Natural Polycystic Ovary Syndrome Treatment Book

The Natural Pcos Diet

The Natural Pcos Diet, By Jenny Blondel, A Leading Australian Naturopath In Response To Thousands Of Requests For Professional Information To Help Women Suffering From Pcos. Real Solutions To Naturally Overcome PCOS. Naturally balance your hormones Increase your chances of conceiving Help you lose weight and feel good Curb your cravings for sugary foods Turn your fatigue around Achieve clearer, glowing skin See improvements in your mood. Do You Feel PCOS Is. Ruling Your Life? At Last! The Natural PCOS Diet. A Naturopath’s Easy Step-by-Step Guide to Overcoming PCOS Is. Now Available! Read more...

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Role of Oxidative Stress in Polycystic Ovary Syndrome

A recent study by Kusgu et al. 209 demonstrated that PCOS subjects have significantly elevated concentration of plasma MDA independent of obesity. The results showed that MDA level is significantly higher in young, nonobese PCOS patients, even in the absence of IR when compared with controls. Protein oxidation status often is assessed with a colorimetric assay that measures protein carbonyl (PC) content, after extracting the serum with dinitrophenylhydra-zine. Fenkci et al. 210 demonstrated that the PC level was significantly higher in PCOS patients with normal BMI compared with controls. This observation of higher protein oxidation suggested that free radicals damage proteins in PCOS patients 210 Furthermore, protein carbonyls were shown to have a positive correlation with fasting insulin, suggesting a strong association between insulin resistance and protein oxidation in PCOS. Measuring plasma concentration of NO3 and NO2 assesses NO concentration. The sum of NO3 and NO2 is assumed...

Polycystic Ovary Syndrome

Polycystic ovary syndrome is the clinical condition seen most frequently with androgen excess. Women with PCOS present with complaints of abnormal menses, infertility, hirsutism, acne, and obesity, all of which are related to excess androgen. PCOS is the single most common endocrine abnormality of women of reproductive age and affects 6 to 8 of women worldwide. The definition of PCOS is constantly being revised. The Task Force on the Phenotype of the Poly-cystic Ovary Syndrome from the Androgen Excess and PCOS Society (AE-PCOS Society) defines PCOS by the presence of hyperandrogenism (clinical and or biochemical), ovarian dysfunction (oligo-anovulation and or polycystic ovaries), Box 35-11 Causes of Androgen Excess in Women I. Adrenal hyperandrogenism B. Functional adrenal hyperandrogenism II. Gonadal hyperandrogenism A. Ovarian hyperandrogenism 1. Functional ovarian hyperandrogenism polycystic ovary syndrome C. Pregnancy-related hyperandrogenism From Ehrmann DA, Barnes RB, Rosenfield...

Possible Role Of Egvegf In Pathological Conditions

EG-VEGF may have considerable pathophysiological and therapeutic significance for several endocrine disorders characterized by excessive angiogenesis and for certain endocrine gland tumors. We have recently evaluated the expression of EG-VEGF in a panel of human ovary specimens isolated from patients diagnosed with poly-cystic ovary syndrome (PCOS) (N. Ferrara et al., in prep.). This condition is a major cause of infertility, affecting 5-10 of women of reproductive age (Goldziher and Green 1962 Dunaif and Thomas 2001). It is known that the increase in ovary mass in PCOS is accompanied by extensive angiogenesis in the stroma and theca (Yen 1999). Our previous studies have demonstrated that ade-novirus-mediated delivery of EG-VEGF in the ovary elicits an angiogenic response and cyst formation, similar to that induced by VEGF (LeCouter et al. 2001). Although both EG-VEGF and VEGF are expressed in the PCOS ovaries, their expression patterns are very distinct, essentially nonoverlapping....

What Additional Effects May Aeds Have On Reproductive Function In Women

Sodium valproate may be associated with increased occurrence of PCOS.80 In PCOS, the patient has anovulatory cycles and hyperandrogenism. Characterized by hirsutism and menstrual disorders, the condition is more frequent in obese women (see Refs. 29 and 81 for reviews). Isojarvi et al.m have noted PCOS to be more common in epileptic women treated with sodium valproate (approximately 45 ) than in those who are treated with CBZ (20 ). They suggest that valproate causes weight gain, insulin resistance, and hyperinsulinemia, which then cause hyperandrogenism,82 which leads to PCOS. Hyperinsulinemia may indeed cause hyperandrogenism by directly stimulating ovarian steroidogenesis29 and by inhibiting the synthesis of SHBG with a consequent increase in the availability ofbioactive androgens. Interestingly, for poorly understood reasons, weight gain is much more likely to occur if valproate treatment is started before the age of 20 than after that age, irrespective of the duration of...

Taxonomy Of Clinical Trials

There are other differences between the two types of trials. Blinding is more likely to be used in an explanatory trial such as one comparing oral metformin with placebo in women with polycystic ovarian syndrome. Pragmatic trials may also be blinded, but this is often not feasible (for example, in surgical versus medical trials), nor always desirable. There is also less of a compulsion to use placebos, as the objective is to compare the new intervention, not with a placebo, but with the 'gold standard' or best of the existing treatments. Clinician and patient biases caused by the absence of blinding may not necessarily be detrimental to the trial, but could actually be seen to be part of the response to treatment. The outcome in a pragmatic trial such as one comparing oral clomiphene citrate (a drug treatment) versus expectant management in unexplained infertility incorporates the total difference between the interventions that are being evaluated. This may include the effect of the...

Effects of exogenous testosterone on cardiovascular risk factors

On the one hand, insulin sensitivity contributes to the patho-genesis of hyperandrogenemia in polycystic ovary syndrome. Insulin stimulates androgen synthesis in the ovaries via its cognate receptor and the inositolglycan pathway (Nestler et al. 1998). Since the ovaries remain sensitive to insulin when other tissues such as fat and muscle are resistant, hyperinsulinemia can augment the LH-dependent hyperandrogenism in insulin resistant women with polycystic ovary syndrome (Dunaif and Thomas 2001). In support of this, treatment of insulin resistance in women with polycystic ovary syndrome with metformin or the insulin sensitizer troglitazone significantly decreased serum levels of insulin as well as testosterone, independently of body mass index or gonadotropin levels (Kolodziejczyk et al. 2000 Pasquali and Filicori 1998). Concomittantly, plasma levels of HDL-cholesterol increased and plasma levels of PAI-1 decreased. These data imply that hyperinsulinemia...

The paradoxical effects of androgens on human hair growth

Vellus Hair

Androgenetic alopecia has also been described in women, but the pattern of expression is normally different. Women generally do not show the frontal recession, but retain the frontal hairline and exhibit thinning on the vertex which may lead to balding (Ludwig 1977) (Fig. 6.3). Post-menopausal women may exhibit the masculine pattern (Venning and Dawber 1988). The progression of balding in women is normally slow and a full endocrinological investigation is recommended if a rapid onset is seen (Dawber and Van Neste 1995). Although female pattern hair loss is seen frequently in association with hyperandrogenism, other women frequently have no other symptoms of androgen abnormality. Therefore, there is some debate about whether androgen is essential for this hair loss in women (Birch etal. 2002) though this is still generally assumed. If, as occurs in men, the changes develop due to the genetically influenced, specific follicular responses within the scalp follicles themselves, it is not...

Endocrine and Metabolic Factors

Polycystic Ovary Syndrome More than 50 of women affected by this relatively common disorder are obese. Some controversy surrounds whether PCOS is a cause or consequence of obesity, although most evidence points to the latter. Other common features include menstrual irregularities, hirsutism, and elevated testosterone and luteinizing hormone blood levels. Insulin resistance is a consistent finding, even in the absence of obesity. This resistance is thought to be associated with other findings in PCOS, although exact mechanisms are unclear.

The treatment of androgenpotentiated hair disorders

The most common endocrine treatment, outside the USA, is the antiandrogen, cyproterone acetate, given with estrogen if the woman is premenopausal spiro-lactone or flutamide can be used as an alternative (Fruzzetti 1997 Lumachi and Rondinome 2003). Patients have to be well-motivated because hair growth on the face generally takes at least nine months before a noticeable effect occurs, although any acne will be cleared in a couple of months and effects on thigh hair growth will be seen in four to six months (Sawers etal. 1982). Facial responses are seen first on the sides of the face and last on the upper lip, in reverse order to the appearance of facial hair in men (personal observations). Finasteride has also been used for hirsutism with some success (Lacryc etal. 2003). This seems logical as 5a-reductase type 2 is necessary for male pattern body hair growth (see Section 6.4.1). Contraception is still required with all endocrine treatments due to the potential to affect the...

Reproductive Age Women

Anovulation is the most common cause of abnormal vaginal bleeding in reproductive-age women. The majority of anovulation is related to hypothalamic abnormalities or polycystic ovarian syndrome (PCOS) (Box 25-2). By definition, anovulatory cycles are unpredictable and cannot be classified by any one type of vaginal bleeding pattern. A woman may experience 14 days of heavy bleeding one month, light spotting intermittently for the next month, and then go for 3 months without a cycle. The pathologic abnormality in these cycles is a lack of ovulation, which produces an unopposed-estrogen state. The lack of progesterone Excessive exercise Polycystic ovarian syndrome Thyroid disorders Hyperprolactinemia Idiopathic chronic anovulation

Genetics vs Lifestyle

Central obesity suggests increased visceral fat deposits, likely caused by increased production of peptides and other metabolic messengers. Hormonal influences most likely play a role in the distribution of fat. Central obesity is believed to result partly from increased androgenic effects, which is why men have a greater tendency for central obesity. Central obesity is also associated with hyperandrogenic states in women, such as polycystic ovary syndrome (PCOS). The increase in visceral deposition of fat that can occur after menopause in women may be related to a decrease in growth hormone and estrogen production (see Chapter 35).

Pharmacologic Therapy

On increasing SHBG and antiandrogenic effects. However, to date there is no consensus as to the best OC choice for these women (e.g., those with PCOS). Specifically, for women with PCOS, the use of depot and intermittent oral MPA sup- The use of metformin and the thiazolidinediones pioglitazone and rosiglitazone results in improved insulin sensitivity. In patients with PCOS, this is associated with reduced circulating androgen concentrations, increasing ovulation rates, and improving glucose tolerance. These improvements can be attributed to the increase in SHBG that

Patient Encounter 4 Hormonal Contraceptives and Interactions With AEDs

As noted above, many of the AEDs induce hepatic microsomal enzyme systems and thus reduce the effectiveness of hormonal contraceptives. Women taking AEDs that may reduce the effectiveness of hormonal contraceptives should be encouraged to also use other forms of birth control. In contrast to these interactions, hormonal contraceptives induce glucoronidation of lamotrigine and valproate. Oral contraceptives that cycle hormones cause reductions in serum concentrations of lamotrigine or valproate during days of the cycle when hormones are taken serum concentrations increase during days when hormones are not taken. Due to induction or inhibition of sex hormone metabolism and changes in binding of hormones to sex hormone binding globulin, some AEDs may reduce fertility. For example, valproate has been associated with a drug-induced polycystic ovarian syndrome. Women who experience difficulties with fertility should seek the advice of health care professionals with expertise in fertility.

Nonpharmacologic Therapy

Nonpharmacologic treatment options for anovulatory bleeding depend on the underlying cause. In a woman of reproductive age with PCOS, weight loss may be beneficial. In women who have completed childbearing or who have failed medical management, endometrial ablation or resection and hysterectomy are surgical options. It is unclear as to which procedure is preferred. Short term, it appears that ablation or resection results in less morbidity and shorter recovery periods.18 However, a significant number of these women eventually undergo hysterectomy in the 5 years that follow.5

Female Infertility The Obstruction to Reproduction

Getting pregnant isn't as easy as it looks. Indeed, there are a host of intricate processes that must be completed during ovulation, fertilization, and implantation of eggs into the uterus. Most of the couples I see have already been through a battery of tests to determine the possible causes of infertility. These conditions range from failure to ovulate properly to polycystic ovaries, blocked fallopian tubes, endometriosis, uterine fibroids, sexually transmitted disease, and pituitary, thyroid, or adrenal disorders. Emotions such as fear, anxiety, anger, and resentment are often by-products of this stressful time in a couple's inability to conceive.

Genetic Disorders of Insulin Resistance

These genetic defects may cause diabetes varying from mild to severe. Marked hyperinsulinemia activates epidermal growth factor receptors in skin, resulting in acanthosis nigricans, a darkening of skin folds at the nape of the neck or in the axilla. Marked hyperinsulinemia stimulates ovarian steroidogenesis, which can result in enlarged ovaries and a virilizing syndrome. This condition provided insight into the connection of insulin resistance to polycystic ovarian syndrome, which is now routinely treated with metformin to attenuate hirsutism and stimulate ovulation. The genetic defects in patients with generalized lipoatrophy have not been fully defined, but these patients are extremely insulin resistant because energy substrates can be stored only in liver and muscle. Impairment in fatty acid storage compromises muscle uptake and glucose oxidation.

Can You Prevent Diabetes

So far, despite a number of research studies now underway, there are no definitive answers on how to prevent Type 1 diabetes. Type 2 diabetes is another story. You can reduce many of the risk factors that increase your chances for developing the condition. Poor lifestyle habits such as a bad diet and lack of exercise can increase your chances for getting diabetes. Other nonnutrition related risk factors for Type 2 diabetes include being over the age of 45, having a parent or sibling with the disease, being of Latino, Native American, African American, or Pacific Islander descent, and, in a woman, having polycystic ovarian syndrome.

Associations of endogenous testosterone with cardiovascular risk factors

Women present the opposite relationships between endogenous androgens and obesity, insulin and cardiovascular risk factors. In cross-sectional studies, serum levels of testosterone were found to have significant positive correlations with BMI and leptin levels. Low serum levels of SHBG, which is an indirect measure of female hyperandrogenism, were associated with high BMI and WHR as well as with high serum levels of leptin and insulin and low serum levels of HDL-C (Hergenc etal. 1999). Moreover, in a prospective study, 20 of women with SHBG-levels below the 5th percentile developed diabetes mellitus type 2 within the 12-year follow-up period (Lindstedt et al. 1991). Thus, in women, hyperandrogenism, rather than hypoandrogenism as in men, is a component of the insulin resistance syndrome. In agreement with this, women with PCOS frequently present with hypercholes-terolemia, low HDL-C, hypertriglyceridemia, elevated fibrinogen and PAI-1, and a family history of diabetes mellitus....

Testosterone and cardiovascular disease in women

More frequently than control women by clinical symptoms of androgen excess such as hirsutism and polycystic ovaries (Amowitz and Sobel 1999 Dunaif 1997 Lobo and Carmina 2000 Rajkhova etal. 2000). Cross-sectional data consistently showed a strong obesity-independent association with a cluster of cardiovascular risk factors including insulin resistance, dyslipidaemia and impaired fibrinolysis. It was therefore suggested that the chronically abnormal hormonal and metabolic milieu in the polycystic ovary syndrome (PCOS), starting from adolescence, may predispose these women to premature atherosclerosis. Based on calculated risk profiles, women with polycystic ovary syndrome were predicted to have a 7-fold increased relative risk for myocardial infarction. In agreement with this concept, a combined angiography and pelvic ultrasound study of 143 women aged < 60 years observed significant associations between the presence of polycystic ovaries with the presence and severity of coronary...

Infancy through Adolescence

Although malnutrition is still a problem in the United States, inappropriate nutrition, especially calorie-nutrient imbalance leading to overweight and obesity, has become commonplace. Recent NHANES studies demonstrate that the prevalence of overweight (BMI > 95 ) in girls 2 to 19 years old increased from 13.8 in 1999-2000 to 16 in 2003-2004, and the prevalence of overweight in boys 2 to 19 years old increased from 14 to 18.2 (Ogden et al., 2006). Increased pediatric BMI is associated with high blood pressure, sleep apnea, asthma, polycystic ovarian syndrome, type 2 diabetes, gastroesophageal reflux, and orthopedic problems (Benson et al., 2009). A nationwide survey of more than 6000 children and adolescents found that at least 30 consumed fast food on a typical day. These children consumed more total fat, total carbohydrate, more added sugars and sugar-sweetened beverages, less milk, and fewer fruits and nonstarchy vegetables than children who did not eat fast food (Bowman, 2004)....

Ovarian and Testicular Disorders

Sexual development in both males and females is driven by the hypothalamic-pituitary axis. The normal process is the result of pulsatile release of GnRH from the hypothalamus, which stimulates the pituitary to release FSH and LH (GHRH and GH also play a role). Release of FSH and LH activates the ovary and testis to produce estrogen and testosterone and is responsible for stimulation of gametogenesis. This process is assisted by conversion of adrenal androgens from the adrenal cortex into androstenedione and subsequently into potent androgens (testosterone) or estrogens (estradiol) in the peripheral tissues (see Adrenal Glands). Errors can occur along this complex pathway, resulting in early sexual development (precocity), delayed sexual development (delayed menarche), errors of translation (male feminization syndrome), early loss of reproductive function (premature menopause), and inappropriate response to stimuli (polycystic ovary syndrome).

Valproate

Valproate (VPA) is FDA-approved in the prevention of episodic migraine. Although it is a very effective preventive therapy, VPA should not be used in women in their childbearing years because of teratogenicity and increased risk of developing polycystic ovarian syndrome. It can cause weight gain and hair breakage. Hair breakage may be prevented in some patients with supplementation of selenium 10-20 mcg daily and zinc 25-50 mg daily.

Hypercalcemia

Figure 35-8 Therapeutic algorithm for management of polycystic ovary syndrome. (Modified from Samraj GPN, Kuritzky L. Polycystic ovary syndrome comprehensive management in primary care. Comp Ther 2002 28 208-22iq.) Figure 35-8 Therapeutic algorithm for management of polycystic ovary syndrome. (Modified from Samraj GPN, Kuritzky L. Polycystic ovary syndrome comprehensive management in primary care. Comp Ther 2002 28 208-22iq.)

Special Populations

Short Dick Syndrome

There are several lifestyle factors that may predispose to obesity. When calorie intake continuously exceeds requirements, obesity results. The converse is likewise true. Fewer than 1 of all cases of obesity are related to neuroendocrine causes, and these conditions rarely cause massive obesity. These syndromes include hypothyroidism, hypopituitarism, adrenocortical excess, polycystic ovary syndrome, and hypothalamic tumors or other damage to this part of the brain, as well as some rare inherited conditions. Prader-Willi syndrome is a rare chromosomal microdeletion syndrome associated with childhood massive obesity, mental retardation, and failure of sexual development. A patient with Prader-Willi syndrome and morbid obesity is pictured in Figure 5-2. An obesity-focused history should include a chronologic history of the patient's weight, identifying age at onset, description of weight gain, and inciting events. For women, weight gain often occurs during adolescence, pregnancy,...

Turners Syndrome

Evaluate anovulation estrogen present (polycystic ovary syndrome) Modified from Brassard M, AinMelk Y, Baillargeon JP. Basic infertility including polycystic ovary syndrome. Med Clin North Am 2008 92 1163-1192. Treatment should be directed toward the underlying cause. For tubal disease, surgery and in vitro fertilization are options. Endometriosis can be managed with conservative surgery based on the degree of disease or can be circumvented through intrauterine insemination or in vitro fertilization. Ovulatory dysfunction is treated based on the underlying cause bromocriptine for prolactinoma, metformin or clomi-phene citrate for PCOS, human menopausal gonadotropin for hypogonadotropic hypogonadism, clomiphene citrate plus glucocorticoids for adrenal hyperplasia with elevated levels of androgens, and antibiotics for infection. The family physician should strongly consider early referral to a reproductive specialist if the patient or couple have complex medical histories or advanced...

Male Hypogonadism

Clinical diagnosis again begins with history, including information about sexual developmental milestones, current symptoms, ambiguous genitalia at birth, cryptorchidism, behavioral abnormalities, anosmia, surgeries, sexually transmitted diseases (STDs), and medications. History should include the presence of acute and chronic medical conditions and neurologic symptoms. Physical examination is directed toward sexual characteristics, body habitus, gyne-comastia, and signs of hypogonadism. Testis should be measured for length and width with an orchidometer. Consistency of the testes should be noted and a scrotal examination done for the presence of varicocele. A nonpalpable prostate may imply testosterone deficiency. A low morning (8-10 am) serum testosterone level confirms hypogonadism. Serum LH and FSH levels are elevated in primary hypogo-nadism and are normal to low in secondary hypogonadism. Semen analysis will assess the capability of spermatogenesis. An increase in sex...

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