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Current Hypertension Reports Jul 2023Puberty is a complex process leading to physical, sexual, and psychosocial maturation. The changes in morphology and organ function during puberty also affect blood... (Review)
Review
Puberty is a complex process leading to physical, sexual, and psychosocial maturation. The changes in morphology and organ function during puberty also affect blood pressure (BP) regulation, and as a consequence (BP) values change noticeably, reaching values often higher than after reaching full maturity. In children entering puberty, BP, especially systolic, increases and then reaches adult values by the end of puberty. The mechanisms responsible for this process are complex and not fully understood. Sex hormones, growth hormone, insulin-like growth factor-1, and insulin, whose production increases during puberty, significantly regulate BP through complex and overlapping mechanisms. During puberty, the incidence of arterial hypertension also increases, especially in children with excess body weight. The present paper presents the current state of knowledge regarding the influence of processes occurring during puberty on blood pressure.
Topics: Child; Adult; Humans; Blood Pressure; Hypertension; Body Mass Index; Puberty; Gonadal Steroid Hormones
PubMed: 37071287
DOI: 10.1007/s11906-023-01241-9 -
Hormones and Behavior Jul 2013This article is part of a Special Issue "Puberty and Adolescence". Adolescence is characterized by a variety of behavioral alterations, including elevations in... (Review)
Review
This article is part of a Special Issue "Puberty and Adolescence". Adolescence is characterized by a variety of behavioral alterations, including elevations in novelty-seeking and experimentation with alcohol and other drugs of abuse. Some adolescent-typical neurobehavioral alterations may depend upon pubertal rises in gonadal hormones, whereas others may be unrelated to puberty. Using a variety of approaches, studies in laboratory animals have not revealed clear relationships between pubertal-related changes and adolescent- or adult-typical behaviors that are not strongly sexually dimorphic. Data reviewed suggest surprisingly modest influences of gonadal hormones on alcohol intake, alcohol preference and novelty-directed behaviors. Gonadectomy in males (but not females) increased ethanol intake in adulthood following surgery either pre-pubertally or in adulthood, with these increases in intake largely reversed by testosterone replacement in adulthood, supporting an activational role of androgens in moderating ethanol intake in males. In contrast, neither pre-pubertal nor adult gonadectomy influenced sensitivity to the social inhibitory or aversive effects of ethanol when indexed via conditioned taste aversions, although gonadectomy at either age altered the microstructure of social behavior of both males and females. Unexpectedly, the pre-pubertal surgical manipulation process itself was found to increase later ethanol intake, decrease sensitivity to ethanol's social inhibitory effects, attenuate novelty-directed behavior and lower social motivation, with gonadal hormones being necessary for these long-lasting effects of early surgical perturbations.
Topics: Adolescent; Adolescent Behavior; Adult; Castration; Female; Gonadal Hormones; Humans; Male; Mental Disorders; Puberty
PubMed: 23998677
DOI: 10.1016/j.yhbeh.2012.11.012 -
International Journal of Molecular... Mar 2021Chronic stress is encountered in our everyday life and is thought to contribute to a number of diseases. Many of these stress-related disorders display a sex bias.... (Review)
Review
Chronic stress is encountered in our everyday life and is thought to contribute to a number of diseases. Many of these stress-related disorders display a sex bias. Because glucocorticoid hormones are the main biological mediator of chronic stress, researchers have been interested in understanding the sexual dimorphism in glucocorticoid stress response to better explain the sex bias in stress-related diseases. Although not yet demonstrated for glucocorticoid regulation, sex chromosomes do influence sex-specific biology as soon as conception. Then a transient rise in testosterone start to shape the male brain during the prenatal period differently to the female brain. These organizational effects are completed just before puberty. The cerebral regions implicated in glucocorticoid regulation at rest and after stress are thereby impacted in a sex-specific manner. After puberty, the high levels of all gonadal hormones will interact with glucocorticoid hormones in specific crosstalk through their respective nuclear receptors. In addition, stress occurring early in life, in particular during the prenatal period and in adolescence will prime in the long-term glucocorticoid stress response through epigenetic mechanisms, again in a sex-specific manner. Altogether, various molecular mechanisms explain sex-specific glucocorticoid stress responses that do not exclude important gender effects in humans.
Topics: Adolescent; Animals; Child; Child Development; Embryonic Development; Genetic Association Studies; Glucocorticoids; Gonadal Hormones; Humans; Hydrocortisone; Puberty; Sex Characteristics; Sex Factors; Steroids; Stress, Physiological; Stress, Psychological
PubMed: 33808655
DOI: 10.3390/ijms22063139 -
Annals of the New York Academy of... Jun 2004Puberty is accompanied by a number of changes, among them increased risk for development of major depression. The most common etiology of major depression is stressful... (Review)
Review
Puberty is accompanied by a number of changes, among them increased risk for development of major depression. The most common etiology of major depression is stressful life events, being present in approximately 90% of first episodes of depression. The hypothalamic-pituitary-adrenal (HPA) axis is one of the major systems involved in responses to stress, and this system is clearly influenced by ovarian hormones. Normal women demonstrate resistance to negative feedback of both cortisol in the fast-feedback paradigm and dexamethasone in the standard delayed-feedback paradigm. Depressed premenopausal women show greater increases in baseline cortisol than postmenopausal depressed women and than depressed men. Studies in rodents suggest a similar resistance to glucocorticoid feedback but suggest that estradiol can function to inhibit stress responsiveness. Studies of premenopausal depressed women demonstrate lower estradiol, which suggests that there is less inhibitory feedback of estradiol on the HPA axis, while normal progesterone continues to augment stress responses further. The onset of these reproductive hormonal changes modulating stress systems at puberty may sensitize girls to stressful life events, which become more frequent at the transition to puberty and young adulthood.
Topics: Animals; Female; Glucocorticoids; Humans; Hypothalamo-Hypophyseal System; Ovary; Pituitary-Adrenal System; Puberty; Sex Characteristics; Steroids; Stress, Physiological
PubMed: 15251881
DOI: 10.1196/annals.1308.013 -
Annual Review of Psychology Jan 2019The assumption that early stress leads to dysregulation and impairment is widespread in developmental science and informs prevailing models (e.g., toxic stress). An... (Review)
Review
The assumption that early stress leads to dysregulation and impairment is widespread in developmental science and informs prevailing models (e.g., toxic stress). An alternative evolutionary-developmental approach, which complements the standard emphasis on dysregulation, proposes that early stress may prompt the development of costly but adaptive strategies that promote survival and reproduction under adverse conditions. In this review, we survey this growing theoretical and empirical literature, highlighting recent developments and outstanding questions. We review concepts of adaptive plasticity and conditional adaptation, introduce the life history framework and the adaptive calibration model, and consider how physiological stress response systems and related neuroendocrine processes may function as plasticity mechanisms. We then address the evolution of individual differences in susceptibility to the environment, which engenders systematic person-environment interactions in the effects of stress on development. Finally, we discuss stress-mediated regulation of pubertal development as a case study of how an evolutionary-developmental approach can foster theoretical integration.
Topics: Adaptation, Physiological; Allostasis; Biological Evolution; Human Development; Humans; Puberty; Stress, Psychological
PubMed: 30125133
DOI: 10.1146/annurev-psych-122216-011732 -
Deutsches Arzteblatt International Apr 2009Puberty is an extremely important phase in the physical and psychosocial development of the adolescent. (Review)
Review
BACKGROUND
Puberty is an extremely important phase in the physical and psychosocial development of the adolescent.
METHODS
Selective literature review.
RESULTS
The diagnosis of abnormal puberty requires thorough knowledge of normal pubertal development and of the variations of normal puberty as well as its pathology. Variations of normal pubertal development can be expected, by definition, to occur at a frequency of roughly 3%. A detailed history is the first step in the diagnostic evaluation of a normal variant or an abnormal puberty. Further evaluation includes laboratory testing (estradiol, testosterone, and the results of a GnRH test, among others) and imaging studies (x-ray of the left hand and wrist, ultrasonography of the gonads, magnetic resonance imaging). Treatment is directed at both the acute and the long-term consequences of precocious, markedly delayed, or absent pubertal development.
CONCLUSIONS
Disorders of pubertal development should be recognized early, correctly diagnosed by a pediatric endocrinologist, and appropriately treated.
Topics: Adolescent; Adult; Child; Female; Humans; Male; Puberty; Puberty, Delayed; Puberty, Precocious; Young Adult
PubMed: 19547638
DOI: 10.3238/arztebl.2009.0295 -
Molecules and Cells Feb 2019Androgens act in almost all tissues throughout the lifetime and have important roles in skeletal muscles. The levels of androgens increase during puberty and remain... (Review)
Review
Androgens act in almost all tissues throughout the lifetime and have important roles in skeletal muscles. The levels of androgens increase during puberty and remain sustained at high levels in adulthood. Because androgens have an anabolic effect on skeletal muscles and muscle stem cells, these increased levels of androgens after puberty should lead to spontaneous muscle hypertrophy and hyperplasia in adulthood. However, the maintenance of muscle volume, myonuclei number per myofiber, and quiescent state of satellite cells in adulthood despite the high levels of androgens produces paradoxical outcomes. Our recent study revealed that the physiological increase of androgens at puberty initiates the transition of muscle stem cells from proliferation to quiescence by the androgen-Mindbomb1-Notch signaling axis. This newly discovered androgen action on skeletal muscles underscores the physiological importance of androgens on muscle homeostasis throughout life. This review will provide an overview of the new androgen action on skeletal muscles and discuss the paradoxical effects of androgens suggested in previous studies.
Topics: Androgens; Animals; Humans; Models, Biological; Muscle, Skeletal; Myoblasts; Puberty; Signal Transduction
PubMed: 30759971
DOI: 10.14348/molcells.2019.0004 -
Human Reproduction Update Aug 2022Globally, the ages at pubertal onset for girls and boys have been decreasing during recent decades, partly attributed to excess body fat accumulation. However, a growing... (Meta-Analysis)
Meta-Analysis
BACKGROUND
Globally, the ages at pubertal onset for girls and boys have been decreasing during recent decades, partly attributed to excess body fat accumulation. However, a growing body of literature has recognized that endocrine disrupting chemicals (EDCs) may play an important role in this global trend, but the association has not yet been fully established.
OBJECTIVE AND RATIONALE
EDCs can interfere with normal hormone function and metabolism and play a role in pubertal onset. We aimed to systematically identify and evaluate the current evidence on the timing of pubertal onset in girls and boys following prenatal or postnatal exposures to xenobiotic EDCs.
SEARCH METHODS
Following PRISMA guidelines, we performed a systematic literature search of original peer-reviewed publications in the PubMed database through a block search approach using a combination of index MeSH and free text search terms. Publications were considered if they covered biomarkers of prenatal or postnatal exposures to xenobiotic EDCs (European Commission's list of category 1 EDCs) measured in maternal or child biospecimen and pubertal onset defined by the progression of the following milestones (and assessed in terms of the following measures): menarche (age), thelarche (Tanner staging) and pubarche (Tanner staging), in girls, and genital stage (Tanner staging), testicular volume (ml) and pubarche (Tanner staging), in boys.
OUTCOMES
The literature search resulted in 703 references, of which we identified 52 publications fulfilling the eligibility criteria for the qualitative trend synthesis and 23 publications for the meta-analysis. The qualitative trend synthesis provided data on 103 combinations of associations between prenatal or postnatal exposure to EDC compounds groups and puberty outcomes and the meta-analysis enabled 18 summary risk estimates of meta-associations.
WIDER IMPLICATIONS
Statistically significant associations in the qualitative trend synthesis suggested that postnatal exposure to phthalates may be associated with earlier thelarche and later pubarche. However, we did not find consistent evidence in the meta-analysis for associations between timing of pubertal onset in girls and boys and exposures to any of the studied xenobiotic EDCs. We were not able to identify specific pre- or postnatal windows of exposure as particularly critical and susceptible for effects of EDCs. Current evidence is subject to several methodological challenges and inconsistencies and evidence on specific exposure-outcome associations remains too scarce to firmly confirm EDC exposure as a risk factor for changes in age of pubertal onset in the general child population. To create a more uniform foundation for future comparison of evidence and to strengthen pooled studies, we recommend the use of more standardized approaches in the choice of statistical analyses, with exposure transformations, and in the definitions and assessments of puberty outcomes. The impact of mixtures of EDC exposures on the association also remains unestablished and would be valuable to elucidate for prenatal and postnatal windows of exposure. Future large, longitudinal epidemiological studies are needed to clarify the overall association.
Topics: Child; Endocrine Disruptors; Female; Humans; Longitudinal Studies; Male; Menarche; Pregnancy; Puberty; Xenobiotics
PubMed: 35466359
DOI: 10.1093/humupd/dmac013 -
Journal of Clinical Research in... 2011The onset and course of puberty are under the control of the neuroendocrine system. Factors affecting the timing and regulation of the functions of this system may alter... (Review)
Review
The onset and course of puberty are under the control of the neuroendocrine system. Factors affecting the timing and regulation of the functions of this system may alter the onset and course of puberty. Several environmental endocrine disruptors (EDs) with significant influences on the normal course of puberty have been identified. Numerous animal and human studies concerning EDs have been conducted showing that these substances may extensively affect human health; nevertheless, there are still several issues that remain to be clarified. In this paper, the available evidence from animal and human studies on the effects of environmental EDs with the potential to cause precocious or delayed puberty was reviewed.
Topics: Animals; Endocrine Disruptors; Environmental Pollutants; Humans; Puberty
PubMed: 21448326
DOI: 10.4274/jcrpe.v3i1.01 -
The Journal of Endocrinology Sep 2022Girls with obesity are at increased risk of early puberty. Obesity is associated with insulin resistance and hyperinsulinemia. We hypothesized that insulin plays a...
Girls with obesity are at increased risk of early puberty. Obesity is associated with insulin resistance and hyperinsulinemia. We hypothesized that insulin plays a physiological role in pubertal transition, and super-imposed hyperinsulinemia due to childhood obesity promotes early initiation of puberty in girls. To isolate the effect of hyperinsulinemia from adiposity, we compared pre-pubertal and pubertal states in hyperinsulinemic, lean muscle (M)-insulin-like growth factor 1 receptor (IGF-1R)-lysine (K)-arginine (R) (MKR) mice to normoinsulinemic WT, with puberty onset defined by vaginal opening (VO). Our results show MKR had greater insulin resistance and higher insulin levels (P < 0.05) than WT despite lower body weight (P < 0.0001) and similar IGF-1 levels (P = NS). Serum luteinizing hormone (LH) levels were higher in hyperinsulinemic MKR (P = 0.005), and insulin stimulation induced an increase in LH levels in WT. VO was earlier in hyperinsulinemic MKR vs WT (P < 0.0001). When compared on the day of VO, kisspeptin expression was higher in hyperinsulinemic MKR vs WT (P < 0.05), and gonadotropin-releasing hormone and insulin receptor isoform expression was similar (P = NS). Despite accelerated VO, MKR had delayed, disordered ovarian follicle and mammary gland development. In conclusion, we found that hyperinsulinemia alone without adiposity triggers earlier puberty. In our study, hyperinsulinemia also promoted dyssynchrony between pubertal initiation and progression, urging future studies in girls with obesity to assess alterations in transition to adulthood.
Topics: Animals; Female; Humans; Hyperinsulinism; Insulin; Insulin Resistance; Mice; Pediatric Obesity; Puberty
PubMed: 35904489
DOI: 10.1530/JOE-21-0447