Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “PUBERTY”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 163 records · Page 9Linked to original sources
PubMed1994

[The status of the gonadotropin releasing hormone test in differential diagnosis of delayed puberty in adolescents over 14 years of age].

BACKGROUND: In patients with delayed puberty with a bone age less than 11 years in girls or 12 years in boys, the clinical and endocrinological examination allows the differentiation of patients with the various forms of hypergonadotropic hypogonadism, but not of patients with hypogonadotropic hypogonadism from more prevalent constitutional delay in puberty. Therefore, watchful waiting is generally recommended for differential diagnosis in patients with delayed puberty. On the other hand, the late onset of sexual hormone replacement in patients with hypogonadism will worsen their outcome. PATIENTS AND METHOD: Therefore, we decided to carry out a retrospective study in 105 adolescents who were examined because of short stature or delayed puberty, who were aged 14 to 22 years at first visit and in whom the differential diagnosis of delayed puberty was documented after an at least one-year follow-up in order to find out which endocrinological parameters could have effectively predicted the final diagnosis already at the first visit. RESULTS: Patients with hypogonadotropic hypogonadism differed from patients with constitutional delay in puberty by lower responses of luteinizing hormone (LH) and follicle-stimulating hormone (FSH) levels to gonadotropin-releasing hormone stimulation (GnRH, 100 micrograms iv) (p < 0.01) as well as by smaller testicular volume (p < 0.05) and by lower testosterone levels (p < 0.01). Stimulated LH < 10 mU/ml differentiated patients with hypogonadotropic hypogonadism from constitutional delay in puberty with a sensitivity of 82% and a specificity of 98%. CONCLUSION: In patients with delayed puberty aged 14 years and older bone age usually exceeds 11 years in girls or 12 years in boys. It thus is in the range, in which normal adult responses of LH to GnRH can be expected. In contrast to patients aged less than 14 years, therefore, measuring GnRH-stimulated LH levels in these patients allows the rapid and effective differential diagnosis of delayed puberty.

Adolescent↗
PubMedDate not supplied

[Delayed puberty].

Delayed puberty can be defined as the absence of any signs of puberty in subjects that have attained an age at the upper limit (+2DS) for the onset of puberty, that means 13 years in girls and 14 years in boys. The causes of delayed puberty can be classified into three groups, functional temporary impairment in gonadotropin and sex steroid secretion (most frequently constitutional delay of puberty), hypothalamo-pituitary failure with deficiency in gonadotropin secretion, primary gonadal failure with increased gonadotropin levels. The Authors discuss about etiology, diagnostic testing and therapeutic approach in these conditions. The majority of children with delayed puberty are males that have only a constitutional delay of growth and puberty. It is difficult, in teenage years, to distinguish this common and benign condition from true gonadotropin deficiency, in spite of the variety of endocrine tests developed for this purpose. Individuals with constitutional delayed puberty with a bone age greater than 11.5 years, show after triptorelin stimulation an increase in LH capable of distinguishing them from patients with gonadotropin deficiency. In our opinion this could be an important screening test to exclude gonadotropin deficiency in boys with delayed puberty.

Adolescent↗
PubMed1985

Disturbances of puberty.

The initiation and progress of puberty requires progressive pulsatile stimulation of the pituitary by GnRH and of the gonads by LH and FSH. Gonadal maturation continues throughout childhood and is not confined to puberty. We have discussed the events of normal puberty and emphasized the consonance of the acquisition of different components of sexual maturation, including growth acceleration. Departure from this consonance is a sign of abnormality. The method by which constitutional delay of growth and puberty can be distinguished from gonadotrophin deficiency has been discussed as well as the treatment options for both conditions. We have emphasized the significance of pulsatile gonadotrophin secretion and how the development of a multicystic ovarian morphology on ultrasound can be used as a non-invasive assessment of gonadotrophin pulsatility in girls. Pulsatile GnRH therapy mimics normal puberty. The converse of suppressing the clinical signs of central precocious puberty can be achieved by abolishing gonadotrophin pulsatility with GnRH analogue therapy. We now recognize qualitative pulse abnormalities of gonadotrophin secretion which occur in isolated premature thelarche and in some cases of delayed puberty. Although clinical assessment remains the key to the diagnosis of disorders of puberty, studies of gonadotrophin pulsatility have aided our understanding and treatment of these conditions.

Adolescent↗
PubMed1981

Determination of onset of puberty in Zebu bulls under tropical conditions of northern Nigeria.

Age at puberty and related phenomena were investigated in White Fulani (Bunaji - WF), Sokoto Gudali (SG) and Friesian X Bunaji (FRXWF) Zebu bulls from 28 weeks to 72 weeks of age. Pubertal traits studied included body weight, heart girth, scrotal circumference and sperm production. Puberty was defined as the age at which an ejaculated semen contained at least 50 x 10(6) spermatozoa with a minimum of 10% motility. Age at puberty was 66.89 +/- 1.0, 73.4 +/- 2.2 and 62.4 +/- 10.7 weeks for WF, SG and FRXWF bulls respectively. The Bunaji bulls were significantly younger than the Sokoto Gudali bulls at production of first motile sperm cell and also at puberty (P<0.01). The SG bulls were significantly heavier (P<0.01) and had larger heart girth (P<0.05) than the FRxWF at production of first motile sperm cells. Body weight and heart girth for all the breeds were not different at puberty (P>0.1). Scrotal circumference of the bulls between the breeds at production of first motile sperm cells and at puberty, did not differ (P 0.>1), despite the variations in age, weight and heart girth at production of first motile sperm cell and at puberty. It is concluded from the data obtained that the indigenous breeds of bulls (Bos indicus ) seem to attain puberty later than exotic breeds (Bos taurus ). The inter-play of genetic, nutritional and environmental factors as a contribution to this delay in attainment of puberty could not be ruled out.

Journal Article↗
PubMed1985

Body composition of beef heifers at puberty.

Three trials were conducted to study age, weight, percent body fat and protein content of 131 crossbred and purebred beef heifers at puberty, to investigate relationships among various pubertal measurements and to determine if body fat and protein values could be used in combination with age, weight and shoulder height to predict the onset of puberty. Trials 1 and 2 compared heifers on treatments of high (H), medium (M) and low (L) levels of energy. The rations were formulated at 120, 100 and 80 percent of the National Research Council (NRC) recommendation for energy. The protein level was 100 percent of the NRC recommendation for all three treatments. Each animal was examined every two weeks per rectum for the presence of follicles and corpora lutea. The presence of a mature corpus luteum indicated the attainment of puberty. Trial 3 heifers were fed the same level of nutrition but ovulation data were based on weekly rectal palpations and on the presence of greater than 2.0 ng/ml blood plasma progesterone. Percentage of fat and protein were quantified in all trials using a whole body counter. In Trial 1 there was a significant difference (P<0.01) among energy levels for mean weight and percent fat values at puberty, but no differences in age at puberty. Even though heifers in Trial 2 were also fed different energy levels, there were no differences among treatments for the variables measured. The onset of puberty in Trial 2 appeared to be delayed due to cooler than normal weather during that experimental period. Heifers in Trial 2 tended to be older and reached puberty approximately one month later in the year than heifers in Trials 1 and 3, despite similarities in weight gain among the trials. In all trials, high R(2) values for multiple stepwise regression analyses indicated that body composition estimates were useful in predicting weight at puberty in beef heifers. The results of this study do not support a critical body weight or body composition hypothesis in the beef heifer. It was concluded that these data indicate environmental factors may have more effect than nutrition on the onset of puberty.

Journal Article↗
PubMed1997

Relationship between the thymus and neurochemical changes in the hypothalamus-preoptic area and prefrontal cortex in female rats with delayed puberty.

In female rats, aged 55-58 days with delayed puberty due to deficient growth and environmental stress, 5-hydroxyindoleacetic acid levels and serotonin turnover rate in the hypothalamus-preoptic area as well as body weight, body weight gain and relative weight of ovaries, uterus, adrenals and preputial glands were lower while serotonin and 5-hydroxyindoleacetic acid levels in the prefrontal cortex were higher when compared to normal rats with the latest onset of puberty aged 42-52 days. In rats with delayed puberty, multiple regression analysis revealed a significant negative dependence on dopamine turnover in the hypothalamus-preoptic area for body weight gain and, of all organs, for the relative weight of the thymus. A similar negative significant dependence on serotonin turnover rate in the prefrontal cortex was also found for the relative weight of thymus and spleen. The same analysis in the opposite direction revealed a significant negative dependence of 3,4-dihydroxyphenylacetic acid levels and dopamine turnover rate in the hypothalamus-preoptic area as well as serotonin turnover rate in the prefrontal cortex only on thymus weight. After separation of delayed pubertal rats into two groups, based on absolute ovarian weight, the rats in the low ovarian weight range and no signs of puberty exhibited: lower body weight gain, lower body weight, and lower relative weight only of thymus, ovaries and preputial glands in parallel with an increased dopamine turnover rate in the hypothalamus-preoptic area and serotonin turnover rate in the prefrontal cortex compared to the delayed pubertal rats in the high ovarian weight range and early signs of puberty. The results suggest that in rats with delayed puberty: (1) serotonergic activation in the hypothalamus-preoptic area is lower compared to normal puberty rats; (2) dopaminergic activation in the hypothalamus-preoptic area negatively affects body weight gain, thymus weight and initiation of puberty and (3) thymus weight is negatively implicated in dopaminergic activation in the hypothalamus-preoptic area and serotonergic activation in the prefrontal cortex and positively related to ovarian weight and early signs of puberty.

Animals↗
PubMed1998

Puberty in the female tammar wallaby.

The growth and timing of female puberty in a seasonally breeding marsupial, the tammar wallaby, was examined in wild and captive animals. Puberty, defined as the time of first estrus and ovulation, can occur at any time of the year. Sixty percent of young wild females went through puberty in late October-November, 3 mo before the normal adult mating season in late January-February, but puberty was delayed in captive animals kept with a low ratio of males to females. During initial cycles, 19% of these captive animals were infertile as judged by failure to conceive. In the wild, puberty occurred well before the animals were fully grown (body weight 2.0+/-0.3 kg [mean+/-SD], n=23; adult females, 4.7+/-0.6 kg; n=34). Only 3% of animals with a body weight below 1.5 kg had ovulated. Thus, attainment of a minimum body weight was a key prerequisite associated with puberty. Progesterone concentrations in the peripheral plasma of prepubertal females were not significantly different from those of adult females during the nonbreeding season (prepubertal, 142+/-121 pg/ml, n=34; adult, 194+/-105 pg/ml, n=32, p > 0.05). However, there was a significant increase in progesterone (322+/-242 pg/ml, n=32, p < 0.05) in the postpubertal females (ovulating but still < 3.5 kg body weight) even though the corpus luteum was quiescent after its formation. There was no increase in plasma progesterone before the first estrus. These data confirm that estrus does not require a change in the progesterone:estradiol ratio, and that a "silent" ovulation does not precede the first estrus in this species, so that the onset of puberty coincides with the first behavioral estrus and ovulation, when the animals have reached a body weight of 2 kg. Although adult female tammars are strict seasonal breeders, with 6 mo of seasonal quiescence from the winter to the summer solstice, young females can go through puberty at any time of the year. The unique feature of the female tammar wallaby is that it does not become a seasonally breeding mammal until after puberty, when it has acquired a corpus luteum.

Aging↗
PubMed2005

Glucocorticoids and the development of agonistic behaviour during puberty in male golden hamsters.

During puberty, the agonistic behaviour of male golden hamsters undergoes a transition from play fighting to adult aggression. Repeated exposure to social stress early in puberty accelerates this transition. The present study investigated the possible role of glucocorticoids on the maturation of agonistic behaviour. First, we compared serum cortisol levels following a 20-min restraint stress during early puberty, mid-puberty or adulthood. Across puberty, animals exhibited a two-fold increase in post-restraint cortisol levels. We also compared corticotrophin-releasing hormone (CRH) immunoreactive fibres projecting to the median eminence between animals in early puberty and adulthood. The CRH fibre density was two-fold greater in adults compared to juveniles. Furthermore, we investigated the effects of stress hormones on the maturation of agonistic behaviour. Male hamsters were injected daily with dexamethasone, a corticosteroid receptor type II agonist (0, 10 or 40 microg/100 g), early in puberty from postnatal day 31 (P-31) to P-36. When paired with a smaller and younger intruder on P-37, attack frequency did not differ between groups. However, dexamethasone-treated animals showed a dose-dependent decrease in the percentage of play-fighting attacks and an increase in the percentage of adult attacks. In summary, puberty can be described as a period of increasing hypothalamic-pituitary-adrenal activity in male golden hamsters. Moreover, increasing glucocorticoid levels influence the maturation of agonistic behaviour. These data shed new light on the neuroendocrine mechanisms that regulate the maturation of social behaviours during puberty.

Aggression↗
PubMed2001

Delayed puberty and response to testosterone in a rat model of colitis.

Delayed puberty is a frequent complication of inflammatory bowel disease. The precise etiological mechanisms are not known. In this study, we wanted to determine the relative contribution of undernutrition and inflammation to delayed puberty and the effect of inflammation on the reproductive axis. Puberty was assessed in rats with 2,4,6-trinitrobenzenesulfonic acid induced-colitis, healthy controls, and animals pair fed to match the food intake of the colitic group. The response to testosterone administration was assessed in colitic rats. We found that induction of colitis was associated with hypophagia and reduced weight gain, and undernutrition in healthy females (i.e., pair fed) resulted in a delay in the onset (by 4.8 days, P < 0.001) and progression of puberty (normal estrous cycles in 42%, P = 0.04) compared with controls. However, puberty was further delayed in the colitic group (1.4 days after pair fed) with the absence of normal estrous cycling in all rats. In males, the onset of puberty was also delayed, and weights of accessory sex organs were reduced compared with pair-fed controls. Plasma testosterone concentrations were low, and gonadotropin concentrations were normal in colitic rats. Testosterone treatment normalized puberty in male rats with colitis. In conclusion, in rats with experimental colitis, inflammation appears to potentiate the effect of undernutrition on puberty. The weights of secondary sex organs and the onset of puberty were normalized by testosterone treatment.

Animals↗
PubMed1993

Is infancy a quiescent period of testicular development? Histological, morphometric, and functional study of the seminiferous tubules of the cebus monkey from birth to the end of puberty.

The objective of this study was to describe the maturational changes observed in the seminiferous tubules of the monkey Cebus apella, a New World primate species, from birth to the end of puberty. Nineteen animals were subdivided into four groups: neonatal (1-40 days), infantile (4 months to 1 yr), early pubertal (1 yr, 8 months to 2 yr, 9 months), and late pubertal (4-8 yr). Volumetric determinations of different testicular components were made, tubule diameter and length were calculated, and spermatogenic cells, Sertoli cells, and androgen-binding protein secretion were quantified. Testicular and seminiferous tubule volumes increased significantly in the first 5 months of life and during puberty due to the combined increment in seminiferous tubule diameter and length. The total number of spermatogonia increased until late puberty to stabilize subsequently. Spermatocytes and spermatids appeared during puberty and increased dramatically until the end of this period. The germ cell ratios, indicative of spermatogenic efficiency, improved continuously in late puberty coincidentally with a reduction of spermatocyte degeneration. Sertoli cells proliferated in the neonatal and infantile periods, determining a longitudinal growth of the seminiferous tubules, but remained stable during puberty, when androgen-binding protein secretion increased significantly. The multiplication of germ cells is the main factor responsible for the increment in tubule diameter during puberty and determines the most noticeable postnatal modification of testicular volume. During late puberty, the reduction of spermatocyte degeneration leads to an increment in germ cell ratios and a progressive, but slow, improvement of spermatogenic efficiency, explaining why pubertal development of the testis occurs over such a prolonged period in this primate. This is in contrast to what happens in most laboratory animals and suggests that the Cebus is a useful model for studies of human male puberty.

Aging↗
PubMed1990

Effect of selection for growth traits on age and weight at puberty in bovine females.

This 20-yr study, using 584 beef heifers born in the spring of 1984 or 1985, was conducted to determine whether selection for growth traits affected age and weight at puberty. Heifers were from three Hereford lines selected for weaning weight, final weight, and final weight plus muscling score, a control line and a line of Angus cattle. In addition, heifers from reciprocal crosses among the selection lines, control and Angus groups were evaluated. Intact bulls and androgenized heifers fitted with marking harnesses were used to aid in detection of estrus for heifers born in 1984 and 1985, respectively. The time of puberty was identified by the first behavioral estrus. During both years, heifers were weighed at 56-d intervals; these weights were used to calculate weight at puberty. Mean age at puberty was determined using survival analysis; percentages of heifers that were pubertal by the end of the study were transformed to logits for analysis. Heifers born in 1985 were heavier (P less than .05) at puberty than those born in 1984. Heifers in lines selected for growth traits were younger at puberty (P less than .05; 20 d) than were heifers in the control line because of combined direct and maternal genetic effects. Heifers from the final weight, control (P less than .05) and weaning weight lines (P less than .10) weighed less at puberty than Angus heifers; selection line x Angus crossbred heifers were heavier at puberty (P less than .05) than their respective pureline or purebred contemporaries due to heterotic effects. Selection for weaning weight, final weight or final weight plus muscling score did not have a detrimental effect on age at puberty in heifers.

Age Factors↗
PubMed1992

Effects of nutrition and season on the onset of puberty in the beef heifer.

Age at puberty is a major determinant of lifetime reproductive efficiency of beef cows. Research conducted during the past 20 yr has documented the major endocrine events leading to first ovulation in heifers. The critical event seems to be a prepubertal increase in pulsatile LH secretion. Environment influences timing of puberty onset in beef heifers. Nutrition and season are two of the better-defined variables that have been studied. Age at puberty is related inversely to plane of nutrition. The effect of nutrition on sexual maturation involves effects on timing of the prepubertal increase in LH secretion and seems to involve the LH pulse generating system located in the hypothalamus. The precise mechanism by which nutrition influences pulsatile LH secretion has not been elucidated, but signals reflecting metabolic status seem to be involved. Seasonal conditions of the early (birth to 6 mo of age) and late (6 to 12 mo of age) postnatal periods also influence timing of puberty onset in the heifer. Autumn-born heifers attain puberty at younger ages than do spring-born heifers, and exposure to spring-summer temperatures and photoperiods during the second 6 mo of life reduces age at puberty regardless of season of birth. Photoperiod may be the major seasonal cue that influences puberty onset in cattle. Limited evidence suggests that melatonin, a pineal hormone, is involved with transducing photic stimuli into neuroendocrine signals that influence LH secretion. If the physiological mechanisms mediating the effects of nutrition and season on timing of puberty onset are determined, then management strategies for reducing age at puberty can be enhanced.

Animal Nutritional Physiological Phenomena↗
PubMed1993

Effect of prepubertal body weight gain and breed on carcass composition at puberty in beef heifers.

Fourteen prepubertal Angus heifers, all of which reached puberty, and 11 Santa Gertrudis (SG) heifers, eight of which reached puberty, were divided into two treatment groups. There was no breed difference in age at puberty for those that reached puberty. Treatment 1 (T1) heifers, fed to gain .5 kg/d, tended (P < .11) to be older than Treatment 2 (T2) heifers, fed to gain 1 kg/d, at puberty. Body weight and height were greater (P < .01) in SG than in Angus heifers at puberty. Angus heifers in T2 deposited more fat over the rump during the 15 wk before puberty, whereas T1 SG heifers deposited the least amount of fat (P < .05). Heifers in T2 were heavier at puberty (P < .05), had faster growing longissimus muscle areas (P < .05), and deposited more fat over the rib (P < .01) as they approached puberty. The T2 (P < .05) and Angus (P < .05) rib sections had more dissectible subcutaneous fat than did T1 and SG rib sections. Angus heifers had higher marbling scores (P < .05), as well as higher total lipid percentages for seam fat (P < .05), longissimus muscle (P < .01), other lean tissue (P < .05), and subcutaneous fat (P < .01). Predicted total lipid content for the edible portion of the dressed carcass was higher for T2 heifers (P < .09).

Adipose Tissue↗
PubMed1997

Non-classical 21-hydroxylase deficiency in infancy and childhood: the effect of time of initiation of therapy on puberty and final height.

OBJECTIVE: To review the characteristics of children with non-classical 21-hydroxylase deficiency (NC-21-OHD) diagnosed during infancy and childhood, and to evaluate the relationship of pubertal and bone age maturation at initiation of glucocorticoid therapy with the course of puberty and final height. DESIGN: We retrospectively compared the course of puberty, growth pattern and final height in two groups of patients: group A (two males, six females), hydrocortisone (HC) treatment 7.5-15 mg/m2 per 24 h, initiated > or = 1 year before onset of true puberty and group B (seven females), treatment started with the first signs of true puberty present. PARTICIPANTS: Thirteen girls and two boys with NC-21-OHD diagnosed at age range 0.5-10.6 years were followed-up for 9.0 +/- 3.8 years (mean +/- S.D). Therapy with HC was initiated because of signs of hyperandrogenism, accelerated growth and bone maturation, or true precocious puberty. The HC dose was adjusted according to linear growth and basal plasma androgen levels. RESULTS: Puberty and peak height velocity developed significantly earlier in the girls of group B: gonadarche at 7.9 +/- 1.4 years and peak height velocity at 9.2 +/- 1.4 years vs 10.2 +/- 0.4 years (P = 0.002) and 11.5 +/- 0.7 years (P = 0.006) in group A. Menarche, however, occurred only slightly earlier in group B (12.0 +/- 1.1 vs 12.8 +/- 0.5 years, P = 0.068). All eight children in group A achieved a final height within the range of their mean parental height standard deviation scores (SDS) in comparison with only 1/7 in group B (P = 0.0014). Seven of eight patients who started therapy before a bone age of 9 years achieved a final height within the parental height SDS range, compared with 2/7 who started therapy later (P = 0.041). The final height SDS was significantly better for group A (0.05 +/- 0.19, mean +/- S.E.M.) than group B (-1.63 +/- 0.23, P = 0.0007), even when adjusted for a significant effect of the mean parental height SDS (A. -0.63 +/- 0.28; B, -0.89 +/- 0.31, P = 0.0245, ANCOVA). CONCLUSION: Every child with signs of excess androgen activity or early puberty should be studied for the possibility of NC-21-OHD. Screening programs for populations with a high frequency of the gene for NC-21-OHD would facilitate early diagnosis and treatment. Pubertal stage and bone age at the introduction of therapy dictate height prognosis. Initiation of therapy before puberty with careful follow-up and HC dose adjustment can assure the achievement of genetic adult height.

Adrenal Hyperplasia, Congenital↗
PubMed2001

Earlier onset of puberty in girls: relation to increased body mass index and race.

OBJECTIVE: A recent study conducted by the Pediatric Research in Office Settings network provided evidence that girls in the United States, especially black girls, are starting puberty at a younger age than earlier studies had found, but the reasons for this are not known. Because nutritional status is known to affect timing of puberty and there is a clear trend for increasing obesity in US children during the past 25 years, it was hypothesized that the earlier onset of puberty could be attributable to the increasing prevalence of obesity in young girls. Therefore, the objective of this study was to reexamine the Pediatric Research in Office Settings puberty data by comparing the age-normalized body mass index (BMI-ZS; a crude estimate of fatness) of girls who had breast or pubic hair development versus those who were still prepubertal, looking at the effects of age and race. RESULTS: For white girls, the BMI-ZS were markedly higher in pubertal versus prepubertal 6- to 9-year-olds; for black girls, a smaller difference was seen, which was significant only for 9-year-olds. Higher BMI-ZS also were found in girls who had pubic hair but no breast development versus girls who had neither pubic hair nor breast development. A multivariate analysis confirms that obesity (as measured by BMI) is significantly associated with early puberty in white girls and is associated with early puberty in black girls as well, but to a lesser extent. CONCLUSIONS: The results are consistent with obesity's being an important contributing factor to the earlier onset of puberty in girls. Factors other than obesity, however, perhaps genetic and/or environmental ones, are needed to explain the higher prevalence of early puberty in black versus white girls.

Adolescent↗
PubMed1994

The blood-retinal barrier in diabetes during puberty.

OBJECTIVE: To assess the alteration of the blood-retinal barrier in patients with type I diabetes during puberty. DESIGN: A 7-year prospective study evaluated retinal changes occurring in diabetic children during puberty. Patients between the ages of 10 and 20 years underwent annual ophthalmologic examinations that included fluorescein angiography and vitreous fluorophotometry. SETTING: Clinical research facility. PATIENTS: Fifty-seven diabetic children met preset eligibility criteria. During the study, 241 ophthalmologic examinations were scheduled and 210 (87.1%) were performed. MAIN OUTCOME MEASURE: Vitreous fluorophotometry penetration ratio (VFPR) was used to indicate blood-retinal barrier permeability. RESULTS: No sign of retinopathy was detected before puberty (age 13 years for boys and 11 or 12 years for girls). The prevalence of retinopathy in the 4 years immediately after puberty was 6%. In the next 4 years, the prevalence was 29.6% (P = .0003). When all VFPRs were correlated with age, and data for male and female patients were analyzed separately, we found that the lowest VFPRs occurred at the expected time of puberty. When patients were paired by gender and duration of diabetes, there was a significant difference between VFPR values before and after puberty (P = .03). Also, a progressive deterioration of the blood-retinal barrier became apparent when only VFPR values after puberty were considered. CONCLUSIONS: These results support the view that the blood-retinal barrier remains stable until puberty, achieving a maximum of efficiency and protection. A progressive decline then begins, suggesting that this period of growth is associated with factors that, under the influence of diabetes, contribute to the progressive damage of the blood-retinal barrier.

Adolescent↗
PubMed2001

Association between puberty and disordered eating, body image, and other psychological variables.

OBJECTIVE: To examine associations between puberty and disordered eating, body image, and other psychological variables. METHOD: Females were grouped into three categories of age at puberty onset (Study 1; N = 267) as well as three categories of self-perception of prepubertal weight (Study 2; N = 222). Participants in both studies were matched on current body mass index (BMI) across categories. RESULTS: Females who perceived themselves to be overweight prior to puberty scored significantly higher on measures of disordered eating, body dissatisfaction, asceticism, drive for thinness, impulse regulation, interoceptive awareness, and perfectionism. They also perceived their current body figure to be larger when compared with those who believed they were average or underweight prior to puberty. Age at puberty onset was not significantly associated with disordered eating, body dissatisfaction, depression, or self-esteem. However, females who entered puberty at an earlier age scored higher on measures of asceticism, drive for thinness, impulse regulation, and social insecurity. They also chose a more slender ideal body figure than those who entered at an older age. DISCUSSION: Females who believe they are overweight prior to puberty may be at risk for the development of disordered eating, body image dissatisfaction, and related problems. Age at puberty onset is not a consistent risk factor of pathological eating.

Adult↗
PubMed2006

Growth in precocious puberty.

Growth in precocious puberty is a subject of concern to families and clinicians alike. The definition of precocious puberty and the role of obesity in the age of onset have also been areas of debate since the Lawson Wilkins Society recommended a lowering of the age of onset of precocious puberty in US girls. An understanding of growth patterns in normal children with earlier or later onset of puberty and the variable rate of progression between individuals with central precocious puberty as well as the imprecision in available height prediction methods are important in assessing height outcomes in this condition. In the absence of randomised controlled trials in this area, only qualified conclusions about the effectiveness of interventions can be drawn. In general, it appears that height outcome is not compromised in untreated slowly progressive variants of central precocious puberty. In rapidly progressing central precocious puberty in girls, gonadotrophin releasing hormone agonists (GnRH agonists) appear to increase final height by about 5 cm in girls treated before the age of eight, but there is no height benefit in those treated after eight years. Scanly data is available to assess treatment effects in boys. GnRH agonists appear to be relatively safe. The decision to treat central precocious puberty should take into account rate of progression of pubertal changes as well as biochemical markers and may need to address other factors (for example psychosocial and behavioural issues) as well as height outcome.

Child↗