Adiposity Rebound and the Development of Metabolic Syndrome

Koyama, Satomi; Ichikawa, Go; Kojima, Megumi; Shimura, Naoto; Sairenchi, Toshimi; Arisaka, Osamu

doi:10.1542/peds.2013-0966

Cited by 123 publications

(128 citation statements)

References 30 publications

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“…These results suggest that our patients developed AR earlier than normal subjects in whom AR usually occurs around 5-6 years of age [19,21]. As no significant difference was observed in AR onset between male and female patients ( Fig.…”

Section: Ar Was Not Associated With the Sex And The Gestational Ages supporting

confidence: 47%

Lower body weight and BMI at birth were associated with early adiposity rebound in 21-hydroxylase deficiency patients

et al. 2016

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21-HYDROXYLASE DEFICIENCY (21-OHD) isthe most common type of congenital adrenal hyperplasia (CAH). Its major clinical manifestations are adrenal crisis, virilization of external genitalia, short stature, and infertility due to adrenal androgen excess. A major part of the treatment for 21-OHD is glucocorticoid therapy, which reduces the excessive production of androgen and its metabolites by the adrenal gland [1][2][3].Obesity and metabolic syndrome during young adulthood are of serious concern for 21-OHD patients. Body mass index (BMI) is elevated in most 21-OHD patients [4,5] Abstract. 21-hydroxylase deficiency (21-OHD) is the most common type of congenital adrenal hyperplasia. In addition to the clinical problems caused by adrenal insufficiency and androgen excess, a risk for obesity and metabolic syndrome during young adulthood is a major ramification of the disease. Although glucocorticoid therapy is very likely to be one of the contributory factors, the precise causes of the metabolic status of adult 21-OHD patients remain to be clarified.Previously we reported that 21-OHD patients developed early onset AR, a condition which might create a risk for obesity and metabolic syndrome in adulthood. In order to elucidate the association between the onset of AR and factors during the fetal period to early infancy, we conducted a retrospective longitudinal analysis of 29 21-OHD patients (male: 14 cases, female: 15 cases, salt wasting type: 16, simple virilizing type: 13), who were identified by newborn screening and followed up at least until the age 10 years. Body size at birth, lower body weight, and lower BMI were found to precipitate the timing of AR. On the other hand, no significant association was observed between the timing of AR and sex, gestational age, treatment regimen (including cumulative dose of HDC), and disease severity (the type of the disease, the value of DHEA-S and 17-OHP). There are two points to consider: first, in 21-OHD patients treated with glucocorticoid substitution therapy, the risk for early AR cannot be reduced by adjusting the dose of glucocorticoid; second, fetal factors might affect the metabolic status of 21-OHD patients.Key words: 21-hydroxylase deficiency, Adiposity rebound, Glucocorticoid, Metabolic syndrome that adult 21-OHD patients tend to have metabolic syndrome [6,7]. Although the precise factors affecting the metabolic status of 21-OHD adults have not been identified, glucocorticoid therapy is thought to play some role [8,9]. 21-OHD patients require a supra-physiological dose of glucocorticoid in order to reduce the effects of androgen excess [10]. Previous reports including ours showed that the onset of adiposity rebound (AR), the point at which the BMI starts to increase after its nadir, occurred earlier in 21-OHD patients than in normal children [5,11]. Premature AR has been identified as one of the possible contributory factors in adult obesity and metabolic syndrome [9,7,[12][13][14][15][16]. We hypothesized that fetal and early infantile factors, including birth size...

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Section: Ar Was Not Associated With the Sex And The Gestational Ages supporting

confidence: 47%

Lower body weight and BMI at birth were associated with early adiposity rebound in 21-hydroxylase deficiency patients

et al. 2016

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“…Pediatrics 2014;134:e1354-e1361 AUTHORS: Adrienne R. Hughes Adiposity rebound (AR), 1 the period in childhood in which BMI begins to increase from a nadir, historically occurred between 5 and 7 years. 1,2 There is some evidence that early AR (defined as younger age at onset) predicts substantially increased risk of obesity in later life as defined by BMI [1][2][3][4][5][6] and other proxies for fat mass (waist circumference and skinfold thickness). [7][8][9] However, the literature on timing of AR and later risk of obesity is limited in many respects, consisting largely of older studies conducted before the pediatric obesity epidemic and/or of small studies with relatively short follow-up or with a limited range of outcomes (usually only proxies for obesity).…”

Section: Discussionmentioning

confidence: 99%

“…A detailed discussion of the early-life environmental factors associated with timing of AR is beyond the scope of the current study but has been discussed elsewhere. 2,5,24,25 A number of generally smaller and/or older studies have suggested that earlier AR increases obesity risk, as reviewed by Taylor et al 2 Arecentstudy by Koyama et al 6 found that an earlier AR (,4 years of age) was associated with a higher BMI and poorer cardiometabolic health at 12 years; however, the sample size was smaller than in the current study; BMI was measured at 12 years, whereas outcomes measured later in adolescence (as in the current study) are more likely to predict outcomes in adult life 26 ;a n dt h ei nfluence of early AR on directly measured…”

Section: Discussionmentioning

confidence: 99%

Timing of Adiposity Rebound and Adiposity in Adolescence

2014

PEDIATRICS

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This version is available at https://strathprints.strath.ac.uk/50659/ Strathprints is designed to allow users to access the research output of the University of Strathclyde. Unless otherwise explicitly stated on the manuscript, Copyright © and Moral Rights for the papers on this site are retained by the individual authors and/or other copyright owners. Please check the manuscript for details of any other licences that may have been applied. You may not engage in further distribution of the material for any profitmaking activities or any commercial gain. You may freely distribute both the url (https://strathprints.strath.ac.uk/) and the content of this paper for research or private study, educational, or not-for-profit purposes without prior permission or charge.Any correspondence concerning this service should be sent to the Strathprints administrator: strathprints@strath.ac.ukThe Strathprints institutional repository (https://strathprints.strath.ac.uk) is a digital archive of University of Strathclyde research outputs. It has been developed to disseminate open access research outputs, expose data about those outputs, and enable the management and persistent access to Strathclyde's intellectual output. Timing of Adiposity Rebound and Adiposity in AdolescenceWHAT'S KNOWN ON THIS SUBJECT: Earlier adiposity rebound may increase fatness in later life; however, there is limited evidence from large cohorts of contemporary children with direct measures of fatness in adolescence or adulthood. WHAT THIS STUDY ADDS:Early adiposity rebound is strongly associated with increased BMI and fatness in adolescence. Future preventive interventions should consider targeting early childhood to delay timing of adiposity rebound.abstract OBJECTIVES: To investigate associations between timing of adiposity rebound (AR; the period in childhood where BMI begins to increase from its nadir) and adiposity (BMI, fat mass) at age 15 years in the Avon Longitudinal Study of Parents and Children (ALSPAC). METHODS:The sample consisted of 546 children with AR derived in childhood and BMI and fat mass index (FMI; fat mass measured by dual-energy radiograph absorptiometry/height in m 2 ) measured at 15 years. Multivariable linear regression models were based on standardized residuals of log BMI and log FMI to allow comparison of regression coefficients across outcomes.RESULTS: There were strong dose-response associations between timing of AR and both adiposity outcomes at 15 years independent of confounders. BMI was markedly higher in adolescence for those with very early AR (by 3.5 years; b = 0.70; 95% confidence interval [CI]: 0.33-1.07; P # .001) and was also higher for those with early AR (between 3.5 and 5 years; b = 0.34; 95% CI: 0.08-0.59; P = .009) compared with those with later AR (.5 years) after full adjustment for a range of potential confounders. Similar magnitudes of association were found for FMI after full adjustment for confounders (compared with later AR: very early AR b = 0.74; 95% CI: 0.34-1.15; P # .001; early AR b = 0.35; 95% CI...

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“…1,2 There is some evidence that early AR (defined as younger age at onset) predicts substantially increased risk of obesity in later life as defined by BMI [1][2][3][4][5][6] and other proxies for fat mass (waist circumference and skinfold thickness). [7][8][9] However, the literature on timing of AR and later risk of obesity is limited in many respects, consisting largely of older studies conducted before the pediatric obesity epidemic and/or of small studies with relatively short follow-up or with a limited range of outcomes (usually only proxies for obesity).…”

mentioning

confidence: 99%

Timing of Adiposity Rebound and Adiposity in Adolescence

Hughes¹,

Sherriff²,

Ness³

et al. 2014

PEDIATRICS

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WHAT'S KNOWN ON THIS SUBJECT: Earlier adiposity rebound may increase fatness in later life; however, there is limited evidence from large cohorts of contemporary children with direct measures of fatness in adolescence or adulthood. WHAT THIS STUDY ADDS:Early adiposity rebound is strongly associated with increased BMI and fatness in adolescence. Future preventive interventions should consider targeting early childhood to delay timing of adiposity rebound. abstract OBJECTIVES: To investigate associations between timing of adiposity rebound (AR; the period in childhood where BMI begins to increase from its nadir) and adiposity (BMI, fat mass) at age 15 years in the Avon Longitudinal Study of Parents and Children (ALSPAC). METHODS:The sample consisted of 546 children with AR derived in childhood and BMI and fat mass index (FMI; fat mass measured by dual-energy radiograph absorptiometry/height in m 2 ) measured at 15 years. Multivariable linear regression models were based on standardized residuals of log BMI and log FMI to allow comparison of regression coefficients across outcomes.RESULTS: There were strong dose-response associations between timing of AR and both adiposity outcomes at 15 years independent of confounders. BMI was markedly higher in adolescence for those with very early AR (by 3.5 years; b = 0.70; 95% confidence interval [CI]: 0.33-1.07; P # .001) and was also higher for those with early AR (between 3.5 and 5 years; b = 0.34; 95% CI: 0.08-0.59; P = .009) compared with those with later AR (.5 years) after full adjustment for a range of potential confounders. Similar magnitudes of association were found for FMI after full adjustment for confounders (compared with later AR: very early AR b = 0.74; 95% CI: 0.34-1.15; P # .001; early AR b = 0.35; 95% CI: 0.07-0.63; P = .02).CONCLUSIONS: Early AR is strongly associated with increased BMI and FMI in adolescence. Preventive interventions should consider targeting modifiable factors in early childhood to delay timing of AR. Pediatrics

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Adiposity Rebound and the Development of Metabolic Syndrome

Cited by 123 publications

References 30 publications

Lower body weight and BMI at birth were associated with early adiposity rebound in 21-hydroxylase deficiency patients

Lower body weight and BMI at birth were associated with early adiposity rebound in 21-hydroxylase deficiency patients

Timing of Adiposity Rebound and Adiposity in Adolescence

Timing of Adiposity Rebound and Adiposity in Adolescence

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