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PubMed1988

Effects of alcohol abuse on reproductive function in women.

Alcohol abuse and alcoholism are associated with disorders of reproductive function in both men and women. Amenorrhea, anovulation, and luteal phase dysfunction may occur in alcohol-dependent women and alcohol abusers. Yet there has been relatively little research on the consequences of alcohol abuse for female reproductive function. Recent clinical and survey studies of alcohol effects on pituitary gonadotropins and gonadal steroid hormones in women are reviewed. Experimental studies of the acute and chronic effects of alcohol on the hypothalamic-pituitary-gonadal axis in normal women and in animal models are also described. Recent studies of the acute effects of alcohol on opioid antagonist and synthetic LHRH-stimulated pituitary gonadotropins are summarized. Possible mechanisms underlying alcohol-induced disruptions of menstrual cycle regularity are discussed.

Alcoholism↗

PubMed1978

Hypothalamic-pituitary-ovarian interactions during reproductive senescence in the rat.

The neuroendocrine status of Long-Evans female rats was evaluated at several key stages of reproductive senescence. Young (4-8 mo), middle-aged (10-14 mo) and old (24-30 mo) animals were studied according to reproductive state. The reproductive states studied were (1) regularly cycling, (2) constant estrus and (3) pseudopregnant, as determined by vaginal smear cytology. Neuroendocrine parameters at the levels of the hypothalamus, pituitary and steroid-producing organs were compared between each group. DA3, E and NE concentrations in the median eminence of the hypothalamus were determined by a highly sensitive radioenzymatic assay. LRF content in the median eminence was measured by radioimmunoassay. Circulating levels of LH, FSH, PRL and six steroids were determined. Changes in hormone and neurotransmitter concentrations were deomonstrated in association with the various stages of reproductive senescence and with age advancement. These changes involved the hypothalamic, pitiutary and steroid systems. NE content in the median eminence, FSH in serum and circulating androstenedione were all significantly increased in middle-aged, cyclic rats prior to the onset of senescent anovulation. DA concentration in 24 mo. old constant estrous rats (30.7 +/- 7.7 pg/microgram, N = 6) and in 30 mo. old pseudopregnant rats (27.5 +/- 7.1 pg/microgram, N = 6) was significantly reduced compared to young (6 mo. old), cyclic controls on proestrous (55.0 +/- 4.7 pg/microgram, N = 12). This DA reduction was associated with a 3-fold increase in circulating prolactin. The results are discussed in terms of a regulatory cascade model of female reproductive senescence (Finch, 1976).

Aging↗

PubMed1985

Altered hypothalamic-pituitary function in the adult female rat with streptozotocin-induced diabetes.

Infertility associated with anovulation and loss of regular oestrous cyclicity is a consequence of diabetes mellitus in the rat. In an attempt to define loci of altered function, studies were undertaken to examine various aspects of hypothalamic-pituitary function in rats treated with streptozotocin. Medial basal hypothalamic fragments from adult female diabetic rats contained the same amount of gonadotrophin-releasing hormone but, with depolarization, released slightly but insignificantly (p greater than 0.05) more than did those from control animals. Furthermore, release of luteinizing hormone from pituitaries exposed to hypothalamic gonadotrophin-releasing hormone was not altered by diabetes. Removal of the negative feedback effect of gonadal steroids upon the hypothalamic-pituitary axis produced an increase in luteinizing hormone and follicle stimulating hormone concentrations in the serum of normal rats within 6h (p less than 0.05), whereas 24h were required for similar increases in diabetic rats. However, the same concentrations of gonadotrophins were found in diabetic and control animals 120 h after ovariectomy. The inhibitory action of oestradiol benzoate on the secretion of gonadotrophins was more pronounced in ovariectomized diabetic than in control rats. A 74% depression in serum luteinizing hormone (p less than 0.01) was produced by 0.5 microgram oestradiol benzoate per day in diabetic rats, while 5 micrograms was required in control animals. Similar reductions in follicle stimulating hormone concentrations (50%, p less than 0.05) were obtained by injecting 5 micrograms of the oestrogen into diabetic or 50 micrograms into control rats. Increases in serum prolactin were greater in the control animals however.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1990

The effect of laparoscopic treatment of polycystic ovarian disease by CO2-laser or Nd:YAG laser.

The feasibility and efficacy of laparoscopic CO2 laser and Nd:YAG non-contact laser application for the treatment of polycystic ovarian disease (PCOD) were evaluated in 30 patients (19 patients treated with the CO2 laser, and 11 with the Nd:YAG laser). The criteria for inclusion of PCOD in our study were: amenorrhea or oligomenorrhea with chronic anovulation, failure to ovulate in response to clomide or human menopausal gonadotropin, elevated serum levels of luteinizing hormone (LH) or an elevated LH/follicle-stimulating hormone ratio, exaggerated LH response to gonadotrophin-releasing hormone (GnRH), elevated serum androgen levels, and ultrasonographic features of polycystic ovaries. Eight pregnancies after CO2 laser and three after Nd:YAG laser were achieved. Decline of serum androgen concentrations was noted in both groups, but was significantly higher in the Nd:YAG laser group (from 3.4 +/- 0.4 ng/ml to 2.2 +/- 0.2 ng/ml). Nine patients checked before and after laser treatment showed a decrease in the characteristically exaggerated pituitary response to exogenous GnRH injection. There were no consistent findings of the pattern in LH pulsatility studied in 5 patients after Nd:YAG laser treatment. Ovarian status was investigated in 11 patients by second-look laparoscopy or cesarian section. There were absolutely no adhesions after Nd:YAG laser coagulation. Filmy adhesions were seen in 3 patients in the CO2 laser group.

Amenorrhea↗

PubMed1995

Hypotheses: melatonin/steroid combination contraceptives will prevent breast cancer.

The use of the conventional combination oral contraceptives (containing ethinyl-estradiol and a progestin) is associated with reduced risk of ovarian and endometrial cancer. However, prolonged use of these pills before first term pregnancy apparently increases the risk of pre menopausal breast cancer. We propose that the pineal gland hormone melatonin, combined with a progestin, as a new and novel oral contraceptive combination might prevent breast cancer in long term users. This hypothesis is based on the assumption that women have a propensity to develop breast cancer which correlates with number of ovulatory cycles over their lifetime. In evolution, the phylogenetic point at which women became sensitive to breast cancer evolved at a transfer point of the mechanism of ovulation from seasonal ovulation, which is still common in many mammalian species, to the current human pattern of continuous ovulatory cycles. We suggest that melatonin/ovarian-steroid contraceptive will restore the lost mechanism of endogenous anovulation, and thus, by preventing continuous epithelial breast cell proliferation, will reduce the risk of breast cancer in long-term users.

Breast Neoplasms↗

PubMed1987

Gamete intrafallopian transfer: a treatment for long-standing infertility.

Gamete intrafallopian transfer (GIFT) has been described by Asch et al. (1,2) as an alternative technique in the treatment of infertile couples. At the University of the Orange Free State, the GIFT technique was introduced in July 1985, and during phase I, 31 patients were treated by means of GIFT. All patients had had at least six cycles of ovulation induction with human menopausal gonadotropin (hMG) and human chorionic gonadotropin (hCG). Their diagnoses were anovulation (3 patients), mild endometriosis (17 patients), and unexplained infertility (11 patients). All husbands' semen analyses were normal. Of the 31 patients, 3 failed, due to spontaneous ovulation before laparoscopy (1 patient) and unsuccessful follicle aspiration at laparoscopy with no oocytes found (2 patients). Four ongoing pregnancies resulted from the remaining 28 patients. This represents a pregnancy rate of 14.29% per laparoscopy (including the failures). The patients who became pregnant had had infertility treatment for 5, 6, 8, and 8 years, respectively. GIFT therefore appears to be a promising method of treatment for long-standing infertility.

Adult↗

PubMed1997

Intermittent Etidronate partially prevents bone loss in hirsute hyperandrogenic women treated with GnRH agonist.

Treatment with gonadotropin-releasing hormone (GnRH) agonist leads to enhanced bone turnover and accelerated bone loss in premenopausal women with endometriosis, uterine leiomyomatomas and hirsutism. Sodium etidronate is a powerful inhibitor of bone resorption which had been proven efficacious in the prevention and treatment of postmenopausal osteoporosis. The objective of this study was to evaluate the skeletal effects of 6 months of therapy with the depot preparation of the GnRH agonist triptorelin (decapeptil 3.75 mg intramuscularly every 4 weeks) in 24 hirsute patients, aged 24-33 years, with hyperandrogenic chronic anovulation. Ten patients also received cyclical etidronate in an oral dose of 400 mg/day for 2 weeks, followed by an 11-week period of 500 mg/day elemental oral calcium (one cycle). The remaining 14 patients received 500 mg/day of elemental calcium continuously. After 6 months all treatments were discontinued for at least a further 6 months. Bone mineral density (BMD) at lumbar spine and hip (dual-energy X-ray absorptiometry, Sophos LXRA, France) and biochemical markers (serum alkaline phosphatase, osteocalcin, urinary N-telopeptide and hydroxyproline/creatinine ratio) were evaluated at baseline, 6 months and 12 months. In the group given GnRH agonist alone BMD fell significantly at all measured skeletal sites during the first 6 months. In the patients treated with etidronate a significant decrease in BMD was observed at lumbar spine but not in the femoral neck and trochanter, and the changes at lumbar spine and trochanter were significantly smaller than those in the control group. At 6 months bone turnover was also increased in patients treated with GnRH and calcium. Cyclical etidronate prevented the increase in biochemical markers of bone formation and resorption, with the exception of calcium/creatinine excretion, which was significantly increased in both groups. Six months after treatment withdrawal BMD did not recover in either group. Biochemical markers (N-telopeptide, serum alkaline phosphatase) remained increased in those patients previously treated with calcium alone while they remained close to baseline values in the patients treated with cyclical etidronate. Our study indicates that: (1) GnRH agonist therapy causes remarkable bone loss in young individuals with androgen excess who are expected to have increased bone mass; (2) this bone loss can be partially prevented by intermittent cyclical etidronate therapy.

Adult↗

PubMed1984

Anti-tumor and endocrine effects of chronic LHRH agonist treatment (Buserelin) with or without tamoxifen in premenopausal metastatic breast cancer.

Seventeen premenopausal women with metastatic breast cancer were treated with the potent Luteinizing Hormone Releasing Hormone (LHRH) agonist Buserelin as a first-line agent. Twelve patients (group A) were treated with Buserelin alone and five patients (group B) with the combination of Buserelin and tamoxifen from the start of treatment. In nine patients of group A tamoxifen was added to Buserelin later on because of tumor progression or recurrent peaks of plasma estradiol (E2). Chronic intranasal therapy with Buserelin alone, preceeded by parenteral administration, caused an objective remission in four patients (2 X C.R., 2 X P.R.) and stable disease in four further patients without causing side effects. The longest duration of response until now is more than 29 months. After addition of tamoxifen a partial response occurred in two more patients of group A. Anovulation with suppressed progesterone secretion was reached in all patients treated with Buserelin alone, but transient peaks of E2 occurred in the majority (60%) of the patients. Addition of tamoxifen to Buserelin treatment caused disappearance of E2 peaks in 2 patients, but also reappearance of progesterone secretion with recurring E2 peaks in 3 other patients; in one case hyperstimulation of the ovaries was observed without progression of tumor growth. In group B only one woman showed a complete castration effect, while in four patients progesterone secretion was not (completely) suppressed. In two of these five patients an objective response occurred. In conclusion, Buserelin appears effective in the treatment of premenopausal women with metastatic breast carcinoma, but with the regimen used close control of endocrine parameters is necessary because of the variation in hormonal response with a risk of (hyper)stimulation of the ovaries, especially during combination therapy with tamoxifen.

Adult↗

PubMed1986

Effects of norgestimate (0.250 mg) in combination with ethinyl estradiol (0.035 mg) on cervical mucus.

The antifertility effect of norgestimate (Ng), 0.250 mg, in combination with ethinyl estradiol (EE), 0.035 mg, on cervical mucus was investigated. The study was conducted over two consecutive cycles: a control cycle followed by a study cycle during which medication was given. Basal body temperature, cervical mucus and karyopyknotic index of vaginal cells were evaluated during both cycles. Disappearance of cyclicity of these parameters in the study cycle as well as monophasic basal body temperature were suggestive of inhibition of ovulation caused by the combination pill. Deterioration of sperm penetration may be reflective of anovulation and a direct antifertility effect of Ng on cervical mucus.

Adolescent↗

PubMed1997

Gonadotropins and glucocorticoid therapy for "low responders"--a controlled study.

PURPOSE: A randomized, nonplacebo controlled study was conducted to determine the effect of dexamethasone supplementation to a protocol of gonadotropin therapy in 42 "low-responder patients" aged 32 to 43 years. METHODS: All underwent at least two previous cycles treated by gonadotropins for unexplained infertility, or anovulation. Human menopausal gonadotropin was started on day 4 of the menstrual cycle combined with dexamethasone 0.5 mg administered nightly, as an adjuvant. A group of "low responders" who did not receive dexamethasone served as the controls. The number of follicles, total amount of gonadotropins used, time required for stimulation, fertilization, peak estradiol levels and pregnancy rate were evaluated. RESULTS: The number of developing follicles, estradiol levels, fertilization rate and pregnancy rate did not differ significantly. CONCLUSIONS: Although certain beneficial effects were observed in the literature in some of the infertile patients treated with corticosteroids, the overall results did not support daily, low-dose dexamethasone (long-acting corticosteroid) as a clinically useful adjuvant therapy for "low responders" during gonadotropin therapy.

Adult↗

PubMed2001

Exercise-related female reproductive dysfunction.

Clinical or biochemical abnormalities of gonadal function, consisting of delayed puberty, luteal phase deficiency, oligo-amenorrhea or anovulation, occur in girls and women participating in strenuous sports. The evidence of a causal relationship between athletic activity and menstrual dysfunction has led to increased interest, also because the number of women who practice sports has increased rapidly. The pathogenesis of exercise-related female reproductive dysfunction (ERFRD) is not completely clarified. The heterogeneity of sports practice, the role of overtraining and other factors, as adequate calorie balance or the assumption of exogenous steroids, could play a primary role in the comprehension of the pathogenic mechanisms of reproductive dysfunction. The interest of physicians about ERFRD is also due to the consequences of reduced gonadal function on women's health. Apart from some short-term transient effects (i.e. on muscle, genito-urinary tract or behavior), hypoestrogenemia can induce long-term deleterious effects, as premature osteoporosis and lifelong impairment of skeletal structure. In view of the possible short-term (infertility) and long-term (osteoporosis) consequences of ERFRD, correct physical training and adequate diet approach are mandatory to prevent or to revert neuroendocrine abnormalities so frequently reported in girls and women participating in recreational or competitive athletic activities.

Energy Intake↗

PubMed2004

Body composition, fat distribution and metabolic characteristics in lean and obese women with polycystic ovary syndrome.

The polycystic ovary syndrome (PCOS), characterized by chronic anovulation and hyperandrogenism, has many features of metabolic syndrome and can be considered a metabolic disease. Approximately 50% of patients with PCOS are overweight or obese with abdominal fat accumulation. Some metabolic alterations and abdominal fat distribution have also been reported in lean women with PCOS. The aim of this study was to evaluate the effect, if any, of obesity on metabolic features, body composition and fat distribution in patients with PCOS. Body composition and abdominal fat distribution (evaluated by DEXA), waist circumference, blood pressure, lipid profile, glucose tolerance and homeostasis model assessment index were determined in 23 lean [mean age 23 +/- 5 yr, mean body mass index (BMI) 22 +/- 2 kg/m2] and 27 overweight-obese (mean age 21 +/- 5 yr, mean BMI 32 +/- 5 kg/m2) patients with PCOS and in 20 age- and weight-matched eumenorrhoic women. Patients exhibited slight but non-significant differences in metabolic parameters, waist circumference, blood pressure and total and abdominal fat content compared with weight-matched controls. None of the lean subjects suffered from metabolic syndrome according to the National Cholesterol Education Program--Adult Treatment Panel III (NCEP-ATPIII) criteria as opposed to 10 overweight-obese patients and three overweight-obese control subjects (37% and 33.3% of each subgroup, respectively). Our data do not show significant metabolic alterations in lean PCOS women. Results indicate that obesity seems to underpin the metabolic alterations exhibited by the overweight-obese patients. However, since women with PCOS are at increased cardiovascular risk, further studies are needed to evaluate metabolic alterations and body composition in these patients.

Adipose Tissue↗

PubMed2004

Is ovulation induction still a therapeutic problem in patients with polycystic ovary syndrome?

Polycystic ovary syndrome (PCOS) is one of the most common endocrine diseases affecting women of fertile age, and is characterized by hyperandrogenism, chronic anovulatory cycles and oligomenorrhea or amenorrhea. Given the repercussions of chronic anovulation on sterility, PCOS is a heavy social burden. Here we describe the procedures used to induce ovulation in PCOS patients, the surgical approach and medical treatments that are still being experimented.

Aromatase Inhibitors↗

PubMed2005

Circulating nitric oxide in women affected by weight loss amenorrhea during pulsatile gonadotropin-releasing hormone therapy.

No specific markers of the severity or prognosis of hypothalamic-pituitary-gonadal axis disturbances associated with weight loss amenorrhea (WLA) are currently available. Circulating nitric oxide (NO), which is involved in the control of the reproductive function in women and is correlated with body mass index (BMI), at least in over-weight and obese subjects, might be a marker of the severity and/or progression of WLA. To test this hypothesis, we studied circulating NO levels in 11 women (age 27.1 +/- 1.59 yr) affected by WLA for 5.1 +/- 1.0 yr; in all patients hormonal therapy had been discontinued 10.0 +/- 3.15 months earlier. NO, determined by measuring its stable catabolite nitrite/nitrates (NOx), was compared with some clinical parameters and sex hormone levels. Subsequently, changes in NOx during pulsatile GnRH therapy (120 ng/kg bw sc every 120 min) were compared with the clinical and hormonal data. Fifteen normal women (27.3 +/- 1.6 yr) served as a control group. NOx was significantly lower (p<0.01) in WLA (8.8 +/- 2.0 micromol/l) than in control (18.7 +/- 2.5 micromol/l) subjects. No correlation between NOx and clinical parameters was noted in either WLA or control subjects. As a result of GnRH therapy, ovulatory cycles reappeared in 91% of WLA women. During the 1st cycle, periovulatory 17beta-estradiol levels were 110% higher than those noted in controls. During the 2nd cycle, NOx showed a slight increase in the follicular phase (+12% vs 1st cycle) followed by a drop during the luteal phase (-40% from the follicular phase); indeed, at that time, NOx correlated negatively with progesterone in both WLA (rS -0.32, p<0.05) and control (rS -0.48, p<0.05) subjects. NOx correlated with BMI at the time of the 2nd cycle (rS 0.71, p<0.05). In conclusion, this study shows that in WLA patients: 1) NO is low, as in other conditions of chronic anovulation; 2) it does not correlate with clinical data; 3) it takes longer than sex steroids to increase and show normal-like fluctuations; 4) its fluctuations are restored earlier in patients with greater BMI.

Adult↗

PubMed1993

Thyroid autoimmunity and female gender.

Sexual dimorphism exists in regard to the immune response between women and men, and it accounts for the greater prevalence of thyroid autoimmunity in women. Similarly to the human situation a sex-related susceptibility to autoimmune thyroiditis is evident in animal models. A direct influence of genes on sex chromosomes (X or Y) on the immune response has been postulated in some models of autoimmune thyroiditis in rats. On the other hand sex hormones have been implicated to explain the majority of sex differences in the autoimmune response against the thyroid. A state of immune suppression during pregnancy influences the clinical course of autoimmune thyroid diseases, in that a typical amelioration during pregnancy is accompanied by aggravation following delivery. This immunologic rebound phenomenon may also underly the post partum thyroid dysfunction in otherwise healthy women with a genetic predisposition to autoimmune thyroid disease. Thyroid autoimmunity also interferes with the female reproductive function. Hypothyroidism and less frequently hyperthyroidism due to thyroid autoimmune disorders may produce menstrual dysfunction, anovulation and eventually infertility. Maternal hyper- or hypothyroidism can affect the outcome of pregnancy, producing a higher incidence of miscarriages, maternal complications, and congenital malformations. Untreated maternal hypothyroidism produced by Hashimoto's disease during pregnancy can impair the neurological development of the fetus due to a reduced availability of maternal thyroxine during early gestation.2+ More specifically, fetal and/or neonatal hypo- or hyperthyroidism produced by the transplacental passage of maternal thyroid autoantibodies can impair growth and neuropsychological development of affected children.

Female↗

PubMedDate not supplied

Clinical features and hormonal characteristics in a case of ovarian arrhenoblastoma.

We report a case of a 34-year-old woman affected with ovarian arrhenoblastoma characterized by very high testosterone (T) levels (34.0-60.0 ng/ml; n.v.0.2-0.9) and suppressed gonadotropin levels. The physical examination revealed: severe hirsutism, acne, amenorrhea and other virilization signs. Basal hormonal evaluation also showed a markedly elevated 17-hydroxyprogesterone (17-OHP) and a mild delta 4 Androstenedione (A) and dehydroepiandrosterone sulfate (DHEAs) increase. ACTH test induced only slight changes in androgen secretion. By contrast, dexamethasone test greatly decreased A and DHEAs whereas T levels were only partially suppressed. Moreover, hCG test was clearly stimulatory for T and A. Suppressed gonadotropin levels did not respond to LHRH stimulation. The removal of the neoplasia was followed by normalization of T levels and increase of serum gonadotropins with subsequent restoration of a normal responsiveness to LHRH and resumption of an ovulatory menstrual cycle. This observation suggests that the high T levels played a primary role in the pathogenesis of the gonadotropin suppression and anovulation. Recovery of acne was complete whereas hirsutism score was reduced but still elevated after one year. This may be due to postoperative A and DHEAs levels slightly above the normal range, indicating the presence of adrenal hyperandrogenism.

17-alpha-Hydroxyprogesterone↗

PubMed1998

The pathogenesis of polycystic ovary syndrome: lessons from ovarian stimulation studies.

In polycystic ovary syndrome (PCOS) the ovary produces markedly increased amounts of both androgens and estrogens in response to gonadotropin stimulation. Distinctive responses of 17-hydroxyprogesterone and androstenedione to ovarian stimulation testing suggest that ovarian hyperandrogenism is a result of dysregulation of theca cell androgen production which is intrinsic to the ovary. The occurrence of hyperestrogenism together with hyperandrogenism in PCOS suggests that whatever the abnormality of local regulatory factors of steroidogenesis, it affects granulosa as well as theca cells. Dysregulation is often associated with an increase in the number of follicles which evade atresia and reach the 2-8 mm stage of development. Autocrine/paracrine factors, especially those which are FSH-dependent, likely play an important role in the pathogenesis of the ovarian abnormality. Both LH and insulin hypersecretion probably play a secondary role in PCOS by amplifying the preexisting ovarian dysregulation. Because FSH secretion is under tight long-loop negative-feedback control and LH is not, hyperandrogenism is the primary clinical manifestation of dysregulation of steroid production in PCOS. However, anovulation in PCOS is most likely a result of excessive estrogen and inhibin production by multiple, small follicles which inhibit FSH secretory dynamics sufficiently to prevent selection of a dominant follicle.

Androgens↗

PubMed1998

Polycystic ovary syndrome and insulin resistance: thrifty genes struggling with over-feeding and sedentary life style?

Almost two decades of research have greatly increased our knowledge in the complex field of metabolic aberrations in polycystic ovary syndrome, but still many problems remain unsolved. The statistical association between insulin levels and androgens originally put the focus on possible direct cause-and-effect relationships between these factors. Indeed there is evidence that insulin may affect ovarian functions in multiple ways, presumably in some cases causing anovulation and hyperandrogenism. Clearly, insulin may increase biologically active testosterone through reducing SHBG levels. Conversely, major increases in androgen levels may induce muscular changes leading to reduced insulin-mediated glucose uptake. There are suggestions of increased steroidogenesis in both ovarian and adrenal pathways, with the net result of increased androgen production. There are also findings supporting increased corticosteroid production, which could contribute to insulin resistance directly or through promoting accumulation of abdominal fat, a typical feature of over-weight women with PCOS. Free fatty acids, released in great amounts from abdominal fat, may induce insulin resistance. Insulin resistance may also be due to a primary aberration in the insulin receptor. Putatively increased serine phosphorylation may cause both impairment of the insulin signal and increased 17,20 lyase activity, thus suggesting a common cause for insulin resistance and increased androgen production. There are also findings supporting a high prevalence of beta-cell dysfunction in PCOS, ranging from increased insulin secretion, not explained by insulin resistance or BMI, to failing beta-cell function, mainly in obese women during progress to glucose intolerance and NIDDM. Recent genetic findings also support a multifactorial genesis to PCOS, notably with positive findings both in genes regulating steroidogenesis and insulin secretion. It is suggested that PCOS is the result of "thrifty" genes, providing advantages in times of shortage of nutrition such as muscular strength, moderate abdominal fatness and decreased insulin sensitivity, i.e. an anabolic, energy saving constitution. However, when this constitution is exposed to unlimited food supplies and modern sedentary life style a full-blown PCOS with insulin resistance and infertility is triggered, presumably via several mechanisms, which follow a logical amplification system between two basic anabolic hormones, insulin and testosterone.

Body Composition↗