scholarly journals Puberty timing and adiposity change across childhood and adolescence: disentangling cause and consequence

2020 ◽  
Vol 35 (12) ◽  
pp. 2784-2792
Author(s):  
Linda M O’Keeffe ◽  
Monika Frysz ◽  
Joshua A Bell ◽  
Laura D Howe ◽  
Abigail Fraser

Abstract STUDY QUESTION Is earlier puberty more likely a result of adiposity gain in childhood than a cause of adiposity gain in adulthood? SUMMARY ANSWER Pre-pubertal fat mass is associated with earlier puberty timing but puberty timing is not associated with post-pubertal fat mass change. WHAT IS KNOWN ALREADY Age at puberty onset has decreased substantially in the last several decades. Whether reducing childhood adiposity prevents earlier puberty and if early puberty prevention itself also has additional independent benefits for prevention of adult adiposity is not well understood. STUDY DESIGN, SIZE, DURATION Prospective birth cohort study of 4176 participants born in 1991/1992 with 18 232 repeated measures of fat mass from age 9 to 18 years. PARTICIPANTS/MATERIALS, SETTING, METHODS We used repeated measures of height from 5 to 20 years to identify puberty timing (age at peak height velocity, aPHV) and repeated measures of directly measured fat mass from age 9 to 18 years, from a contemporary UK birth cohort study to model fat mass trajectories by chronological age and by time before and after puberty onset. We then examined associations of these trajectories with puberty timing separately in females and males. MAIN RESULTS AND THE ROLE OF CHANCE In models by chronological age, a 1-year later aPHV was associated with 20.5% (95% confidence interval (CI): 18.6–22.4%) and 23.4% (95% (CI): 21.3–25.5%) lower fat mass in females and males, respectively, at 9 years. These differences were smaller at age 18 years: 7.8% (95% (CI): 5.9–9.6%) and 12.4% (95% (CI): 9.6–15.2%) lower fat mass in females and males per year later aPHV. Trajectories of fat mass by time before and after puberty provided strong evidence for an association of pre-pubertal fat mass with puberty timing, and little evidence of an association of puberty timing with post-pubertal fat mass change. The role of chance is likely to be small in this study given the large sample sizes available. LIMITATIONS, REASONS FOR CAUTION Participants included in our analyses were more socially advantaged than those excluded. The findings of this work may not apply to non-White populations and further work examining associations of puberty timing and fat mass in other ethnicities is required. WIDER IMPLICATIONS OF THE FINDINGS Previous research has relied on self-reported measures of puberty timing such as age of voice breaking in males, has lacked data on pre-and post-pubertal adiposity together and relied predominantly on indirect measures of adiposity such as BMI. This has led to conflicting results on the nature and direction of the association between puberty timing and adiposity in females and males. Our work provides important clarity on this, suggesting that prevention of adiposity in childhood is key for prevention of early puberty, adult adiposity and associated cardiovascular risk. In contrast, our findings suggest that prevention of early puberty without prevention of childhood adiposity would have little impact on prevention of adult adiposity. STUDY FUNDING/COMPETING INTEREST(S) The UK Medical Research Council and Wellcome (Grant ref: 102215/2/13/2) and the University of Bristol provide core support for Avon Longitudinal Study of Parents and Children (ALSPAC). L.M.O.K. is supported by a UK Medical Research Council Population Health Scientist fellowship (MR/M014509/1) and a Health Research Board (HRB) of Ireland Emerging Investigator Award (EIA-FA-2019-007 SCaRLeT). J.A.B. is supported by the Elizabeth Blackwell Institute for Health Research, University of Bristol and the Wellcome Trust Institutional Strategic Support Fund (204813/Z/16/Z). L.D.H. and A.F. are supported by Career Development Awards from the UK Medical Research Council (grants MR/M020894/1 and MR/M009351/1, respectively). All authors work in a unit that receives funds from the UK Medical Research Council (grant MC_UU_00011/3, MC_UU_00011/6). No competing interests to declare. TRIAL REGISTRATION NUMBER N/A.

2019 ◽  
Author(s):  
Linda M O’Keeffe ◽  
Monika Frysz ◽  
Joshua A. Bell ◽  
Laura D. Howe ◽  
Abigail Fraser

AbstractObjectiveTo better understand if earlier puberty is more likely a result of adiposity gain in childhood than a cause of adiposity gain in adulthood.DesignProspective birth cohort study.SettingPopulation based study of children born in 1991/1992 in Bristol UK (Avon Longitudinal Study of Parents and Children (ALSPAC)).Participants4,186 participants (2,176 female and 1,990 male) of predominantly White ethnicity with 18,232 repeated measures throughout follow-up.Exposures & outcomesRepeated measures of height from 5y to 20y to identify puberty timing (age at peak height velocity) and repeated measures of dual-energy X-ray absorptiometry-derived fat mass from age 9y to 18y, modelled separately in females and males using models based on chronological age and time before and after puberty onset.ResultsMean age at peak height velocity was 11.7y (standard deviation (SD)=0.8y) for females and 13.6y (SD=0.9y) for males. In adjusted models of fat mass by chronological age, a one-year later age at peak height velocity was associated with 20.4% (95% Confidence Interval (CI): 18.5% to 22.3%) and 22.8% (95% (CI): 20.7% to 24.8%) lower fat mass in females and males respectively at 9y. These differences were smaller at age 18y: 7.8% (95% (CI):5.9% to 9.6%) and 11.9% (95% (CI): 9.1%, to 14.7%) lower fat mass in females and males respectively per year later age at peak height velocity. Trajectories of fat mass by time before and after puberty onset provided strong evidence for an association of pre-pubertal fat mass with puberty timing, and little evidence of an association of puberty timing with post-pubertal changes in fat mass in females. In males, findings were less clear before puberty though there was some evidence for an association of earlier puberty timing with great post-pubertal gain in fat mass.ConclusionsEarlier puberty is more likely a result of adiposity gain in childhood than a cause of adiposity gain in adulthood in females. In males early to puberty, differences in fat mass after puberty are driven partially by tracking of adiposity from early childhood but also greater gains in post-pubertal adiposity. Reducing levels of childhood adiposity may help prevent both earlier puberty, later life adiposity and their associated adverse social, mental and physical health sequelae.


2020 ◽  
Vol 4 (Supplement_2) ◽  
pp. 805-805
Author(s):  
Ebrima Bah ◽  
Frank Michelangeli

Abstract Objectives To find out the overlapping and correlating relationships between serum haptoglobin level, haptoglobin genotype and phenotype, blood haemoglobin level and zinc protoporphyrin (measured in washed RBCs) in association to prevalence of anaemia. It will focus on comparing all the mention components in contrast to each other. The study will also look for the frequency distribution of the major HP alleles. Methods 1278 participants were randomly selected. Blood samples collected by trained nurses. Data generation was done at the Medical research council (keneba field station) research site. Data Analysis was conducted at the university of Chester with the assistance of the computer department team. Results P = 0.000 indicating anaemia prevalence with HP 1 allele. P > 0.05 when ID, IDA and AI relates with HP genotype. Positive correlation between ZnPP and HP serum level, but negative between ZnPP and Hb. P = 0.000 between ZnPP and IDA. P = 0.024 between HP genotype and Hb level. P = 0.013 between HP genotype and HP serum. P = 0.100 between HP genotype and ZnPP. P = 0.000 between ZnPP and IDA. P = 0.024 between HP genotype and Hb. ZnPP shared a positive correlation with HP serum level, and a negative correlation with Hb level. The correlation significant = 0.01 level (2-tailed) P = 0.01. The correlation between HP genotype and HP serum level was significant with P = 0.013, but the correlation between HP genotype and ZnPP was not significant with P = 0.100. Conclusions HP genotype had association with anaemia prevalence and more occurrence was observed in carriers of the type ‘1’ allele. It had no association with ID, IDA and AI. HP genotype had association with HP serum level and Hb level but had no association with ZnPP level. ZnPP level was observed to have had association with HP serum level, Hb level and IDA; but had no association with ID and AI in the region. Funding Sources All the resources used in this study were from MRC Keneba (International Nutrition Group) which is supported by funds from the UK Medical Research Council (MRC) and the UK Department for International Development (DFID) under the MRC/DFID Concordat agreement (Hennig et al., 2015).


2015 ◽  
Vol 33 (15_suppl) ◽  
pp. 4002-4002 ◽  
Author(s):  
Derek Alderson ◽  
Ruth E Langley ◽  
Matthew Guy Nankivell ◽  
Jane M. Blazeby ◽  
Michael Griffin ◽  
...  

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