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Proceedings. Biological Sciences May 2011I apply evolutionary perspectives and conceptual tools to analyse central issues underlying child health, with emphases on the roles of human-specific adaptations and... (Review)
Review
I apply evolutionary perspectives and conceptual tools to analyse central issues underlying child health, with emphases on the roles of human-specific adaptations and genomic conflicts in physical growth and development. Evidence from comparative primatology, anthropology, physiology and human disorders indicates that child health risks have evolved in the context of evolutionary changes, along the human lineage, affecting the timing, growth-differentiation phenotypes and adaptive significance of prenatal stages, infancy, childhood, juvenility and adolescence. The most striking evolutionary changes in humans are earlier weaning and prolonged subsequent pre-adult stages, which have structured and potentiated maladaptations related to growth and development. Data from human genetic and epigenetic studies, and mouse models, indicate that growth, development and behaviour during pre-adult stages are mediated to a notable degree by effects from genomic conflicts and imprinted genes. The incidence of cancer, the primary cause of non-infectious childhood mortality, mirrors child growth rates from birth to adolescence, with paediatric cancer development impacted by imprinted genes that control aspects of growth. Understanding the adaptive significance of child growth and development phenotypes, in the context of human-evolutionary changes and genomic conflicts, provides novel insights into the causes of disease in childhood.
Topics: Adaptation, Biological; Adolescent; Adolescent Development; Biological Evolution; Child; Child Development; Child, Preschool; Genomic Imprinting; Health; Humans; Infant; Puberty; Risk Factors; Time Factors
PubMed: 21288946
DOI: 10.1098/rspb.2010.2627 -
Reproductive Toxicology (Elmsford, N.Y.) Apr 2014Recent studies indicate that the onset of puberty is occurring at increasingly younger ages. Many etiologies have been hypothesized to be involved, but environmental... (Review)
Review
Recent studies indicate that the onset of puberty is occurring at increasingly younger ages. Many etiologies have been hypothesized to be involved, but environmental exposures are among the most worrisome. Multiple organizations have endorsed the need to study and provide clinical awareness regarding the effect of a child's environment on pubertal timing. This review article summarizes the current understanding of the major environmental influences on pubertal timing, focusing on factors for which the most scientific evidence exists. The research reviewed addresses intrinsic factors unique to each individual, naturally occurring endocrine disruptors and chemical endocrine disruptors. In each category, evidence was found for and against the involvement of specific environmental factors on pubertal timing. Ultimately, an individual's environment is likely comprised of many aspects that collectively contribute to the timing of puberty. The need for research aimed at elucidating the effects of numerous specific yet disparate forms of exposures is emphasized.
Topics: Animals; Endocrine Disruptors; Environment; Environmental Exposure; Environmental Pollutants; Humans; Puberty
PubMed: 23602892
DOI: 10.1016/j.reprotox.2013.03.012 -
Biology of Reproduction Jan 2019Acquisition of reproductive maturity involves one of the most important series of developmental events in an organism's life. The beginning of adolescence is marked by... (Review)
Review
Acquisition of reproductive maturity involves one of the most important series of developmental events in an organism's life. The beginning of adolescence is marked by the onset of puberty. Puberty is the continuum of physical changes through which an infantile body matures into an adult capable of reproduction. This is a period of increased brain plasticity, where processes of re-wiring, neuronal proliferation, and pruning are enhanced. The initiation of mammalian puberty requires an increased pulsatile release of gonadotropin-releasing hormone from the hypothalamus. Puberty is regulated by neuroendocrine, genetic, and epigenetic factors. The maturation and function of the reproductive axis are highly sensitive to the energy status of the organism and sophisticated mechanisms exist to inhibit the axis in unfavorable energetic or metabolic conditions.In this review, we will focus on the impact of alcohol and obesity on reproductive outcomes, with emphasis on their effects on the timing of puberty. In the case of obesity, conflictive data are found, and while in females the association of overnutrition with advanced onset of puberty is consistent, in males, discrepant results have been reported. Concerning alcohol exposure, compelling evidence has documented a delay in the onset of puberty. We will present here data from both clinical studies and research involving preclinical models, which do not only delineate the impact of these conditions on the timing of puberty and potential underlying mechanisms, but that may help to define better strategies for the rational management of puberty disorders, especially of metabolic origin.
Topics: Adolescent; Adult; Age of Onset; Alcohol Drinking; Animals; Ethanol; Female; Humans; Male; Pediatric Obesity; Puberty; Sexual Maturation; Time Factors
PubMed: 30052777
DOI: 10.1093/biolre/ioy168 -
Frontiers in Endocrinology 2020The fetal hypothalamus-pituitary gonadal (HPG) axis begins to function during mid-gestation but its activity decreases during late pregnancy due to the suppressive... (Review)
Review
The fetal hypothalamus-pituitary gonadal (HPG) axis begins to function during mid-gestation but its activity decreases during late pregnancy due to the suppressive effects of placental estrogens. Placental hormones drop immediately after birth, FSH and LH surge at around 1 week and peak between 1 and 3 months of life. The HPG axis is activated in both sexes, but a sexual dimorphism is evident with higher LH values in boys, while FSH prevails in girls. Both gonadotrophins decline in boys by around 6 months of age. In girls, LH declines at the same time as in boys, while FSH persists elevated up to 3 or 4 years of age. As a result of gonadotropin activation, testicular testosterone increases in males and ovarian estradiol rises in females. These events clinically translate into testicular and penile growth in boys, enlargement of uterus and breasts in girls. The functional impact of HPG axis activity in infancy on later reproductive function is uncertain. According to the perinatal programming theory, this period may represent an essential programming process. In boys, long-term testicular hormonal function and spermatogenesis seem to be, at least in part, regulated by minipuberty. On the contrary, the role of minipuberty in girls is still uncertain. Recently, androgen exposure during minipuberty has been correlated with later sex-typed behavior. Premature and/or SGA infants show significant differences in postnatal HPG axis activity in comparison to full-term infants and the consequences of these differences on later health and disease require further research. The sex-dimorphic HPG activation during mid-gestation is probably responsible for the body composition differences observed ad birth between boys and girls, with boys showing greater total body mass and lean mass, and a lower proportion of fat mass. Testosterone exposure during minipuberty further contributes to these differences and seems to be responsible for the significantly higher growth velocity observed in male infants. Lastly, minipuberty is a valuable "window of opportunity" for differential diagnosis of disorders of sex development and it represents the only time window before puberty when congenital hypogonadism can be diagnosed by the simple analysis of basal gonadotropin and gonadal hormone levels.
Topics: Child, Preschool; Female; Gonads; Humans; Hypothalamo-Hypophyseal System; Male; Puberty; Sexual Maturation; Signal Transduction
PubMed: 32318025
DOI: 10.3389/fendo.2020.00187 -
The Journal of Adolescent Health :... Sep 2021On average, boys have lower academic achievement than girls. We investigated whether the timing of puberty is associated with academic achievement, and whether later...
PURPOSE
On average, boys have lower academic achievement than girls. We investigated whether the timing of puberty is associated with academic achievement, and whether later puberty among boys contributes to the sex difference in academic achievement.
METHOD
Examination scores at age 16 were studied among 13,477 British twins participating in the population-based Twins Early Development Study. A pubertal development scale, a height-based proxy of growth spurt, and age at menarche were used as indicators of puberty. Associations between puberty, sex, and academic achievement were estimated in phenotypic mediation models and biometric twin models.
RESULTS
Earlier puberty was associated with higher academic achievement both in boys and girls. The exception was early age at menarche in girls, which associated with lower academic achievement. More than half of the sex differences in academic achievement could be linked to sex differences in pubertal development, but part of this association appeared to be rooted in prepubertal differences. The biometric twin modelling indicated that the association between puberty and academic achievement was due to shared genetic risk factors. Genetic influences on pubertal development accounted for 7%-8% of the phenotypic variation in academic achievement.
CONCLUSIONS
Pubertal maturation relates to the examination scores of boys and of girls. This can give genes related to pubertal maturation an influence on outcomes in education and beyond. Sex differences in pubertal maturation can explain parts of the sex difference in academic achievement. Grading students when they are immature may not accurately measure their academic potential.
Topics: Academic Success; Adolescent; Female; Humans; Male; Menarche; Puberty; Sex Characteristics; Twins
PubMed: 33795203
DOI: 10.1016/j.jadohealth.2021.02.001 -
American Journal of Epidemiology Nov 2022Earlier puberty has been associated with numerous adverse mental, emotional, and physical health outcomes. Obesity is a known risk factor for earlier puberty in girls,...
Earlier puberty has been associated with numerous adverse mental, emotional, and physical health outcomes. Obesity is a known risk factor for earlier puberty in girls, but research with boys has yielded inconsistent findings. We examined sex- and race/ethnicity-specific associations between childhood obesity and puberty in a multiethnic cohort of 129,824 adolescents born at a Kaiser Permanente Northern California medical facility between 2003 and 2011. We used Weibull regression models to explore associations between childhood obesity and breast development onset (thelarche) in girls, testicular enlargement onset (gonadarche) in boys, and pubic hair development onset (pubarche) in both sexes, adjusting for important confounders. Clear dose-response relationships were observed. Boys with severe obesity had the greatest risk for earlier gonadarche (hazard ratio = 1.23, 95% confidence limit: 1.15, 1.32) and pubarche (hazard ratio = 1.44, 95% confidence limit: 1.34, 1.55), while underweight boys had delayed puberty compared with peers with normal body mass index. A similar dose-response relationship was observed in girls. There were significant interactions between childhood body mass index and race/ethnicity. Childhood obesity is associated with earlier puberty in both boys and girls, and the magnitude of the associations may vary by race/ethnicity. Prevention of childhood obesity may delay pubertal timing and mitigate health risks associated with both conditions.
Topics: Adolescent; Male; Female; Child; Humans; Pediatric Obesity; Ethnicity; Puberty; Body Mass Index; Puberty, Precocious
PubMed: 35998084
DOI: 10.1093/aje/kwac148 -
Human Reproduction Update 2001The secular changes in growth and maturation can be seen as indicators of socio-economic and health status. In most European countries the age of onset of puberty and of... (Review)
Review
The secular changes in growth and maturation can be seen as indicators of socio-economic and health status. In most European countries the age of onset of puberty and of menarcheal age has been decreasing during the past few decades. The duration of puberty seems also to decrease, though few studies provide sufficient data to support this postulation. The four Dutch nationwide growth surveys are useful examples assessing the secular trend in pubertal development over the past 45 years. Genetic and environmental factors contribute to the secular changes. Environmental factors seem to be the most important. Recently, attention has been given to substances with oestrogen-like actions that are present in nutrients. The possible role of these substances in growth and maturation is discussed.
Topics: Aging; Animals; Europe; Humans; Menarche; Puberty
PubMed: 11392375
DOI: 10.1093/humupd/7.3.287 -
Tidsskrift For Den Norske Laegeforening... May 2008Onset of puberty in boys is more complex than in girls, and delayed onset is the most common puberty complication in boys. This article presents the physiology of normal... (Review)
Review
BACKGROUND
Onset of puberty in boys is more complex than in girls, and delayed onset is the most common puberty complication in boys. This article presents the physiology of normal development of male puberty and the background for commonly associated disturbances.
MATERIAL AND METHOD
The article builds on clinical experience and relevant publications within pediatric endocrinology.
RESULTS AND INTERPRETATION
Mechanisms involved in pubertal development of gonads remain unclear despite intensive research. Height growth as well as the age for onset of puberty are influenced by environmental factors. Genetic factors are however more important determinants within a defined population and one usually inherits the probability for both early and delayed puberty. Gonadotropin releasing hormone (GnRH) neurons in the hypothalamus secrete GnRH in intermittent pulses to the pituitary glands that respond with pulsatile LH and FSH production. These neurons are thus decisive for testicle activity and therefore puberty development. GnRH-neurons are inactive during childhood because many types of hypothalamic neurons suppress them. Puberty starts when this suppression is reduced and kisspeptin-producing neurons stimulate GnRH neuron activity. At a testicle volume of 4 mL the Leydig cells' testosterone production has reached such a level that pubertal changes become apparent. Delayed or incomplete puberty sometimes occurs in certain syndromes, and complete lack of puberty can also be syndrome-related. Klinefelter's syndrome is associated with gonad dysgenesis expressed as gradual reduction of gonadal function starting after puberty. Cancer treatment during childhood; especially radiation therapy of the gonads, may cause hypogonadism and infertility. It is therefore essential to follow gonad function closely in these patients. In conclusion, each doctor treating children should be able to evaluate the degree of puberty development and when needed request adequate laboratory tests.
Topics: Adolescent; Adrenarche; Child; Disorders of Sex Development; Gonadotropin-Releasing Hormone; Growth Hormone; Humans; Hypogonadism; Male; Puberty; Sex Chromosome Disorders; Testis
PubMed: 18511972
DOI: No ID Found -
Annals of Clinical and Translational... Oct 2020To study the impact of gender, puberty, and pregnancy on the expression of POLG disease, one of the most common mitochondrial diseases known.
OBJECTIVE
To study the impact of gender, puberty, and pregnancy on the expression of POLG disease, one of the most common mitochondrial diseases known.
METHODS
Clinical, laboratory, and genetic data were collected retrospectively from 155 patients with genetically confirmed POLG disease recruited from seven European countries. We used the available data to study the impact of gender, puberty, and pregnancy on disease onset and deterioration.
RESULTS
We found that disease onset early in life was common in both sexes but there was also a second peak in females around the time of puberty. Further, pregnancy had a negative impact with 10 of 14 women (71%) experiencing disease onset or deterioration during pregnancy.
INTERPRETATION
Gender clearly influences the expression of POLG disease. While onset very early in life was common in both males and females, puberty in females appeared associated both with disease onset and increased disease activity. Further, both disease onset and deterioration, including seizure aggravation and status epilepticus, appeared to be associated with pregnancy. Thus, whereas disease activity appears maximal early in life with no subsequent peaks in males, both menarche and pregnancy appear associated with disease onset or worsening in females. This suggests that hormonal changes may be a modulating factor.
Topics: DNA Polymerase gamma; Europe; Female; Humans; Menarche; Mitochondrial Diseases; Pregnancy; Puberty; Retrospective Studies
PubMed: 32949115
DOI: 10.1002/acn3.51199 -
European Journal of Nutrition Feb 2022Early puberty is associated with adverse health outcomes. To identify potential modifiable factors for puberty timing, we examined the associations of prepubertal...
PURPOSE
Early puberty is associated with adverse health outcomes. To identify potential modifiable factors for puberty timing, we examined the associations of prepubertal childhood macronutrient intakes with puberty timing in boys and girls.
METHODS
In the Avon Longitudinal Study of Parents and Children, macronutrient intakes at age 6 years were predicted using random intercepts linear regression models of dietary data at 3, 4, 7 (assessed by food frequency questionnaires) and 7.5 years (by 3-day food diaries). Timings of puberty onset (Tanner stage 2 genital or breast (B2) development) and puberty completion (voice breaking (VB) or menarche) were calculated from annual parental and child reports at 8-17 years. Age at peak height velocity (PHV) was derived from repeated height measurements at 5-20 years. Linear regression models were fit to estimate the associations of total energy (TEI) and macronutrient intakes (carbohydrate, fat, protein) with puberty timing traits, adjusting for maternal and infant characteristics.
RESULTS
Among 3811 boys, higher TEI, but no macronutrient, was associated with earlier VB. Among 3919 girls, higher TEI was associated with earlier ages at B2, PHV, and menarche. Higher protein intake but not carbohydrate or fat intake (in energy partition models) and substitution of dietary protein for carbohydrate (in nutrient density and residual models) was associated with earlier B2, PHV, and menarche in girls. Findings were not attenuated on additional adjustment for body fat percentage during adolescence.
CONCLUSIONS
These findings suggest habitual total energy intakes in children, and protein intakes in girls, as potential modifiable determinants of puberty timing.
Topics: Child; Eating; Female; Humans; Longitudinal Studies; Male; Menarche; Puberty; United Kingdom
PubMed: 34232374
DOI: 10.1007/s00394-021-02629-6