The pubertal growth spurt is diminished in children with severe obesity

Holmgren, Anton; Martos‐Moreno, Gabriel Ángel; Niklasson, Aimon; Martínez‐Villanueva, Julián; Argente, Jesús; Albertsson‐Wikland, Kerstin

doi:10.1038/s41390-020-01234-3

Cited by 13 publications

(19 citation statements)

References 35 publications

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“…We have confirmed previous observations pointing to accelerated skeletal maturation in children with obesity, resulting in a standardized height over their target height and directly correlated with the severity of obesity [12,13]. Interestingly, the follow up of a significant number of our patients over an extended period of time, some of them encompassing their entire pubertal development and growth spurt, confirms the lack of impairment of obesity-oriented intervention on growth and the attainment of adult height, which was equal to or slightly above that expected according to parental heights [13,14]. Additionally, we observed that the mean pubertal growth spurt in obesity is lower and inversely correlated with the severity of obesity.…”

Section: Influence Of Bmi On Puberty and Growthsupporting

confidence: 89%

“…At the same time the presence of obesity seems to abolish the differences between sexes in the degree of the growth spurt observed in physiological conditions. This could be related to the acceleration in skeletal maturation and the relative childhood overgrowth observed in these patients [12,13]. In contrast, the mean pubertal duration (3.23 years) and time from Tanner stage II to menarche in girls (1.65 years) were similar to that of the general population, despite the inverse correlation observed between obesity severity and duration of puberty.…”

Section: Influence Of Bmi On Puberty and Growthmentioning

confidence: 68%

“…An additional concern of parents upon intervention for childhood obesity is the potential effect on growth and pubertal development of their child. These patients usually exhibit some degree of advancement in skeletal maturation and overgrowth in relation to their target height [12,13] and this is directly correlated with the severity of their obesity and inversely proportional to the magnitude of their pubertal growth spurt [13] but does not impair the attainment of their predicted adult height [13][14][15]. Consequently, although severe caloric restriction is not usually included in childhood and adolescent obesity interventions [2,3] and evidence indicates that conventional strategies for weight control in this age range do not impair growth or puberty [15], this can be a factor underlying the reluctance of some parents to intervene.…”

Section: Introductionmentioning

confidence: 99%

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Conservative Treatment for Childhood and Adolescent Obesity: Real World Follow-Up Profiling and Clinical Evolution in 1300 Patients

et al. 2021

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Background: Limited therapeutic tools and an overwhelming clinical demand are the major limiting factors in pediatric obesity management. The optimal protocol, environment, body mass index (BMI) change targets and duration of obesity-oriented interventions remain to be elucidated. Aims: We aimed to characterize the singularities of follow-up, anthropometric and metabolic evolution of a large cohort of pediatric patients with obesity in a specialized university hospital outpatient obesity unit. Patients and methods: Follow-up duration (up to seven years), attrition rate and anthropometric and metabolic evolution of 1300 children and adolescents with obesity were studied. An individualized analysis was conducted in patients attaining a high level of weight loss (over 1.5 BMI-SDS (standard deviation score) and/or 10% of initial weight; n = 252; 19.4%) as well as in “metabolically healthy” patients (n = 505; 38.8%). Results: Attrition rate was high during the early stages (11.2% prior to and 32.5% right after their initial metabolic evaluation). Mean follow-up time was 1.59 ± 1.60 years (7% of patients fulfilled 7 years). The highest BMI reduction occurred in the first year (−1.11 ± 0.89 SDS, p < 0.001 in 72.5% of patients). At the end of the follow-up, improvements in glucose and lipid metabolism parameters were observed (both p < 0.05), that were highest in patients with the greatest weight reduction (all p < 0.01), independent of the time spent to achieve weight loss. The pubertal growth spurt negatively correlated with obesity severity (r = −0.38; p < 0.01) but patients attaining adult height exceeded their predicted adult height (n = 308, +1.6 ± 5.4 cm; p < 0.001). “Metabolically healthy” patients, but with insulin resistance, had higher blood pressure, glucose, uric acid and triglyceride levels than those without insulin resistance (all p < 0.05). Preservation of the “metabolically healthy” status was associated with BMI improvement. Conclusions: Behavioral management of children with obesity can be effective and does not impair growth but is highly conditioned by high attrition. The best results regarding BMI reduction and metabolic improvement are achieved in the first year of intervention and can be preserved if follow-up is retained.

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Section: Influence Of Bmi On Puberty and Growthsupporting

confidence: 89%

Section: Influence Of Bmi On Puberty and Growthmentioning

confidence: 68%

Section: Introductionmentioning

confidence: 99%

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Conservative Treatment for Childhood and Adolescent Obesity: Real World Follow-Up Profiling and Clinical Evolution in 1300 Patients

et al. 2021

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“…Bone age was also related to pubertal growth, and a strong linear correlation between accelerated bone age and low specific pubertal height gain was seen. 52…”

Section: Pubertal Growth Related To Bmi In Childhoodmentioning

confidence: 99%

The Quadratic‐Exponential‐Pubertal‐Stop model is valid for analysing human growth patterns and developing novel growth references

Holmgren

2021

Acta Paediatrica

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Like most important aspects of human life, human growth depends on both nature and nurture and this review mainly relates to height and changes in height and growth patterns over time. 1 Broadly speaking, human growth periods can be divided into foetal, infancy, childhood and puberty. 1,2 The most rapid period is during foetal life, and then, height velocity starts to decline after birth. Growth continues to be rapid during early infancy, then reduces in velocity until the pubertal growth spurt. Once adolescent peak height velocity

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“…En la obesidad infantil es habitual una EO acelerada respecto a la EC (19). En contraposición, la presencia de talla alta junto con la referida aceleración de la maduración esquelética, pueden ayudar a evaluar correctamente el patrón de crecimiento de los niños y adolescentes afectos de obesidad, en los que la aceleración de crecimiento durante la pubertad («estirón puberal») se correlaciona negativamente con la gravedad de su obesidad y con el grado de aceleración de su maduración esquelética (22,25).…”

Section: Exámenes Complementariosunclassified

Precision medicine in childhood obesities

Martos‐Moreno

Argente

2021

an. ranm

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Obesity is currently one of the most common consultations in pediatrics due to its high prevalence rate in our environment. Even though an impaired balance between caloric intake and energy expenditure underlies the excessive accumulation of adipose tissue in most cases of childhood and adolescent obesity, there is a high interindividual variability in the susceptibility to develop obesity, which is based largely on each person’s singular genetic background. Advances in our understanding of the latter arise from the progressive unravelling of the pathophysiological bases of the mechanisms involved in the control of appetite, satiety, and energy expenditure. An important body of evidence in this field has derived from the study of an increasing number of cases of obesity with proven genetic (either syndromic or not), endocrinological or secondary etiology. Consequently, we now need to speak in term of «childhood obesities» when referring to the common phenotypic trait of excessive adipose tissue accumulation as the underlying pathophysiological bases are widely different between subjects; thus, individualized diagnostic and management approaches both, for obesity itself as for its associated comorbidities are required. Furthermore, the advances made in identifying patients with monogenic diseases cosegregating with the phenotype of obesity have considerably increased the modern pathophysiological bases of obesity. Therefore, it is imperative to individualize the diagnostic strategy, thus leading to a relevant change in the therapeutic approach. In fact, the results obtained by using the analog of melanocortin, setmelanotide, in patients with POMC (proopiomelanocortin), LEPR (leptin receptor) and PCSK1 (proprotein concertase subtilisin-kexin type 1) deficiency, and more recently studies of the structure and architecture of the MC4R (melanocortin receptor number 4), may allow a more precise analysis of the effects of the loss-of-function mutations in MC4R associated to obesity, as well as structural prediction of their responsiveness to setmelanotide, leading to a personalized therapy based on precision medicine.

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The pubertal growth spurt is diminished in children with severe obesity

Cited by 13 publications

References 35 publications

Conservative Treatment for Childhood and Adolescent Obesity: Real World Follow-Up Profiling and Clinical Evolution in 1300 Patients

Conservative Treatment for Childhood and Adolescent Obesity: Real World Follow-Up Profiling and Clinical Evolution in 1300 Patients

The Quadratic‐Exponential‐Pubertal‐Stop model is valid for analysing human growth patterns and developing novel growth references

Precision medicine in childhood obesities

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