Tim D Spector

The Kings College, TWF, Idaho, United States

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Publications (423)3611.49 Total impact

  • Andrea Burri, Tim Spector, Qazi Rahman
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    ABSTRACT: Homosexuality is a stable population-level trait in humans that lowers direct fitness and yet is substantially heritable, resulting in a so-called Darwinian "paradox." Evolutionary models have proposed that polymorphic genes influencing homosexuality confer a reproductive benefit to heterosexual carriers, thus offsetting the fitness costs associated with persistent homosexuality. This benefit may consist of a "sex typicality" intermediate phenotype. However, there are few empirical tests of this hypothesis using genetically informative data in humans. This study aimed to test the hypothesis that common genetic factors can explain the association between measures of sex typicality, mating success, and homosexuality in a Western (British) sample of female twins. Here, we used data from 996 female twins (498 twin pairs) comprising 242 full dizygotic pairs and 256 full monozygotic pairs (mean age 56.8) and 1,555 individuals whose co-twin did not participate. Measures of sexual orientation, sex typicality (recalled childhood gender nonconformity), and mating success (number of lifetime sexual partners) were completed. Variables were subject to multivariate variance component analysis. We found that masculine women are more likely to be nonheterosexual, report more sexual partners, and, when heterosexual, also report more sexual partners. Multivariate twin modeling showed that common genetic factors explained the relationship between sexual orientation, sex typicality, and mating success through a shared latent factor. Our findings suggest that genetic factors responsible for nonheterosexuality are shared with genetic factors responsible for the number of lifetime sexual partners via a latent sex typicality phenotype in human females. These results may have implications for evolutionary models of homosexuality but are limited by potential mediating variables (such as personality traits) and measurement issues. Burri A, Spector T, and Rahman Q. Common Genetic Factors among Sexual Orientation, Gender Nonconformity, and Number of Sex Partners in Female Twins: Implications for the Evolution of Homosexuality. J Sex Med **;**:**-**. © 2015 International Society for Sexual Medicine.
    Journal of Sexual Medicine 02/2015; · 3.15 Impact Factor
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    ABSTRACT: The degree and the origins of quantitative variability of most human plasma proteins are largely unknown. Because the twin study design provides a natural opportunity to estimate the relative contribution of heritability and environment to different traits in human population, we applied here the highly accurate and reproducible SWATH mass spectrometry technique to quantify 1,904 peptides defining 342 unique plasma proteins in 232 plasma samples collected longitudinally from pairs of monozygotic and dizygotic twins at intervals of 2–7 years, and proportioned the observed total quantitative variability to its root causes, genes, and environmental and longitudinal factors. The data indicate that different proteins show vastly different patterns of abundance variability among humans and that genetic control and longitudinal variation affect protein levels and biological processes to different degrees. The data further strongly suggest that the plasma concentrations of clinical biomarkers need to be calibrated against genetic and temporal factors. Moreover, we identified 13 cis-SNPs significantly influencing the level of specific plasma proteins. These results therefore have immediate implications for the effective design of blood-based biomarker studies.
    Molecular Systems Biology 02/2015; 11(2). · 14.10 Impact Factor
  • Tess Pallister, Tim D Spector, Cristina Menni
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    ABSTRACT: Investigations into the genetic architecture of diet-disease relationships are particularly relevant today with the global epidemic of obesity and chronic disease. Twin studies have demonstrated that genetic makeup plays a significant role in a multitude of dietary phenotypes such as energy and macronutrient intakes, dietary patterns, and specific food group intakes. Besides estimating heritability of dietary assessment, twins provide a naturally unique, case-control experiment. Due to their shared upbringing, matched genes and sex (in the case of monozygotic (MZ) twin pairs), and age, twins provide many advantages over classic epidemiological approaches. Future genetic epidemiological studies could benefit from the twin approach particularly where defining what is 'normal' is problematic due to the high inter-individual variability underlying metabolism. Here, we discuss the use of twins to generate heritability estimates of food intake phenotypes. We then highlight the value of discordant MZ pairs to further nutrition research through discovery and validation of biomarkers of intake and health status in collaboration with cutting-edge omics technologies.
    Nutrition Research Reviews 12/2014; · 3.86 Impact Factor
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    ABSTRACT: Carotid-femoral pulse-wave velocity (PWV) is a measure of aortic stiffness that is strongly associated with increased risk of cardiovascular morbidity and mortality. The aim of the current study was to identify the molecular markers and the pathways involved in differences in PWV in women, in order to further understand the regulation of arterial stiffening. A total of 280 known metabolites were measured in 1797 female twins (age range: 18-84 years) not on any antihypertensive medication. Metabolites associated with PWV (after adjustment for age, BMI, metabolite batch, and family relatedness) were entered into a backward linear regression. Transcriptomic analyses were further performed on the top compounds identified. Twelve metabolites were associated with PWV (P < 1.8 × 10). One of the most strongly associated metabolites was uridine, which was not associated with blood pressure (BP) and traditional risk factors but correlated significantly with the gene-expression levels of the purinergic receptor P2Y (Beta = 0.29, standard error = 0.12, P = 0.013), suggesting that it may play a role in regulating endothelial nitric oxide synthase phosphorylation. On the other hand, phenylacetylglutamine was strongly associated with both PWV and BP. Circulating levels of uridine, phenylacetylglutamine, and serine appear strongly correlated with PWV in women.This is an open-access article distributed under the terms of the Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 License, where it is permissible to download and share the work provided it is properly cited. The work cannot be changed in any way or used commercially. http://creativecommons.org/licenses/by-nc-nd/4.0.
    Journal of Hypertension 12/2014; · 4.22 Impact Factor
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    ABSTRACT: IntroductionFemale sexual desire and arousal problems have been shown to have a heritable component of moderate size. Previous molecular genetic studies on sexual desire have mainly focused on genes associated with neurotransmitters such as dopamine and serotonin. Nevertheless, there is reason to believe that hormones with more specific functions concerning sexuality could have an impact on sexual desire and arousal.AimThe aim of the present study was to investigate the possible effects of 17 single nucleotide polymorphisms (SNPs) located in estrogen receptor genes on female sexual desire and subjective and genital arousal (lubrication). Based on previous research, we hypothesized that ESR1 and ESR2 are relevant genes that contribute to female sexual desire and arousal.Main Outcome MeasuresThe desire, arousal, and lubrication subdomains of the Female Sexual Function Index self-report questionnaire were used.Methods The present study involved 2,448 female twins and their sisters aged 18–49 who had submitted saliva samples for genotyping. The participants were a subset from a large-scale, population-based sample.ResultsWe found nominally significant main effects on sexual desire for three ESR2-linked SNPs when controlled for anxiety, suggesting that individuals homozygous for the G allele of the rs1271572 SNP, and the A allele of the rs4986938 and rs928554 SNPs had lower levels of sexual desire. The rs4986938 SNP also had a nominally significant effect on lubrication. No effects for any of the SNPs on subjective arousal could be detected.Conclusions The number of nominally significant results for SNPs in the ESR2 gene before correcting for multiple testing suggests that further studies on the possible influence of this gene on interindividual variation in female sexual functioning are warranted. In contrast, no support for an involvement of ESR1 was obtained. Our results should be interpreted with caution until replicated in independent, large samples. Gunst A, Jern P, Westberg L, Johansson A, Salo B, Burri A, Spector T, Eriksson E, Sandnabba NK, and Santtila P. A study of possible associations between single nucleotide polymorphisms in the estrogen receptor 2 gene and female sexual desire. J Sex Med **;**:**–**.
    Journal of Sexual Medicine 12/2014; · 3.15 Impact Factor
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    ABSTRACT: Because of the dearth of biomarkers of aging, it has been difficult to test the hypothesis that obesity increases tissue age. Here we use a novel epigenetic biomarker of aging (referred to as an "epigenetic clock") to study the relationship between high body mass index (BMI) and the DNA methylation ages of human blood, liver, muscle, and adipose tissue. A significant correlation between BMI and epigenetic age acceleration could only be observed for liver (r = 0.42, P = 6.8 × 10(-4) in dataset 1 and r = 0.42, P = 1.2 × 10(-4) in dataset 2). On average, epigenetic age increased by 3.3 y for each 10 BMI units. The detected age acceleration in liver is not associated with the Nonalcoholic Fatty Liver Disease Activity Score or any of its component traits after adjustment for BMI. The 279 genes that are underexpressed in older liver samples are highly enriched (1.2 × 10(-9)) with nuclear mitochondrial genes that play a role in oxidative phosphorylation and electron transport. The epigenetic age acceleration, which is not reversible in the short term after rapid weight loss induced by bariatric surgery, may play a role in liver-related comorbidities of obesity, such as insulin resistance and liver cancer.
    Proceedings of the National Academy of Sciences 10/2014; · 9.81 Impact Factor
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    ABSTRACT: Changes in an individual’s human metabolic phenotype (metabotype) over time can be indicative of disorder-related modifications. Studies covering several months to a few years have shown that metabolic profiles are often specific for an individual. This “metabolic individuality” and detected changes may contribute to personalized approaches in human health care. However, it is not clear whether such individual metabotypes persist over longer time periods. Here we investigate the conservation of metabotypes characterized by 212 different metabolites of 818 participants from the Cooperative Health Research in the Region of Augsburg; Germany population, taken within a 7-year time interval. For replication, we used paired samples from 83 non-related individuals from the TwinsUK study. Results indicated that over 40 % of all study participants could be uniquely identified after 7 years based on their metabolic profiles alone. Moreover, 95 % of the study participants showed a high degree of metabotype conservation (>70 %) whereas the remaining 5 % displayed major changes in their metabolic profiles over time. These latter individuals were likely to have undergone important biochemical changes between the two time points. We further show that metabolite conservation was positively associated with heritability (rank correlation 0.74), although there were some notable exceptions. Our results suggest that monitoring changes in metabotypes over several years can trace changes in health status and may provide indications for disease onset. Moreover, our study findings provide a general reference for metabotype conservation over longer time periods that can be used in biomarker discovery studies.
    Metabolomics 10/2014; 10(5). · 3.97 Impact Factor
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    ABSTRACT: Abstract Smoking is a major risk factor in many diseases. Genome wide association studies have linked genes for nicotine dependence and smoking behavior to increased risk of cardiovascular, pulmonary, and malignant diseases. We conducted an epigenome wide association study in peripheral-blood DNA in 464 individuals (22 current smokers and 263 ex-smokers), using the Human Methylation 450K array. Upon replication in an independent sample of 356 twins (41 current and 104 ex-smokers), we identified 30 probes in 15 distinct loci, all of which reached genome-wide significance in the combined analysis P< 5 × 10(-8). All but one probe (cg17024919) remained significant after adjusting for blood cell counts. We replicated all nine known loci and found an independent signal at CPOX near GPR15. In addition, we found six new loci at PRSS23, AVPR1B, PSEN2, LINC00299, RPS6KA2, and KIAA0087. Most of the lead probes (13 out of 15) associated with cigarette smoking, overlapped regions of open chromatin (FAIRE and DNaseI hypersensitive sites) or / and H3K27Ac peaks (ENCODE data set), which mark regulatory elements. The effect of smoking on DNA methylation was partially reversible upon smoking cessation for longer than 3 months. We report the first statistically significant interaction between a SNP (rs2697768) and cigarette smoking on DNA methylation (cg03329539). We provide evidence that the metSNP for cg03329539 regulates expression of the CHRND gene located circa 95 kb downstream of the methylation site. Our findings suggest the existence of dynamic, reversible site-specific methylation changes in response to cigarette smoking , which may contribute to the extended health risks associated with cigarette smoking.
    Epigenetics: official journal of the DNA Methylation Society 09/2014; · 5.11 Impact Factor
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    ABSTRACT: Epigenetic regulation of gene expression has been shown to change over time and may be associated with environmental exposures in common complex traits. Age-related hearing impairment is a complex disorder, known to be heritable, with heritability estimates of 57-70%. Epigenetic regulation might explain the observed difference in age of onset and magnitude of hearing impairment with age. Epigenetic epidemiology studies using unrelated samples can be limited in their ability to detect small effects, and recent epigenetic findings in twins underscore the power of this well matched study design. We investigated the association between venous blood DNA methylation epigenome-wide and hearing ability. Pure-tone audiometry (PTA) and Illumina HumanMethylation array data were obtained from female twin volunteers enrolled in the TwinsUK register. Two study groups were explored: first, an epigenome-wide association scan (EWAS) was performed in a discovery sample (n = 115 subjects, age range: 47-83 years, Illumina 27 k array), then replication of the top ten associated probes from the discovery EWAS was attempted in a second unrelated sample (n = 203, age range: 41-86 years, Illumina 450 k array). Finally, a set of monozygotic (MZ) twin pairs (n = 21 pairs) within the discovery sample (Illumina 27 k array) was investigated in more detail in an MZ discordance analysis. Hearing ability was strongly associated with DNA methylation levels in the promoter regions of several genes, including TCF25 (cg01161216, p = 6.6×10-6), FGFR1 (cg15791248, p = 5.7×10-5) and POLE (cg18877514, p = 6.3×10-5). Replication of these results in a second sample confirmed the presence of differential methylation at TCF25 (p(replication) = 6×10-5) and POLE (p(replication) = 0.016). In the MZ discordance analysis, twins' intrapair difference in hearing ability correlated with DNA methylation differences at ACP6 (cg01377755, r = -0.75, p = 1.2×10-4) and MEF2D (cg08156349, r = -0.75, p = 1.4×10-4). Examination of gene expression in skin, suggests an influence of differential methylation on expression, which may account for the variation in hearing ability with age.
    PLoS ONE 09/2014; 9(9):e105729. · 3.53 Impact Factor
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    Nature Communications 09/2014; 5:4871. · 10.74 Impact Factor
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    Nature Communications 09/2014; 5:4871. · 10.74 Impact Factor
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    ABSTRACT: To elucidate the proteomic features of aging in plasma, the subproteome targeted by the SOMAscan assay was profiled in blood samples from 202 females from the TwinsUK cohort. Findings were replicated in 677 independent individuals from the AddNeuroMed, Alzheimer's Research UK, and Dementia Case Registry cohorts. Results were further validated using RNAseq data from whole blood in TwinsUK and the most significant proteins were tested for association with aging-related phenotypes after adjustment for age. Eleven proteins were associated with chronological age and were replicated at protein level in an independent population. These were further investigated at gene expression level in 384 females from the TwinsUK cohort. The two most strongly associated proteins were chordin-like protein 1 (meta-analysis β [SE] = 0.013 [0.001], p = 3.66 × 10(-46)) and pleiotrophin (0.012 [0.005], p = 3.88 × 10(-41)). Chordin-like protein 1 was also significantly correlated with birthweight (0.06 [0.02], p = 0.005) and with the individual Framingham 10-years cardiovascular risk scores in TwinsUK (0.71 [0.18], p = 9.9 × 10(-5)). Pleiotrophin is a secreted growth factor with a plethora of functions in multiple tissues and known to be a marker for cardiovascular risk and osteoporosis. Our study highlights the importance of proteomics to identify some molecular mechanisms involved in human health and aging.
    The Journals of Gerontology Series A Biological Sciences and Medical Sciences 08/2014; · 4.31 Impact Factor
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    ABSTRACT: Oxidative stress and inflammation are major contributors to accelerated age-related relative telomere length (RTL) shortening. Both conditions are strongly linked to leptin and adiponectin, the most prominent adipocyte-derived protein hormones. As high leptin levels and low levels of adiponectin have been implicated in inflammation, one expects adiponectin to be positively associated with RTL while leptin should be negatively associated. Within the ENGAGE consortium, we investigated the association of RTL with adiponectin and leptin in seven independent cohorts with a total of 11,448 participants. We performed partial correlation analysis on Z-transformed RTL and LN-transformed leptin/adiponectin, adjusting for age and sex. In extended models we adjusted for body mass index (BMI) and C-reactive protein (CRP). Adiponectin showed a borderline significant association with RTL. This appeared to be determined by a single study and when the outlier study was removed, this association disappeared. The association between RTL and leptin was highly significant (r = -0.05; p = 1.81 × 10(-7)). Additional adjustment for BMI or CRP did not change the results. Sex-stratified analysis revealed no difference between men and women. Our study suggests that high leptin levels are associated with short RTL.
    European Journal of Epidemiology 07/2014; · 5.15 Impact Factor
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    ABSTRACT: Hearing function is known to be heritable but few significant and reproducible associations of genetic variants have been identified to date in the adult population. In this study, genome-wide association results of hearing function from the G-EAR consortium and TwinsUK were used for meta-analysis. Hearing ability in 8 population samples of Northern and Southern European ancestry (n=4591) and the Silk Road (n=348) was measured using pure-tone audiometry, and summarized using principal component (PC) analysis. Genome-wide association analyses for PC1-3 were conducted separately in each sample assuming an additive model adjusted for age, sex and relatedness of subjects. Meta-analysis was performed using 2.3 million single nucleotide polymorphisms (SNPs) tested against each of the three PCs of hearing ability in 4939 individuals. A single SNP lying in intron 6 of the salt-inducible kinase 3 (SIK3) gene was found to be associated with hearing PC2 (p=3.7x10(-8)) and further supported by whole genome sequence in a subset. To determine the relevance of this gene in the ear, expression of the Sik3 protein was studied in mouse cochlea of different ages. Sik3 was expressed in murine hair cells during early development and in cells of the spiral ganglion during early development and adulthood. Our results suggest a developmental role of Sik3 in hearing and may be required for maintenance of adult auditory function.
    Human Molecular Genetics 07/2014; · 6.68 Impact Factor
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    ABSTRACT: Research for the use of biomarkers in osteoarthritis (OA) is promising, however, adequate discrimination between patients and controls may be hampered due to innate differences. We set out to identify loci influencing levels of serum cartilage oligomeric protein (sCOMP) and urinary C-telopeptide of type II collagen (uCTX-II).
    Journal of medical genetics. 07/2014;
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    ABSTRACT: Monozygotic (MZ) twins share nearly all of their genetic variants and many similar environments before and after birth. However, they can also show phenotypic discordance for a wide range of traits. Differences at the epigenetic level may account for such discordances. It is well established that epigenetic states can contribute to phenotypic variation, including disease. Epigenetic states are dynamic and potentially reversible marks involved in gene regulation, which can be influenced by genetics, environment, and stochastic events. Here, we review advances in epigenetic studies of discordant MZ twins, focusing on disease. The study of epigenetics and disease using discordant MZ twins offers the opportunity to control for many potential confounders encountered in general population studies, such as differences in genetic background, early-life environmental exposure, age, gender, and cohort effects. Recently, analysis of disease-discordant MZ twins has been successfully used to study epigenetic mechanisms in aging, cancer, autoimmune disease, psychiatric, neurological, and multiple other traits. Epigenetic aberrations have been found in a range of phenotypes, and challenges have been identified, including sampling time, tissue specificity, validation, and replication. The results have relevance for personalized medicine approaches, including the identification of prognostic, diagnostic, and therapeutic targets. The findings also help to identify epigenetic markers of environmental risk and molecular mechanisms involved in disease and disease progression, which have implications both for understanding disease and for future medical research.
    Genome Medicine 07/2014; 6(7):60. · 4.94 Impact Factor
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    ABSTRACT: HMIP-2 is a human quantitative trait locus affecting peripheral numbers, size and hemoglobin composition of red blood cells, with a marked effect on the persistence of the fetal form of hemoglobin, HbF, in adults. The locus consists of multiple common variants in an enhancer region for MYB (chr 6q23.3), which encodes the hematopoietic transcription factor cMYB. Studying a European population cohort and four African-descended groups of patients with sickle cell anemia, we found that all share a set of two spatially separate HbF-promoting alleles at HMIP-2, termed “A” and “B.” These typically occurred together (“A–B”) on European chromosomes, but existed on separate homologous chromosomes in Africans. Using haplotype signatures for “A” and “B,” we interrogated public population datasets. Haplotypes carrying only “A” or “B” were typical for populations in Sub-Saharan Africa. The “A–B” combination was frequent in European, Asian, and Amerindian populations. Both alleles were infrequent in tropical regions, possibly undergoing negative selection by geographical factors, as has been reported for malaria with other hematological traits. We propose that the ascertainment of worldwide distribution patterns for common, HbF-promoting alleles can aid their further genetic characterization, including the investigation of gene–environment interaction during human migration and adaptation.
    Annals of Human Genetics 07/2014; 78(6). · 1.93 Impact Factor
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    ABSTRACT: Background Low plasma 25-hydroxyvitamin D (25[OH]D) concentration is associated with high arterial blood pressure and hypertension risk, but whether this association is causal is unknown. We used a mendelian randomisation approach to test whether 25(OH)D concentration is causally associated with blood pressure and hypertension risk. Methods In this mendelian randomisation study, we generated an allele score (25[OH]D synthesis score) based on variants of genes that affect 25(OH)D synthesis or substrate availability (CYP2R1 and DHCR7), which we used as a proxy for 25(OH)D concentration. We meta-analysed data for up to 108 173 individuals from 35 studies in the D-CarDia collaboration to investigate associations between the allele score and blood pressure measurements. We complemented these analyses with previously published summary statistics from the International Consortium on Blood Pressure (ICBP), the Cohorts for Heart and Aging Research in Genomic Epidemiology (CHARGE) consortium, and the Global Blood Pressure Genetics (Global BPGen) consortium. Findings In phenotypic analyses (up to n=49 363), increased 25(OH)D concentration was associated with decreased systolic blood pressure (β per 10% increase, −0·12 mm Hg, 95% CI −0·20 to −0·04; p=0·003) and reduced odds of hypertension (odds ratio [OR] 0·98, 95% CI 0·97—0·99; p=0·0003), but not with decreased diastolic blood pressure (β per 10% increase, −0·02 mm Hg, −0·08 to 0·03; p=0·37). In meta-analyses in which we combined data from D-CarDia and the ICBP (n=146 581, after exclusion of overlapping studies), each 25(OH)D-increasing allele of the synthesis score was associated with a change of −0·10 mm Hg in systolic blood pressure (−0·21 to −0·0001; p=0·0498) and a change of −0·08 mm Hg in diastolic blood pressure (−0·15 to −0·02; p=0·01). When D-CarDia and consortia data for hypertension were meta-analysed together (n=142 255), the synthesis score was associated with a reduced odds of hypertension (OR per allele, 0·98, 0·96—0·99; p=0·001). In instrumental variable analysis, each 10% increase in genetically instrumented 25(OH)D concentration was associated with a change of −0·29 mm Hg in diastolic blood pressure (−0·52 to −0·07; p=0·01), a change of −0·37 mm Hg in systolic blood pressure (−0·73 to 0·003; p=0·052), and an 8·1% decreased odds of hypertension (OR 0·92, 0·87—0·97; p=0·002). Interpretation Increased plasma concentrations of 25(OH)D might reduce the risk of hypertension. This finding warrants further investigation in an independent, similarly powered study.
    The Lancet Diabetes and Endocrinology. 06/2014;
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    ABSTRACT: Low weight at birth has previously been shown to be associated with a number of adult diseases such as type 2 diabetes, cardiovascular disease, high blood pressure, and obesity later in life. Genome-wide association studies (GWAS) have been published for singleton-born individuals, but the role of genetic variation in birth weight (BW) in twins has not yet been fully investigated. A GWAS was performed in 4,593 female study participants with BW data available from the TwinsUK cohort. A genome-wide significant signal was found in chromosome 9, close to the NTRK2 gene (OMIM: 600456). QIMR, an Australian twin cohort (n = 3,003), and UK-based singleton-birth individuals from the Hertfordshire cohort (n = 2,997) were used as replication for the top two single nucleotide polymorphism (SNPs) underpinning this signal, rs12340987 and rs7849941. The top SNP, rs12340987, was found to be in the same direction in the Australian twins and in the singleton-born females (fixed effects meta-analysis beta = -0.13, SE = 0.02, and p = 1.48 × 10-8) but not in the singleton-born males tested. These findings provide an important insight into the genetic component of BW in twins who are normally excluded due to their lower BW when compared with singleton births, as well as the difference in BW between twins. The NTRK2 gene identified in this study has previously been associated with obesity.
    Twin Research and Human Genetics 06/2014; · 1.92 Impact Factor
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    ABSTRACT: Understanding the links between genetic, epigenetic and non-genetic factors throughout the lifespan and across generations and their role in disease susceptibility and disease progression offer entirely new avenues and solutions to major problems in our society. To overcome the numerous challenges, we have come up with nine major conclusions to set the vision for future policies and research agendas at the European level
    BMC Genomics 06/2014; · 4.04 Impact Factor

Publication Stats

17k Citations
3,611.49 Total Impact Points


  • 2006–2014
    • The Kings College
      TWF, Idaho, United States
  • 2002–2014
    • King's College London
      • Department of Twin Research and Genetic Epidemiology
      Londinium, England, United Kingdom
  • 2013
    • Universitair Medisch Centrum Groningen
      Groningen, Groningen, Netherlands
    • Harvard Medical School
      Boston, Massachusetts, United States
    • University of Glasgow
      • Institute of Cardiovascular and Medical Sciences
      Glasgow, SCT, United Kingdom
    • Skåne University Hospital
      Malmö, Skåne, Sweden
  • 2010–2013
    • Erasmus MC
      • Department of Internal Medicine
      Rotterdam, South Holland, Netherlands
    • University of St. Thomas
      Saint Paul, Minnesota, United States
    • National Heart, Lung, and Blood Institute
      • Division of Cardiovascular Sciences (DCVS)
      Maryland, United States
    • CSU Mentor
      Long Beach, California, United States
    • University of Michigan
      • Department of Biostatistics
      Ann Arbor, MI, United States
  • 2009–2013
    • ICL
      Londinium, England, United Kingdom
    • University of Leicester
      • • Department of Health Sciences
      • • Department of Cardiovascular Sciences
      Leiscester, England, United Kingdom
    • University of Otago
      • Department of Human Nutrition
      Dunedin, Otago, New Zealand
    • University Hospital Regensburg
      Ratisbon, Bavaria, Germany
  • 2012
    • Mokpo National University
      • Department of Education
      Mokuho, South Jeolla, South Korea
    • Johns Hopkins Bloomberg School of Public Health
      Baltimore, Maryland, United States
  • 2009–2012
    • McGill University
      • Department of Epidemiology, Biostatistics and Occupational Health
      Montréal, Quebec, Canada
  • 2006–2012
    • University of East Anglia
      • Norwich Medical School
      Norwich, ENG, United Kingdom
  • 2003–2012
    • Queen Mary, University of London
      • School of Biological and Chemical Sciences
      London, ENG, United Kingdom
    • University of Helsinki
      • • Department of Food Technology
      • • Department of Dental Public Health
      Helsinki, Southern Finland Province, Finland
    • Queen Elizabeth Hospital Birmingham
      Birmingham, England, United Kingdom
  • 2011
    • King College
      Twin Falls, Idaho, United States
  • 2009–2011
    • Erasmus Universiteit Rotterdam
      • Department of Epidemiology
      Rotterdam, South Holland, Netherlands
  • 2008–2011
    • Guy's and St Thomas' NHS Foundation Trust
      Londinium, England, United Kingdom
    • Westmead Millennium Institute
      Sydney, New South Wales, Australia
    • University of Missouri - Kansas City
      • School of Medicine
      Kansas City, MO, United States
    • The University of Western Ontario
      • Department of Psychology
      London, Ontario, Canada
    • National Public Health Institute
      Helsinki, Uusimaa, Finland
    • Duke University
      Durham, North Carolina, United States
  • 2009–2010
    • Sir Charles Gairdner Hospital
      Perth City, Western Australia, Australia
  • 2000–2010
    • Case Western Reserve University
      • Department of Epidemiology and Biostatistics
      Cleveland, Ohio, United States
  • 2008–2009
    • St George's, University of London
      Londinium, England, United Kingdom
  • 2006–2009
    • VU University Amsterdam
      • Department of Biological Psychology
      Amsterdam, North Holland, Netherlands
  • 2002–2008
    • University of Southampton
      Southampton, England, United Kingdom
  • 2007
    • Tel Aviv University
      • Department of Anatomy and Anthropology
      Tell Afif, Tel Aviv, Israel
    • Procter & Gamble
      Cincinnati, Ohio, United States
    • University of Liège
      • Department of Public Health, Epidemiology and Health Economics
      Luik, Walloon Region, Belgium
  • 2006–2007
    • Rutgers New Jersey Medical School
      Newark, New Jersey, United States
  • 2002–2007
    • University of Leeds
      Leeds, England, United Kingdom
  • 2004–2006
    • University of California, Irvine
      • Department of Medicine
      Irvine, CA, United States
    • Virginia Commonwealth University
      • Virginia Institute for Psychiatric and Behavioral Genetics
      Richmond, VA, United States
    • Georgia Health Sciences University
      • Department of Pediatrics
      Augusta, GA, United States
    • CHU de Lyon - Groupement Hospitalier Edouard Herriot
      Lyons, Rhône-Alpes, France
  • 2005
    • Karolinska Institutet
      Solna, Stockholm, Sweden
  • 2003–2004
    • St. Vincent's Hospital Sydney
      • Department of Cardiology
      Sydney, New South Wales, Australia
  • 1997
    • Alfred Hospital
      • Department of Department of Epidemiology and Preventive Medicine (DEPM)
      Melbourne, Victoria, Australia
  • 1993
    • Barnet and Chase Farm Hospitals NHS Trust
      Endfield, England, United Kingdom