C Osmond

University of Southampton, Southampton, England, United Kingdom

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Publications (419)2831.79 Total impact

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    ABSTRACT: Maternal obesity has long-term consequences for the offspring's later health, including an increased risk of type 2 diabetes and cardiovascular disease. The underlying mechanisms explaining these associations are, however, not fully understood. A total of 2003 individuals from the Helsinki Birth Cohort Study born 1934-44, underwent measurements of body size, body composition, and clinical characteristics at a mean age of 62 years. Data on maternal anthropometry were available from hospital records. Maternal BMI was positively associated with BMI in the offspring. Higher maternal BMI was associated with less favorable body composition in the offspring. There was a significant interaction between birth weight and maternal BMI on offspring body fat percentage (P for interaction 0.003). In mothers with low BMI, a higher offspring birth weight was associated with lower fat percentage, while among those with maternal BMI in the highest fourth, higher offspring birth weight predicted higher body fat percentage. Our findings suggest that a disadvantageous body composition is programmed in early life. This may in part underlie the association between maternal obesity and later cardio-metabolic health of the offspring. These findings support the importance of prevention of overweight in women of child-bearing age.
    Annals of Medicine 03/2015; 47(2):1-6. DOI:10.3109/07853890.2015.1004360 · 4.73 Impact Factor
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    ABSTRACT: We studied if late preterm birth (34 weeks 0 days-36 weeks 6 days of gestation) is associated with performance on the Consortium to Establish a Registry for Alzheimer's Disease Neuropsychological Battery (CERAD-NB) in late adulthood and if maximum attained lifetime education moderated these associations. Participants were 919 Finnish men and women born between 1934 and 1944, who participated in the Helsinki Birth Cohort Study. They underwent the CERAD-NB at a mean age of 68.1 years. Data regarding gestational age (late preterm versus term) were extracted from hospital birth records, and educational attainment data were gathered from Statistics Finland. After adjustment for major confounders, those born late preterm scored lower on word list recognition (mean difference: -0.33 SD; P = .03) than those born at term. Among those who had attained a basic or upper secondary education, late preterm birth was associated with lower scores on word list recognition, constructional praxis, constructional praxis recall, clock drawing, Mini-Mental State Examination, and memory total and CERAD total 2 compound scores (mean differences: >0.40 SD; P values <.05), and had a 2.70 times higher risk of mild cognitive impairment (Mini-Mental State Examination score: <26 points) (P = .02). Among those with tertiary levels of education, late preterm birth was not associated with CERAD-NB scores. Our findings offer new insight into the lifelong consequences of late preterm birth, and they add late preterm birth as a novel risk factor to the list of neurocognitive impairment in late adulthood. Our findings also suggest that attained lifetime education may mitigate aging-related neurocognitive impairment, especially among those born late preterm. Copyright © 2015 by the American Academy of Pediatrics.
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    ABSTRACT: The Åland Islands were recently ranked as Finland's healthiest region with lower prevalence of several non-communicable diseases compared with the national mean. We have compared birth characteristics of 1697 individuals born on the Åland Islands between 1937 and 1944 with contemporaneous data from the Helsinki Birth Cohort Study (HBCS; n=11,808). This is a first step towards a potential future analysis of Ålandic health from a life-course perspective. Mean birth weight and length were calculated for both cohorts. Birth weight was entered into a multiple linear regression model with sex, maternal age, marital status and birth year as predictors. Mean birth weight in the Åland cohort was 3499 g, 87 g (95% CI 62; 111) higher compared with the HBCS. Sex and maternal marital status were the strongest predictors of birth weight. More detailed studies are needed to explore the potential effects of this difference in average birth weight between cohorts.
    Journal of Developmental Origins of Health and Disease 02/2015; DOI:10.1017/S2040174415000136 · 0.77 Impact Factor
  • Bo Abrahamsen, Clive Osmond, Cyrus Cooper
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    ABSTRACT: Osteoporosis is a chronic disease, carrying an elevated risk of fractures, morbidity and death. Long term treatment may be required but the long term risks with osteoporosis drugs remain incompletely understood. The competing risk of death may be a barrier to treating the oldest, yet this may not be rational if the risk of death is reduced by treatment. It is difficult to devise goal directed long term strategies for managing osteoporosis without firm information about residual lifetime expectancy in treated patients. We conducted an observational study in Danish national registries tracking prescriptions for osteoporosis drugs, comorbid conditions and deaths. We included 58,637 patients and 225,084 age- and gender matched control subjects. Information on deaths until the end of 2013 was retrieved, providing a follow-up period of 10-17 years. In men below age 80 and women below age 60, the relative risk of dying declined from being strongly increased in the first year to a stable but elevated level in subsequent years. In women older than 65-70 years of age there was only a small elevation in risk in the first year of treatment followed by lower than background mortality. The residual life expectancy of a 50-year old man beginning osteoporosis treatment was estimated to be 18.2 years and 7.5 years in a 75-year old man. Estimates in women were 26.4 years and 13.5 years. This study shows an excess mortality in men and in women below age 70 who are treated for osteoporosis, compared with the background population. This excess risk is more pronounced in the first few years on treatment. The average life expectancy of osteoporosis patients is in excess of fifteen years in women below the age of 75 and in men below the age of 60, highlighting the importance of developing tools for long term management. This article is protected by copyright. All rights reserved. This article is protected by copyright. All rights reserved.
    Journal of bone and mineral research: the official journal of the American Society for Bone and Mineral Research 02/2015; DOI:10.1002/jbmr.2478 · 6.59 Impact Factor
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    ABSTRACT: Objective Type 2 diabetes (T2D) is a heterogeneous disorder. The aim of this study was to examine the trajectories of childhood growth associated with T2D.Design and subjectsA total of 13,345 individuals born in Helsinki, Finland between 1934 and 1944 were included in the study. The participants’ growth had been recorded in detail during childhood, and 11.7% (n = 1558) had been diagnosed with T2D. We divided the cohort around the median body mass index (BMI) at 11 years. Body composition and glucose tolerance were assessed in a clinical subsample (n = 2003) in adulthood.ResultsTwo pathways of growth were associated with T2D. Both began with low weight and BMI at birth. In one, persistent low BMI through infancy was followed by a rapid increase in BMI in childhood. Among individuals with a BMI at 11 years above the median value, the odds ratio for T2D associated with a one z-score increase in BMI between 2 and 11 years was 1.31 (95% confidence interval 1.21 to 1.42, P < 0.001). In the other pathway, low BMI at birth, accompanied by short length at birth, was followed by low BMI in childhood. Most women who developed diabetes followed this trajectory; they developed T2D at a lower BMI and lower fat percentage than women with a BMI above the median at 11 years of age.Conclusions Two pathways of early growth trigger T2D. Low fat deposition leading to thinness at birth and during infancy results in fat acquisition during childhood. Reduced linear growth leading to short length at birth is associated with lower body fat percentage in adulthood but increased risk of developing diabetes.This article is protected by copyright. All rights reserved.
    Journal of Internal Medicine 02/2015; DOI:10.1111/joim.12354 · 5.79 Impact Factor
  • Journal of Developmental Origins of Health and Disease 02/2015; · 0.77 Impact Factor
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    ABSTRACT: Objective Associations between parental and offspring size at birth are well established, but the relative importance of parental growth at different ages as predictors of offspring birthweight is less certain. Here we model parental birthweight and postnatal conditional growth in specific age periods as predictors of offspring birthweight.Methods We analyzed data from 3,392 adults participating in four prospective birth cohorts and 5,506 of their offspring.ResultsThere was no significant heterogeneity by study site or offspring sex. 1SD increase in maternal birthweight was associated with offspring birthweight increases of 102 g, 1SD in maternal length growth 0–2 year with 46 g, and 1SD in maternal height growth Mid-childhood (MC)-adulthood with 27 g. Maternal relative weight measures were associated with 24 g offspring birth weight increases (2 year- MC) and 49 g for MC-adulthood period but not with earlier relative weight 0–2 year. For fathers, birthweight, and linear/length growth from 0–2 year were associated with increases of 57 and 56 g in offspring birthweight, respectively but not thereafter.Conclusions Maternal and paternal birthweight and growth from birth to 2 year each predict offspring birthweight. Maternal growth from MC-adulthood, relative weight from 2-MC and MC-adulthood also predict offspring birthweight. These findings suggest that shared genes and/or adequate nutrition during early life for both parents may confer benefits to the next generation, and highlight the importance of maternal height and weight prior to conception. The stronger matrilineal than patrilineal relationships with offspring birth weight are consistent with the hypothesis that improving the early growth conditions of young females can improve birth outcomes in the next generation. Am. J. Hum. Biol., 2014. © 2014 The Authors American Journal of Human Biology Published by Wiley Periodicals, Inc.
    American Journal of Human Biology 01/2015; 27(1). DOI:10.1002/ajhb.22614 · 1.93 Impact Factor
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    ABSTRACT: Previous studies have shown that maternal grand multiparity may predict an increased risk of mental disorders in young adult offspring, but whether such effects persist throughout adulthood remains unknown. The current study examined if maternal grand multiparity predicts the risks of severe mental disorders, suicides, suicide attempts and dementias throughout adult life. Our study sample comprised 13243 Helsinki Birth Cohort Study 1934-1944 participants (6905 men and 6338 women). According to hospital birth records, 341 offspring were born to grand multiparous mothers. From Finnish national hospital discharge and causes of death registers, we identified 1682 participants diagnosed with mental disorders during 1969-2010. Maternal grand multiparity predicted significantly increased risks of mood disorders (Hazard Ratio = 1.64, p = 0.03), non-psychotic mood disorders (Hazard Ratio = 2.02, p = 0.002), and suicide attempts (Hazard Ratio = 3.94, p = 0.01) in adult offspring. Furthermore, women born to grand multiparous mothers had significantly increased risks of any severe mental disorder (Hazard Ratio = 1.79, p = 0.01), non-psychotic substance use disorders (Hazard Ratio = 2.77, p = 0.02) schizophrenia, schizotypal and delusional disorders (Hazard Ratio = 2.40, p = 0.02), mood disorders (Hazard Ratio = 2.40, p = 0.002), non-psychotic mood disorders (Hazard Ratio = 2.91, p<0.001), and suicide attempts (Hazard Ratio = 5.05, p = 0.01) in adulthood. The effects of maternal grand multiparity on offspring psychopathology risk were independent of maternal age and body mass index at childbirth, and of year of birth, sex, childhood socioeconomic position, and birth weight of the offspring. In contrast, no significant effects were found among men. Women born to grand multiparous mothers are at an increased risk of severe mental disorders and suicide attempts across adulthood. Our findings may inform the development of preventive interventions for mental disorders.
    PLoS ONE 12/2014; 9(12):e114679. DOI:10.1371/journal.pone.0114679 · 3.53 Impact Factor
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    ABSTRACT: Context: Altered endocrinal and autonomic nervous system responses to stress may link impaired intra-uterine growth with later cardiovascular disease. Objective: To test the hypothesis that offspring of gestational diabetic mothers (OGDM) have high cortisol and cardio-sympathetic responses during the Trier Social Stress Test for Children (TSST-C). Design: Adolescents from a birth cohort in India (N=213, mean age:13.5 years) including 26 OGDM, 22 offspring of diabetic fathers (ODF) and 165 offspring of non-diabetic parents (controls) completed five minutes each of public speaking and mental arithmetic tasks in front of two unfamiliar 'evaluators' (TSST-C). Salivary cortisol concentrations were measured at baseline and at regular intervals after the TSST-C. Heart rate, blood pressure (BP), stroke volume, cardiac output and total peripheral resistance (TPR) were measured continuously at baseline, during and for 10 minutes after the TSST-C using a finger cuff; the beat-to-beat values were averaged for these periods. Results: Cortisol and cardio-sympathetic parameters increased from baseline during stress (P<0.001). OGDM had greater systolic BP (mean difference: 5.6 mmHg), cardiac output (0.5 L/min), and stroke volume (4.0 mL) rises and a lower TPR rise (125 dyn.s/cm(5)) than controls during stress. ODF had greater systolic BP responses than controls (difference: 4.1 mmHg); there was no difference in other cardio-sympathetic parameters. Cortisol responses were similar in all three groups. Conclusions: Maternal diabetes during pregnancy is associated with higher cardio-sympathetic stress-responses in the offspring, which may contribute to their higher cardiovascular disease risk. Further research may confirm stress-response programming as a predictor of cardiovascular risk in OGDM.
    Journal of Clinical Endocrinology &amp Metabolism 12/2014; 100(3):jc20143239. DOI:10.1210/jc.2014-3239 · 6.31 Impact Factor
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    ABSTRACT: Background Growth and feeding during infancy have been associated with later life BMI. However, the associations of infant feeding, linear growth and weight gain relative to linear growth with separate components of body composition remain unclear.Methods Of 5551 children with collected growth- and infant feeding data in a prospective cohort study (Amsterdam Born Children and their Development), body composition measured using bioelectrical impedance analysis at age 5-6 years was available for 2227 children. We assessed how feeding (duration of full breastfeeding and timing of introduction of complementary feeding), and conditional variables representing linear growth and relative weight gain were associated with childhood Fat Free Mass (FFM) and Fat Mass (FM).ResultsBirth weight was positively associated with both fat-free mass (FFM) and fat mass (FM) in childhood, and more strongly with FFM than FM. Faster linear growth and faster relative weight gain at all ages in infancy were positively associated with childhood FFM and FM. The associations with FM were stronger for relative weight gain than for linear growth (FM z score: β coefficient 0.23 (95% CI 0.19 to 0.26), P<0.001 and 0.14 (0.11 to 0.17), P<0.001 per SD change in relative weight gain and linear growth between 1-3 months respectively). Compared to full breastfeeding <1 month, full breastfeeding >6 months was associated with lower FM (FM z score: -0.17 (-0.28 to -0.05), P=0.005) and lower FFM (FFM z score: -0.13 (-0.23 to -0.03), P=0.015), as was introduction of complementary feeding >6 months (FM z score: -0.22 (-0.38 to -0.07), P=0.004), compared to <4 months.Conclusions Faster infant weight gain is associated with a healthier childhood body composition when it is caused by faster linear growth. Full breastfeeding >6 months and introduction of complementary feeding >6 months are associated with lower childhood FM.International Journal of Obesity accepted article preview online, 01 December 2014. doi:10.1038/ijo.2014.200.
    International journal of obesity (2005) 12/2014; DOI:10.1038/ijo.2014.200 · 5.39 Impact Factor
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    ABSTRACT: Background. Overweight and obesity in childhood have been linked to an increased risk of adult mortality, but evidence is still scarce. Methods. We identified trajectories of body mass index (BMI) development in early life and investigated their mortality risk. Data come from the Helsinki Birth Cohort Study, in which 4943 individuals, born 1934-1944, had serial measures of weight and height from birth to 11 years extracted from health care records, weight and height data in adulthood, and register-based mortality data for 2000-2010. Results. Three early BMI trajectories (increasing, average, and average-to-low for men and increasing, average, and low-to-high BMI for women) were identified. Women with an increasing or low-to-high BMI (BMI lower in early childhood, later exceeded average) trajectory had an increased risk of all-cause mortality compared to those with an average BMI trajectory (HR 1.55, 95% CI 1.07-2.23; and HR 1.57, 95% CI 1.04-2.37, respectively). Similar associations were observed for cancer mortality. Among men, BMI trajectories were not associated with all-cause mortality, but those with average-to-low BMI (BMI first similar then dropped below average) had an increased risk of cancer mortality. Conclusions. An increasing BMI in early life may shorten the lifespan of maturing cohorts as they age, particularly among women.
    Annals of Medicine 10/2014; 47(1):1-6. DOI:10.3109/07853890.2014.963664 · 4.73 Impact Factor
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    ABSTRACT: Late preterm births constitute the majority of preterm births. However, most evidence suggesting that preterm birth predicts the risk of mental disorders comes from studies on earlier preterm births. We examined if late preterm birth predicts the risks of severe mental disorders from early to late adulthood. We also studied whether adulthood mental disorders are associated with post-term birth or with being born small (SGA) or large (LGA) for gestational age, which have been previously associated with psychopathology risk in younger ages.
    Psychological Medicine 09/2014; 45(05):1-15. DOI:10.1017/S0033291714001998 · 5.43 Impact Factor
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    ABSTRACT: Malnutrition below 5 years remains a global health issue. Severe acute malnutrition (SAM) presents in childhood as oedematous (kwashiorkor) or nonoedematous (marasmic) forms, with unknown long-term cardiovascular consequences. We hypothesized that cardiovascular structure and function would be poorer in SAM survivors than unexposed controls. We studied 116 adult SAM survivors, 54 after marasmus, 62 kwashiorkor, and 45 age/sex/body mass index-matched community controls who had standardized anthropometry, blood pressure, echocardiography, and arterial tonometry performed. Left ventricular indices and outflow tract diameter, carotid parameters, and pulse wave velocity were measured, with systemic vascular resistance calculated. All were expressed as SD scores. Mean (SD) age was 28.8±7.8 years (55% men). Adjusting for age, sex, height, and weight, SAM survivors had mean (SE) reductions for left ventricular outflow tract diameter of 0.67 (0.16; P<0.001), stroke volume 0.44 (0.17; P=0.009), cardiac output 0.5 (0.16; P=0.001), and pulse wave velocity 0.32 (0.15; P=0.03) compared with controls but higher diastolic blood pressures (by 4.3; 1.2-7.3 mm Hg; P=0.007). Systemic vascular resistance was higher in marasmus and kwashiorkor survivors (30.2 [1.2] and 30.8 [1.1], respectively) than controls 25.3 (0.8), overall difference 5.5 (95% confidence interval, 2.8-8.4 mm Hg min/L; P<0.0001). No evidence of large vessel or cardiac remodeling was found, except closer relationships between these indices in former marasmic survivors. Other parameters did not differ between SAM survivor groups. We conclude that adult SAM survivors had smaller outflow tracts and cardiac output when compared with controls, yet markedly elevated peripheral resistance. Malnutrition survivors are thus likely to develop excess hypertension in later life, especially when exposed to obesity.
    Hypertension 09/2014; 64(3):664-71. DOI:10.1161/HYPERTENSIONAHA.114.03230. · 7.63 Impact Factor
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    ABSTRACT: Abstract This article looks at the association of maternal blood pressure with the blood pressure of the offspring from birth to childhood. The Barker hypothesis states that maternal and "in utero" attributes during pregnancy affect a child's cardiovascular health throughout life. We present an analysis of a unique dataset that consists of three distinct developmental processes: maternal cardiovascular health during pregnancy; fetal development; and child's cardiovascular health from birth to 14 years. This study explored whether a mother's blood pressure reading in pregnancy predicts fetal development and determines if this in turn is related to the future cardiovascular health of the child. This article uses data that have been collected prospectively from a Jamaican cohort which involves the following three developmental processes: (1) maternal cardiovascular health during pregnancy which is the blood pressure and anthropometric measurements at seven time-points on the mother during pregnancy; (2) fetal development which consists of ultrasound measurements of the fetus taken at six time-points during pregnancy; and (3) child's cardiovascular health which consists of the child's blood pressure measurements at 24 time-points from birth to 14 years. The inter-relationship of these three processes was examined using linear mixed effects models. Our analyses indicated that attributes later in childhood development, such as child's weight, child's baseline systolic blood pressure (SBP), age and sex, predict the future cardiovascular health of children. The results also indicated that maternal attributes in pregnancy, such as mother's baseline SBP and SBP change, predicted significantly child's SBP over time.
    Journal of Perinatal Medicine 08/2014; DOI:10.1515/jpm-2014-0038 · 1.43 Impact Factor
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    ABSTRACT: One previous, preliminary study reported that the length of the umbilical cord at birth is related to the risk of developing chronic rheumatic heart disease in later life. We sought to replicate this finding.
    European Journal of Preventive Cardiology 07/2014; DOI:10.1177/2047487314544082 · 2.68 Impact Factor
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    ABSTRACT: Background: Disturbed one-carbon (1-C) metabolism in the mother is associated with poor fetal growth but causality of this relationship has not been established. Methods: We studied the association between maternal total homocysteine and offspring birthweight in the Pune Maternal Nutrition Study (PMNS, Pune, India) and Parthenon Cohort Study (Mysore, India). We tested for evidence of causality within a Mendelian randomization framework, using a methylenetetrahydrofolatereductase (MTHFR) gene variant rs1801133 (earlier known as 677C -> T) by instrumental variable and triangulation analysis, separately and using meta-analysis. Results: Median (IQR) homocysteine concentration and mean (SD) birthweight were 8.6 mu mol/l (6.7,10.8) and 2642 g (379) in the PMNS and 6.0 mu mol/l (5.1,7.1) and 2871 g (443) in the Parthenon study. Offspring birthweight was inversely related to maternal homocysteine concentration-PMNS: -22 g/SD [95% confidence interval (CI): (-50, 5), adjusted for gestational age and offspring gender]; Parthenon: -57 g (-92, -21); meta-analysis: -40 g (-62, -17)]. Maternal risk genotype at rs1801133 predicted higher homocysteine concentration [PMNS: 0.30 SD/allele (0.14, 0.46); Parthenon: 0.21 SD (0.02, 0.40); meta-analysis: 0.26 SD (0.14, 0.39)]; and lower birthweight [PMNS: -46 g (-102, 11, adjusted for gestational age, offspring gender and rs1801133 genotype); Parthenon: -78 g (-170, 15); meta-analysis: -61 g (-111, -10)]. Instrumental variable and triangulation analysis supported a causal association between maternal homocysteine concentration and offspring birthweight. Conclusions: Our findings suggest a causal role for maternal homocysteine (1-C metabolism) in fetal growth. Reducing maternal homocysteine concentrations may improve fetal growth.
    International Journal of Epidemiology 07/2014; 43(5). DOI:10.1093/ije/dyu132 · 9.20 Impact Factor
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    ABSTRACT: ContextEarly life factors (including intrauterine growth retardation) may influence the development of type 2 diabetes. We postulated that birth size is associated with cortisol levels, which itself could alter serum (i.e. adiponectin, IGF-I, myostatin) and glucose metabolism.DesignAn observational study with 60 Afro-Caribbean young adults from a birth cohort.MeasurementsFasting blood was drawn for serum adiponectin, IGF-I and myostatin. A frequently sampled intravenous glucose tolerance test measured insulin sensitivity (SI), acute insulin response (AIRg), disposition index (DI) and glucose effectiveness (Sg). Body composition was assessed by dual energy x-ray absorptiometry. Salivary cortisol was collected at home at 0800 and 2300 h. Sex-adjusted correlations were used to explore the relationships between birth size, cortisol and the metabolic variables.ResultsThe participants were 55% male, mean age 23.1 ± 0.5 years. Birth weight correlated positively with 2300 h cortisol (P = 0.04), though not after adjusting for gestational age. Gestational age correlated with 2300 h cortisol (r = 0.38, P = 0.03), even after adjusting for birth weight (P = 0.02). 2300 h cortisol was not associated with adiponectin, IGF-I, myostatin, SI, AIRg or DI but was negatively correlated with Sg (r = -0.30; P = 0.05) even after adjusting for birth and adult anthropometry. Adiponectin, IGF-I and myostatin were unrelated to glucose metabolism.Conclusions Gestational age is associated with higher nocturnal cortisol, which in turn is associated with lower glucose effectiveness in adulthood. Higher glucose effectiveness could therefore be a compensatory mechanism to improve glucose uptake.This article is protected by copyright. All rights reserved.
    Clinical Endocrinology 07/2014; 82(3). DOI:10.1111/cen.12537 · 3.35 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.
    06/2014; DOI:10.1016/S2213-8587(14)70113-5
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    ABSTRACT: Introduction. Obesity has reached epidemic proportions worldwide. Maternal obesity has consequences for the offspring's later health. Only few studies have focused upon the long-term consequences of maternal obesity on the offspring's later health. Methods. A total of 13,345 men and women born in Helsinki during 1934-44 belonging to the Helsinki Birth Cohort Study were included in the study. Data on maternal weight and height in late pregnancy were available from hospital records. Using validated national registers we report on the following outcomes in relation to maternal BMI: death, cancer, coronary heart disease, stroke, and diabetes among the offspring. Results. Maternal BMI was positively associated with each of the later health outcomes of the offspring. The associations were strongest for cardiovascular disease and type 2 diabetes. The association with type 2 diabetes was stronger in women. Discussion. Our findings stress the importance of early prevention of overweight and obesity in women of child-bearing age.
    Annals of Medicine 06/2014; DOI:10.3109/07853890.2014.919728 · 4.73 Impact Factor
  • Journal of Developmental Origins of Health and Disease 06/2014; 5(3):161-3. DOI:10.1017/S2040174414000099 · 0.77 Impact Factor

Publication Stats

32k Citations
2,831.79 Total Impact Points


  • 1983–2015
    • University of Southampton
      • • MRC Lifecourse Epidemiology Unit
      • • Developmental Origins of Health and Disease
      Southampton, England, United Kingdom
  • 2003–2014
    • The University of the West Indies at Mona
      • • Tropical Medicine Research Institute (TMRI)
      • • Department of Obstetrics, Gynaecology and Child Health
      Kingston, Kingston, Jamaica
  • 2012–2013
    • WWF United Kingdom
      Londinium, England, United Kingdom
  • 2009–2012
    • National Institute for Health and Welfare, Finland
      • Department of Chronic Disease Prevention
      Helsinki, Province of Southern Finland, Finland
    • London School of Hygiene and Tropical Medicine
      Londinium, England, United Kingdom
  • 2001–2012
    • University of Helsinki
      • • Institute of Behavioural Sciences
      • • The Hospital for Children and Adolescents
      • • Department of Dental Public Health
      • • Department of Obstetrics and Gynaecology
      • • Department of Psychiatry
      Helsinki, Southern Finland Province, Finland
  • 2011
    • University of the Witwatersrand
      • Faculty of Health Sciences
      Johannesburg, Gauteng, South Africa
  • 2010
    • Oregon Health and Science University
      • Heart Research Center
      Portland, OR, United States
  • 2008
    • Circumcision Resource Center
      Boston, Massachusetts, United States
  • 1999–2008
    • University of Amsterdam
      • Department of Clinical Epidemiology and Biostatistics
      Amsterdamo, North Holland, Netherlands
  • 1997–2008
    • National Public Health Institute
      Helsinki, Southern Finland Province, Finland
    • The Princess Grace Hospital
      Londinium, England, United Kingdom
  • 2007
    • The University of Edinburgh
      Edinburgh, Scotland, United Kingdom
  • 2001–2006
    • Academisch Medisch Centrum Universiteit van Amsterdam
      • Department of Clinical Epidemiology and Biostatistics
      Amsterdam, North Holland, Netherlands
  • 2005
    • Sunder Lal Jain Hospital
      Old Delhi, NCT, India
  • 1992–2003
    • Medical Research Council (UK)
      Londinium, England, United Kingdom
  • 2000
    • Medical University of South Carolina
      Charleston, South Carolina, United States