Natural Polycystic Ovary Syndrome Treatment Ebook

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...

The Natural Pcos Diet Summary

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Causes of Hyperandrogenism

As far as hyperandrogenisms due to an excess of androgen production are concerned, tumoral causes and Cushing's syndrome are rare. The most common endocrine disorders are polycys-tic ovary syndrome (PCOS) and non-classic adrenal hyperplasia (NCAH) with 21-hydroxylase deficiency. Hyperandrogenism is associated with high levels of circulating androgens and decreased SHBG levels. PCOS also requires morphological and ultrasound criteria an increased number of subcapsular follicles and stromal hyperplasia. Plasma levels of 17-hydroxyproges-terone (17-HP) are increased in NCAH. If NCAH is only suspected with moderately increased 17-HP, an adrenocorticotropic hormone (ACTH) test must be performed 1, 6, 7 .

HS and Biological Hyperandrogenism

Furthermore, as far as serum levels of andro-gens and SHBG are concerned, there is no clear evidence for biochemical hyperandrogenism. On average, androgen levels (total plasma testosterone and free testosterone index due to a low SHBG) were increased, but were normal in many individual patients, and no significant decrease of SHBG could be detected 13 . In fact, SHBG is known to be regulated by factors that influence body weight and this study was not controlled for body weight, and neither was a second one which found hyperandrogenism in a subgroup of women who did not experience a premenstrual flare in their disease 9 . In a further group of 66 women with HS, among which 23 had acne, 23 were significantly obese and 19 were hirsute testosterone and DHEAS were normal in all subjects 3 . In obese subjects, SHBG was reduced, consistent with body-mass-index-matched controls. No evidence for biochemical hyperandrogenism could be found in women with HS when compared with controls matched...

Physical examination

Hair distribution may reveal signs of androgen excess. The absence of both axillary and pubic hair in a phenotypically normal female suggests androgen insensitivity. 4. External genitalia and vagina should be inspected for atrophy from estrogen deficiency or clitoromegaly from androgen excess. An imperforate hymen or vaginal septum can block the outflow tract.

Lack of Association between HS and Endocrinopathies

In women HS has not been reported in association with ovarian or adrenal tumours, Cush-ing' syndrome, PCOS or NCAH, all known causes of hyperandrogenism with increased or abnormal androgen production. In fact, a possible association of HS with functional hyperan-drogenism (ovarian or adrenal dysfunction) merits investigation with modern biological and ultrasound markers 7 . HS usually begins after puberty when the apocrine glands are fully developed. A few cases have been reported in children, as clinical manifestations of premature adrenarche or early puberty 11, 12, 15 . This represents in fact the strongest evidence for an influence of andro-gens on HS. However, HS is more common in women and usually affects premenopausal women, although it may appear after menopause 3 . The rare incidence of HS in post-menopausal women does not stand in favour of a role for androgens, since hyperandrogenism after the menopause has yet to be demonstrated. On the other hand, improvement during and...

End Organ Androgen Sensitivity

All the above data suggest that the main mechanism for the possible role of sex hormones in HS lies in end-organ sensitivity rather than in the plasma levels. Women can develop HS while taking oral contraceptives especially when an-drogenic progestins are used, and this also suggests, as in acne, a possible androgen dependence of the disease 19 . In acne, not only sebocytes but also other epithelial cells are involved in the skin hyperandrogenism that is responsible for the formation of the comedo. Keratinocytes from the acroinfundibulum express the key enzymes involved in the in situ metabolism of androgens (in situ synthesis of the weaker androgens, their transformation into testosterone and its reduction into DHT) 5 . Investigation for the activity of these enzymes in the epithelial cells that are presumed to be involved in the first stage, i.e. follicular occlusion, of HS remains to be conducted. cal skin hyperandrogenism in women with HS. On the other hand, a genetic polymorphism...

Female Reproductive System

Hormonal control of the menstrual cyclc. The hypothalamus secretes gonadotropin-relcasing hormone (GnRH). In response to GnRH, the adenohypophysis secretes follicle-stimulating hormone (FSH) and luteinizing hormone (LH). In response to FSH, the development of a secondary follicle to a Graafian follicle is stimulated in the ovary. The granulosa cells within the secondary follicle and Graafian follicle secrete estrogen (E). In response to estrogen, the endometrium of the uterus enters (he proliferative phase. In response to LH (LH surge), ovulation occurs. After ovulation, the granulosa lutein cells of the corpus luteum secrete progesterone (P). In response to progesterone, the endometrium of the uterus enters the secretory phase. Conditions that impair the secretion of GnRH from the hypothalamus will prevent the secretion of FSH that is necessary for follicle development and will resulr in inferriliry. In such cases, the drug clomiphene (an estrogen receptor antagonist) is...

Modeling Human Disease through Targeted Overexpression

Several clinical studies have shown a correlation between hypersecretion of LH and functional ovarian hyperandrogenism (FOH), infertility, and miscarriage in women (Barnes et al., 1994 Ehrmann et al, 1995 Franks, 1995 Regan et al., 1990 Shoham et al., 1993), suggesting that chronically elevated LH impairs fertility. Unfortunately, no studies show a direct relationship between hypersecreted LH and reproductive abnormalities. Because LH is secreted in regulated pulses (Gibson et al., 1991) and its serum half-life is short (20-30 min Niswender et al., 1974), it is difficult to devise protocols for chronic administration of exogenous LH that mimic endogenous pulse patterns of LH. To circumvent this limitation, the authors devised a transgenic approach where elevated hormone levels are maintained chronically, without requiring multiple injections, supraphysiologic dosing, or appreciable dampening of the hypothalamic-pituitary-gonadal axis. In summary, a transgenic strategy has been...

Nonneoplastic Conditions

Stromal hyperthecosis this rare condition is often associated with signs of hyperandrogenism. Oestrogenic manifestations, coexistent endometrial hyperplasia or adenocarcinoma may also occur. Typically, both ovaries are enlarged and yellow white in colour with a vague nodular pattern. Histologically, there is usually accompanying stromal hyperplasia, but in addition luteinised stromal cells are present singly or in small groups. Massive oedema this is a rare cause of unilateral ovarian enlargement and is probably secondary to partial torsion of the ovary. Presentation is often with abdominal pain and a palpable ovarian mass. There may be evidence of androgen excess. On sectioning the ovary it is typically oedematous and pale in colour and watery fluid exudes from the cut surface. Histologically, there is separation of the stromal cells by oedema fluid which surrounds residual ovarian structures. Luteinised stromal cells may be present. The outer cortex is typically not oedematous but...

Androgen Metabolism

The causes of hyperandrogenism are multiple (Table 12.1). Skin androgenization in women may be due to abnormal production of andro-gens by the ovaries and or the adrenal glands, and or to an excessive response of target cells in the pilosebaceous unit (peripheral androgen-ism) 6 . Table 12.1. Causes of hyperandrogenism 1. Polycystic ovary syndrome (PCOS) 3. Skin hypersensitivity peripheral hyperandrogenism

Neoplastic Disease

And thus may influence carcinogenesis (Giovannucci, 2001). Conditions associated with hyperinsulinemia, such as obesity, sedentary lifestyle, or chronic insulin therapy, are also related to high risk (Yang et al., 2004). Hyperinsulinemia can be associated hyperandrogenism and hyperestrogenic conditions, which may play a role in the onset of some malignancies, such as endo-metrial cancer, breast cancer, and prostate cancer (Guastamacchia et al., 2004).

Regulation

Sex hormone-binding globulin is regulated in a complex fashion, which is poorly understood. Originally, it was thought that the major regulators of SHBG biosynthesis were estrogens and androgens. This hypothesis was based on the observation that normal women have significantly higher serum SHBG levels than normal men. However, subsequently, a number of studies showed that estrogens and androgens do not always account for the significant changes in circulating SHBG levels observed in clinical situations. For example, although patients with polycystic ovarian syndrome generally have elevated androgens and decreased SHBG levels, some have normal SHBG levels.87,88 Similarly, the effect of estrogens on SHBG levels is inconsistent. During the latter half of pregnancy, SHBG levels rise dramatically as estrogens increase. However, in infancy, SHBG levels also rise in spite of low circulating estrogens and in puberty, levels fall as estrogens increase in girls.

Hormonal Treatment

Contraindications to testosterone therapy include androgenic alopecia, seborrhea, or acne, hirsutism as well as a history of polycystic ovary syndrome, and estrogen depletion. Oral methyl testosterone therapy is contraindicated in women with hyperlipidemia or liver dysfunction. Regular follow up is both clinical inspection of skin and hair for seborrhea, acne, hirsutism, and alopecia and biochemical through monitoring of free bioavailable testosterone and SHBG, keeping these values within the normal range for premenopausal women. Of note, methyl-T is not included in the usual assays for T. Possibly, the target level for older women should be even lower but this remains unclear. Lipid profile and glucose tolerance are also monitored. The current recommendation is to prescribe only for 12 months owing to lack of long-term safety data (92).

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