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Influence of blindness on plasma luteinizing hormone, follicle-stimulating hormone, prolactin, and testosterone levels in prepubertal boys.

The aim of this study was to determine if changes in LH, FSH, PRL, and testosterone (T) secretion occur in blind prepubertal boys. Eight blind and six normal boys, aged 7-10 yr, living at an institute for blind subjects in Naples, Italy, were studied. Each had a combined GnRH (100 micrograms) and TRH (200 micrograms) test at 0800 h after nocturnal rest. Plasma LH, FSH, PRL, and T levels were measured by RIA. The blind boys had basal plasma LH, FSH, and T levels significantly lower than those in the normal boys (P less than 0.01 for all three); plasma PRL basal levels were similar to those in the normal boys. The blind boys, moreover, had lower peak LH, FSH, and PRL (P less than 0.01 for all three peaks) levels in response to GnRH-TRH. Our results, similar to those found by others in patients with delayed puberty or with hypogonadotropic hypogonadism, suggest that light stimuli influence neuroendocrine-gonadal activity in humans, as in other mammals; and in blind prepubertal boys, impaired hormone secretion could cause a delay of pubertal development or more severe hypogonadism.

Blindness↗

Twenty-four hour profiles of circulating androgens and oestrogens in male puberty with and without gynaecomastia.

The possible mechanisms involved in the development of transient gynaecomastia during male puberty have been investigated by studying 24 h profiles of circulating androstenedione (Ao) and testosterone (T) and their oestrogen pairs oestrone (E1) and oestradiol(E2), in eight boys with simple delayed puberty, eleven boys with pubertal gynaecomastia (three of whom were re-tested after its spontaneous resolution), and two normal adult men. No differences were observed between the 24h T and Ao profiles of pubertal boys with or without gynaecomastia; we confirmed that the initial T rise was nocturnal, associated with sleep. Late in puberty daytime T levels also rise. A small rise in 24 h Ao was seen, but this was not closely related to the stage of puberty. The major new finding was that E2 and to a lesser extent E1 levels are high relative to T for prolonged periods of the afternoon and evening (when T levels are lowest) in male puberty. A frequent finding, seen only in boys with gynaecomastia and one who later developed it, was of elevated and markedly fluctuating levels of plasma E2, and an absolute increase in the area under the 24 h E2 profile and between the E2 and T profiles. These fell towards normal in three boys who were re-tested after resolution of gynaecomastia. In a minority of subjects T and E2 were quite closely correlated, suggesting that in them rapid aromatization of T was occurring within or outside the testis. We conclude that normal male puberty is associated with relative oestrogen dominance particulary in the daytime. In boys with gynaecomastia there is in addition often an absolute elevation of E2 with or without E1, while 24 h T levels are submaximal. Normal men probably require sustained adult circulating T levels to prevent their oestrogens from stimulating breast development.

Adolescent↗

Effects of active immunization against growth-hormone releasing factor on puberty and reproductive development in gilts.

Hormones within the somatotropin cascade influence several physiological traits, including growth and reproduction. Active immunization against growth hormone-releasing factor (GRFi) initiated at 3 or 6 mo of age decreased weight gain, increased deposition of fat, and delayed puberty in heifers. Two experiments were conducted to investigate the effects of GRFi on puberty and subsequent ovulation rate in gilts. Crossbred gilts were actively immunized against GRF-(1-29)-(Gly)2-Cys-NH2 conjugated to human serum albumin (GRFi) or against human serum albumin alone (HSAi). In Exp. 1, gilts were immunized against GRF (n = 12) or HSA (n = 12) at 92 +/- 1 d of age. At 191 d of age, antibody titers against GRF were greater (P < .05) in GRFi (55.5 +/- 1.3%) than in HSAi (.4 +/- 2%) gilts. The GRFi decreased (P < .05) BW (86 +/- 3 vs 104 +/- 3 kg) by 181 d of age and increased (P < .05) backfat depth (15.7 +/- .4 vs 14.8 +/- .4 mm) by 130 d of age. At 181 d of age, GRFi reduced the frequency of ST release (1.0 +/- .5 vs 5.0 +/- .5, peaks/24 h; P < .0001) and decreased (P < .01) ST (1.1 +/- .06 vs 1.7 +/- .06 ng/mL), IGF-I (29 +/- 2 vs 107 +/- 2 ng/mL), and insulin concentrations (3.5 +/- .2 vs 6.3 +/- .2 ng/mL). The GRFi decreased (P < .05) feed conversion efficiency but did not alter age at puberty (GRFi = 199 +/- 5 d vs HSAi = 202 +/- 5 d) or ovulation rate after second estrus (GRFi = 10.7 +/- .4 vs HSAi = 11.8 +/- .5). In Exp. 2, gilts were immunized against GRF (n = 35) or HSA (n = 35) at 35 +/- 1 d of age. The GRFi at 35 d of age did not alter the number of surface follicles or uterine weight between 93 and 102 d of age, but GRFi decreased (P < .05) ovarian weight (.41 +/- .08 vs 1.58 +/- .4 g) and uterine length (17.2 +/- 1.1 vs 25.3 +/- 2.3 cm). Immunization against GRF reduced (P < .05) serum IGF-I (GRFi = 50 +/- 4 vs HSAi = 137 +/- 4 ng/mL) and BW (GRFi = 71 +/- 3 vs HSAi = 105 +/- 3 kg) and increased (P < .05) backfat depth (GRFi = .38 +/- .03 vs HSAi = .25 +/- .02 mm/kg). Age at puberty was similar in GRFi and HSAi gilts, but ovulation rate was lower (P < .05) after third estrus in GRFi (11.3 +/- .8) than in HSAi (13.8 +/- .8) gilts. Thus, GRFi at 92 or 35 d of age decreased serum ST, IGF-I, and BW in prepubertal gilts without altering age of puberty. However, GRFi at 35 d of age, but not 92 d of age, decreased ovulation rate. These results indicate that alterations in the somatotropic axis at 1 mo of age can influence reproductive development in pubertal gilts.

Animals↗

Growth and pubertal disorders in neurofibromatosis type 1.

The first textbook of Pediatric Endocrinology in the early 1950s reported an association of neurofibromatosis type 1 (NF1) and precocious puberty (PP) and/or short stature. Recent studies have indicated that children with NF1 grow normally until puberty; thereafter height velocity and relative height (SDS or percentiles) decreases with respect to healthy peers, reaching a mean adult height close to the 25th percentile for the general population. Moreover, the percentage of patients with true short stature (<3rd percentile) increases from childhood (5%) to late puberty (20-30% in literature, 18% in our study), and final height is significantly below the genetic target and predicted adult height calculated just before or at the beginning of puberty. Finally, among the shortest patients (<10th percentile) there is a high incidence of severe complications, such as CNS tumors, huge plexiform neurofibromas and severe scoliosis. Precocious puberty is a frequent complication of NF1, and occurs mainly in association with optic pathway tumors (OPT); however, occasionally it has been reported in the absence of optic gliomas, probably with a similar incidence as in the general population. GnRH agonist therapy must be decided individually as in some patients further growth could be normal and/or treatment would not improve final height. In the presence of early pubertal signs, an OPT must be ruled out. In addition to PP, delayed puberty has been frequently reported in NF1. In a study of 123 girls with NF1, we found that the mean age at menarche (13.0 +/- 1.9 yr) was later than in their mothers (12.7 +/- 1.4 yr) and in the general population (12.4 +/- 1.2 yr; p <0.05), with a very high incidence of delayed menarche (>2 SD): 16% vs 6.8% (mothers) vs 3.4% (controls) (p <0.01). In conclusion, growth and puberty present unusual patterns in NF1, often with true pathological findings increasing medical and psychological problems.

Body Height↗

Mutations along the pituitary-gonadal axis affecting sexual maturation: novel information from transgenic and knockout mice.

During the last 10 years, numerous activating and inactivating mutations have been detected in the genes encoding the two gonadotrophins, luteinising hormone (LH) and follicle-stimulating hormone (FSH), as well as their cognate receptors (R), LHR and FSHR. Because activation of the hypothalamic-pituitary-gonadal axis is a crucial event in the onset and progression of puberty, mutations affecting gonadotrophin action have major influence on this developmental process. Many of the phenotypic effects observed have been expected on the basis of the existing information about gonadotrophin action (e.g. delayed puberty), but also many unexpected findings have been made, including the lack of phenotype in women with activating LHR mutations, and the discrepancy in phenotypes of men with inactivating mutations of FSHbeta (azoospermia and infertility) and FSHR (oligozoospermia and subfertility). Some of the possible mutations, such as inactivating LHbeta and activating FSHR mutations in women, have not yet been detected. Genetically modified mice provide relevant phenocopies for the human mutations and serve as good models for studies on molecular pathogenesis of these conditions. They may also predict phenotypes of the mutations that have not yet been detected in humans. We review here briefly the effects of gonadotrophin subunit and receptor mutations on puberty in humans and contrast the information with findings on genetically modified mice with similar mutations.

Animals↗

Puberty in chronically diseased patients.

Delayed onset of puberty and a reduced pubertal growth spurt are often reported in patients suffering from chronic diseases. The basis of abnormal puberty in these patients is multifactorial. Nutritional deficiency may contribute to growth disorders and delayed puberty. Insufficient food supply and/or eating disorders and/or malabsorption of nutrients can be observed in these patients. Moreover, increased energy supplies are often needed in patients with chronic lung disease, infection or inflammation. More specific factors due to the disease itself may be involved in growth and puberty disorders. Abnormalities of the growth hormone (GH)-insulin-like growth factor (IGF)1 axis and gonadotrophin secretion have been described in patients with chronic renal failure, cystic fibrosis and Crohn's disease. More recently, it has been shown that cytokines produced during chronic diseases such as juvenile idiopathic arthritis may affect the GH-IGF1 axis. Finally, concomitant medication, namely corticosteroids, which are often given to these patients, may contribute to delayed puberty and poor pubertal growth.

Adolescent↗

Alpha-difluoromethylornithine modifies FSH secretion and puberty onset in the female rat.

FSH secretion is high in immature female rats from Postnatal Day 5 to 18 and decreases thereafter. This is a relatively steroid-independent event of cerebral origin and of importance for puberty onset. Polyamines, a group of ubiquitous amines, play an essential role in tissue growth and differentiation, body weight increment, brain organization, and molecular mechanisms of hormonal action. Polyamine levels as well as the activity of ornithine decarboxylase, the limiting enzyme in polyamines biosynthesis, are highest during development. Inhibition of their synthesis during this period by alpha- difluoromethylornithine (DFMO), a specific and irreversible inhibitor of ornithine decarboxylase, impairs normal brain development. The present study tested the hypothesis that polyamines play a role during brain organization of reproduction. DFMO was administered following different schedules in female newborn rats, and the effect on pituitary secretion, puberty onset, and fertility was evaluated. In three groups (daily injections from Day 1 to 9, or from Day 1 to 6, or injections on alternative days from Day 1 to 9), a delay in vaginal opening and first estrous was observed. When vaginal opening was plotted against body weight, it was evident that in groups daily injected with DFMO vaginal opening occurred at a lower body weight. In the group treated on alternate days, a delay occurred but at a higher body weight than in controls. In this group, serum FSH levels on Day 10 and 20, but not on Day 30, were higher in DFMO rats. In the group treated from Day 1 to 6 daily, DFMO increased serum FSH on Postnatal Day 20. After vaginal opening, estrous cyclicity in control and DFMO injected rats was similar. There was no significant effect of treatment on fertility and litter weight or number of offspring at birth. It is concluded that DFMO, an inhibitor of ornithine decarboxylase, administered during the first week of life in female rats is followed by prolonged high FSH serum levels and delayed puberty, but once puberty occurs, fertility is normal.

Animals↗

Gonadal function after testicular radiation for acute lymphoblastic leukaemia.

Pubertal maturation, growth, and gonadal function were assessed in 13 boys with acute lymphoblastic leukaemia who had received direct testicular irradiation three to nine years earlier as treatment for testicular relapse or prophylaxis against this complication. Six boys had reached Tanner stage III-V puberty, five of whom had normal growth velocities and bone ages equivalent to chronological age. One boy exhibited maturational arrest on entering stage IV. The remaining seven children (54%) showed evidence of complete pubertal delay or arrested development in stage II, with absence of the pubertal growth spurt and often with delayed bone age. Basal gonadotrophins were abnormally high in all 13 boys, and those with delayed puberty had prepubertal concentrations of testosterone. Testicular irradiation given before puberty causes permanent Leydig cell damage in a high proportion of subjects, necessitating testosterone supplementation. The extent of damage may be related to the age at which radiation is delivered.

Adolescent↗

Transforming growth factor-alpha gene expression in the hypothalamus is developmentally regulated and linked to sexual maturation.

Hypothalamic injury causes female sexual precocity by activating luteinizing hormone-releasing hormone (LHRH) neurons, which control sexual development. Transforming growth factor-alpha (TGF-alpha) has been implicated in this process, but its involvement in normal sexual maturation is unknown. The present study addresses this issue. TGF-alpha mRNA and protein were found mostly in astroglia, in regions of the hypothalamus concerned with LHRH control. Hypothalamic TGF-alpha mRNA levels increased at times when secretion of pituitary gonadotropins--an LHRH-dependent event--was elevated, particularly at the time of puberty. Gonadal steroids involved in the control of LHRH secretion increased TGF-alpha mRNA levels. Blockade of TGF-alpha action in the median eminence, a site of glial-LHRH nerve terminal association, delayed puberty. These results suggest that TGF-alpha of glial origin is a component of the developmental program by which the brain controls mammalian sexual maturation.

Animals↗

[Ambulatory diagnostic methods in disorders of sex maturation].

The most important investigative methods for study of disorders of pubertal development are simple. However, they require a detailed knowledge of the normal course of puberty. In most cases the family history (height of the parents, course of puberty in the father, age at menarche of the mother), personal history (growth curve, height velocity) and physical examination (height measurement, evaluation of stage of pubertal development, bone age) make it possible to decied whether there is benign delayed growth and development (a variation of normal) or whether the patient is suffering from one of the rare types of true hypogonadism (hormonal disorder or types of true hypogonadism (hormonal disorder or chromosomal anomaly). Only when there is strong suspicion of hypogonadism should the expensive and complicated laboratory and chromosome studies be carried out. They serve to detect a disorder of the end organ or of the hypothalamus-pituitary system (determination of testosterone or estradiol, determination of LH and FSH before and after stimulation with the releasing hormone LHRH, determination of growth hormone before and after insulin and arginine, determination of TSH before and after TRH). Although endocrine disorders are rarely the cause of delayed puberty, their diagnosis is important with a view to causal treatment.

Adolescent↗

Childhood obesity, adipose tissue distribution, and the pediatric practitioner.

The prevalence of pediatric obesity is increasing in the United States. Sequelae from pediatric obesity are increasingly being seen, and long-term complications can be anticipated. Obesity is the most common cause of abnormal growth acceleration in childhood. Obesity in females is associated with an early onset of puberty and early menarche. Puberty is now occurring earlier in females than in the past, and this is probably related either directly or indirectly to the population increase in body weight. The effect of obesity on male pubertal maturation is more variable, and obesity can lead to both early and delayed puberty. Pubertal gynecomastia is a common problem in the obese male. Many of the complications of obesity seen in adults appear to be related to increased accumulation of visceral fat. It has been proposed that subcutaneous fat may be protective against the adverse effects of visceral fat. Males typically accumulate fat in the upper segment of the body, both subcutaneously and intraabdominally. In females, adiposity is usually subcutaneous and is found particularly over the thighs, although visceral fat deposition also occurs. Gender-related patterns of fat deposition become established during puberty and show significant familial associations. There are no reliable means for assessing childhood and adolescent visceral fat other than radiologically. Noninsulin-dependent diabetes is being seen more commonly in the pediatric population. Diabetes and impaired glucose tolerance are noted particularly in obese children with a family history of diabetes. In this situation, a glucose tolerance test may be indicated, even in the presence of fasting normoglycemia. Hypertriglyceridemia and low high-density lipoprotein-cholesterol levels are the primary lipid abnormalities of obesity and are related primarily to the amount of visceral fat. Low-density lipoprotein-cholesterol levels are not typically elevated in simple obesity. The offspring of parents with early coronary disease tend to be obese. Very low-density lipoprotein and intermediate-density lipoprotein particles, which are small in size, may be important in atherogenesis but they cannot be identified in a fasting lipid panel. The propensity to atherogenesis cannot be interpreted readily from a fasting lipid panel, which therefore should be interpreted in conjunction with a family history for coronary risk factors. Hypertriglyceridemia may be indicative of increased visceral fat, familial combined hyperlipidemia, familial dyslipidemic hypertension, impaired glucose tolerance, or diabetes. Almost half of adult females with polycystic ovary syndrome are obese and many have a central distribution of body fat. This condition frequently has its origins in adolescence. It is associated with increased androgen secretion, hirsutism, menstrual abnormalities, and infertility, although these may not be present in every case. Adults with polycystic ovary syndrome adults are hyperlipidemic, have a high incidence of impaired glucose tolerance and noninsulin-dependent diabetes, and are at increased risk for coronary artery disease. Weight reduction and lipid lowering therefore are an important part of therapy. Obstructive sleep apnea with daytime somnolence is a common problem in obese adults. Pediatric studies suggest that obstructive sleep apnea occurs in approximately 17% of obese children and adolescents. Sleep disorders in the obese may be a major cause of learning disability and school failure, although this remains to be confirmed. Symptoms suggestive of a sleep disorder include snoring, restlessness at night with difficulty breathing, arousals and sweating, nocturnal enuresis, and daytime somnolence. Questions to exclude obstructive sleep apnea should be part of the history of all obese children, particularly for the morbidly obese. For many children and adolescents with mild obesity, and particularly for females, one can speculate that obesity may not be a great health risk

Adipose Tissue↗

Different reproductive strategies in males and females.

The claim for a connection between stressful, unstable childhood environments and early pubertal maturation has only modest empirical support. However, granting the claim for purposes of discussion, and taking an evolutionary perspective, it is argued here that early puberty need not imply a shift from a "quality" toward a "quantity" reproductive strategy. Indeed, for females to make such a shift when they cannot count on secure pair bonding or paternal investment from a male would not serve their inclusive fitness interests; indeed, probably the reverse. Delayed puberty among juveniles with secure, long-continued bonds with the parental generation may serve a different evolutionary function: to minimize inbreeding. Nonevolutionary factors are more than adequate to account for precocious sexuality in individuals with stressful childhood histories.

Animals↗

Delayed sexual maturation during prepubertal cannabinoid treatment: importance of the timing of treatment.

Treatment of prepubertal female rats with delta-9-tetrahydrocannabinol (THC) delays first estrus and ovulation. The present study was conducted to determine if treatments initiated at different prepubertal ages would be equally effective in delaying sexual maturation and if changes in prepubertal hormone secretion accompanied the delay. Treatments with THC (10 mg/kg) or vehicle were initiated at 24, 27 or 30 days of age and continued until first estrus was detected by vaginal smears. In one experiment, serum luteinizing hormone (LH) and prolactin (PRL) were measured at 24, 27 or 30 days of age after different durations of treatment. First estrus was delayed (4.8 +/- 1.1 days) when THC treatment started at 27 days of age, but not when treatment started at 24 or 30 days of age. Serum LH was reduced after 1 or 4, but not 7, days of treatment; however, LH suppression was associated with pubertal delay only when it occurred at 27 to 30 days of age. Serum PRL, which increased with age, was suppressed after 1 day of THC treatment at 27 or 30 days of age, but only the former was associated with delayed puberty. Suppression was not evident at 24 days of age after 1 day of THC, or at other ages after treatment for longer than 1 day. These results define a narrow interval, encompassing the ages of 27 to 30 days, during which THC exposure resulted in pubertal delay. Such treatment reduced serum LH and PRL levels, but reductions also occurred with treatments that did not result in maturational delay. The relationship of hormone suppression to the delay thus remains unclear, although the timing of suppression might be a factor.

Analysis of Variance↗

Gestational and lactational exposure to heptachlor does not alter reproductive system development in rats.

Like other organochlorine insecticides, heptachlor is lipophilic and accumulates in fatty tissues. Earlier studies suggested that in utero exposure to heptachlor decreased fertility in the offspring; neonatal exposure to the closely related insecticide chlordane reportedly delayed puberty and disrupted estrous cycling in females. We hypothesized that in utero and lactational exposure to heptachlor would disrupt the development of the reproductive system in males and females, resulting in altered timing of puberty and abnormal gonadal histology and reproductive hormone levels. Timed pregnant Sprague-Dawley rats were treated by oral gavage with heptachlor in corn oil at doses of 0.5 and 5.0 mg/kg or an equivalent volume of corn oil alone daily from gestational day 8 through post-natal day (PND) 21, the day of weaning (n = 7-8/group). Litters were standardized to 4 males and 4 females on the day of birth. Two of the dams in the 5.0 mg/kg/d group died. Pups in the highest dose group weighed significantly less than those in the other 2 groups on PND 0. All but 1 litter of the 5.0 mg/kg/d group died within the first 4 post-natal days. Age at eye opening was delayed with increasing heptachlor dose. There was no effect of treatment on pup weight gain in the surviving litters, on anogenital distance, age at puberty, nipple retention past the infantile period in males, estrous cycling, serum sex steroid concentrations, reproductive organ weights, or testicular or ovarian histology. These results suggest that heptachlor exposure during gestation and lactation does not disrupt development of the reproductive system in rats.

Animals↗

Menstrual disorders in adolescence.

Current concepts of normal and pathologic puberty have been reviewed because menstrual abnormalities are usually due to abnormal maturation of the reproductive endocrine system. Schema are presented for the initial evaluation of patients with amenorrhea or oligomenorrhea based upon whether they are hypoestrogenic or estrogenized. The role of the bone age in the differential diagnosis of delayed puberty is emphasized. The differential diagnosis and management of excessive genital bleeding and dysmenorrhea in adolescence are given.

Adolescent↗

Gonadotropin releasing hormone analogue therapy in children with isolated growth hormone deficiency: final height benefit from postponing puberty?

Although growth hormone (GH) treatment has improved final height prognosis in children with GH deficiency (GHD), adult heights are still disappointing. Final height could be improved by increasing the duration of puberty and in this way increasing total pubertal height gain. Many studies have been published on the effect of gonadal suppression, mostly by gonadotropin releasing hormone (GnRH) analogues, on final height in children with GHD. Because of the different methodologies used in these studies, results are difficult to compare. Both positive and marginal effects on final height have been reported; however, patient numbers are limited. Children with GHD who start puberty at a relatively young age and who have a poor predicted adult height, can benefit from the addition of GnRH analogues. From previous studies, we might conclude that when there is a positive effect, height benefit is marginal. However, additional prospective, randomized controlled trials are needed to further elucidate whether delaying puberty is indicated in children with GHD to improve final height.

Adolescent↗

The steroid receptor coactivator SRC-3 (p/CIP/RAC3/AIB1/ACTR/TRAM-1) is required for normal growth, puberty, female reproductive function, and mammary gland development.

Steroid receptor coactivator-3 (SRC-3) is a coactivator of nuclear receptors in the SRC family as assayed in vitro. Here, we show that mouse SRC-3 is expressed in a tissue-specific fashion and distributed mainly in the oocytes, mammary glands, hippocampus, olfactory bulb, smooth muscle, hepatocytes, and vaginal epithelium. Genetic disruption of SRC-3 in mice results in a pleiotropic phenotype showing dwarfism, delayed puberty, reduced female reproductive function, and blunted mammary gland development. Hormonal analysis indicates that SRC-3 plays a role in both the growth hormone regulatory pathway and the production of estrogen, which may explain the observed phenotypes. These results suggest that the physiological role of SRC-3 is different from that of SRC-1 and prove the diversity among coactivator family members.

Animals↗

Flaxseed and its lignan precursor, secoisolariciresinol diglycoside, affect pregnancy outcome and reproductive development in rats.

Flaxseed is the richest source of the mammalian lignan precursor secoisolariciresinol diglycoside (SDG). Because lignans have estrogen agonist or antagonist properties, the objective of this study was to determine whether feeding flaxseed to rats during a hormone-sensitive period has reproductive effects. Rat dams were fed a basal diet or the basal diet supplemented with 10% flaxseed, 5% flaxseed or SDG at the level in 5% flaxseed during pregnancy and lactation. At weaning, the offspring were fed the basal diet. Flaxseed had no effect on pregnancy outcome except that the 10% flaxseed diet lowered birth weight (P < 0.05), compared with other treatments, and produced hormonal effects. The female offspring had shortened anogenital distance, greater uterine and ovarian relative weights, earlier age and lighter body weight at puberty, lengthened estrous cycle and persistent estrus (P < 0.05), whereas the males had reduced postnatal weight gain and, at postnatal d 132, greater sex gland and prostate relative weights (P < 0.05), suggesting estrogenic effects. In contrast, compared with the basal diet, 5% flaxseed reduced immature ovarian relative weight by 29% (P < 0.05), delayed puberty by approximately 5 d (P < 0.05) and tended to lengthen diestrus, indicating an antiestrogenic effect. The SDG produced results similar to those of 5% flaxseed, suggesting that lignans were responsible for the observed effects. Lignans were transferred to the offspring via rat dam's milk as indicated by the recovery of radioactivity in the offspring of lactating dams given 3H-SDG. Because flaxseed affects the reproductive development of offspring, caution is suggested when consuming flaxseed during pregnancy and lactation.

Anal Canal↗