Pubertal timing and adult obesity and cardiometabolic risk in women and men: a systematic review and meta-analysis.
01 Aug 2013-International Journal of Obesity (Nature Publishing Group)-Vol. 37, Iss: 8, pp 1036-1043
TL;DR: Earlier pubertal development appears to also be inversely correlated with risk of other cardiometabolic risk factors and cardiovascular mortality, hypertension, metabolic syndrome (MetS) and abnormal glycaemia.
Abstract: Pubertal timing and adult obesity and cardiometabolic risk in women and men: a systematic review and meta-analysis
Citations
More filters
30 Oct 1999
TL;DR: This paper found a strong consistent relationship between low socioeconomic status (SES) in early life and increased fatness in adulthood, but in studies which attempted to address potential confounding by gestational age, parental fatness, or social group, the relationship was less consistent.
Abstract: OBJECTIVE
To identify factors in childhood which might influence the development of obesity in adulthood.
BACKGROUND
The prevalence of obesity is increasing in the UK and other developed countries, in adults and children. The adverse health consequences of adult obesity are well documented, but are less certain for childhood obesity. An association between fatness in adolescence and undesirable socio-economic consequences, such as lower educational attainment and income, has been observed, particularly for women. Childhood factors implicated in the development of adult obesity therefore have far-reaching implications for costs to the health-services and economy.
SEARCH STRATEGY
In order to identify relevant studies, electronic databases--Medline, Embase, CAB abstracts, Psyclit and Sport Discus-were searched from the start date of the database to Spring 1998. The general search structure for electronic databases was (childhood or synonyms) AND (fatness or synonyms) AND (longitudinal or synonyms). Further studies were identified by citations in retrieved papers and by consultation with experts.
INCLUSION CRITERIA
Longitudinal observational studies of healthy children which included measurement of a risk factor in childhood (<18 y), and outcome measure at least 1 y later. Any measure of fatness, leanness or change in fatness or leanness was accepted. Measures of fat distribution were not included. Only studies with participants from an industrialized country were considered, and those concerning minority or special groups, e.g. Pima Indians or children born preterm, were excluded.
FINDINGS
Risk factors for obesity included parental fatness, social factors, birth weight, timing or rate of maturation, physical activity, dietary factors and other behavioural or psychological factors. Offspring of obese parent(s) were consistently seen to be at increased risk of fatness, although few studies have looked at this relationship over longer periods of childhood and into adulthood. The relative contributions of genes and inherited lifestyle factors to the parent-child fatness association remain largely unknown. No clear relationship is reported between socio-economic status (SES) in early life and childhood fatness. However, a strong consistent relationship is observed between low SES in early life and increased fatness in adulthood. Studies investigating SES were generally large but very few considered confounding by parental fatness. Women who change social class (social mobility) show the prevalence of obesity of the class they join, an association which is not present in men. The influence of other social factors such as family size, number of parents at home and childcare have been little researched. There is good evidence from large and reasonably long-term studies for an apparently clear relationship for increased fatness with higher birth weight, but in studies which attempted to address potential confounding by gestational age, parental fatness, or social group, the relationship was less consistent. The relationship between earlier maturation and greater subsequent fatness was investigated in predominantly smaller, but also a few large studies. Again, this relationship appeared to be consistent, but in general, the studies had not investigated whether there was confounding by other factors, including parental fatness, SES, earlier fatness in childhood, or dietary or activity behaviours. Studies investigating the role of diet or activity were generally small, and included diverse methods of risk factor measurement. There was almost no evidence for an influence of activity in infancy on later fatness, and inconsistent but suggestive evidence for a protective effect of activity in childhood on later fatness. No clear evidence for an effect of infant feeding on later fatness emerged, but follow-up to adulthood was rare, with only one study measuring fatness after 7y. Studies investigating diet in childhood were limited and inconc
1,196 citations
TL;DR: In this article, the authors used genome-wide and custom-genotyping arrays in up to 182,416 women of European descent from 57 studies and found robust evidence for 123 signals at 106 genomic loci associated with age at menarche.
Abstract: Age at menarche is a marker of timing of puberty in females. It varies widely between individuals, is a heritable trait and is associated with risks for obesity, type 2 diabetes, cardiovascular disease, breast cancer and all-cause mortality. Studies of rare human disorders of puberty and animal models point to a complex hypothalamic-pituitary-hormonal regulation, but the mechanisms that determine pubertal timing and underlie its links to disease risk remain unclear. Here, using genome-wide and custom-genotyping arrays in up to 182,416 women of European descent from 57 studies, we found robust evidence (P < 5 × 10(-8)) for 123 signals at 106 genomic loci associated with age at menarche. Many loci were associated with other pubertal traits in both sexes, and there was substantial overlap with genes implicated in body mass index and various diseases, including rare disorders of puberty. Menarche signals were enriched in imprinted regions, with three loci (DLK1-WDR25, MKRN3-MAGEL2 and KCNK9) demonstrating parent-of-origin-specific associations concordant with known parental expression patterns. Pathway analyses implicated nuclear hormone receptors, particularly retinoic acid and γ-aminobutyric acid-B2 receptor signalling, among novel mechanisms that regulate pubertal timing in humans. Our findings suggest a genetic architecture involving at least hundreds of common variants in the coordinated timing of the pubertal transition.
498 citations
TL;DR: Earlier or later puberty timing in women or men was associated with higher risks for 48 adverse outcomes, across a range of cancers, cardio-metabolic, gynaecological/obstetric, gastrointestinal, musculoskeletal, and neuro-cognitive categories.
Abstract: Early puberty timing is associated with higher risks for type 2 diabetes (T2D) and cardiovascular disease in women and therefore represents a potential target for early preventive interventions. We characterised the range of diseases and other adverse health outcomes associated with early or late puberty timing in men and women in the very large UK Biobank study. Recalled puberty timing and past/current diseases were self-reported by questionnaire. We limited analyses to individuals of White ethnicity (250,037 women; 197,714 men) and to disease outcomes with at least 500 cases (~ 0.2% prevalence) and we applied stringent correction for multiple testing (corrected threshold P < 7.48 × 10(-5)). In models adjusted for socioeconomic position and adiposity/body composition variables, both in women and men separately, earlier puberty timing was associated with higher risks for angina, hypertension and T2D. Furthermore, compared to the median/average group, earlier or later puberty timing in women or men was associated with higher risks for 48 adverse outcomes, across a range of cancers, cardio-metabolic, gynaecological/obstetric, gastrointestinal, musculoskeletal, and neuro-cognitive categories. Notably, both early and late menarche were associated with higher risks for early natural menopause in women. Puberty timing in both men and women appears to have a profound impact on later health.
358 citations
TL;DR: The results of this study suggest that childhood obesity may be a risk factor for selected adult CVD risk factors, but a need exists for additional, higher-quality studies that include, but are not limited to, both unadjusted and adjusted measures such as BMI before any definitive conclusions can be reached.
Abstract: Overweight and obesity is a major public health concern that includes associations with the development of cardiovascular disease (CVD) risk factors during childhood and adolescence as well as premature mortality in adults. Despite the high prevalence of childhood and adolescent obesity as well as adult CVD, individual studies as well as previous systematic reviews examining the relationship between childhood obesity and adult CVD have yielded conflicting results. The purpose of this study was to use the aggregate data meta-analytic approach to address this gap. Studies were included if they met the following criteria: (1) longitudinal and cohort studies (including case-cohort), (2) childhood exposure and adult outcomes collected on the same individual over time, (3) childhood obesity, as defined by the original study authors, (4) English-language articles, (5) studies published up to June, 2015, (6) one or more of the following CVD risk factors [systolic blood pressure (SBP), diastolic blood pressure (DBP), total cholesterol (TC), high-density lipoprotein cholesterol (HDL), low-density lipoprotein cholesterol (LDL), non-high-density lipoprotein cholesterol (non-HDL), and triglycerides (TG)], (7) outcome(s) not self-reported, and (8) exposure measurements (child’s adiposity) assessed by health professionals, trained investigators, or self-reported. Studies were retrieved by searching three electronic databases as well as citation tracking. Fisher’s r to z score was calculated for each study for each outcome. Pooled effect sizes were calculated using random-effects models while risk of bias was assessed using the STROBE instrument. In order to try and identify sources of heterogeneity, random-effects meta-regression was also performed. Of the 4840 citations reviewed, a total of 23 studies were included in the systematic review and 21 in the meta-analysis. The findings suggested that childhood obesity is significantly and positively associated with adult SBP (Zr = 0.11; 95% CI: 0.07, 0.14), DBP (Zr = 0.11; 95% CI: 0.07, 0.14), and TG (Zr =0.08; 95% CI: 0.03, 0.13), and significantly and inversely associated with adult HDL (Zr = −0.06; 95% CI: -0.10, −0.02). For those studies that adjusted for adult body mass index (BMI), associations were reversed, suggesting that adult BMI may be a potential mediator. Nine studies had more than 33% of items that placed them at an increased risk for bias. The results of this study suggest that childhood obesity may be a risk factor for selected adult CVD risk factors. However, a need exists for additional, higher-quality studies that include, but are not limited to, both unadjusted and adjusted measures such as BMI before any definitive conclusions can be reached. PROSPERO 2015: CRD42015019763
.
329 citations
Cites background from "Pubertal timing and adult obesity a..."
...From our perspective, it is important to adjust for these variables as well as socio-demographic variables given previous research suggesting an association between pubertal timing and adult cardio-metabolic risk factors [94] as well as an association between energy intake, energy expenditure and adult CVD [95]....
[...]
TL;DR: Current challenges involving the precise diagnosis and adequate treatment of central precocious puberty are described, which remain challenging for paediatric endocrinologists.
261 citations
References
More filters
Journal Article•
TL;DR: The QUOROM Statement (QUality Of Reporting Of Meta-analyses) as mentioned in this paper was developed to address the suboptimal reporting of systematic reviews and meta-analysis of randomized controlled trials.
Abstract: Systematic reviews and meta-analyses have become increasingly important in health care. Clinicians read them to keep up to date with their field,1,2 and they are often used as a starting point for developing clinical practice guidelines. Granting agencies may require a systematic review to ensure there is justification for further research,3 and some health care journals are moving in this direction.4 As with all research, the value of a systematic review depends on what was done, what was found, and the clarity of reporting. As with other publications, the reporting quality of systematic reviews varies, limiting readers' ability to assess the strengths and weaknesses of those reviews.
Several early studies evaluated the quality of review reports. In 1987, Mulrow examined 50 review articles published in 4 leading medical journals in 1985 and 1986 and found that none met all 8 explicit scientific criteria, such as a quality assessment of included studies.5 In 1987, Sacks and colleagues6 evaluated the adequacy of reporting of 83 meta-analyses on 23 characteristics in 6 domains. Reporting was generally poor; between 1 and 14 characteristics were adequately reported (mean = 7.7; standard deviation = 2.7). A 1996 update of this study found little improvement.7
In 1996, to address the suboptimal reporting of meta-analyses, an international group developed a guidance called the QUOROM Statement (QUality Of Reporting Of Meta-analyses), which focused on the reporting of meta-analyses of randomized controlled trials.8 In this article, we summarize a revision of these guidelines, renamed PRISMA (Preferred Reporting Items for Systematic reviews and Meta-Analyses), which have been updated to address several conceptual and practical advances in the science of systematic reviews (Box 1).
Box 1
Conceptual issues in the evolution from QUOROM to PRISMA
46,935 citations
TL;DR: A checklist contains specifications for reporting of meta-analyses of observational studies in epidemiology, including background, search strategy, methods, results, discussion, and conclusion should improve the usefulness ofMeta-an analyses for authors, reviewers, editors, readers, and decision makers.
Abstract: ObjectiveBecause of the pressure for timely, informed decisions in public health
and clinical practice and the explosion of information in the scientific literature,
research results must be synthesized. Meta-analyses are increasingly used
to address this problem, and they often evaluate observational studies. A
workshop was held in Atlanta, Ga, in April 1997, to examine the reporting
of meta-analyses of observational studies and to make recommendations to aid
authors, reviewers, editors, and readers.ParticipantsTwenty-seven participants were selected by a steering committee, based
on expertise in clinical practice, trials, statistics, epidemiology, social
sciences, and biomedical editing. Deliberations of the workshop were open
to other interested scientists. Funding for this activity was provided by
the Centers for Disease Control and Prevention.EvidenceWe conducted a systematic review of the published literature on the
conduct and reporting of meta-analyses in observational studies using MEDLINE,
Educational Research Information Center (ERIC), PsycLIT, and the Current Index
to Statistics. We also examined reference lists of the 32 studies retrieved
and contacted experts in the field. Participants were assigned to small-group
discussions on the subjects of bias, searching and abstracting, heterogeneity,
study categorization, and statistical methods.Consensus ProcessFrom the material presented at the workshop, the authors developed a
checklist summarizing recommendations for reporting meta-analyses of observational
studies. The checklist and supporting evidence were circulated to all conference
attendees and additional experts. All suggestions for revisions were addressed.ConclusionsThe proposed checklist contains specifications for reporting of meta-analyses
of observational studies in epidemiology, including background, search strategy,
methods, results, discussion, and conclusion. Use of the checklist should
improve the usefulness of meta-analyses for authors, reviewers, editors, readers,
and decision makers. An evaluation plan is suggested and research areas are
explored.
17,663 citations
TL;DR: The Strengthening the Reporting of Observational Studies in Epidemiology (STROBE) initiative developed recommendations on what should be included in an accurate and complete report of an observational study, resulting in a checklist of 22 items (the STROBE statement) that relate to the title, abstract, introduction, methods, results, and discussion sections of articles.
Abstract: Much biomedical research is observational. The reporting of such research is often inadequate, which hampers the assessment of its strengths and weaknesses and of a study's generalisability. The Strengthening the Reporting of Observational Studies in Epidemiology (STROBE) Initiative developed recommendations on what should be included in an accurate and complete report of an observational study. We defined the scope of the recommendations to cover three main study designs: cohort, case-control, and cross-sectional studies. We convened a 2-day workshop in September 2004, with methodologists, researchers, and journal editors to draft a checklist of items. This list was subsequently revised during several meetings of the coordinating group and in e-mail discussions with the larger group of STROBE contributors, taking into account empirical evidence and methodological considerations. The workshop and the subsequent iterative process of consultation and revision resulted in a checklist of 22 items (the STROBE Statement) that relate to the title, abstract, introduction, methods, results, and discussion sections of articles. 18 items are common to all three study designs and four are specific for cohort, case-control, or cross-sectional studies. A detailed Explanation and Elaboration document is published separately and is freely available on the Web sites of PLoS Medicine, Annals of Internal Medicine, and Epidemiology. We hope that the STROBE Statement will contribute to improving the quality of reporting of observational studies.
15,454 citations
30 Oct 1999
TL;DR: This paper found a strong consistent relationship between low socioeconomic status (SES) in early life and increased fatness in adulthood, but in studies which attempted to address potential confounding by gestational age, parental fatness, or social group, the relationship was less consistent.
Abstract: OBJECTIVE
To identify factors in childhood which might influence the development of obesity in adulthood.
BACKGROUND
The prevalence of obesity is increasing in the UK and other developed countries, in adults and children. The adverse health consequences of adult obesity are well documented, but are less certain for childhood obesity. An association between fatness in adolescence and undesirable socio-economic consequences, such as lower educational attainment and income, has been observed, particularly for women. Childhood factors implicated in the development of adult obesity therefore have far-reaching implications for costs to the health-services and economy.
SEARCH STRATEGY
In order to identify relevant studies, electronic databases--Medline, Embase, CAB abstracts, Psyclit and Sport Discus-were searched from the start date of the database to Spring 1998. The general search structure for electronic databases was (childhood or synonyms) AND (fatness or synonyms) AND (longitudinal or synonyms). Further studies were identified by citations in retrieved papers and by consultation with experts.
INCLUSION CRITERIA
Longitudinal observational studies of healthy children which included measurement of a risk factor in childhood (<18 y), and outcome measure at least 1 y later. Any measure of fatness, leanness or change in fatness or leanness was accepted. Measures of fat distribution were not included. Only studies with participants from an industrialized country were considered, and those concerning minority or special groups, e.g. Pima Indians or children born preterm, were excluded.
FINDINGS
Risk factors for obesity included parental fatness, social factors, birth weight, timing or rate of maturation, physical activity, dietary factors and other behavioural or psychological factors. Offspring of obese parent(s) were consistently seen to be at increased risk of fatness, although few studies have looked at this relationship over longer periods of childhood and into adulthood. The relative contributions of genes and inherited lifestyle factors to the parent-child fatness association remain largely unknown. No clear relationship is reported between socio-economic status (SES) in early life and childhood fatness. However, a strong consistent relationship is observed between low SES in early life and increased fatness in adulthood. Studies investigating SES were generally large but very few considered confounding by parental fatness. Women who change social class (social mobility) show the prevalence of obesity of the class they join, an association which is not present in men. The influence of other social factors such as family size, number of parents at home and childcare have been little researched. There is good evidence from large and reasonably long-term studies for an apparently clear relationship for increased fatness with higher birth weight, but in studies which attempted to address potential confounding by gestational age, parental fatness, or social group, the relationship was less consistent. The relationship between earlier maturation and greater subsequent fatness was investigated in predominantly smaller, but also a few large studies. Again, this relationship appeared to be consistent, but in general, the studies had not investigated whether there was confounding by other factors, including parental fatness, SES, earlier fatness in childhood, or dietary or activity behaviours. Studies investigating the role of diet or activity were generally small, and included diverse methods of risk factor measurement. There was almost no evidence for an influence of activity in infancy on later fatness, and inconsistent but suggestive evidence for a protective effect of activity in childhood on later fatness. No clear evidence for an effect of infant feeding on later fatness emerged, but follow-up to adulthood was rare, with only one study measuring fatness after 7y. Studies investigating diet in childhood were limited and inconc
1,196 citations