Poly Cystic Ovary (PCO) & PCO Syndrome (PCOS)
Polycystic Ovary Syndrome (PCOS) is now recognized as a spectrum of varying signs and symptoms. At one end of the spectrum a woman may ovulate and have no symptoms. At the other end of the spectrum there may be women with menstrual disturbances, increased hair growth, acne, baldness and insulin resistance. The manifestations of PCOS can be predetermined by genetic, lifestyle and dietary factorsiA woman severely affected by PCOS symptoms with a high BMI(Body Mass Index) can return to the other end of the spectrum through weight reduction and a woman with no symptoms needs to maintain her BMI to prevent the implications of PCOS later in life.
The metabolic and reproductive aspects of PCOS interact and intertwine and are influenced by nutrition. It is acknowledged by medical practitioners that treatment of PCOS including the short-term problems such as acne or infertility, and long-term risk factors such as obesity, diabetes mellitus, atherosclerosis, and even breast cancer must include a nutritional component.
Polycystic ovaries
The diagnosis of Polycystic ovaries is the observation of 12 or more discrete follicles of <10mm3 by ultrasoundii. A finding of polycystic ovaries by ultrasound, does not mean you have the syndrome. Many healthy women can show polycystic formation around her ovaries upon ultrasound at any given time. Only when there are the other accompanying signs and symptoms is it true Polycystic Ovarian Syndrome.
Polycystic Ovary Syndrome
To diagnose Polycystic Ovarian Syndrome, in addition to the presence of polycystic ovaries a woman will have an irregular and lengthened menstrual cycles or not be ovulating, as well as biochemical markers such as hyperandrogenism (high androgens), raised insulin and other variations in hormones.iii
What causes PCO & PCOS?
Polycystic Ovary Syndrome depends on a combination of genetic and environmental factors. A woman may be genetically predisposed to PCOS and then exposed to poor diet and a sedentary lifestyle and then PCOS may appear.
Hormones & PCOS
Hormones work in positive and negative feedback cycles. This means that high levels of one hormone result in higher or lower levels of another hormone. For example, we know that high levels of insulin result in the ovaries producing more androgen in the majority of PCOS patients. This is complicated by the fact that different women express different levels of hormone receptors. Therefore women respond differently to the same level of circulating hormones.
Insulin resistance & PCOS
Hyperinsulinemia (high insulin) is a major metabolic feature of PCOS. Insulin resistance has been demonstrated in the majority (80%) of obese patients with PCOS, and 30-40% of lean patients with PCOS.iv Insulin causes an increase in the production of androgens from the ovaries and the adrenal glands. In response to high levels of insulin the liver reduces output of a hormone called Sex Hormone Binding Globulin (SHBG) which binds to testosterone. In PCOS patients SHBG is lower, which results in higher levels of free testosterone. Free testosterone causes the associated symptoms such as hair growth, baldness and acne found in patients with extreme PCOS.
What blood tests should I have if polycystic ovaries are detected by ultrasound?
Your practitioner should request a blood test for the following hormones; Luteinizing Hormone (LH), Follicle Stimulating Hormone (FSH), Oestradiol, Progesterone and Prolactin. If you are cycling regularly the timing of these blood tests is important. In addition the following blood tests help to identify if you have PCOS and insulin resistance; Total Testosterone, Sex Hormone Binding Globulin, DHEA-S, A Glucose Tolerance Test and Pre and Post Serum Insulin, Liver function, Lipid Studies (Cholesterol and Triglycerides), C – reactive protein and Homocysteine.
Polycystic ovaries and fertility
Due to the irregularity or absence of menstrual cycles falling pregnant is more difficult in women with PCO and PCOS. In addition PCO is associated with a greater incidence of recurrent miscarriage, possibly due to raised luteinizing hormone that leads to production of poor quality oocytes (eggs).v In IVF procedures, women with PCOS respond more slowly to treatment, and have a greater risk of ovarian hyperstimulation and cyst formation.vi. PCO patients produce more oocytes at collection, however fewer of these oocytes fertilize.vii. In addition PCO is associated with poor embryo quality.viii In clinical studies weight reduction alone induced ovulation and pregnancy by reducing insulin levels, androgen concentrations and an increase in SHBG.ix.
Medical treatment of PCOS & fertility
The antidiabetic drug Metformin improves the frequency of ovulation in PCOS patients with insulin resistance and irregular menstrual cycles eight to ten fold.x. Studies on women with PCOS using Metformin in the early part of their pregnancy appear to reduce the incidence of miscarriage and the rate of gestational diabetes. The other drug clomipherine or clomid is also used to improve ovulation frequency. Generally, clomid will be used for 3-6 cycles before patients are referred for assisted reproductive treatment (IUI, IVF or ICSI). Research shows that a combination of both drugs is more effective.
Natural therapies, PCOS and fertility
Natural therapies present a good alternative to Metformin or Clomid for patients who experience mild to severe side effects with these medications. The aim of natural therapies for PCOS patients is management of lowering blood sugar and correcting raised insulin levels, as well as regulating menstrual cycle. Some herbs have been studies for their effectiveness in regulating blood sugar such as Gymnema, licorice, cinnamon and bitter melon. See Our Approach to PCO & PCOS for further information.
References
i | Balen A.H. Conway G.S., Kaltas G., et al (1995) Polycystic Ovarian Syndrome” The Spectrum of the Disorder in 1741 patients” Hum. Reprod. 10:2107-2111 |
ii | The Rotterdam ESHRE/ASRM-Sponsored PCOS Consensus Workshop Group 2004 |
iii | The Rotterdam ESHRE/ASRM-Sponsored PCOS Consensus Workshop Group 2004 |
iv | Dunaif A., Segal K., Futterweit W., and Dobrjanksky A. (1989) Profound peripheral resistance independent of obesity in polycystic ovary syndrome. Diabetes 38:1165-1174. |
v | Homburg R. (1996) Polycystic ovarian syndrome: from gynaecological curiosity to multisystem endocrinopathy. Hum. Reprod. 11:29-39. |
vi | Balen A.H., Tan S.L., Macdougall J., and Jacobs (1993) Hypersecretion of Lutienizing Hormone: a significant cause of infertility and miscarriage. Br J. Obstet. Gynaecol. 100:1082:1089. |
vii | Child T., Phillips S., Abdul-Jajil A., Guleki B., and Tan S., (2002) A comparison of in vitro maturation and in vitro fertilization for women with polycystic ovaries. Am J. Obstet. Gynaecol. 100:665 |
viii | Homburg R. (1996) Polycystic ovarian syndrome: from gynaecological curiosity to multisystem endocrinopathy. Hum. Reprod. 11:29-39. |
ix | Clarke A.M., Thornley et al (1995) Weight loss in obese infertile women results in significant improvement in pregnancy and ovulation rates in anovulatory obese women. Hum. Reprod. 10:2705-2712. |
x | Palomba S., Orio Jr. F., Falbo A., et al. (2005) Prospective Parallel Randomized, double blind, double dummy controlled trials using clomiphene citrate and Metformin as the first line of treatment for ovulation induction in non-obese anovulatory women with PCOS. J. Clin, Endocrinol. Metab 90:4068-4074.” |