary protein intake and offer insight into potential link between FTO, dietary protein intake and adiposity.
    Human Molecular Genetics 08/2014; · 7.69 Impact Factor
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    ABSTRACT: Sleep duration is genetically regulated, but the genetic variants are largely unknown. We aimed to identify such genes using a genome-wide association study (GWAS) combined with RNA expression at the population level, and with experimental verification. A GWAS was performed in a Finnish sample (n = 1941), and variants with suggestive association (P < 5 × 10−5) were tested in a follow-up sample from the same population with sleep duration (n = 6834) and time in bed (n = 1720). Variants with pointwise association of P < 0.05 in the follow-up sample were analysed further. First, we correlated genotypes with transcript expression levels with sleep duration (n = 207). The expression levels of significant transcripts were further studied in experimental sleep restriction. Of the 31 variants with P < 5 × 10−5 in the discovery sample, three variants showed nominal allelic association (P < 0.05) in the follow-up sample: rs10914351, near PTPRU (P = 0.049), rs1037079 in PCDH7-CENTD1 (P = 0.011) and rs2031573 near KLF6 (P = 0.044). The risk alleles for shorter sleep (rs2031573 and rs1037079) were also associated with higher KLF6 and PCDH7 expression levels (P < 0.05). Experimental sleep restriction increased the expression of KLF6 (P < 0.01). These data suggest that rs2031573 near KLF6 or related loci and rs1037079 between PCDH7-CENTD1 or related loci may contribute to the regulation of sleep duration via gene expression. These results illustrate the utility of combining different analytical approaches to identify genetic determinants for traits related to sleep physiology. However, additional studies are needed in order to understand the roles of KLF6 and PCDH7 in sleep regulation.
    Journal of Sleep Research 08/2014; Early View. · 3.04 Impact Factor
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    ABSTRACT: Aims: Cardiovascular risk factor levels in 2011 and 4-year changes between 2007 and 2011 were examined using data collected in follow-ups of the Cardiovascular Risk in Young Finns Study. Methods: The study population comprised 2063 Finnish adults aged 34-49 years (45% male). Lipid and blood pressure levels, glucose and anthropometry were measured and life style risk factors examined with questionnaires. Results: Mean total cholesterol level in 2011 was 5.19 mmol/l, low density lipoprotein (LDL)-cholesterol 3.27 mmol/l, high density lipoprotein (HDL)-cholesterol 1.33 mmol/l, and triglycerides 1.34 mmol/l. Using American Diabetes Association criteria, Type 2 diabetes (T2D) was observed in 4.1% and prediabetes (fasting glucose 5.6-6.9 mmol/l or glycated hemoglobin 5.7-6.4%) diagnosed for 33.8% of the participants. Significant changes (P < 0.05) between 2007 and 2011 included an increase in waist circumference (3.3%) in women. In both sexes, systolic (-3.0% in women, -4.0% in men) and diastolic (-3.0% in women, -3.3% in men) blood pressure and triglycerides (-3.4% in women, -6.5% in men) decreased during follow-up. CONCLUSIONS PREVIOUSLY OBSERVED FAVORABLE TRENDS IN LDL-CHOLESTEROL LEVELS HAVE LEVELED OFF AMONG A SAMPLE OF YOUNG AND MIDDLE-AGED ADULTS IN FINLAND TRIGLYCERIDE AND BLOOD PRESSURE LEVELS HAVE DECREASED OVER ONE-THIRD OF THE STUDY POPULATION HAD PREDIABETES AND MAY BE AT INCREASED RISK FOR T2D:
    Scandinavian journal of public health. 07/2014;

Publication Stats

15k Citations
4,099.30 Total Impact Points

Institutions

  • 1994–2014
    • University of Turku
      • • Research Centre of Applied and Preventive Cardiovascular Medicine
      • • Department of Clinical Neurophysiology
      Turku, Province of Western Finland, Finland
  • 2013
    • Uppsala University
      Uppsala, Uppsala, Sweden
    • University of Wuerzburg
      Würzburg, Bavaria, Germany
  • 2008–2013
    • LIKES - Foundation for Sport and Health Sciences
      Jyväskylä, Province of Western Finland, Finland
    • The Royal Children's Hospital
      Melbourne, Victoria, Australia
    • University of Leicester
      • Department of Cardiovascular Sciences
      Leicester, ENG, United Kingdom
  • 2006–2013
    • University of Tasmania
      • Menzies Research Institute
      Hobart, Tasmania, Australia
  • 2002–2013
    • University of Oulu
      • Institute of Clinical Medicine
      Oulu, Oulu, Finland
  • 1998–2013
    • Turku University Hospital
      • • Turku PET Centre
      • • Department of Pediatrics
      Turku, Province of Western Finland, Finland
  • 1995–2013
    • University of Helsinki
      • • Department of Psychology
      • • Department of Food and Environmental Sciences
      • • Division of Nutrition
      • • Department of Oral Medicine
      Helsinki, Southern Finland Province, Finland
  • 2012
    • Ludwig-Maximilians-University of Munich
      München, Bavaria, Germany
  • 2008–2012
    • Tampere University Hospital (TAUH)
      Tammerfors, Province of Western Finland, Finland
  • 2006–2012
    • Finnish Institute of Occupational Health
      • • Centre of Expertise for Health and Work Ability
      • • Centre of Expertise for Work Organizations
      Helsinki, Province of Southern Finland, Finland
  • 2002–2012
    • Turku PET Centre
      Turku, Province of Western Finland, Finland
    • University of Tampere
      • • Medical School
      • • Department of Clinical Physiology
      • • Department of Clinical Chemistry
      Tampere, Western Finland, Finland
  • 2001–2012
    • University of Jyväskylä
      • • Department of Sport Sciences
      • • LIKES-Research Center
      Jyväskylä, Province of Western Finland, Finland
  • 2011
    • The University of Warwick
      Coventry, England, United Kingdom
    • Tulane University
      • Department of Epidemiology
      New Orleans, LA, United States
  • 2003–2011
    • University of Sydney
      Sydney, New South Wales, Australia
    • Children's Hospital at Westmead
      Sydney, New South Wales, Australia
  • 2010
    • Broad Institute of MIT and Harvard
      Cambridge, Massachusetts, United States
    • Baker IDI Heart and Diabetes Institute
      Melbourne, Victoria, Australia
    • University Hospital Regensburg
      Ratisbon, Bavaria, Germany
  • 2007–2010
    • University College London
      • Department of Epidemiology and Public Health
      London, ENG, United Kingdom
    • University of Texas Health Science Center at San Antonio
      • Department of Pathology
      San Antonio, TX, United States
  • 2009
    • National Institute for Health and Welfare, Finland
      • Nutrition Unit
      Helsinki, Southern Finland Province, Finland
  • 2008–2009
    • Kuopio University Hospital
      • Department of Obstetrics and Gynaecology
      Kuopio, Province of Eastern Finland, Finland
  • 2006–2009
    • University of Kuopio
      • Department of Obstetrics and Gynecology
      Kuopio, Eastern Finland Province, Finland
  • 1999–2009
    • Royal Prince Alfred Hospital
      Camperdown, New South Wales, Australia
  • 2005
    • Satakunta Hospital District
      Björneborg, Province of Western Finland, Finland
  • 2004
    • Karolinska Institutet
      • Avdelningen för klinisk fysiologi
      Stockholm, Stockholm, Sweden