Polycystic Ovarian Syndrome (PCOS)

Polycystic ovarian syndrome (PCOS) Part 2

Polycystic ovarian syndrome (PSOC) is a complex endocrine disorder, with multiple theorised causes and long term health effects not only related to fertility but other metabolic health complications such as cardiovascular disease or diabetes.

Exact cause for PCOS is unknown, with multiple theories being put forward, yet it appears to have strong links insulin resistance and elevated androgens. In a normal menstrual cycle the hypothalamus secretes gonadotrophin-releasing hormone (GnRH), this hormone then stimulates the pituitary gland to release follicle stimulating hormone (FSH) and luteninzing hormone (LH). These two hormones then cause the ovaries to produce steroid hormones, resulting in follicular development. LH stimulates the theca cells of the developing follicle to produce androgens and progesterone and FSH stimulates the granulose cells to produce aromatase, aromatase converts androgen to oestrogen which nourishes the developing follicle. As the follicle matures and the level of oestrogen rises the ovary regulates the release of FSH from the pituitary through a positive feedback loop, resulting in declining FSH levels and a spike in LH levels. The LH spike causes the follicle to rupture, i.e. ovulate, the corpus luteum (which are the cells left once the egg has been released) secrete progesterone. This is called the luteal stage of the menstrual cycle and lasts 14 days, during which the endometrial cells grow, if fertilisation doesn’t occur the levels of progesterone decreases and menstration begins 1.

In PCOS, the exact pathophysiology is unknown yet in all cases there is an excess of androgen production, thought to be a result of either or a combination of:

  • metabolic dysfunction resulting in insulin resistance and hyperandrogenism2
  • Inappropriate secretion of GnRH, which disrupts the normal balance of LH:FSH2
  • Hyperactive CYP17 enzyme1

Hyperinsulinaemia, i.e. high levels of insulin circulating in the blood due to insulin resistance, causes androgen secretion from the ovaries. Excess androgens inhibit follicular development resulting in anovulation. Hyperinsulinemia also decreases the hepatic production of the sex hormone binding globulin (SHBG), which in turn further increases the amounts of circulating androgens in the blood.1,3

In PCOS, the hypothalamus increases production and frequency of GnRH release, resulting in increased levels of LH relative to FSH. This hormonal imbalance further results in increased levels of androgens, which also increases the levels of circulating oestrogen as androgens are converted by peripheral tissues. The lack of progesterone stimulates the increase in GnRH creating a cycle of elevated LH to FSH.1,3

One theory for elevated androgens in PCOS women is a hyperactive CYP17 enzyme in the ovaries and adrenal glands, which is responsible for converting DHEA-S to androgens. DHEA is created due to stimulation by adrenocorticotropic hormone (ACTH), which is produced by the pituitary gland in response to stress. In over half of women with PCOS, DHEA levels are found to be elevated.

 Treatment

Lifestyle changes are one of the most important ways to manage and effect change.  A 5% weight loss  will reduce central obesity and insulin resistance and improve endocrinological abnormalities and menstrual irregularity4. A low carbohydrate or paleo type diet has been shown to help insulin resistance and be beneficial in PCOS. Mind body practices such as yoga, meditation, aromatherapy are beneficial in PCOS as they help reduce stress, and stress plays a significant role in PCOS.

There are also a good variety of herbs available that can help to regulate the hormones and improve the stress response. A good medical herbalist or naturopath is essential in choosing the right herbs for you. Accupuncture is also shown to be of benefit for PCOS, in that it reduces the level of  plasma β-endorphin and sympathetic nerve activity.6

As you can see it is not a straight forward condition and manifests differently depending on the individual, if you have this condition I stronly recommend that you see a natural health care practitioner as most often your doctor will recommend the oral contraceptive pill. This will ameliorate your symptoms however it is not going to address the underlying cause.

References:

1. Romm, A. (2010). Botanical medicine for women’s health. St Louis:Churchill Livingstone.

2. Rooney, S. & Pendry, B. (2014). Phytotherapy for Polycystic Ovarian Syndrome: A review of the literature and evaluation ofpractitioners’ experiences. Journal of Herbal Medicine,4, 159-171.

3. Craft, J., Gordon, C., Tiziani, A., Huether, S.E., McCance, K.L., Brashers, V.L., & Rote, N.S.(2014). Understanding pathophysiology (2nd ed.). Sydney, Australia: Elsevier. ISBN 9780729541602

4. Farquhar, C. & Johnson, N.(2008).Understanding polycystic ovary syndrome. Better Practice Journal, 12. Retrived from http://www.bpac.org.nz/BPJ/2008/April/docs/bpj12_polycystic_pages_7-13.pdf.

5. Hay, L. (1984). You can heal your life. Hay House.

6. Johansson, J., & Stener-Victorin, E. (2013). Polycystic Ovary Syndrome: Effect and mechanisms of acupuncture for ovulation induction. Evidence-Based Complementary and Alternative Medicine : eCAM, 2013, 762615. http://doi.org/10.1155/2013/762615

 

2 thoughts on “Polycystic ovarian syndrome (PCOS) Part 2

  1. Great article – Also recent Listener has some interesting thoughts on PCOS, being related to anti-Mullerian hormone thought to over-excites the follicular cells. Amazing read!

  2. Thanks Amelia, for those that are interested in Anti-Mullerian hormone, here is a link to an interview from the Otago University who did that research.
    http://www.radionz.co.nz/national/programmes/summerreport/audio/201785405/otago-uni-involved-in-cure-to-polycystic-ovary-syndrome and
    and news on their website http://www.otago.ac.nz/news/news/otago440203.html
    as well as a research paper exploring this further:
    Anti-Müllerian hormone: correlation with testosterone and oligo- or amenorrhoea in female adolescence in a population-based cohort study

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