Poly-cystic ovarian syndrome

Description of condition

 

PCOS is a complex condition that is located in the reproductive system, involves the endocrine system, but is primarily a metabolic condition.  The term polycystic refers to the appearance of many small cysts on the ovaries when examined by ultrasound.  These ‘cysts’ are actually undeveloped follicles and will appear on approximately 20% of all ovarian ultrasounds.  

Presence of these cysts is diagnosed as polycystic ovaries (PCO), which differs from PCOS in that the latter condition includes hormonal and metabolic abnormalities.  Of the women diagnosed with PCO only about 7-8% will have PCOS, although 80% of women that do not ovulate regularly will have PCOS. [1]

 

It is estimated that between 5-10% of women have PCOS.  Many women will start to experience menstrual irregularities 3-4 years after menarche, with most cases being diagnosed between the age of 20-29. [9]

 

Aetiology

 

It is thought that the primary cause of PCOS is insulin resistance and chronic hyperinsulinaemia which lead to ovarian and adrenal hyperandrogenism.  Insulin resistance can be acquired or amplified due to central obesity, a sedentary lifestyle, smoking or corticosteroid use. [1]  Oestrogen dominance is also a significant causative factor, and may occur due to the following reasons:

 

  • Increased activity of the ovarian enzyme cytochrome P450c17α which is responsible for forming androgens in both the ovaries and adrenal glands. [2]

  • Stress and low blood sugar levels (BSLs) → release of ACTH (adrenocorticotropic hormone) from the pituitary which stimulates the adrenal glands to produce elevated levels of DHEA (dehydroepiandrosterone), an androgen which is converted into oestrone (a type of oestrogen).[2]

  • Excess weight has been shown to increase the rate of aromatisation in fatty tissue – that is the conversion of androgens into oestrone. [3]  The levels of the carrier protein for oestrogen and testosterone, SHBG (sex hormone binding globulin) are also reduced in obese women, resulting in increased circulation of these hormones. [1]

  • Adrenal or hypothalamic-pituitary dysfunction can cause inappropriate stimulation of hormones that are able to increase the level oestrogen in the body. [3]

  • Imbalance of oestrogen relative to progesterone.

 

Women with a family history of PCOS have a 40% chance of developing the condition, clearly illustrating a genetic link. [3]

 

The hormone leptin which is secreted by adipocytes is responsible for the regulation of body weight by its effect on metabolism, satiety and energy metabolism.  The presence of leptin receptors on ovarian follicles indicates that this hormone is also involved in the regulation of follicular development.  In obese women the levels of leptin are greatly increased, this may cause leptin resistance and lead to persistently high levels of LH (luteinising hormone), which is a significant factor in PCOS. [1]

 

Pathophysiology

 

Before looking at the Pathophysiology, let’s first have a quick review of normal physiology.  Firstly, there are two main oestrogens in the body: Oestradiol and Oestrone. 

 

Oestradiol is low during the follicular phase and high during the luteal phase due to ovulation.  Anovulation results in decreased levels of oestradiol. 

 

Oestrone is primarily derived from the peripheral conversion of androgens in fat and muscle tissue in a process called aromatisation.  Increased body fat increases the level of oestrone.  Irregular menstruation also increases oestrone levels.  [1]

 

To limit confusion, I will just refer to oestrogen in general.  The female reproductive cycle typically lasts from 24-35days and is divided into four phases (based on a 28 day cycle):

 

  • Menstrual phase – lasts for about 5 days, is the shedding of the endometrium.  The hypothalamus secretes GnRH (gonadotropin releasing hormone) → pituitary releases FSH (follicle stimulating hormone) → follicular growth in the ovary is initiated.

  • Follicular or pre-ovulatory phase, days 6-13 – FSH is still high, the follicles continue to grow and begin to secrete oestrogen which stimulates growth of the endometrium.  One dominant follicle continues to develop and the others undergo atrophy, FSH levels decline and oestrogen rises due to stimulation from LH.

  • Ovulation, day 14 – the mature oocyte is released into the pelvic cavity.  There is a dramatic drop in FSH levels and a gradual decline in LH.

  • Luteal or postovulatory phase, day 15-28 – LH causes the corpus luteum to secrete progesterone and oestrogen, other hormones such as prolactin are also released during this phase.  As the endometrium prepares for embryo development the level of progesterone increases, and LH continues to slowly decrease.  If the oocyte is not fertilised then the levels of progesterone and oestrogen will decrease, stimulating the release of FSH and LH.  Follicular growth begins again and the endometrium will shed (menses). [1, 4]

 

Hyperinsulinaemia increases the production of androgens in the ovaries by stimulating the secretion of LH, by directly stimulating ovarian tissue or by indirectly enhancing the adrenal production of androgens. [1]

 

A high androgen environment alters the hypothalamic release of GnRH and increases the sensitivity of the pituitary to GnRH.  This causes an increase in the secretion of LH while at the same time inhibiting FSH .  This means that the new follicles cannot fully mature and ovulation can not occur and no corpus luteum develops. [5]  The lack of corpus luteum means that progesterone levels do not increase as they normally would, this results in the absence of negative feed back to the hypothalamus-pituitary unit and results in persistent acyclic oestrogens .  Once again LH comes into play, as it becomes chronically elevated it stimulates the production of more ovarian androgens. [1]  Chronic anovulation results in amenorrhea and an oestrogen environment, eventually causing bilaterally enlarged ovaries. [5]

 

High oestrogen levels during the luteal phase stimulate prolactin, because oestrogen levels do not drop as they would in a normal cycle this causes abnormal negative feedback mechanism whereby prolactin continues to be secreted.  High levels of prolactin then further stimulate the release of more oestrogen.  Approximately 25% of women with PCOS have elevated prolactin levels. [1, 2]

 

Essentially, the reproductive cycle of a woman with PCOS has the following alterations:

 

Menstrual phase – FSH is inhibited, follicular growth is still initiated.

  • Follicular phase – FSH inhibition means that no dominant follicle will develop and mature.  LH is high which increases the level of oestrogen.

  • Ovulation – No mature follicle means there is no ovulation.  LH levels continue to be elevated, which keeps increasing the levels of oestrogen.

  • Luteal phase – No ovulation means that no corpus luteum develops, therefore progesterone is not secreted.  Continued elevated LH levels means that oestrogen is still secreted leading to excessive levels of oestrogen in relation to progesterone.  Lack of fertilisation would normally inhibit oestrogen, however, as there is no oocyte present, the level of oestrogen does not drop as it normally would.  The high levels of oestrogen inhibit FSH.  Menstruation may or may not occur.

 

Clinical manifestations

 

♀ Secondary amenorrhoea or oligomenorrhoea will be experienced in 90% of cases. 

    50% of women will not menstruate. 

♀ Hyperinsulinaemia occurs in 90% of cases, regardless of the woman’s weight.

♀ Ultrasounds will show multiple ovarian follicles in between 65-85% of PCOS

    women.

♀ Infertility or recurrent miscarriages will affect 75% of these women.

♀ Hirsutism – excess body hair and/or androgenic alopecia will affect 50-60% of

    Women.  

♀ Obesity is observed in 40% of cases. [3]  Women with PCOS have significantly lower

    Postprandial thermogenesis which means that they store fat more efficiently and burn

    calories more slowly, making weight loss very difficult. [6]

♀ Adult acne occurs in 40% of cases.

♀ Abnormal bleeding patterns have been recorded in 30% of cases.

♀ Hyperprolacinaemia occurs in 25% of women with PCOS.

♀ Only 15% of women with PCOS will be experiencing ovular cycles if they are

    menstruating. [3]

♀ Acanthosis nigricans – this refers to the thickening and pigmentation of the skin,

    these lesions can be found on the vulva, nape of the neck, inner thigh and below the

    breast.  They are caused by severe insulin resistance. [2]

 

Excess levels of androgens are the cause of most of these manifestations – such as acne, hirsutism, androgenic alopecia and menstrual irregularities.  Reduced levels of SHBG caused by increased androgens, insulin resistance and obesity increase the level of unbound active androgens (primarily testosterone) in the body. [1]  The presence and activity of androgens on the skin are responsible for hirsutism. [2]

 

Excess weight can make many of the symptoms associated with PCOS more pronounced, particularly menstrual irregularities, infertility and hirsutism.  Increased fatty tissue in the body allows for the increased aromatisation of androgens into oestrone.  Excess abdominal weight in both obese and non-obese women with PCOS contributes to insulin resistance. [1]

 

Further to the above manifestations, these women are at an increased risk of developing type II diabetes, high cholesterol, hypertension, cardiovascular disease, endometriosis, endometrial cancer, eating disorders.  If these women are able to conceive, they have a much higher risk of miscarriage before 14 weeks gestation. [6]

 

Of the many herbs that will help with PCOS, the following appeared most prominently in my research and would combine well in a formula:

 

  • Vitex agnus-castus: this herb is very well known for its hormone balancing capability.  It has been shown to reduce excess prolactin and androgens, thereby promoting normal luteal phases and increasing progesterone levels.  The production of prolactin is inhibited by this herbs ability to act as a dopaminergic agonist. [2]  There have been numerous clinical trials and case studies that have demonstrated this herbs ability to reduce various PMS symptoms, increase fertility and correct menstrual disorders [1]0  Vitex should be taken first thing in the morning for at least 3-6 months to see any benefit.  It is more effective when it is used in conjunction with Tribulus and Paeonia. [2]  It is important to note that some practitioners recommend against using Vitex in the treatment of PCOS as in some cases they have found it to worsen menstrual irregularity.  Many other practitioners use it frequently for PCOS and infertility and have found it to be very successful. [3]

 

  • Glycyrrhiza glabra: this versatile herb is important for supporting adrenal function, reducing testosterone levels and initiating ovulation.  It is also useful in the treatment of hirsutism and may be of assistance in weight loss. [2, 3, 8]  Women with PCOS are suspected to have increased peripheral cortisol metabolism, resulting in raised ACTH secretion which maintains blood cortisol levels and increases adrenal androgen production.  Glycyrrhiza supports the adrenal cortex and endogenous corticosteroids; in doing this it exerts a peripheral antiandrogenic activity. [2]  For long term use of this herb it is recommended that the dosage be kept low and that the patients blood pressure be monitored closely.  A diet high in potassium will help to minimise the risk of increased blood pressure. [11] 

 

  • Paeonia lactiflora: has a positive influence on progesterone, reduces elevated androgens and modulates oestrogen and prolactin.  In vitro it has been shown to assist in follicular maturation and corpus luteum function, thereby initiating ovulation and improving fertility.  It is also useful in the treatment of hirsutism. [2, 3]

 

  • The combination of Glycyrrhiza and Paeonia has been studied in the treatment of PCOS, the synergistic effect of these two herbs is much more potent than the collective effect of these herbs when used individually. [2]  The combined use of these herbs on infertile, hyperandrogenic and oligomenorrhoeic women and women with PCOS were successful in lowering serum testosterone levels and regulating ovulation, with some of the patients subsequently becoming pregnant.  A later study found that it was the paeoniflorin and glycurrhetinic acid that were responsible for decreasing the ovarian testosterone production. [11]  Other trials have shown this herbal combination to be effective in the treatment of acne and in lowering raised prolactin levels.  Moreover, there have not been any side effects noted in these studies. [2]

 

  • Gymnema sylvestre: this is the primary insulin modulating herb, it has traditionally been used to lower BSL and lipid levels and also assist in weight loss by reducing carbohydrate/sugar cravings. [2, 3]   Gymnema regulates BSLs by increasing the activity of the enzymes involved in the use of glucose and by increasing the uptake of glucose in the liver, muscles and kidneys. [10]  The absorption of glucose into the intestine is also reduced with the use of this herb. [2]

 

  • Schisandra chinensis: is a great liver herb that improves the livers ability to conjugate sex hormones, thereby reducing the circulating levels of testosterone and oestrogen. [2, 3]   It is thought that Schisandra may also help in depression and mental and physical fatigue. [10]

 

  • Tribulus terrestris: this is an oestrogen and androgen modulator and as such it has been used to restore menstrual regularity, initiate ovulation, normalise follicle development and to improve fertility. [2, 3]  Other benefits of Tribulus include improved muscle strength, endurance and stamina through enhanced protein synthesis and enzymatic activity, all of which may assist in weight loss.  For the treatment of PCOS Tribulus is best used on days 5-14 of the menstrual cycle (the follicular phase).  [2] 

 

Therapeutic considerations – Lifestyle

 

Obtaining and maintaining ideal body weight is really important in the long term management of PCOS.  Losing weight, if necessary will help to reduce insulin levels, which in turn will reduce the ovarian production of testosterone; also, when there are less fat cells the level of aromatisation will decrease and the number of SHBG proteins will increase. [6]  

 

Regular exercise that increases the heart rate will help with weight loss, reduce the risk of CVD and increase the amount of SHBG. [1] 

 

Come off the OCP.  The OCP can cause a deficiency of many micronutrients, particularly the B vitamins, vitamins C and E and Zinc.  It has also been shown to affect insulin metabolism. [6]

 

Alleviate stress!!! Stress triggers the release of insulin and the secretion of testosterone from the adrenal glands and can eventually cause insulin resistance, weight gain, depression, irregular periods and high blood pressure. [6]

 

A good diet can do much to alleviate many problems associated with PCOS; ensuring the diet includes plenty of water, fresh fruit and vegetables, fibre, essential fatty acids, phytoestrogen foods, low glycaemic index foods and good quality proteins will assist greatly with blood sugar management and in the balancing of hormones.  Avoiding caffeine, alcohol refined foods, saturated fats and xenoestrogens will also help. [6]

 

Summary: by following the above herbal medicine protocols and by undertaking the lifestyle recommendations, insulin levels will decrease, androgen and oestrogen levels will decrease, oestrogen/progesterone ratio will become more balanced, menstrual cycles and ovulation will start to become regular and fertility will improve.  As these are the underlying factors of PCOS, the resulting symptoms and potential complications will also be greatly reduced.

 

References

 

1 Trickey, R. (2003), Women, Hormones & The Menstrual Cycle: Herbal and medical solutions from adolescence to menopause, 2nd ed, Allen & Unwin, Crows Nest, NSW

 

2 Hywood, A & Bone, K. (2004, November), “Phytotherapy for Polycystic Ovarian Syndrome (PCOS)”, A Phytotherapist’s Perspective, no. 46

 

3 Bulloch, S. (2004), “Phytotherapy for Polycystic Ovarian Syndrome”, Modern Phytotherapist, vol. 8, no. 2

4 Tortora, G and Grabowski, S (Ed) (2003) Principles of Anatomy and Physiology, 10th Edition, John Wiley & Sons Inc., New York

5 Porth, C. (2005), Pathophysiology: Concepts of Altered Health States, 7th ed, Lippincott Williams & Wilkins, Philadelphia, pp 1465-1467

 

6 Harris, C. (2002), PCOS Diet Book: How you can use the nutritional approach to deal with polycystic ovary syndrome, Thorsons, London

 

7 “Polycystic Ovary Syndrome” (2005, August 4), (Mayo Clinic), Available:  http://www.mayoclinic.com/health/polycystic-ovary-syndrome/DS00423  (Accessed: 2006, October 10)

 

8 Morgan, M. (2005, February), “Herbal Treatment of Polycystic Ovary Syndrome: Focus on Hyperandrogenism & Anovulation”, A Phytotherapist’s Perspective, no. 49

 

9 NZ PCOS Support, Available: http://www.nzpcos.org/forum/faq.php?faq=welcome#faq_whoisaffected

(Accessed: 2006, October 21)

 

10 Bone, K. (2003), A Clinical Guide to Blending Liquid Herb, Churchill Livingtone, St. Louis, Missouri

 

11. Bone, K. and Mills, S. (2000), Principles and Practice of Phytotherapy, Churchill Livingstone

 

JULIE WILSON

021-933-667

julie@nzyogamama.com

 

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