Showing papers by "Debbie A Lawlor published in 2006"
TL;DR: This glossary presents a comprehensive list of indicators of socioeconomic position used in health research, with a description of what they intend to measure and how data are elicited and the advantages and limitation of the indicators.
Abstract: This glossary presents a comprehensive list of indicators of socioeconomic position used in health research. A description of what they intend to measure is given together with how data are elicited and the advantages and limitation of the indicators. The glossary is divided into two parts for journal publication but the intention is that it should be used as one piece. The second part highlights a life course approach and will be published in the next issue of the journal.
2,271 citations
TL;DR: Findings provide some support for the fetal overnutrition hypothesis by examining the associations between parental prepregnancy body mass index and offspring BMI in 3,340 parent-offspring trios from a birth cohort based in Brisbane, Australia.
Abstract: The fetal overnutrition hypothesis proposes that greater maternal adiposity results in increased obesity throughout life in the offspring. The authors examined the associations between parental prepregnancy body mass index (BMI; weight (kg)/height (m)(2)), based on height and weight reported by the mother at her first antenatal clinic visit, and offspring BMI (height and weight measured at age 14 years) in 3,340 parent-offspring trios from a birth cohort based in Brisbane, Australia (mothers were recruited in 1981-1984). The maternal-offspring BMI association was stronger than the paternal-offspring BMI association. In the fully adjusted model, the increase in standardized offspring BMI at age 14 for a one-standard-deviation (SD) increase in maternal BMI was 0.362 SD (95% confidence interval: 0.323, 0.402), and the corresponding result for a one-SD increase in paternal BMI was 0.239 SD (95% confidence interval: 0.197, 0.282). There was statistical support for a difference in the magnitude of the association between maternal-offspring BMI and paternal-offspring BMI in all confounder-adjusted models tested (all p's < 0.0001). In sensitivity analyses taking account of different plausible levels of nonpaternity (up to 15%), the greater maternal effect remained. These findings provide some support for the fetal overnutrition hypothesis.
270 citations
TL;DR: It is confirmed that not all teenage mothers and their offspring have adverse outcomes, and that many if not the majority have good outcomes.
181 citations
TL;DR: A direct effect of maternal smoking during pregnancy on adolescent overweight and obesity is suggested and provides yet another incentive for pregnant women to be persuaded not to smoke and for young women to been encouraged to never take up smoking.
Abstract: The authors used a population-based birth cohort of 3,253 children (52% males) born in Brisbane, Australia, between 1981 and 1984 to prospectively examine whether maternal smoking during pregnancy was associated with offspring overweight and obesity. The authors compared mean body mass indexes (weight (kg)/height (m)2) and levels of overweight and obesity at age 14 years among offspring by patterns of maternal smoking (never smoked, smoked before and/or after pregnancy but not during pregnancy, or smoked during pregnancy). Adolescent body mass index and prevalences of overweight and obesity were greater in offspring whose mothers had smoked during pregnancy than in those whose mothers had never smoked. Body mass index and levels of overweight and obesity among adolescent offspring whose mothers stopped smoking during pregnancy but smoked at other times in the child's life were similar to those among offspring whose mothers had never smoked. These results were independent of a range of potentially confounding factors and suggest a direct effect of maternal smoking during pregnancy on adolescent overweight and obesity. They provide yet another incentive for pregnant women to be persuaded not to smoke and for young women to be encouraged to never take up smoking.
181 citations
TL;DR: High alcohol consumption may underlie the association between low blood cholesterol and increased risk of haemorrhagic stroke.
Abstract: Objective To investigate risk factors, such as heavy alcohol consumption, that might explain any increased risk of haemorrhagic stroke associated with low blood cholesterol.
Design Prospective cohort study.
Setting Korea.
Participants 787 442 civil servants (661 700 men, 125 742 women) aged 30-64.
Main outcome measures Cardiovascular risk factors were assessed at biennial health check. Data on morbidity and mortality were ascertained from 1990 to 2001 using hospital admissions and mortality surveillance systems.
Results 6328 cases of ischaemic stroke (6021 men, 307 women), 3947 cases of haemorrhagic stroke (3748 men, 199 women), 3170 cases of undefined stroke (2902 men, 268 women), and 4417 cases of myocardial infarction (4305 men, 112 women) occurred. Ischaemic stroke and myocardial infarction were strongly and positively associated with blood cholesterol (hazard ratio per 1 mmol/l cholesterol 1.20 (95% confidence 1.16 to 1.24) and 1.48 (1.43 to 1.53), respectively). Haemorrhagic stroke showed an inverse association in fully adjusted models (0.91, 0.87 to 0.95). This inverse association was confined to participants with hypertension. When stratified by concentration of γ glutamyl transferase (GGT), an indicator of alcohol consumption, the association was not seen in participants with low concentrations of GGT, and it was independent of hypertension in those with high concentrations of GGT (> 80 U/l).
176 citations
TL;DR: There is a need to develop findings from epidemiological research into coherent decisions regarding prevention and treatment interventions and ultimately appropriate polices for the improvement of public health, and a themed issue on obesity in the International Journal of Epidemiology would contribute towards this aim.
Abstract: Both professionals and the public view obesity, increasingly apparent in childhood, and already highly prevalent in adults in the Western world, as one of, if not, the most important public health problem of our times. The considerable effort expended on researching risk factors for obesity (a Medline search for studies examining risk factors for obesity conducted at the time of writing this editorial (November 2005) resulted in 264 326 hits) contrasts starkly with the simplicity of the key underlying problem, that obesity is largely a consequence of over-nutrition and under-activity. Despite the clarity of this message, there is little evidence-based guidance on successful, viable long-term strategies to prevent or treat obesity.We believe there is a need to develop findings from epidemiological research into coherent decisions regarding prevention and treatment interventions and ultimately appropriate polices for the improvement of public health. Our intention was that a themed issue on obesity in the International Journal of Epidemiology would contribute towards this aim. In the first half of this editorial we review the current evidence for the treatment of adult obesity and conclude that to date there is no strong evidence that such treatments have long-term benefits in terms of health gain. Clearly, lack of evidence does not equate to lack of effect and there is no doubt that most trials to date have not been large enough or had sufficiently long-term follow-up to answer these questions. On the other hand treating established obesity in adulthood may be ‘shutting the gate after the horse has bolted’. Further, epidemiology tells us that obesity is socially patterned, varies between countries, but in recent years has shown marked increases in all countries, and that what we eat and the exercise we take is largely determined by the food industry, transport policy, and the built environment (see for example the piece by Cummins and Macintyre in this issue 1 ). Thus, a population approach to the primary prevention of obesity and to the prevention of its associated diseases is more likely to be beneficial than an individual or small group level approach such as treating established obesity. Animal studies suggest that brief interventions during critical or sensitive periods of development can have lasting effects in terms of disease prevention. This seems such an exciting prospect to us that we spend the second half of this editorial considering whether there is sufficient evidence relating critical/sensitive periods of development to the risk of later obesity and its associated diseases to warrant trials in humans of such interventions.
170 citations
TL;DR: The metabolic syndrome, defined by any of the three methods, is only modestly associated withCHD risk in this study of older women, and life-course socioeconomic position appears to be an important confounder in the association of the metabolic syndrome with CHD risk.
Abstract: Aims/hypothesis
We compared the associations between three definitions of the metabolic syndrome and CHD risk. The definitions studied were the new International Diabetes Federation (IDF) definition, and those of the World Health Organization (WHO) and the National Cholesterol Education Programme (NCEP). Our aim was to determine whether the magnitudes of the associations for any of the syndrome definitions are greater than for the individual components.
158 citations
TL;DR: BMI-suicide associations were similar in relation to suicide deaths occurring in the first 5 years of follow-up, indicating that weight loss as a consequence of mental illness does not explain the BMI-su suicide association and that factors influencing BMI may be causally implicated in the etiology of mental disorders leading to suicide.
Abstract: The authors investigated the association of body mass index (BMI) with suicide in a record linkage study based on the Swedish Military Service Conscription Register, the Population and Housing Censuses, and the Cause of Death Register. The cohort studied consisted of 1,299,177 Swedish men who were conscripted in 1968-1999, had their BMI measured at age 18-19 years, and were followed up for as long as 31 years. A strong inverse association was found between BMI and suicide. For each 5-kg/m2 increase in BMI, the risk of suicide decreased by 15% (95% confidence interval: 9, 21). The association was similar when subjects with mental disorder at baseline were excluded from the analysis. BMI-suicide associations were similar in relation to suicide deaths occurring in the first 5 years of follow-up (hazard ratio for each 5-kg/m2 increase in BMI = 0.84, 95% confidence interval: 0.73, 0.96) compared with associations > or = 10 years after baseline (hazard ratio = 0.87, 95% confidence interval: 0.79, 0.96), indicating that weight loss as a consequence of mental illness does not explain the BMI-suicide association and that factors influencing BMI may be causally implicated in the etiology of mental disorders leading to suicide.
145 citations
TL;DR: Evidence of an increased risk of ever being diagnosed as depressed in MTHFR C677T TT individuals compared with CC individuals is found and suggest that folate or its derivatives may be causally related to risk of depression.
Abstract: Low dietary folate intake has been implicated as a risk factor for depression. However, observational epidemiological studies are plagued by problems of confounding, reverse causality and measurement error. A common polymorphism (C677T) in MTHFR is associated with methyltetrahydrofolate reductase (MTHFR) activity and circulating folate and homocysteine levels and offers insights into whether the association between low folate and depression is causal. We genotyped this polymorphism in 3478 women in the British Women's Heart and Health Study. In these women, we looked at the association between genotype and three indicators of depression; ever diagnosed as depressed, currently taking antidepressants and the EuroQol mood question. We also carried out a systematic review and meta-analysis of all published studies which have looked at the association between MTHFR C677T genotype and depression. In the British Women's Heart and Health Study, we found evidence of an increased risk of ever being diagnosed as depressed in MTHFR C677T TT individuals compared with CC individuals, odds ratio (OR) 1.35(95% CI: 1.01, 1.80). Furthermore, we identified eight other studies, which have examined the association between depression and MTHFR C677T. We were able to include all of these studies in our meta-analysis together with our results, obtaining an overall summary OR of 1.36 (95% CI: 1.11, 1.67, P=0.003). Since this genotype influences the functioning of the folate metabolic pathway, these findings suggest that folate or its derivatives may be causally related to risk of depression.
143 citations
TL;DR: Assessment of associations of parental social class at age 0-16 years with mortality among Swedes born in 1944-1960 found poorer social class in early life was associated with diseases largely caused by behavioral risk factors such as smoking, physical inactivity, and an unhealthy diet.
Abstract: Previous studies have lacked sufficient power to assess associations between early-life socioeconomic position and adult cause-specific mortality. The authors examined associations of parental social class at age 0-16 years with mortality among 1,824,064 Swedes born in 1944-1960. Females and males from manual compared with nonmanual childhood social classes were more likely to die from smoking-related cancers, stomach cancer, respiratory disease, cardiovascular disease, and diabetes. Males from manual compared with nonmanual social classes were more likely to die from unintentional injury, homicide, and alcoholic cirrhosis. The association with stomach cancer was little affected by adjustment for parental later-life and own adult social class or education. For other outcomes, educational attainment resulted in greater attenuation of associations than did adjustment for adult social class. Early-life social class was not related to suicide or to melanoma, colon, breast, brain, or lymphatic cancers or to leukemia. With the exception of stomach cancer, caused by Helicobacter pylori infection acquired in childhood, poorer social class in early life was associated with diseases largely caused by behavioral risk factors such as smoking, physical inactivity, and an unhealthy diet. Educational attainment may be important in reducing the health inequalities associated with early-life disadvantage.
141 citations
TL;DR: The objective was to examine the effect of reverse causality and confounding on the association of BMI with all‐cause and cause‐specific mortality.
Abstract: Objective: To examine the effect of reverse causality and confounding on the association of BMI with all-cause and cause-specific mortality.
Research Methods and Procedures: Data from two large prospective studies were used. One (a community-based cohort) included 8327 women and 7017 men who resided in two Scottish towns at the time of the baseline assessment in 1972–1976; the other (an occupational cohort) included 4016 men working in the central belt of Scotland at the time of the baseline assessment in 1970–1973. Participants in both cohorts were ages 45 to 64 years at baseline; the follow-up period was 28 to 34 years.
Results: In age-adjusted analyses that did not take account of reverse causality or smoking, there was no association between being overweight (BMI 25 to <30 kg/m2) and mortality, and weak to modest associations between obesity (BMI ≥30 kg/m2) and mortality. There was a strong association between smoking and lower BMI in women and men in both cohorts (all p < 0.0001). Among never-smokers and with the first 5 years of deaths removed, overweight was associated with an increase in all-cause mortality (relative risk ranging from 1.12 to 1.38), and obesity was associated with a doubling of risk in men in both cohorts (relative risk, 2.10 and 1.96, respectively) and a 60% increase in women (relative risk, 1.56). In both never-smokers and current smokers, being overweight or obese was associated with important increases in the risk of cardiovascular disease.
Discussion: These findings demonstrate that with appropriate control for smoking and reverse causality, both overweight and obesity are associated with important increases in all-cause and cause-specific mortality, and in particular with cardiovascular disease mortality.
TL;DR: A comprehensive analysis of common variation of the glucokinase gene shows that this is the first gene to be reproducibly associated with fasting glucose and fetal growth.
Abstract: Fasting glucose is associated with future risk of type 2 diabetes and ischemic heart disease and is tightly regulated despite considerable variation in quantity, type, and timing of food intake. In pregnancy, maternal fasting glucose concentration is an important determinant of offspring birth weight. The key determinant of fasting glucose is the enzyme glucokinase (GCK). Rare mutations of GCK cause fasting hyperglycemia and alter birth weight. The extent to which common variation of GCK explains normal variation of fasting glucose and birth weight is not known. We aimed to comprehensively define the role of variation of GCK in determination of fasting glucose and birth weight, using a tagging SNP (tSNP) approach and studying 19,806 subjects from six population-based studies. Using 22 tSNPs, we showed that the variant rs1799884 is associated with fasting glucose at all ages in the normal population and exceeded genomewide levels of significance ( P =10 −9 ). rs3757840 was also highly significantly associated with fasting glucose ( P =8×10 −7 ), but haplotype analysis revealed that this is explained by linkage disequilibrium ( r 2 =0.2) with rs1799884. A maternal A allele at rs1799884 was associated with a 32-g (95% confidence interval 11–53 g) increase in offspring birth weight ( P =.002). Genetic variation influencing birth weight may have conferred a selective advantage in human populations. We performed extensive population-genetics analyses to look for evidence of recent positive natural selection on patterns of GCK variation. However, we found no strong signature of positive selection. In conclusion, a comprehensive analysis of common variation of the glucokinase gene shows that this is the first gene to be reproducibly associated with fasting glucose and fetal growth.
TL;DR: The results demonstrate the importance of indicators of socio-economic position as predictors of intelligence, and illustrate the need to consider the role of such factors in generating the association of childhood intelligence with adult disease risk.
Abstract: Growing evidence linking childhood intelligence with adult health outcomes suggests a need to identify predictors of this psychological characteristic. In this study, we have examined the early life determinants of childhood intelligence in a population-based birth cohort of individuals born in Brisbane, Australia between 1981 and 1984. In univariable analyses, family income in the year of birth, maternal and paternal education, maternal age at birth, maternal ethnicity, maternal smoking during pregnancy, duration of labour, birthweight, breast feeding and childhood height, and body mass index were all associated with intelligence at age 14. In multivariable analyses, the strongest and most robust predictors of intelligence were family income, parental education and breast feeding, with these three variables explaining 7.5% of the variation in intelligence at age 14. Addition of other variables added little further explanatory power. Our results demonstrate the importance of indicators of socio-economic position as predictors of intelligence, and illustrate the need to consider the role of such factors in generating the association of childhood intelligence with adult disease risk.
TL;DR: Results do not provide strong evidence that being overweight or obese in childhood is associated with future cardiovascular disease risk, and no association was found between overweight or obesity and stroke risk.
TL;DR: The data suggest that early socioeconomic disadvantage influences later blood pressure through an effect on blood pressure in early life, which tracks into adulthood, and in part through a effect on BMI.
Abstract: Studies have found an association between low socioeconomic position in childhood and high adult blood pressure. It is unclear whether this association is explained by a pathway directly linking disadvantage to elevated blood pressure in childhood and adolescence, which then tracks into adulthood. We assessed parental socioeconomic position and systolic blood pressure in 1807 children and adolescents ages 3 to 18 years at baseline. Adult systolic blood pressure was measured 21 years later at ages 24 to 39 years. There was strong tracking of blood pressure from childhood to adulthood. Lower parental socioeconomic position was associated with higher blood pressure in childhood, adolescence (P<0.01), and adulthood (P<0.0001), with the mean age- and sex-adjusted systolic pressure differences between the highest and lowest socioeconomic groups varying between 2.9 and 4.3 mm Hg. With adjustment for blood pressure in childhood and adolescence, the regression coefficient between parental socioeconomic position and adult blood pressure attenuated by 32%. A similar level of attenuation (28%) occurred with adjustment for adult body mass index (BMI). With adjustment for both preadult blood pressure and adult BMI, the association between parental socioeconomic position and adult blood pressure was attenuated by 45%. Other factors, including birth weight and BMI in childhood and adolescence, had little impact on the association between parental socioeconomic position and adult blood pressure. These data suggest that early socioeconomic disadvantage influences later blood pressure in part through an effect on blood pressure in early life, which tracks into adulthood, and in part through an effect on BMI.
TL;DR: In this population, who were born in the 1950s, poor intrauterine growth and preterm birth are associated with an increased risk of diabetes.
Abstract: Aims/hypothesis
The aim of this study was to examine the associations of birthweight, gestational age and childhood BMI (assessed at a mean age of 5 years) with a self-report of a doctor diagnosis of diabetes in middle age.
TL;DR: An alternative risk assessment based on only a simple routine examination and a small number of pertinent questions may be more useful in the primary care setting, and appears to perform well but needs to be tested in different populations.
Abstract: Objectives: To develop a cardiovascular risk assessment tool that is feasible and easy to use in primary care (general practice (GP) model). Design: Prospective cohort study. Setting: 23 towns in the United Kingdom. Participants: 3582 women aged 60 to 79 years who were free of coronary heart disease (CHD) at entry into the British Women’s Heart and Health Study. Main outcome measures: Predictive performance of a GP model compared with the standard Framingham model for both CHD and cardiovascular disease (CVD). Results: The Framingham tool predicted CHD events over 5 years accurately (predicted 5.7%, observed 5.5%) but overpredicted CVD events (predicted 10.5%, observed 6.8%). In higher-risk groups, Framingham overpredicted both CHD and CVD events and was poorly calibrated for this cohort. Including C-reactive protein and fibrinogen with standard Framingham risk factors did not improve discrimination of the model. The GP model, which used age, systolic blood pressure, smoking habit and self-rated health (all of which can be easily obtained in one surgery visit) performed as well as the Framingham risk tool: area under the receiver operating curve discrimination statistic was 0.66 (95% confidence interval (CI) 0.62 to 0.70) for CHD and 0.67 (95% CI 0.64 to 0.71) for CVD compared with 0.65 (95% CI 0.61 to 0.68) and 0.66 (95% CI 0.62 to 0.69) for the corresponding Framingham models. Conclusions: An alternative risk assessment based on only a simple routine examination and a small number of pertinent questions may be more useful in the primary care setting. This model appears to perform well but needs to be tested in different populations.
TL;DR: The association of birth weight with adult symptoms of depression was examined in an Australian prospective birth cohort and it is suggested that the association is not explained by maternal mental health characteristics during pregnancy.
Abstract: It is unclear whether there is a fetal origin of adult depression. In particular, previous studies have been unable to adjust for the potential effect of maternal depression during pregnancy on any association. The association of birth weight with adult symptoms of depression was examined in an Australian prospective birth cohort, the Mater University Study of Pregnancy and its outcomes. Depressive symptoms were assessed with the Center for Epidemiologic Studies Depression Scale among 3,719 participants at the 21-year follow-up in 2002-2005. In multivariable analyses, there were a weak inverse association between birth weight and symptoms of depression in the whole cohort and some evidence of sex differences in this association. Among females, there was a graded inverse association: In the fully adjusted model, the odds ratio for a high level of depressive symptoms for a 1-standard deviation increase in birth weight (gestational age-standardized z score) was 0.82 (95% confidence interval: 0.73, 0.92). Among males, there was no association (with sex in all models: p(interaction) < 0.004). Study results provide some support for a fetal origin of adult depression and suggest that the association is not explained by maternal mental health characteristics during pregnancy. Further research is needed to better understand the mechanisms underlying the association.
TL;DR: These results provide some evidence for a sex difference in the birth weight-total cholesterol association, consistent with studies of fetal growth which suggest that birth size reflects different biological processes for females and males.
TL;DR: The lack of any association within singleton sibling pairs from the same family suggests that the association between birth weight and childhood intelligence in the general population of singletons is largely explained by fixed family factors that are closely matched in siblings of a similar age.
Abstract: OBJECTIVE The objective of this study was to examine whether the established positive association between birth weight and childhood psychometric intelligence is seen within singleton sibling pairs from the same family as well as between nonsiblings METHODS We examined the association of intrauterine growth (measured as birth weight standardized for gender and gestational age) with psychometric intelligence (measured using the Moray House picture test) at 7 years old in a birth cohort of 9792 individuals who were singleton births occurring in Aberdeen, Scotland, between 1950 and 1956 We further compared this association within siblings with that between nonsiblings in the cohort; this family-based analysis included 1645 sibling pairs (N = 3290 individuals) RESULTS There was a positive linear association between birth weight and childhood psychometric intelligence at age 7 in the whole cohort, which remained with adjustment for a range of potential confounding factors A one standard deviation increase in birth weight for gestational age z score was associated with a greater intelligence score in a regression model adjusting for sex, year of birth, paternal social class, maternal height, age, gravidity, and birth outside of marriage The mean age difference between the siblings within each family pair was 22 years In the family-based analysis there was no strong association between birth weight for gestation age z score and intelligence within sibling pairs from the same family, but there was a positive association between nonsiblings; the difference in these effects being unlikely to be due to chance With additional adjustment for social class, maternal height, age, gravidity, and birth outside of marriage, the within-sibling pair effect was unaltered and the nonsibling effect attenuated, although an apparently robust positive association remained In these adjusted analyses there was still evidence that the within-sibling effect differed from that between nonsiblings We found no evidence that the main effects or the family-based analyses differed between males and females DISCUSSION Our family-based analyses are consistent with one previous large family-based study that included >2500 sibling pairs and found no within-sibling-pairs association between birth weight and childhood intelligence, but did not make a direct statistical comparison between the within-sibling-pairs association and that between nonsiblings In a second large study that included only sibling pairs of the same sex, in males there was a within-sibling-pairs association between birth weight and childhood intelligence However, for females there was no within-sibling-pairs association The authors commented that this sex difference was puzzling and needed replication Although we had less power than this earlier study to assess sex differences, the point estimates and statistical tests in our study suggested that there was no sex difference CONCLUSIONS The lack of any association within sibling pairs from the same family suggests that the association between birth weight and childhood intelligence in the general population of singletons is largely explained by fixed family factors that are closely matched in siblings of a similar age These factors include family socioeconomic characteristics, parental education and intelligence, genetic factors and fixed maternal factors, such as her behaviors, size, and metabolic and cardiovascular health that are constant from one pregnancy to the next and could therefore affect her offspring growth and intelligence across all pregnancies
TL;DR: The Aberdeen Children of the 1950s cohort study 1 is a follow-up into adult life of 12 150 individuals born in Aberdeen 1950–56, and is based on the Aberdeen Child Development Survey (ACDS).
Abstract: The Aberdeen Children of the 1950s cohort study 1 was established in 1999. It is a follow-up into adult life of 12 150 individuals born in Aberdeen 1950–56, and is based on the Aberdeen Child Development Survey (ACDS). The ACDS was a population-based cross-sectional study of 14 939 Aberdeen school children conducted 1962–64 to estimate the prevalence of mental subnormality in childhood and to investigate its aetiology in a well-defined community. It was funded by a US charity: the American Association for the Aid of the Crippled Child (AAACC). They had been searching for a suitable site to research the causes of cognitive problems in childhood. In the 1950s there was considerable public health and scientific interest in the fetal and obstetric determinants of ‘mental disorders’ and ‘mental retardation’ in particular. 2,3
TL;DR: Family analyses suggest that fixed family and neighbourhood factors, which are closely matched in siblings of a similar age, explain much of the association between greater educational attainment and lower adult BMI.
Abstract: The mechanisms underlying the observed association of childhood intelligence with body mass index (BMI) are unclear and few studies of this association have been prospective in design. Prospective study in a birth cohort of 5467 individuals who were born in Aberdeen, Scotland between 1950 and 1956 and who responded to a follow-up survey in 2001. Comparison of associations within sibling pairs of the same family to associations between different families in 643 sibling pairs (1286 individuals) who are participants in the main cohort. Childhood intelligence (age 7 years) and educational attainment were both inversely associated with adult BMI (mean age 48 years): the sex- and age-adjusted mean change in adult BMI per s.d. of intelligence was −0.35 kg/m2 (95% CI: −0.49, −0.21 kg/m2) and per unit increase in educational category (seven categories) was −0.28 kg/m2 (95% CI: −0.34, −0.22). On adjustment for education the association between childhood intelligence and adult BMI attenuated to the null (−0.03 kg/m2 (−0.19, 0.13 kg/m2)); other potential confounding or mediating factors had little or only modest effects on this association. The association between education and adult BMI was not affected by adjustment for childhood intelligence or other potential covariates. The within sibling-pair effect of education on adult BMI (−0.06 kg/m2 (95% CI: −0.26, 0.14)) was weaker than the effect between different families (−0.37 kg/m2 (95%CI: −0.58, −0.17)), P-value for difference of within sibling and between family effect=0.03. The association of childhood intelligence with adult BMI is attenuated to the null on adjustment for educational attainment, whereas the association of educational attainment with adult BMI appears to be independent of childhood intelligence and other measured covariates. However, our family analyses suggest that fixed family and neighbourhood factors, which are closely matched in siblings of a similar age, explain much of the association between greater educational attainment and lower adult BMI.
TL;DR: This issue finds that adding CRP to predictive models containing conventional cardiovascular risk factors leads to minor improvement in measures of discrimination (receiver-operator characteristic curve properties or c-statistics), in line with the findings of the most recent study on this issue.
Abstract: In this issue, 2 articles express widely divergent views regarding the role of C-reactive protein (CRP) in cardiovascular disease risk stratification. The place of CRP in the cardiovascular disease...
TL;DR: Any variation in mean childhood intelligence by season of birth is weak and largely explained by age at school entry and age relative to class peers.
Abstract: Background. In this study, 2 main hypotheses have been put forward to explain the variation in childhood intelligence or school performance by season of birth. In the first hypothesis, it is suggested that it is due to school policy concerning school entry, whereas the second suggests that a seasonally patterned exposure such as temperature, maternal nutrition, or infection during critical periods of brain development have a lasting effect on intelligence.
Aims. To determine whether childhood performance on tests of different domains of intelligence is patterned by season of birth and to examine possible mechanisms for any associations.
Sample. 12,150 individuals born in Aberdeen, Scotland between 1950 and 1956.
Methods. Birth cohort study in which the variation in different domains of childhood intelligence measured at ages 7, 9, and 11 by season of birth were examined.
Results. Reading ability at age 9 and arithmetic ability at age 11 varied by season of birth, with lowest scores among those born in autumn or early winter (September–December) and highest scores among those born in later winter or spring (February–April); p = .002 for joint sine-cosine functions for reading ability at age 9 and p = .05 for sine-cosine function for arithmetic ability at age 11. The child's perception and understanding of pictorial differences at age 7, verbal reasoning at 11, and English language ability at 11 did not vary by season of birth. Age at starting primary school and age relative to class peers were both associated with the different measurements of childhood intelligence and both attenuated the association between month of birth and reading ability at age 9 and arithmetic ability at age 11 towards the null. Both adjusted and unadjusted differences in reading ability at age 9 and arithmetic ability at age 11 between those born from September to December compared with other times of the year were less than 0.1 of a standard deviation of the test scores. Ambient temperature around the time of conception, during gestation, and around the time of birth did not affect intelligence.
Conclusion. Any variation in mean childhood intelligence by season of birth is weak and largely explained by age at school entry and age relative to class peers.
TL;DR: Being overweight at any point during life is associated with an increased risk of adult-onset diabetes, and the cumulative nature of this association reinforces the need to prevent the development of excess weight at an early age to reduce diabetes prevalence in coming decades.
Abstract: Objective: To examine the association between body weight measures across the lifecourse and the risk of adult-onset diabetes. Methods: We analysed data from the Glasgow Alumni Cohort and the British Women's Heart and Health Study (BWHHS). The former included 5571 men and women who had height and weight measured at university, and reported birthweight, mid- and later-life weight in a postal questionnaire. The BWHHS analysis included 4280 women who had height and weight measured in later adulthood and recalled their birthweight and early adult height and weight. Adult-onset diabetes was defined as doctor-diagnosed disease after age 30, either self-reported or abstracted from medical records. Results: Thirty nine women and 209 men (Glasgow Alumni study) and 314 women (BWHHS) had diabetes. Those with diabetes had lower mean birthweight than those without, although the differences were small. Individuals with diabetes were also shorter and heavier at all ages than those without diabetes. Being overweight during at least one time period in adult life was associated with an increased risk of diabetes, compared to those who were never overweight. While there was no age at which being overweight was particularly detrimental, the risk associated with being overweight was cumulative across the lifecourse. Conclusions: Being overweight at any point during life is associated with an increased risk of adult-onset diabetes. The cumulative nature of this association reinforces the need to prevent the development of excess weight at an early age to reduce diabetes prevalence in coming decades.
TL;DR: It is found that social class at birth was associated with risk of fatal and nonfatal cardiovascular disease among individuals born in the 1950s, a period of relative prosperity and after the introduction of the welfare state in Britain.
Abstract: Objectives. We assessed the association of father’s social class, recorded at the time of birth, with coronary heart disease and stroke in a British cohort of 11106 individuals born in the 1950s.
Methods. Survival analysis was used to relate social class at birth to the occurrence of either fatal or nonfatal coronary heart disease or stroke.
Results. Rates of coronary heart disease and stroke increased across the social class distribution from highest to lowest, and patterns of association were similar for the 2 outcomes. The gender-adjusted hazard ratio of experiencing either coronary heart disease or stroke comparing the manual and nonmanual social class categories was 1.52 (95% confidence interval [CI]=1.14, 2.02). This ratio fell to 1.41 (95% CI = 1.05, 1.88) after adjustment for indicators of intrauterine and childhood growth. Further adjustment for educational attainment reduced the ratio to 1.28 (95% CI=0.94, 1.75).
Conclusions. We found that social class at birth was associated with risk of fatal and nonfatal cardiovascular disease among individuals born in the 1950s, a period of relative prosperity and after the introduction of the welfare state in Britain. This relation appeared to be mediated in part through educational attainment.
TL;DR: Climate variables act as an instrumental variable for the association of early-life dehydration with later blood pressure and provide some evidence in favor of the hypothesis that dehydration in infancy is associated with higher adult blood pressure.
Abstract: The authors hypothesized that individuals born in the early 20th century who experienced the hottest and driest summers during infancy would be more likely to have suffered severe infant diarrhea and dehydration, and consequently have had higher blood pressure in adulthood, than those who experienced cooler and wetter summers. In this context, these climate data act as an instrumental variable for the association of early-life dehydration with later blood pressure. For 3,964 randomly selected British women born between 1919 and 1940 and whose blood pressure was measured at age 60-79 years, a one standard deviation (1.3 degrees C) higher mean summer temperature in the first year of life was associated with a 1.12-mmHg (95% confidence interval: 0.33, 1.91) higher adult systolic blood pressure, and a one standard deviation higher mean summer rainfall (33.9 mm) was associated with lower systolic blood pressure (-1.65 mmHg, 95% confidence interval: -2.44, -0.85). Equivalent results for diastolic blood pressure were 0.11 (95% confidence interval: -0.65, 0.86) and -0.32 (95% confidence interval: -0.71, 0.05). The climate variables were not associated with potential confounding factors such as socioeconomic position or lifestyle risk factors. These findings provide some evidence in favor of the hypothesis that dehydration in infancy is associated with higher adult blood pressure.
TL;DR: Between 1998-2001 and 2003, statin uptake and the use of combined drug treatment in elderly men and women increased markedly, and further potential exists for reducing the risk of recurrent coronary heart disease in older patients.
Abstract: Objective To examine the extent of uptake of medication for secondary prevention of coronary heart disease in older British men and women before (1998-2001) and after (2003) the implementation of the national service framework Design Two population based, longitudinal studies of men and women aged 60-79 in 1998-2001, based in one general practice in each of 24 British towns Participants Men and women with established coronary heart disease at the two time points (respectively 817 and 465 in 1998-2001, 857 and 548 in 2003), aged 60-79 in 1998-2001 Main outcome measures Prevalence of use of antiplatelet medication, statins, β blockers, angiotensin converting enzyme (ACE) inhibitors, and other blood pressure lowering treatments (individually and in combination) assessed in 1998-2001 and 2003 Results Between 1998-2001 and 2003, the use of all individual drugs had increased in both men and women, especially for statins (from 34% to 65% in men and from 48% to 67% in women with myocardial infarction) However, less than half received β blockers and ACE inhibitors, even by 2003 Prevalences of medication use were lower in patients with angina than in those with myocardial infarction The proportions of patients receiving more than one drug increased over time; by 2003 about half of patients with myocardial infarction and a third of those with angina were receiving antiplatelet medication, statins, and blood pressure lowering treatments Conclusions Between 1998-2001 and 2003, statin uptake and the use of combined drug treatment in elderly men and women increased markedly Further potential exists, however, for reducing the risk of recurrent coronary heart disease in older patients, particularly by improving the uptake of medication among angina patients, and by more extensive use of blood pressure lowering treatment (particularly with β blockers and ACE inhibitors)
TL;DR: There was no association between PON1 Q192R and either self-report of pregnancy-induced hypertension or gestational hyperglycaemia but the prevalence of reporting having a preterm birth increased with each R allele: per allele odds ratio 1.20.
Abstract: It has been hypothesised that paraoxonase genes would be related to adverse pregnancy outcomes, via a maternal or fetal effect on placental hypoperfusion and thrombosis. To date only two studies have assessed this possibility. In this study we assessed the associations of the PON1 Q192R polymorphism with self-report of having pregnancy-induced hypertension, gestational hyperglycaemia and a preterm offspring birth. The associations were assessed in 3266 white women who were randomly selected from 23 British towns. There was no association between PON1 Q192R and either self-report of pregnancy-induced hypertension or gestational hyperglycaemia but the prevalence of reporting having a preterm birth increased with each R allele: per allele odds ratio 1.20 [95% confidence interval (CI) 1.03, 1.41]. When our results were pooled with the one previous study of the association of this polymorphism with preterm birth, the pooled per allele odds ratio was 1.19 [95% CI 1.02, 1.39]. Our findings provide some further evidence to suggest that PON1 Q192R is associated with preterm birth; they invite further investigation of both maternal and fetal genotype for PON1 Q192R in relation to preterm birth.
TL;DR: Among older British women, preventive services for cardiovascular disease are not socially patterned, however, those from lower socio-economic groups are less likely to have recent flu vaccinations and dental, eye and chiropody examinations.
Abstract: [odds ratio (OR) 0.85, 95% confidence interval (CI) 0.74, 0.98] and dental (OR 0.42, 95% CI 0.36, 0.49), eye (OR 0.77, 95% CI 0.67, 0.88) or chiropody examinations (OR 0.88, 95% CI 0.77, 1.01). Manual social class was not related to having recent blood pressure or cholesterol checks. Conclusions. Among older British women, preventive services for cardiovascular disease are not socially patterned. However, those from lower socio-economic groups are less likely to have recent flu vaccinations and dental, eye and chiropody examinations.