Risk Factors Affecting Puberty: Environment, Obesity, and Lifestyles

Abstract

Puberty is a crucial developmental stage marked by the gradual transition from childhood to adulthood, initiated by the activation of the hypothalamus–pituitary–gonadal axis, and gonadal stimulation by rising levels of gonadotropins in response to an increased pulsatility of hypothalamic gonadotropin-releasing hormone, terminating with attainment of sexual maturity and accompanied by growth spurt, changes in physical aspect and behavior, and appearance of secondary sexual characteristics. Interconnections between genetic, endocrine, environmental, lifestyle-related and nutritional cues are involved in the complex control of the normal onset and/or progression of puberty; nevertheless, although risk factors of aberrant pubertal development have been widely investigated in girls, studies in boys are scarce. Sparse and uncertain associations between prenatal to adolescent exposure to polychlorinated biphenyls, dioxin and dioxin-like compounds, phthalates, bisphenol A, pesticides and lead and delayed genital and pubertal development have been provided, but no definitive causal inferences may be drawn at present. An equivocal relationship of obesity with pubertal timing has been reported in boys, partly explained by the paucity of studies and methodological drawbacks, as well as by contrasting actions on the hypothalamus–pituitary–gonadal axis exerted by hormonal changes occurring in obesity. Indeed, despite a beneficial effect of physiological increase of leptin levels on pubertal onset, obesity-induced leptin resistance at the hypothalamic–pituitary level determines central inhibition of the hypothalamus–pituitary–gonadal axis; moreover obesity-related hyperleptinemia might directly inhibit testicular steroidogenesis therefore potentially further delaying pubertal progression. On the other hand, reduced adiponectin levels might favor earlier pubertal onset and/or accelerate pubertal progression. Although increased adrenal androgens might accelerate the androgenic manifestations of puberty irrespective of the activation of the hypothalamus-pituitary-gonadal axis, excessive obesity-induced greater peripheral conversion of adrenal androgens to estrogens after pubertal onset might result in the inhibition of hypothalamus–pituitary–gonadal axis and delayed pubertal completion. Defective growth hormone-insulin-like growth factor 1 system signaling might also be called into question with a potential role of increased insulin-like growth factor 1 in anticipating pubertal onset and progression. A tendency to an earlier or a delayed onset of puberty has been associated with maternal cigarette smoking and alcohol consumption during pregnancy, in line with evidence suggesting delayed appearance of pubertal signs in boys consuming alcohol in pre-pubertal stage. Lastly, very scant evidence seems to suggest an association of higher animal protein dietary intake with earlier puberty in boys, whereas a potential malnutrition-related and negative energy balance-related delay in pubertal development might be speculated, based on evidence from girls suffering from anorexia nervosa or practicing vigorous physical activity, respectively.