Risk factors and preventive strategies for precocious puberty: a narrative review

Abstract

Precocious puberty (PP) is a common pediatric endocrine disorder with rising global incidence, significantly compromising children's quality of life and long-term health. Current therapeutic options remain limited in applicability, leaving many patients inadequately controlled. Prevention targeting known risk factors is substantially more cost-effective than post-diagnosis treatment; however, the available evidence on PP risk factors remains fragmented. This review systematically synthesizes the risk factors for PP across seven age stages—preconception period, fetal period, infancy, toddlerhood, preschool age, school age, and adolescence—and eight domains: genetic predisposition and family history, maternal conditions and prenatal factors, delivery mode and early feeding patterns, dietary behaviors and nutritional status, individual lifestyle habits, family/school/community environments, early clinical signs and indicators, and pre-existing and idiopathic medical conditions. Corresponding preventive strategies, including optimizing parental reproductive health, promoting balanced nutrition, physical activity, and psychosocial well-being, and fostering multi-sector collaboration, are briefly discussed. This review aims to raise awareness of PP risk factors and facilitate the implementation of preventive strategies.

1. Introduction

Precocious puberty (PP) is a common endocrine disorder in children and is typically defined as the onset of secondary sexual characteristics before 7.5 years of age in girls and 9.0 years in boys (1). The adverse effects of PP during childhood are mainly manifested by the early appearance of secondary sexual characteristics (e.g., breast development and menarche in girls and testicular enlargement in boys) and associated psychological problems (e.g., depression and anxiety) (2). These adverse effects may persist into adulthood and are primarily manifested as reduced final adult height. In addition, PP may increase the risk of reproductive system cancers and cardiovascular diseases, posing a potential threat to long-term health (3, 4). During the COVID-19 pandemic, children and adolescents experienced prolonged home confinement, and their lifestyles changed markedly, including increased use of electronic devices, reduced physical activity space, disrupted sleep patterns, and extended time spent with parents or caregivers. Many studies worldwide have reported a significant increase in the incidence of PP, and a substantial rise in cases has been observed globally during this period (5, 6). Therefore, the prevention and management of PP have become important public health concerns (7).

The pathogenesis of PP is complex and influenced by multiple factors, including intracranial diseases, endocrine disorders, and environmental risk factors. In clinical practice, most cases of PP are idiopathic; however, recent studies suggest that genetic background plays an increasingly important role and represents a congenital factor that should not be overlooked (8). In addition, the incidence of PP increased more rapidly during the COVID-19 pandemic than before, suggesting that lifestyle factors are also important acquired determinants of the onset and progression of PP (9, 10) The primary treatment for central precocious puberty (CPP) currently involves gonadotropin-releasing hormone analogues, such as triptorelin and leuprolide (11). However, the clinical use of these agents is limited by strict indications and contraindications, a treatment duration that typically exceeds two years, and high costs, which restrict their widespread application (12).

Compared with clinical treatment after diagnosis, preventive interventions targeting potential risk factors for PP may provide greater economic and public health benefits (13). However, significant gaps remain in the prevention of PP. To date, studies on the risk factors for PP remain fragmented, and a clear and systematic framework has not yet been established, which hinders the development and implementation of effective prevention strategies (14). Therefore, this narrative review systematically summarizes the various influencing factors of PP and proposes that its risk factors should be considered across seven age groups and eight levels in Figure 1. Based on these risk factors, corresponding preventive measures are also briefly discussed to improve public awareness and promote the implementation of prevention strategies for PP. Ultimately, these efforts aim to support the physical and mental health of children and adolescents.

Figure 1.

Hierarchy of risk factors for precocious puberty in children.

2. Genetic factors and familial predisposition

Genetic factors play a key role in endocrine diseases. CPP, caused by premature activation of the hypothalamic–pituitary–gonadal axis (HPGA), may result from pathogenic mutations in a single gene or the additive effects of multiple gene variants (15, 16). Similarly, family history, including familial CPP and neurodevelopmental disorders, may serve as potential clinical predictors of PP (17). According to the characteristics of genetic defects, the genetic factors associated with PP can be categorized into four groups: gene variants, epigenetic regulation, chromosomal variations, and gene regulatory networks. The most well-characterized single-gene functional mutations include gain-of-function mutations in the KISS1 and KISS1R genes and loss-of-function mutations in the MKRN3, DLK1, and LIN28 genes (15–18). Common gene variants, including non-functional or missense variants, have been identified in genes such as NAA10, PORCN, NR0B1, ABCD1, LHCGR, MECP2, and GATA4 (19–25). Large-scale genome-wide association studies (GWAS) have shown that single nucleotide polymorphisms in these genes are also closely associated with PP (26, 27). As shown in Table 1, studies on the genetic etiology of PP have shown that epigenetic mechanisms (such as DNA methylation and microRNA regulation), syndromes caused by chromosomal variations (structural or numerical), and the synergistic effects of multiple variant genes within gene regulatory networks also play important roles in the early onset of puberty (15, 28–38). Familial CPP is influenced by genetic factors and can be defined by early onset of sexual development or a clinical history of CPP in first-, second-, or third-degree relatives of affected individuals (39), which is an important factor for clinical consultation and screening of PP (Table 2). Familial CPP accounts for approximately 20–27.5% of CPP cases, with similar frequencies of maternal and paternal transmission (40).

Table 1.

The heredity factors of PP.

Classification		Hereditary factors associated with PP	Refs.
Category	Subcategory
Genetic variation	Functional gene mutation	Gain-of-function mutations (KISS1, KISS1R), Loss-of-function mutations (MKRN3, DLK1, LIN28), Gain-of-function mutations in the GNAS gene (McCune-Albright syndrome)	(15–18)
	Non-functional variant or missense variant	NAA10 (p.Arg83Cys), PORCN, NR0B1, ABCD1, LHCGR, MECP2 (Rett syndrome), GATA4	(19–25)
	Single nucleotide polymorphism (SNP)	KISS1 gene polymorphism (rs5780218、rs12998、rs10158616、rs10159082、rs7538038), SIRT1 gene polymorphism (rs7895833、rs3758391、rs3740051), VDR gene polymorphism (rs1544410、rs1544410、rs7975232 、rs731236), LIN28B gene polymorphism (rs7759938), ERα gene polymorphism(rs2234693)	(26–27)
Epigenetics	DNA methylation or demethylation	Methylation of the EED and CBX7 promoters, hypomethylation of the DLK1 gene, differentially methylated genes encoding zinc finger proteins, and loss of methylation at 11p15 ICR1 (Silver Russell syndrome)	(15, 28–29)
	MicroRNAs	Let-7、MiR-200/429、MiR-155、MiR-29 family、MiR-375、MiR-505-3p、MiR-199-3p、MiR-664-2、MiR-30b	(30)
Chromosomal variation	Structural or numerical variation	Temple syndrome(14q32.2 deletion)、Williams-Beuren syndrome (7q11.2 deletion)、Simpson–Golabi–Behmel syndrome (Xq26.2 deletion)、Prader-Willi syndrome (15.11q3 deletion)、Myhre syndrome (18q21.2 deletion)、Beckwith-Wiedemann syndrome (11p15.5 deletion)	(31–36)
Gene regulatory network	Regulatory network of chromatin, transcription factor, and gene interactions	G protein-coupled receptor network (KISS1R, TACR3, PROKR2, GNRHR, LHCGR, and FSHR), Combined regulation of TTF1 and EAP1	(37, 38)

Table 2.

Risk factors of PP and related mechanism.

Classification		Certain risk factors of PP (Decrease ↓/Increase ↑)	Related mechanism	Refs.
Genetic Factors and Familial Predisposition	Genes and family history	Susceptibility genes ↑	Involving chromosomal inheritance, gene expression, and epigenetic regulation	(15–40)
		First-, second-, and third-degree relatives with PP ↑
		Maternal menarche ≤10 years↑
Maternal and Prenatal Factors	Maternal preconception health	Maternal overweight/obesity ↑	Maternal abnormal conditions, through intrauterine exposure and intergenerational transmission, induce precocious activation of the HPG axis or adrenarche	(41, 42)
		Maternal polycystic ovary syndrome ↑
	Mode of conception	ART conception (in girls) ↑ Primiparity ↑	Infants conceived via ART have a higher risk of low birth weight than those conceived without ART, thereby indirectly increasing the risk of precocious puberty	(43)
	Prenatal living environment	Elevated EDC exposure (e.g., phthalates, parabens, BPA) ↑	Endocrine-disrupting chemicals interfere with estrogen and androgen signaling pathways, thereby accelerating pubertal development	(44–46)
	Maternal prenatal behavior	Prenatal healthy diet ↓ prenatal malnutrition ↑ prenatal circadian rhythm disruption ↑ prenatal anxiety ↑	Prenatal adverse behaviors exert long-term adverse effects on Kisspeptin-neurokinin B-dynorphin A neurons in the hypothalamic reproductive center of offspring	(47–50)
Delivery Mode and Infant Feeding Patterns	Delivery Mode	Cesarean section ↑ vaginal delivery ↓	Involving neonatal gut microbiota colonization	(51)
	Perinatal status	SGA ↑	During catch-up growth, SGA infants exhibit changes including increased visceral fat, decreased insulin sensitivity, and elevated IGF-1 concentrations	(52–55)
	Infant Feeding Patterns	Breastfeeding (for >6 months) ↓ formula feeding (especially soy-based formula) ↑	Breast milk indirectly shapes the early gut microbiota, whereas soy-based formula contains high concentrations of isoflavones that may exert potential estrogenic effects on infant development	(56, 57)
Dietary Behaviors and Nutritional Status	Dietary pattern	Traditional dietary pattern ↓	Unhealthy dietary behaviors or specific nutritional components induce adipose conversion and hormonal dysregulation	(58, 59)
		High-vegetable and high-protein dietary pattern ↓
		High-animal-food and high-fruit dietary pattern ↑
	Dietary habits	Poor overall dietary habits ↑		(60, 61)
		Binge eating ↑
		High-frequency consumption of sugar-sweetened beverages ↑
		Probiotic beverages ↓
	Nutrients	Dietary fat ↑		(62–73)
		Polyunsaturated fatty acids
		High carbohydrate ↑
		Food additives (e.g., tartrazine, propolis, acesulfame K) ↑
		Food additives (e.g., aspartame, glycyrrhizic acid, EGCG) ↓
		Pesticide residues in food ↑
Lifestyle Behaviors	Exercise habits	Prolonged use of electronic devices or sedentary behavior ↑	Through its effects on energy metabolism, hormone secretion, and related functions, a comprehensive influence is exerted on the timing of pubertal onset	(74–76)
		Aerobic training ↓
	Sleep habits	Sleep disorder (narcolepsy type 1) ↑		(77–80)
		Longer sleep duration ↑
		Insufficient sleep ↑
	Psychological behavior	Depressive and anxiety status ↑Abnormal psychological behavior ↑		(81–86)
		ADHD ↑
		ASD ↑
Family, School, and Community Environments	Family environments	Family breakdown ↑	Common major environmental stressors can induce changes in childrens brain structure and physiological status	(87–92)
		Internationally adopted children ↑
		Frequent interparental conflict ↑
		Parental alcoholism ↑
		Maternal anxiety and stress ↑
		Childhood emotional abuse ↑
		Child neglect ↑
		Negative parenting styles ↑
	School environments	Socioeconomic deprivation of the school area		(93)
	Community environments	Vulnerable community groups ↑		(14, 94–95)
		Residence near chemical industrial parks ↑
Clinical Signs, Symptoms, and Indicators	Clinical Signs and Symptoms	Breast enlargement (in girls) ↑Vaginal bleeding (in girls) ↑ Testicular enlargement (in boys) ↑	Abnormal timing or sequence of pubertal development	(96–108)
		Hoarseness ↑
		Growth spurt ↑
		Overweight or obesity ↑
		Fat mass index (in girls) ↑Increased systolic blood pressure (in boys) ↑
		Childhood acne ↑
	Indicators	Sudden increase in pituitary volume ↑		(109–115)
		Sudden increase in bone age ↑
		Abnormal findings on breast, uterus, and adnexal ultrasonography ↑ abnormal serum biomarkers ↑
Pre-existing Diseases and Idiopathic Diseases	Pre-existing Diseases	Antibiotic exposure ↑	Specific diseases directly or indirectly cause premature activation of the HPG axis	(116–118)
		Chronic kidney disease ↑Hidradenitis suppurativa ↑
	Idiopathic Diseases	Thyroid dysfunction ↑ premature adrenarche ↑ congenital adrenal hyperplasia ↑ adrenocortical tumor ↑		(119–131)
		Leydig cell tumor ↑ granulosa cell tumor of the ovary ↑ ovarian cyst ↑ hypothalamic hamartoma ↑ pineal cyst ↑
		Rathkes cleft cyst ↑ postoperative status of intracranial tumor ↑

3. Maternal and prenatal factors

Hormonal imbalance in the intrauterine environment caused by abnormal maternal conditions or adverse prenatal factors may disrupt reproductive processes and directly affect the growth and development of offspring. Maternal conditions—including preconception health status, mode of conception, prenatal environment, and maternal behaviors—have been associated with the risk of PP in offspring (as shown in Table 2). Several epidemiological studies have shown that maternal overweight or obesity and polycystic ovary syndrome before pregnancy are two common factors associated with early menarche in daughters and earlier pubertal development in both sexes (41, 42). A cohort study based on Danish national data from 1985 to 2015 found that children conceived by assisted reproductive technology had a higher risk of developmental disorders during adolescence, with PP more commonly observed in girls and delayed puberty more frequently observed in boys (43). Environmental endocrine-disrupting chemicals, such as phthalates, are widely present in flexible plastic products, leading to widespread human exposure (44). Prenatal maternal exposure to phthalates and parabens may affect early pubertal development in boys, whereas prenatal exposure to bisphenol A may increase the risk of PP in girls (45, 46). Prenatal adverse maternal behaviors, such as malnutrition, circadian rhythm disruption, and anxiety, may have long-term effects on kisspeptin–neurokinin B–dynorphin neurons in the reproductive center of the hypothalamic arcuate nucleus in offspring, thereby indirectly contributing to the development of PP (47–49). In addition, several case–control studies have reported that certain factors are not significantly associated with PP or show inconsistent effects, including maternal hypertension, diabetes, maternal age, prenatal smoking, and alcohol consumption (50).

4. Delivery mode and infant feeding patterns

The mode of delivery may also influence the risk of PP in offspring. Cesarean section has been identified as a risk factor for PP, whereas vaginal delivery may have a protective effect (51). This may be because infants delivered by cesarean section are not exposed to maternal vaginal microbiota during birth, which may hinder the early establishment of a balanced gut microbiota. Several studies have shown that preterm birth is not significantly associated with early puberty (52). However, being born small for gestational age (SGA) or having low birth weight (<1 SD) has been identified as a risk factor for earlier pubertal onset. This association may be related to metabolic changes during catch-up growth in small-for-gestational-age infants, including increased visceral fat, decreased insulin sensitivity, and elevated IGF-1 concentrations (53–55). Differences between human milk and formula feeding have long been studied and may influence pubertal development (56). Existing studies, primarily focused on girls (as shown in Table 2), have found that formula-fed girls tend to experience earlier menarche than breastfed girls, whereas exclusive breastfeeding during the first 6 months of life appears to be an important protective factor against CPP. Girls fed soy-based formula, which contains high concentrations of isoflavones with potential estrogenic activity, may experience earlier breast development and earlier menarche (57).

5. Dietary behaviors and nutritional Status

Similar to infant feeding, the dietary behaviors and nutritional status of preschool- and school-aged children play important roles in determining the timing of pubertal onset (132). A cross-sectional study of Chinese primary school students aged 6–9 years found that, compared with Westernized and high-protein dietary patterns, the traditional dietary pattern was protective against PP (58). Another case–control study reported that dietary patterns rich in vegetables and protein were protective against PP, whereas dietary patterns high in animal foods and fruits were associated with an increased risk of PP in Chinese girls (59). Regarding dietary habits, unhealthy eating behaviors, such as binge eating and frequent consumption of sugar-sweetened beverages, may increase the risk of PP (60, 61). This may occur because such behaviors promote adiposity and hormonal imbalances, which can indirectly trigger premature activation of the HPGA. With socioeconomic development, overnutrition among children has become increasingly prevalent (62–64). Excessive intake of energy-dense nutrients, particularly fats and sugars, has been identified as a risk factor for PP (65, 66). Food safety issues may also contribute to the risk of PP (as shown in Table 2). On the one hand, certain food additives, such as tartrazine, propolis, and acesulfame potassium, have been reported as potential risk factors for PP (67–69), whereas others, including aspartate and glycyrrhizic acid, may exert protective effects (70–72). On the other hand, pesticide residues in food may act as endocrine-disrupting chemicals and contribute to the early onset of puberty in children (73).

6. Lifestyle behaviors

Similar to the mechanisms underlying obesity, prolonged use of electronic devices (>2 h/day) and a sedentary lifestyle may increase the risk of PP in school-aged children (74). Conversely, increased physical activity, regardless of exercise intensity, may help reduce the risk of PP, particularly in girls (73). A randomized controlled trial showed that 12 weeks of aerobic exercise had positive effects on improving pubertal development in children with CPP (75). Similarly, treatment with triptorelin combined with aerobic and resistance exercise demonstrated greater improvements in CPP than pharmacological therapy alone (76). Narcolepsy, a neurological disorder characterized by disturbed nocturnal sleep, is often comorbid with endocrine disorders, including obesity and CPP (77). An epidemiological survey conducted during the COVID-19 lockdown found that children with CPP had higher rates of sleep disorders and later bedtimes than healthy controls (78). Multiple cohort studies have shown that longer sleep duration is associated with a lower risk of premature puberty in children, whereas insufficient sleep increases the risk of PP, particularly in girls (79, 80). Notably, adverse psychological conditions, such as persistent depression and anxiety, or psychosocial stress, such as low self-esteem and low self-confidence, may contribute to PP and are often comorbid with childhood mental disorders, including attention-deficit/hyperactivity disorder and autism spectrum disorder (81–86).

7. Family, school, and community environments

Early puberty in children is considered to result from complex interactions between biological and environmental factors operating at the individual, family, school, and community levels (as shown in Table 2). Many clinicians and psychologists believe that childhood adversity may influence brain structure and physiological regulation in children, thereby contributing to the earlier onset of PP (87, 88). Separation from the family of origin (e.g., family breakdown or international adoption), adverse family environments (e.g., frequent parental conflict, family alcohol misuse, or maternal anxiety and stress), and negative parenting styles (e.g., emotional abuse, neglect, or harsh parenting) are common risk factors for PP (89–92). Currently, relatively few studies have examined the associations between school and community environments and PP, and most rely on questionnaire-based surveys. A survey based on the Korean Adolescent Risk Behavior Web-based Survey conducted between 2007 and 2015 showed that socioeconomic deprivation in school districts was associated with earlier pubertal development (93). A study examining the influence of community characteristics, race, and socioeconomic status on pubertal onset among females in the United States reported that disadvantaged community environments were associated with an increased risk of PP (94, 95). Another case–control study conducted in China suggested that living near a chemical industrial park was associated with an increased risk of PP (14).

8. Clinical signs, symptoms, and indicators

Normal puberty develops in stages, with relatively stable timing and sequence of characteristic developmental events, as shown in Figure 2. Clinically, breast enlargement or prepubertal vaginal bleeding may be the first signs of PP in girls (96, 97), whereas testicular enlargement is often the earliest sign in boys (98). Voice changes and rapid height growth are also noticeable indicators of pubertal development (99–101). Therefore, early recognition of these clinical manifestations, which may indicate the initiation of pubertal development, is critical for the early detection and prevention of PP. Several meta-analyses have demonstrated that long-term overweight and obesity during childhood are independent risk factors for PP, and weight control is an important strategy for its prevention (102, 103). This may occur because obesity-induced hypothalamic inflammation can promote the premature activation of gonadotropin-releasing hormone neurons, thereby contributing to the development of PP (104). However, the effects of fat mass index on PP differ between sexes, showing a positive association with sexual development in girls but a negative association in boys (105). Elevated systolic blood pressure and childhood acne have also been reported as risk factors for PP in boys (106–108). Consistent with current guidelines and consensus statements on PP (as shown in Table 2), increases in pituitary volume and bone age, breast enlargement detected by ultrasonography, uterine and adnexal enlargement on pelvic ultrasonography, and abnormalities in serum biomarkers—including sex hormones, vitamin D, IGF-1, IGFBP-3, inhibin B, dehydroepiandrosterone sulfate, and leptin—are important clinical indicators and diagnostic criteria for PP (109–115).

Figure 2.

Diagram of normal pubertal development.

9. Pre-existing diseases and idiopathic factors

The HPGA is the core component of the endocrine regulatory network in children. It interacts with, and is regulated by, other neuroendocrine axes, including the hypothalamic–pituitary–adrenal axis, hypothalamic–pituitary–thyroid axis, and the growth hormone–insulin-like growth factor-1 axis. Through these interactions, the HPGA integrates nutritional, metabolic, and energy signals and ultimately regulates the initiation and progression of puberty. Consequently, disorders affecting these regulatory systems during childhood may contribute to the development of PP. Therefore, careful evaluation of pre-existing diseases and idiopathic conditions in children is important for the early screening and diagnosis of PP. Previous clinical reports have identified several medical conditions associated with an increased risk of PP, including antibiotic exposure (116), chronic kidney disease (117), hidradenitis suppurativa (118), thyroid dysfunction (119, 120), premature adrenarche (121), congenital adrenal hyperplasia (122), adrenocortical tumors (123), Leydig cell tumors of the testis (124), ovarian granulosa cell tumors (125), ovarian cysts (126), hypothalamic hamartoma (127), pineal cysts (128), Rathke cleft cysts (129), and a history of intracranial tumor surgery (130, 131).

10. Prevention strategies for PP based on risk factors

At present, the clinical understanding of PP and its prevention and management remains limited. Therefore, coordinated efforts among families, schools, healthcare systems, and communities are essential to reduce the occurrence of PP. With increasing knowledge of the pathogenesis and risk factors of PP, and considering the developmental characteristics of children at different ages, the following prevention strategies are proposed (some strategies still require further confirmation through evidence-based studies).

• (1)Genetic screening and family history assessment

PP shows a genetic predisposition, with similar maternal and paternal inheritance patterns. A family history of early pubertal onset among third-degree relatives (e.g., early maternal menarche or early paternal spermarche), as well as syndromes caused by chromosomal abnormalities such as Williams–Beuren syndrome and Prader–Willi syndrome, may increase the risk of PP. Therefore, prenatal screening for genetic diseases and birth defects should be performed when appropriate and ethically permissible. In addition, obtaining a detailed family history of pubertal timing should be included as a routine component of clinical screening.

• (2)Maternal health and prenatal care

Maternal health before and during pregnancy plays a critical role in the growth and development of offspring. Particular attention should be paid to maternal overweight/obesity and polycystic ovary syndrome, both of which may affect fetal endocrine programming. Appropriate medical interventions should be undertaken to restore normal reproductive and metabolic conditions before conception. During pregnancy, adopting a balanced diet, regular sleep–wake patterns, avoidance of environmental endocrine disruptors, and effective management of prenatal stress and anxiety may support placental function and promote healthy fetal development.

• (3)Perinatal factors and early-life feeding

Natural conception without assisted reproductive technologies, vaginal delivery, and breastfeeding may help reduce the risk of PP. A balanced vaginal microbiota supports early neuroendocrine development, while breast milk provides essential nutrients and may delay exposure to exogenous estrogenic substances. Infants born SGA or with low birth weight should undergo long-term monitoring of growth and development until puberty. Particular attention should be paid to catch-up growth, during which Tanner staging of sexual development should be regularly assessed.

• (4)Healthy lifestyle during childhood

The preschool and school-age periods are critical stages for establishing dietary, physical activity, sleep, and psychological habits. Maintaining balanced nutrition, healthy eating behaviors, regular sleep patterns, moderate physical activity, and psychological well-being are essential for preventing PP. From a nutritional perspective, it is important to prevent overnutrition, excessive caloric intake, and consumption of foods with high pesticide residues. In terms of physical activity, children should avoid prolonged sedentary behavior, particularly excessive use of electronic devices, and engage in regular aerobic exercise. Following established pediatric sleep hygiene guidelines can help ensure sufficient sleep duration and quality. Psychologically, children should be encouraged to maintain a positive emotional state, and professional medical support should be sought if mental health problems arise.

• (5)Active health management and community involvement

The concept of active health, which emphasizes the transition from passive disease treatment to proactive prevention and health management, represents a new paradigm in modern medicine. Families, schools, communities, and healthcare institutions play key roles in children's active health management. The family environment is particularly important. Harmonious family relationships and positive parenting styles can reduce psychosocial stress and support healthy development. Parents also play a crucial role in monitoring children's growth and pubertal development. Meanwhile, schools and communities should provide safe, healthy, and environmentally friendly environments. Public health education activities—such as lectures and informational materials—can improve awareness of PP and promote active health management (as shown in Figure 1).

• (6)Early detection and comprehensive prevention

The prevention of PP requires a multidisciplinary and systematic approach. Improving public awareness of the normal timing and sequence of pubertal development (as shown in Figure 2) can help parents, teachers, and community healthcare providers recognize early signs of abnormal development. Given the limited time window for pubertal development and the complex etiology of PP, early detection, early intervention, and early treatment remain the most effective strategies for prevention and management.

11. Summary

This review systematically summarizes the risk factors associated with PP in children. Multiple factors contribute to the susceptibility to PP, including genetic predisposition and family history, maternal conditions and prenatal factors, delivery mode and early feeding patterns, dietary behaviors and nutritional status, individual lifestyle habits, family, school and community environments, early clinical signs and indicators, as well as pre-existing and idiopathic medical conditions. Although certain determinants—such as genetic background, chromosomal variations, and fetal sex—cannot currently be modified, parents can reduce the risk of PP by maintaining a healthy reproductive status and lifestyle before and during pregnancy. In addition, establishing balanced nutritional intake, regular physical activity, and adequate sleep during childhood may help prevent early pubertal onset while also reducing the risk of other chronic diseases. Furthermore, promoting psychological well-being in children and improving their living and learning environments are important societal measures for the prevention of PP. Collaborative efforts from families, schools, healthcare systems, and communities are essential to reduce the incidence of PP and alleviate the long-term health and economic burden associated with endocrine disorders. Future large-scale prospective studies are needed to further clarify the causal relationships between environmental, metabolic, and genetic factors and the onset of precocious puberty, which may provide stronger evidence for targeted prevention strategies.

Funding Statement

The authors declare financial support was received for the research and/or publication of this article. The implementation and publication processes of this research were financed by the General Project of National Natural Science Foundation of China (82675864), Key Research and Development Project of Technology Innovation Plan of Hubei Province (2025BCB023), Qi-Huang Scholar Training Program of State Administration of Traditional Chinese Medicine - Leading Talents Training Program of Traditional Chinese Medicine (Letter of Teaching of Traditional Chinese Medicine (2025) No. 182), Hubei Provincial Administration of Traditional Chinese Medicine key discipline Construction Project of Traditional Chinese Medicine Pediatrics of Traditional Chinese Medicine (No. 2 of Hubei Traditional Chinese Medicine Tong [2023]), Hubei Province “Chutian Talents Plan” Medical and health Talent Project (No. 1 of Hubei Wei-hua [2024]).

Author contributions

JL: Writing – original draft, Formal analysis, Data curation, Conceptualization. TH: Writing – original draft, Software, Visualization, Formal analysis, Data curation. JZ: Formal analysis, Validation, Software, Writing – original draft. XT: Writing – original draft, Software, Visualization, Methodology. YC: Visualization, Software, Writing – original draft. XW: Data curation, Writing – original draft, Visualization. XZ: Visualization, Methodology, Funding acquisition, Supervision, Writing – review & editing. EL: Resources, Writing – review & editing, Conceptualization, Methodology.

Conflict of interest

The author(s) declared that this work was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.

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