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Background: The purpose of this study was to examine the association of birth weight and infant growth with childhood autonomic nervous system (ANS) activity and to assess whether ANS activity mediates the associations of birth weight and infant growth with energy-balance-related behaviours, including energy intake, satiety response, physical activity and screen time.Methods: In 2089 children, we prospectively collected birth weight, infant growth defined as conditional weight and height gain between birth and 12 months and-at 5 years-indices of cardiac ANS activity and parent-reported energy-balance-related behaviours. A mediation analysis was conducted, based on MacKinnon's multivariate extension of the product-of-coefficients strategy.Results: Birth weight and infant height gain were inversely associated with sympathetic, but not parasympathetic, activity at age 5. Infant weight gain was not associated with childhood ANS activity. Infant weight gain was predictive of increased childhood screen time and infant height gain of diminished childhood energy intake, but sympathetic activity did not mediate these associations.Conclusions: Low-birth-weight children have higher sympathetic activity, which is considered a risk factor for cardiovascular disease. Height gain in infancy seems to be beneficial for childhood sympathetic activity. However, sympathetic activity was no mediator of the associations of infant growth with childhood energy-balance-related behaviours. As individual differences in ANS activity predict increased risk of cardiovascular disease, these differences may offer insight into the early-life origins of chronic diseases and provide further basis for public health strategies to optimize birth weight and infant growth. [ABSTRACT FROM AUTHOR]

Background: Lifelong inflammation - known to be associated with many non-communicable diseases - has not been thoroughly investigated in hearing. We aimed to determine if glycoprotein A (GlycA), a novel biomarker of chronic inflammation, is associated with hearing acuity in mid-childhood and mid-life.Methods: Population-based cross-sectional study within the Longitudinal Study of Australian Children with plasma GlycA and audiometry data (1169 children and 1316 parents). We calculated high Fletcher Index (mean threshold across 1, 2 and 4 kHz), defining hearing loss as threshold >15 decibel hearing level (dB HL) (better ear). Linear/logistic regression quantified associations of GlycA with hearing threshold/loss.Results: Mean [standard deviation (SD)] high Fletcher Indices (dB HL) were 8.0 (5.7) for children and 13.1 (6.9) for adults, with 8.7% and 26.1% respectively showing hearing loss. 1-SD rise in GlycA (children 0.13 mmol/L, adults 0.17 mmol/L) predicted higher hearing thresholds for the lower individual frequencies [1 kHz: children β 0.8, 95% confidence interval (CI) 0.3-1.3; adults β 0.8, 95% CI 0.2-1.4]. This same pattern was evident for the high Fletcher Index (children β 0.7, 95% CI 0.3-1.1; adults β 0.8, 95% CI 0.3-1.4). This translated into 1-SD rise in GlycA predicting adult hearing loss [odds ratio (OR) 1.2, 95% CI 1.0-1.5] with similar but attenuated patterns in children.Conclusions: GlycA is associated with poorer hearing by mid-childhood. This potentially reframes hearing loss as a life-course condition with inflammatory antecedents common to other non-communicable diseases. Replication and mechanistic studies could inform causal inference and early prevention efforts. [ABSTRACT FROM AUTHOR]

Background: Socioeconomic experiences are recognized determinants of health, and recent work has shown that social disadvantages in early life may induce sustained biological changes at molecular level that are detectable later in life. However, the dynamics and persistence of biological embedding of socioeconomic position (SEP) remains vastly unexplored.Methods: Using the data from the ALSPAC birth cohort, we performed epigenome-wide association studies of DNA methylation changes at three life stages (birth, n = 914; childhood at mean age 7.5 years, n = 973; and adolescence at mean age 15.5 years, n = 974), measured using the Illumina HumanMethylation450 Beadchip, in relation to pregnancy SEP indicators (maternal and paternal education and occupation).Results: Across the four early life SEP metrics investigated, only maternal education was associated with methylation levels at birth, and four CpGs mapped to SULF1, GLB1L2 and RPUSD1 genes were identified [false discovery rate (FDR)-corrected P-value <0.05]. No epigenetic signature was found associated with maternal education in child samples, but methylation levels at 20 CpG loci were found significantly associated with maternal education in adolescence. Although no overlap was found between the differentially methylated CpG sites at different ages, we identified two CpG sites at birth and during adolescence which are 219 bp apart in the SULF1 gene that encodes an heparan sulphatase involved in modulation of signalling pathways. Using data from an independent birth cohort, the ENVIRONAGE cohort, we were not able to replicate these findings.Conclusions: Taken together, our results suggest that parental SEP, and particularly maternal education, may influence the offspring's methylome at birth and adolescence. [ABSTRACT FROM AUTHOR]

Background Early exposure to socioeconomic disadvantage is associated with obesity. Here we investigated how early, and conducted mediation analyses to identify behavioural factors in adulthood that could explain why. Methods Among 931 participants in the New England Family Study, we investigated the associations of family socioeconomic disadvantage measured before birth and at age 7 years with the following measures of adiposity in mid-adulthood (mean age = 44.4 years): body mass index (BMI), waist circumference and, among 400 participants, body composition from dual-energy X-ray absorption scans. Results In linear regressions adjusting for age, sex, race and childhood BMI Z-score, participants in the highest tertile of socioeconomic disadvantage at birth had 2.6 additional BMI units in adulthood [95% confidence interval (CI) = 1.26, 3.96], 5.62 cm waist circumference (95% CI = 2.69, 8.55), 0.73 kg of android fat mass (95% CI = 0.25, 1.21), and 7.65 higher Fat Mass Index (95% CI = 2.22, 13.09). Conditional on disadvantage at birth, socioeconomic disadvantage at age 7 years was not associated with adult adiposity. In mediation analyses, 10–20% of these associations were explained by educational attainment and 5–10% were explained by depressive symptoms. Conclusions Infancy may be a sensitive period for exposure to socioeconomic disadvantage, as exposure in the earliest years of life confers a larger risk for overall and central adiposity in mid-adulthood than exposure during childhood. Intervention on these two adult risk factors for adiposity would, if all model assumptions were satisfied, only remediate up to one-fifth of the excess adult adiposity among individuals born into socioeconomically disadvantaged households. [ABSTRACT FROM AUTHOR]

Background: Whereas most studies have reported prior history/diagnosis of asthma as an independent risk factor for chronic obstructive pulmonary disease (COPD) development in later life, no systematic review and meta-analysis has been conducted to synthesize these observational studies. The aim of this review is to investigate associations between prior history of asthma and later development of COPD.Methods: We conducted a comprehensive search in PubMed, CINAHL and EMBASE for studies related to prior history of asthma and COPD diagnosis. Articles were screened for relevance by two independent reviewers. Methodological quality was independently assessed and data extracted for qualitative and quantitative review. We explored heterogeneity and performed a publication bias check.Results: From the 1260 articles retrieved, 9 were included in the qualitative review and 7 in the meta-analysis. History of asthma was associated with developing COPD in later life (Inverse Variance Random-effects model, odds ratio: 7.87, 95% confidence interval: 5.40-11.45, p < 0.00001).Conclusions: Studies with high methodological quality provided sufficient evidence to suggest that individuals with previous history of asthma have an increasing likelihood of developing COPD in later life. [ABSTRACT FROM AUTHOR]

Background: Limited evidence suggests that exposure to maternal smoking in utero or early life might be associated with chronic obstructive pulmonary disease (COPD), but whether this is independent of later own smoking remains unclear. Our objective was to examine the independent and combined association of maternal and own smoking with adult lung function and COPD.Methods: We used UK Biobank to examine associations of maternal smoking around delivery, and pack-years of own smoking, with lung function (n = 502 626) and hospitalization/death from COPD (n = 433 863). We calculated the additive interaction between maternal and own smoking on the outcomes of interest, and estimated the association with maternal smoking within categories of own smoking.Results: There was no strong evidence that maternal smoking influenced adult lung health among never smokers. Exposure to both maternal and own smoking was associated with lower Forced expiratory volume (FEV1)/ forced vital capacity (FVC) and greater risk of hospitalization/death from COPD than expected from their independent associations. For FEV1/FVC, the mean difference according to maternal smoking was -0.02 (-0.06, 0.02), -0.01 (-0.05, 0.03), -0.11 (-0.16, -0.05) and -0.11 (-0.19, -0.04) among women who smoked ≤10, 11-20, 21-30 and >30 pack-years, respectively. The association between maternal smoking and COPD also varied by pack-years of own smoking, with a hazard ratio of 2.25 (1.30, 3.89) for ≤10 years, 1.23 (0.80, 1.89) for 11-20 years, 1.30 (0.85, 2.01) for 21-30 years and 1.14 (0.91, 1.43) for >30 years.Conclusions: Our findings indicate an excess reduction in FEV1/FVC and risk of COPD due to maternal smoking that is heterogeneous across levels of own smoking. [ABSTRACT FROM AUTHOR]

Background: Mothers' smoking during pregnancy increases asthma risk in their offspring. There is some evidence that grandmothers' smoking may have a similar effect, and biological plausibility that fathers' smoking during adolescence may influence offspring's health through transmittable epigenetic changes in sperm precursor cells. We evaluated the three-generation associations of tobacco smoking with asthma.Methods: Between 2010 and 2013, at the European Community Respiratory Health Survey III clinical interview, 2233 mothers and 1964 fathers from 26 centres reported whether their offspring (aged ≤51 years) had ever had asthma and whether it had coexisted with nasal allergies or not. Mothers and fathers also provided information on their parents' (grandparents) and their own asthma, education and smoking history. Multilevel mediation models within a multicentre three-generation framework were fitted separately within the maternal (4666 offspring) and paternal (4192 offspring) lines.Results: Fathers' smoking before they were 15 [relative risk ratio (RRR) = 1.43, 95% confidence interval (CI): 1.01-2.01] and mothers' smoking during pregnancy (RRR = 1.27, 95% CI: 1.01-1.59) were associated with asthma without nasal allergies in their offspring. Grandmothers' smoking during pregnancy was associated with asthma in their daughters [odds ratio (OR) = 1.55, 95% CI: 1.17-2.06] and with asthma with nasal allergies in their grandchildren within the maternal line (RRR = 1.25, 95% CI: 1.02-1.55).Conclusions: Fathers' smoking during early adolescence and grandmothers' and mothers' smoking during pregnancy may independently increase asthma risk in offspring. Thus, risk factors for asthma should be sought in both parents and before conception.Funding: European Union (Horizon 2020, GA-633212). [ABSTRACT FROM AUTHOR]

Background: Non-communicable diseases are increasing in sub-Saharan Africa and are estimated to account for 32% of adult deaths in The Gambia. Worldwide, prevalence of hypertension is highest in the African region (46%) and a very high proportion is undiagnosed. This study examined diagnosed and undiagnosed hypertension in The Gambian adult population.Methods: Data were collected in 2010 from a nationally representative random sample of 4111 adults aged 25-64 years, using the World Health Organization STEPwise cross-sectional survey methods. Analyses were restricted to non-pregnant participants with three valid blood pressure measurements (n = 3573). We conducted gender-stratified univariate and multivariate regression analyses to identify the strongest sociodemographic, behavioural and biological risk factors associated with hypertension.Results: Almost one-third of adults were hypertensive; a high proportion were undiagnosed, particularly among men (86% of men vs 71% of women with hypertension, P < 0.001). Rural and semi-urban residents and overweight/obese persons had increased odds of hypertension. Compared with urban residents, participants from one of the most rural regions had higher odds of hypertension among both men [adjusted odds ratio (AOR) 3.2; 95% CI: 1.6-6.4] and women (AOR 2.5; 95% CI: 1.3-4.6). Other factors strongly associated with hypertension in multivariate analyses were age, smoking, physical inactivity and ethnicity.Conclusions: Rural and semi-urban residence were strongly associated with hypertension, contrary to what has been found in similar studies in sub-Saharan Africa. Intervention to reduce the burden of hypertension in The Gambia could be further targeted towards rural areas. [ABSTRACT FROM AUTHOR]

Background: Our objective was to examine the associations of parental body mass index (BMI) and maternal gestational weight gain with childhood-onset type 1 diabetes. Comparing the associations of maternal and paternal BMI with type 1 diabetes in the offspring will provide further insight into the role of unmeasured confounding by characteristics linked to BMI in both parents.Methods: We studied 132 331 children participating in the Norwegian Mother and Child Cohort Study (MoBa) and the Danish National Birth Cohort (DNBC) who were born between February 1998 and July 2009. Exposures of interest included parental BMI and maternal gestational weight gain obtained by maternal report. We used Cox-proportional hazards regression to examine the risk of type 1 diabetes (n=499 cases), which was ascertained by national childhood diabetes registers.Results: The incidence of type 1 diabetes was 32.7 per 100 000 person-years in MoBa and 28.5 per 100 000 person-years in DNBC. Both maternal pre-pregnancy obesity, adjusted hazard ratio (HR) 1.41 [95% confidence interval (CI): 1.06, 1.89] and paternal obesity, adjusted HR 1.51 (95% CI: 1.11, 2.04), were associated with childhood-onset type 1 diabetes. The associations were similar after mutual adjustment. In contrast, maternal total gestational weight gain was not associated with childhood-onset type 1 diabetes, adjusted HR 1.00 (95% CI: 0.99, 1.02) per kilogram increase.Conclusions: Our study suggests that the association between maternal obesity and childhood-onset type 1 diabetes is not likely explained by intrauterine mechanisms, but possibly rather by unknown environmental factors influencing BMI in the family. [ABSTRACT FROM AUTHOR]

Background: We investigate patterns of neurodevelopmental trajectories in infants, using a representative population, and identify risk factors that predict delayed growth.Methods: Participating infants (n = 952; 82.8% of the total sample) were assessed by Mullen Scales of Early Learning at seven time points, from 1 month to 24 months of age. Mothers were recruited in early pregnancy and data on demographic characteristics were collected during pregnancy. Trajectory patterns were investigated using latent class growth analysis, and risk factors for the derived trajectory classes were investigated by multinomial logistic regression.Results: Participants were found to be a fairly representative sample with respect to their demographic characteristics. Five classes of high normal (11.5%), normal (49.2%), low normal (21.2%), delayed (14.1%), and markedly delayed (4.0%) were identified. The markedly delayed class was characterized by overall delay from the early developmental stages; notably, such delay first became salient in motor domains and was then exceeded by language domains, especially receptive language. This class was predicted by male sex (odds ratio 4.0; 95% confidence interval 1.7-9.1), small for gestational age (2.8; 1.0-7.5), low placenta-to-birthweight ratio (2.8; 1.2-6.4) and low maternal education (4.7; 1.2-19.0). The delayed class was characterized by gradual downward deviation after the first birthday, and was predicted by male sex (2.5; 1.5-4.2), preterm birth (4.4; 1.6-12.6) and advanced paternal age (1.9; 1.0-3.5).Conclusions: Our results demonstrate that about 1 out of 5 infants exhibits delayed neurodevelopment. Infants with distinct patterns of delayed trajectories and varying risk factors are considered to have different pathophysiological mechanisms. [ABSTRACT FROM AUTHOR]

Background: Several studies have investigated the effect of known adult body mass index (BMI) associated single nucleotide polymorphisms (SNPs) on BMI in childhood. There has been no genome-wide association study (GWAS) of BMI trajectories over childhood. Methods: We conducted a GWAS meta-analysis of BMI trajectories from 1 to 17 years of age in 9377 children (77 967 measurements) from the Avon Longitudinal Study of Parents and Children (ALSPAC) and the Western Australian Pregnancy Cohort (Raine) Study. Genome-wide significant loci were examined in a further 3918 individuals (48 530 measurements) from Northern Finland. Linear mixed effects models with smoothing splines were used in each cohort for longitudinal modelling of BMI. Results: A novel SNP, downstream from the FAM120AOS gene on chromosome 9, was detected in the meta-analysis of ALSPAC and Raine. This association was driven by a difference in BMI at 8 years (T allele of rs944990 increased BMI; PSNP=1.52×10-8), with a modest association with change in BMI over time (PWald(Change)=0.006). Three known adult BMI-associated loci (FTO, MC4R and ADCY3) and one childhood obesity locus (OLFM4) reached genome-wide significance (PWald<1.13×10-8) with BMI at 8 years and/or change over time. Conclusions: This GWAS of BMI trajectories over childhood identified a novel locus that warrants further investigation. We also observed genome-wide significance with previously established obesity loci, making the novel observation that these loci affected both the level and the rate of change in BMI. We have demonstrated that the use of repeated measures data can increase power to allow detection of genetic loci with smaller sample sizes. [ABSTRACT FROM AUTHOR]

The Mysore Parthenon Birth Cohort was established to examine the long-term effects of maternal glucose tolerance and nutritional status on cardiovascular disease risk factors in the offspring. During 1997–98, 830 of 1233 women recruited from the antenatal clinics of the Holdsworth Memorial Hospital (HMH), Mysore, India, underwent an oral glucose tolerance test. Of these, 667 women delivered live babies at HMH. Four babies with major congenital anomalies were excluded, and the remaining 663 were included for further follow-up. The babies had detailed anthropometry at birth and at 6–12-monthly intervals subsequently. Detailed cardiovascular investigations were done at ages 5, 9.5 and 13.5 years in the children, and in the parents at the 5-year and 9.5-year follow-ups. This ongoing study provides extensive data on serial anthropometry and body composition, physiological and biochemical measures, dietary intake, nutritional status, physical activity measures, stress reactivity measures and cognitive function, and socio-demographic parameters for the offspring. Data on anthropometry, cardiovascular risk factors and nutritional status are available for mothers during pregnancy. Anthropometry and risk factor measures are available for both parents at follow-up. [ABSTRACT FROM PUBLISHER]

Background Adult height is known to be inversely related to coronary heart disease (CHD) risk. We sought to investigate transgenerational influence of parental height on offspring’s CHD risk.Methods Parents took part in a cardiorespiratory disease survey in two Scottish towns during the 1970s, in which their physical stature was measured. In 1996, their offspring were invited to participate in a similar survey, which included an electrocardiogram recording and risk factor assessment.Results A total of 2306 natural offspring aged 30–59 years from 1456 couples were subsequently flagged for notification of mortality and followed for CHD-related hospitalizations. Taller paternal and/or maternal height was associated with socio-economic advantage, heavier birthweight and increased high-density lipoprotein cholesterol in offspring. Increased height in fathers, but more strongly in mothers (risk ratio for 1 SD change in maternal height = 0.85; 95% confidence interval: 0.76 to 0.95), was associated with a lower risk of offspring CHD, adjusting for age, sex, other parental height and CHD risk factors.Conclusion There is evidence of an association between taller parental, particularly maternal, height and lower offspring CHD risk. This may reflect an influence of early maternal growth on the intrauterine environment provided for her offspring. [ABSTRACT FROM PUBLISHER]

Background Social disparities in obesity are often more marked among women than men, possibly due to social factors. Taking a life-history perspective, we hypothesized that childhood infections could be relevant via sex-specific effects of immune system activation on sexual development and, hence, body shape.Methods We used multivariable linear regression to assess the sex-specific, adjusted associations of ‘childhood’ pathogens [0 (n = 1002), 1 (n = 2199), 2 (n = 3442) or 3 (n = 4833) of HSV1, CMV and hepatitis A antibodies] and ‘adult’ pathogens [0 (n = 5836), 1 (n = 3018) or &geq;2 (n = 720) of HSV2, HHV8 and hepatitis B or C) with waist–hip ratio (WHR) and body mass index (BMI) standard deviations (SDs) using NHANES III (1988–94). As validation, we assessed associations with height.Results ‘Childhood’ pathogens were positively associated with WHR among women [0.18 SD, 95% confidence interval (95% CI) 0.04–0.32 for 3, compared with 0], but not men (−0.04 SD, 95% CI −0.15 to 0.08), adjusted for age, education, race/ethnicity, smoking and alcohol. Further adjustments for leg length barely changed the estimates. There were no such sex-specific associations for BMI or for adult pathogens. ‘Childhood’, but not ‘adult’, pathogens were negatively associated with height, adjusted for age, sex, education and race/ethnicity.Conclusions These observations are consistent with the lifecourse hypothesis that early exposure to infections makes women vulnerable to central obesity. This hypothesis potentially sheds new light on the developmental origins of obesity, and is consistent with the generally higher levels of central obesity among women than men in developing populations. [ABSTRACT FROM PUBLISHER]

Background: In utero exposure to tobacco smoking has been suggested to cause persistent alterations in cognitive functioning. We examined if mothers' smoking during pregnancy (SDP) is associated with long-term impairment in offspring stress coping and the causal mechanism behind a possible link.Methods: We used a large cohort (n = 187,106) of young males in Sweden (mean age = 18.2 years), who underwent a semi-structured psychological assessment in 1997-2006, including an evaluation of stress coping ability, as part of the compulsory military conscript examination. We compared differentially exposed siblings within nuclear families and cousins in extended families and used multilevel structural equation models to disentangle genetic from environmental contributions to the association between SDP and stress coping.Results: SDP and offspring stress coping was moderately strongly associated when comparing unrelated individuals [regression coefficient (b) = -0.38 on a nine-point scale; 95% confidence interval (CI) -0.40 to -0.36, P < 0.0001]. In contrast, it disappeared when siblings were compared (b = 0.11; 95% CI -0.01 to 0.23, P = 0.071). This familial confounding was entirely due to genetic influences.Conclusions: SDP is an established risk factor for pregnancy- and birth-related complications. However, we found no long-term effect of SDP on offspring stress coping. Rather, the observed association was due to familial confounding of genetic origin; women prone to SDP also transmit genes to their children that are associated with poorer coping with stress. [ABSTRACT FROM AUTHOR]

Background: In Caucasian populations, adult height is inversely associated with cardiovascular disease (CVD) risk and positively related to some cancers. However, there are few data from Asian populations and from women. We sought to determine the sex- and region-specific associations between height and cardiovascular outcomes, and deaths due to cancer, respiratory and injury in populations from the Asia-Pacific region.Methods: Thirty-nine studies from the Asia Pacific Cohort Studies Collaboration database were included. We used Cox proportional hazard regression models to estimate the associations between height and pre-specified outcomes.Results: A total of 510,800 participants with 21,623 deaths were included. Amongst men, inverse linear associations were observed between height and coronary heart disease (CHD), stroke, CVD, injury and total mortality. The hazard ratios [95% confidence intervals, (CI)] for a 1-SD (= 6 cm) increment in height ranged from 0.85 (0.80-0.91) for injury to 0.97 (0.95-0.98) for total mortality. Similar trends were found between height and CHD, haemorrhagic stroke and CVD in women. A positive linear association was observed between height and cancer mortality. For each standard deviation greater height, the risk of cancer was increased by 5% (2-8%) and 9% (5-14%) in men and women, respectively. No regional difference was observed between Asian and Australasian cohorts. Adjusting for markers of education did not alter the results.Conclusions: The opposing relationships of height with CVD and cancer suggest that care is required in setting national policies on childhood nutrition lest they have unintended consequences on the incidence of major non-communicable diseases. [ABSTRACT FROM AUTHOR]

Twin studies have long been recognized for their value in learning about the aetiology of disease and specifically for their potential for separating genetic effects from environmental effects. The recent upsurge of interest in life-course epidemiology and the study of developmental influences on later health has provided a new impetus to study twins as a source of unique insights. Twins are of special interest because they provide naturally matched pairs where the confounding effects of a large number of potentially causal factors (such as maternal nutrition or gestation length) may be removed by comparisons between twins who share them. The traditional tool of epidemiological ‘risk factor analysis’ is the regression model, but it is not straightforward to transfer standard regression methods to twin data, because the analysis needs to reflect the paired structure of the data, which induces correlation between twins. This paper reviews the use of more specialized regression methods for twin data, based on generalized least squares or linear mixed models, and explains the relationship between these methods and the commonly used approach of analysing within-twin-pair difference values. Methods and issues of interpretation are illustrated using an example from a recent study of the association between birth weight and cord blood erythropoietin. We focus on the analysis of continuous outcome measures but review additional complexities that arise with binary outcomes. We recommend the use of a general model that includes separate regression coefficients for within-twin-pair and between-pair effects, and provide guidelines for the interpretation of estimates obtained under this model. [ABSTRACT FROM AUTHOR]

Background Although low birthweight has been related to higher mean blood pressure in individuals, there have been very few studies on the contribution of the ‘fetal origins hypothesis’ to international variations in mean blood pressure.Methods Standardized data on mean blood pressure levels in adults aged 20–29 years (available from the INTERSALT study countries) were related to data on mean birthweight and infant mortality rates (IMRs) ∼25 years earlier (available from the World Health Organization and the United Nations statistics for 24 of these countries).Results Population mean systolic pressure was inversely correlated with IMR (r = −0.66, P < 0.001) and positively correlated with mean birthweight (r = 0.36, P = 0.108). These correlations were little affected by adjustment either for current body mass index or for current sodium, potassium, and alcohol intake.Conclusions The directions of these associations suggest that low mean birthweight and high infant mortality are not important determinants of high population mean adult blood pressure levels. [ABSTRACT FROM AUTHOR]

Background Although the detrimental effect of overweight and obesity has been extensively reported in Western populations, little is known on the association between body weight, weight change and mortality in Asian populations whose weight distribution and mortality differ considerably from the West. Methods A cohort of 75 868 subjects aged 35 years and above, participants of the Trivandrum Oral Cancer Study—a cluster-randomized controlled trial originally implemented to evaluate the efficacy of visual inspection on oral cancer, in Kerala State, South India—were followed up from 1995 to 2004. Weight and height were measured both at baseline and in 3.5-year follow-up surveys. Early years of follow-up were excluded from the analyses. Relative risks of overall death and cause-specific death were estimated according to the body mass index (BMI) category of the WHO Asian population definitions, and to weight changes between two surveys. Results Low BMI was a predictor of mortality, while high BMI was not. Mortality risks in men adjusted for age, smoking habits and other potential confounders, as compared with a BMI 18.5–22.9 kg/m2, were 1.26 (95% CI 1.03–1.55) for BMI < 16 kg/m2; 1.16 (1.03–1.32) for BMI = 16–18.4 kg/m2; 0.95 (0.81–1.12) for BMI = 23–24.9 kg/m2; 0.85 (0.69–1.05) for BMI = 25–27.4 kg/m2; and 0.89 (0.65–1.21) for BMI ≥ 27.5 kg/m2. Similar findings were observed in women. BMI was not associated with deaths from cancer, cardiovascular and cerebrovascular diseases, and diabetes. A low BMI (<16 kg/m2) was associated with increased deaths from chronic respiratory diseases. Smoking and socio-economical status did modify the association. A moderate weight gain of 4–10% between the two surveys was associated with decreased risk of death, while moderate and severe weight loss were predictive factors of death. Similar results were observed in both men and women. Conclusions Among this Indian rural population, mild to severe leanness (BMI < 16 kg/m2) and weight loss were important determinants of mortality, especially from chronic respiratory diseases, while overweight and above (BMI > 23 kg/m2) did not show any detrimental effect. [ABSTRACT FROM AUTHOR]

Background: Most studies of associations between child growth and cognitive ability were based on size at one or two ages and a single measure of cognition. We aimed to characterize different aspects of early growth and their associations with cognitive outcomes in childhood through adolescence.Methods: In a sample of 12 368 Belarusian children born at term, we examined associations of length/height and weight trajectories over the first 6.5 years of life with cognitive ability at 6.5 and 16 years and its change over time. We estimated growth trajectories using two random-effects models-the SuperImposition by Translation and Rotation to model overall patterns of growth and the Jenss-Bayley to distinguish growth in infancy from post infancy. Cognitive ability was measured using the Wechsler Abbreviated Scales of Intelligence at 6.5 years and the computerized NeuroTrax test at 16 years.Results: Higher length/height between birth and 6.5 years was associated with higher cognitive scores at 6.5 and 16 years {2.7 points [95% confidence interval (CI): 2.1, 3.2] and 2.5 points [95% CI: 1.9, 3.0], respectively, per standard deviation [SD] increase}. A 1-SD delay in the childhood height-growth spurt was negatively associated with cognitive scores [-2.4 (95% CI: -3.0, -1.8) at age 6.5; -2.2 (95% CI: -2.7, -1.6) at 16 years]. Birth size and post-infancy growth velocity were positively associated with cognitive scores at both ages. Height trajectories were not associated with the change in cognitive score. Similar results were observed for weight trajectories.Conclusions: Among term infants, the overall size, timing of the childhood growth spurt, size at birth and post-infancy growth velocity were all associated with cognitive ability at early-school age and adolescence. [ABSTRACT FROM AUTHOR]