PCOS (Polycystic Ovarian Syndrome) is one of the most common heterogeneous endocrine & metabolic disorders in women of reproductive age (Abu Hashim 2012). Between 12-21% of women of reproductive age are affected with PCOS with potentially 70% of cases remaining undiagnosed (March et al 2010, NHMRC 2015). This is due to changing definitions over time and a very complex and diverse range of symptoms that may or may nor be recognised as “typically PCOS”.
“In fact, 6 different women with PCOS, may all present differently, with different clinical features, different biochemical markers and different symptoms. Eight of the 12 key symptoms of PCOS is a strong indicator of the likelihood of the condition”.
The cardinal features of PCOS are hyperandrogenism (excess male hormone production) and oligo-ovulation (irregular ovulation). The metabolic abnormalities include obesity, insulin resistance, hyperinsulinemia and dyslipidemia. Other significant endocrine features include irregular menstrual cycles, amenorrhoea (absence of cycles) and oligomenorrhoea (infrequent cycles), sub-optimal infertility/infertility, polycystic ovary morphology on ultrasound (Rotterdam 2004, Showell et al 2016), hirsutism and acne.
- Insulin resistance/hyperinsulinaemia
- Metabolic syndrome
- Impaired glucose tolerance
- Type 2 diabetes
- Increased CVD risk factors- elevated markers of early CVD including elevated blood pressure and abnormal lipid profile- Altered lipid profile & hyperlidiaemia: Increased LDL and decreased HDL
- Hirsutism and/or acne
- Ovulatory and menstrual dysfunction – Amenorrhea, oligomenorrhea, irregular menstruation, Anovulation, irregular, infrequent ovulation
PCOS is a complex syndrome with no single defining clinical symptom. It is a syndrome, a cluster of symptoms and one individual may present with all, or only a few of the symptoms and may still be classified as PCOS. This of course has lead over the years to much confusion for practitioners in correctly and efficiently diagnosing PCOS.
A unifying definition was presented at a consensus workshop Revised 2003 consensus (Rotterdam 2004, Azziz et al 2006), jointly proposed by the European Society for Human Reproduction and Embryology and the American Society for Reproductive Medicine and use HA, oligo-anovulation and polycystic ovarian morphology (PCOM) at ultrasound as markers. In order to make a diagnosis of PCOS a woman must exhibit at least two of the following three criteria;
oligo-ovulation (infrequent ovulation) or anovulation (absence of ovulation), or both (clinically presenting as amenorrhoea, oligo-menorrhea or occasional chaotic bleeding;
hyperandrogenism (high levels of male hormones), either clinically with acne or excessive hair growth (hirsutism), or biochemically with raised blood serum androgen levels;
polycystic ovaries, defined as the “presence of 12 or more follicles in each ovary measuring 2 mm to 9 mm in diameter and/or increased ovarian volume (> 10 ml)” (Showell 2016).
According to these criteria, it is not necessary for a woman to have polycystic ovaries (PCO) on ultrasound to be diagnosed with PCOS. The name ‘polycystic’ suggests you might have multiple ‘cysts’ on your ovaries, but not all women who have PCOS have multiple ‘cysts’ and not all women who have multiple ‘cysts’ have PCOS. The term ‘cysts’ is a bit misleading. The cysts are actually not cysts but partially formed follicles that each contain an egg (Jean Hailles)
You also do not have to have high levels of androgens (male hormones such as testosterone and androstenedione) to be diagnosed with PCOS. That means you do not have to have male pattern hair growth, or excessive hair growth to have PCOS.
PCOS VS PCO
There is so much confusion around PCO and PCOS, amongst the public and medical community. The terms are incorrectly used interchangeably, contributing to the confusion~ PCO and PCOS are different; they are not one and the same. Different incidence, diagnostic criteria, aetiology, symptomatology, hormonal profiles, risk factors, health implications…VERY DIFFERENT!
PCO simply refers to the appearance of the ovaries, marked by many cysts (partially mature follicles) diagnosed on ultrasound.
By “many” the latest diagnostic criteria suggests for PCO is more than 25 cysts on each ovary ranging in size from 2-9mm. (This supersedes the former Rotterdam criteria of 12 or more cysts). So a woman with PCOS may or may not have polycystic ovaries; and not all women with polycystic ovaries have PCOS.
PCO is more common than PCOS. About one in four (~25%) women of reproductive age have PCO; about one in seven (~15-18%) have PCOS.
In PCO there may be excess unopposed oestrogen (ostrogen dominance). Ovulation and periods tend to remain regular. In POCS, blood sugar dysregualtion and insulin resistance is the driver of PCOS leading to abnormal ovarian function & excess ovarian androgen production disrupting both ovulation and menstruation.
PCO may in fact be considered a normal ovarian variant, is not considered a disease, does not have an associated risk profile, nor should it affect fertility PCOS is a polyglandular endocrine & metabolic syndrome with short and long term fertility and heath implications. Associated risks include sub-infertility, infertility, gestational diabetes, obesity, thyroid issues and cardiovascular disease risk. If PCOS is not adequately managed, it may be associated with a higher miscarriage risk.
If polycystic ovaries are found on ultrasound, associated with irregular cycles, hirsutism, acne, blood sugar dysregulation (such as sugar cravings), then further investigations need to be conducted to rule out an endocrine or metabolic abnormality.
There may be a genetic component in both and both may start during adolescence, but neither may be found until later in life.
Symptoms of PCOS tend to begin early in teenage years- acne, hirsuitism, insulin resistance & irregular cycles. To “fix it”, and “regulate their cycles”, many teenagers are then prescribed the pill, investigations are not done, and the condition continues until the pill is ceased, often when the woman thinks about wanting to conceive. By this time, she may have been on the pill for up to 15 years or more and the condition has been there that long. Remember, how a period was when a woman started the pill (as a teenager) will pretty much will be how it is once the pill is stopped. The pill doesn’t fix anything, and thus the condition is not discovered until later in life.
PCO may also begin during adolescence, however, as there are no overt PCO symptoms, the polycystic ovaries are often found incidentally on ultrasound during other health screening (such as in preparation for pregnancy)
- Family History of diabetes
- Iatrogenic (valproate for epilepsy and bipolar disorder: 10-20% incidence) (Morrell & Montouris 2004)
- Low birth weight & history of early puberty
- Androgen exposure in utero
With PCOS, it is very difficult to absolutely know where the problem first started. It is hypothesized that insulin resistance, susceptibility to elevated androgens (male sex hormones such as testosterone) and disordered luteinizing hormone (LH) activity are the underlying mechanisms that lead to the ovulatory failure and hyperandrogensim – the hallmarks of PCOS
HIGH LH, LOW FSH
Normally our FSH:LH ratio is 2:1. PCOS is confirmed if elevated LH:FSH ratio of 2:1 or 3:1. This increased secretion of luteinising hormone (LH) is associated with ovulatory failure and hyperandrogenism
Hyperinsulinaemia is intimately related to PCOS and blood sugar dysregulation drives PCOS. Insulin resistance occurs in both obese and lean individuals, so you do not need to be obese to have PCOS! High insulin leads to high androgens (testosterone) potentially leading to infertility or problems getting pregnant due to anovulation (Balen 2017)
BODY WEIGHT – LIPOTOXICITY / OBESITY
Evidence is increasing that suggests that lipotoxicity which is a key mechanism in the development of insulin resistance, pancreatic beta-cell dysfunction and type 2 diabetes, could also explain the androgen overproduction. The more fat, the more androgens are produced. However, it is really important to understand that you do not need to be obese to develop PCOS.
ELEVATED ANDROGENS (TESTOSTERONE, ANDROSTENEDIONE, DHEA-S)
Free testosterone can be up to twice the normal range than what a female would normally have.
From the ovaries:
The theca cells of the ovaries are the primary source of androgens in PCOS. Overactivity of 17β-hydroxysteroid (17β-OHSD) in the theca cells of the ovary converts androstenedione to testosterone. Simultaneously, aromatase activity in the ovarian granulosa cells is reduced, resulting in poor conversion of androgens into oestradiol.
Thus, high androgens and low oestradiol (oestrogen) is the result. The high androgens interfere with normal follicular development and small cystic immature follicles form and ovulation fails.
From the adrenal glands:
“Stress has a direct impact and drives PCOS”
The pituitary gland produces ACTH (adrenocorticotrophic hormones) during stress, in turn overproducing DHEA. Excess DHEA is converted to androgens via the adrenals. So, if you are a stress-head, sympathetically dominant with high cortisol, that can lead to excess adrenal and ovarian stimulation and increased androgens.
ACYCLIC OESTROGEN DOMINANCE
Did you know we have 3 different types of oestrogen? We have:
E1: Oestrone (this is the one that is elevated in PCOS)
E2: Oestradiol (this is the one we want during our reproductive years)
PCOS is often described as a condition of relative oestrogen dominance. This is true, however, it is not oestradiol dominance, but rather acyclic oestrone dominance, the wrong type of oestrogen.
The oestrone is made from the high levels of androgens (androstenedione) in fat and muscle cells (via aromatase and 17β-OHSD hydroxysteroid activities). The abnormal oestrogen levels ultimately results in high prolactin, low progesterone and the symptoms include delayed ovulation, long cycles, pre-Mx breast tenderness (chaste-tree, B6 and peony are really good for this)
So the picture now is elevated androgens, little oestradiol, elevated acyclic oestrogens (oestrone), little progesterone which leads to elevated LH, in turn perpetuating the cycle.
- Bloods: E2, FSH, LH, Prolactin, Pg, FAI, SHBG, free & total testosterone, DHEA-S
- Elevated LH:FSH ratio of 2:1 or 3:1
- Low oestradiol (E2), high oestrone (E1), or may appear as just high oestrogen on blood depending what was tested
- Elevated prolactin
- Low Pg (failure to ovulate)
- Low SHBG
- High free testosterone, androgens, high DHEA-S
- Prolactin normal range 85-500 mlU/L. > 400 mIU/L can indicate prolactin secreting tumour on the pituitary gland (Hywood, 2012)
- Glucose tolerance test (OGTT), fasting insulin, fasting glucose
- AMH (Anti-Mullerian Hormone): >35 is diagnostic
- Thyroid panel: TSH, fT3, fT4, rT3, thyroid antibodies, urinary iodine, spot iodine (Lugols Iodine- colour should last >24 hours)
- Blood lipids: We expect elevated total cholesterol, LDL & trigylcerides & low HDL
- DUTCH (dried urine test for comprehensive hormones): Comprehensive & thorough investigation of Urinary Oestrogens, Progestogens, Androgens & Cortisol
- Pelvic ultrasound: Presence of >12 cysts on each ovary, 2-9 mm in size is condsidered diagnostic
Please have all medical tests interpreted by a health care professional that is well-versed in PCOS. Not all of the above tests may be required, but these are the potentials
There are a few standard treatment options for you in PCOS. Please speak with you health care professional about symptoms and side-effects associated with them. Included are:
- OCP to improve acne & hirsutism, regulate menstrual cycles
- Insulin-sensitizing drugs (Metformin, Diabex, Glucophage) to improve to treat insulin resistance, acne & hirsutism (Carreau & Baillargeon 2015)
- Clomiphene (Clomid or Serophene) is the mot common prescription medication used to improve ovulation and is used in any situation where ovulation is not occurring. If it fails, is is at this point you will be referred for IVF.
- Spironolactone (Aldactone) is an anti-androgen drug, used to treat hirsutism and acne in women and can increase the frequency of menstrual bleeding.
PCOS does not mean INFERTILITY and it does not necessarily mean never having kids (despite what you may have been told). Treatment generally aims to reduce insulin sensitivity, lower weight, reduce androgens, improve oestrogen and progesterone levels, re-establish ovulation and your period, and get you pregnant!
We would like menstruation to occur every three to four months to prevent abnormal thickening of the womb lining (Balen 2017). Ideally 5-6 menstrual cycles per year are considered sufficient for a healthy endometrium and to prevent the risk of endometrial cancer that is associated with excess body weight (Trickey 2011)
There are a myriad of beautiful herbs that are used successfully to treat PCOS. This is best done under the supervision of a qualified Naturopath, Herbalist, or Traditional Chinese Medicine practitioner with an expertise in treating women’s health and reproductive issues. Herbs are used to reduce androgen production, decrease LH:FSH ratio, decrease insulin resistance, improve oestrogen:progesterone ratio, improve ovuPCOS and peonieslation and re-establish menstrual cycle, support stress & emotional symptoms associated with PCOS, resolve the cysts, improve liver clearance of hormones and improve your fertility. I have written a detailed online webinar for Optimal Rx covering the treatment options in detail which is available to all health care practitioners and students through Oborne Health Supplies.
Herbs that are effective and should be considered for treatment, and are available through your practitioner include:
Peony, Licorice, Tribulus, Saw palmetto, Black cohosh, Hops, Wild Yam, Vitex, True Unicorn Root, False Unicorn Root, Shatavari, Nettle root, Cinnamon, Galega, Gymnema, Panax ginseng, Siberian ginseng, Poke root, Red root, Thuja, Withania
DIET & WEIGHT MNAGEMENT
The right diet for an individual is one that is practical, sustainable and compatible with your lifestyle but that still is effective treatment strategy in PCOS. Again, this is probably most effective and best done with a qualified health care professional.
- Higher protein & higher (good) fat diet (no trans fats, or saturated fats)
- Lower carbohydrates- cut out everything white, refined and sugary!
- Complex carbs only
- Eat regularly, every 2-3 hours to maintain blood sugar
- 5-6 small meals daily
- Avoid refined sugar, coffee, stimulants
- Protein snacks, not fruit snacks
- Re-learn individual circadian rhythms of appetite, hunger & satiety
- High fibre
- Magnesium-deficiency results in insulin resistance- 400-800 mg daily
- Chromium- blood sugar regulation & insulin resistance- 200-800 mcg daily
- Vitamin B6 250 mg daily, P5P 40 mg- improves progesterone levels and helps to reduce prolactin
- Iodine 220-500 mcg daily, beneficial for reducing ovarian cysts
- Inositol 1200-2500 mg daily
- Improves insulin action and reduces insulin resistance
- May relieve the emotional distress associated with PCOS
- Improves liver metabolism of fats (Hywood, 2012)
- Zinc 25-50 mg daily blood sugar regulation and insulin sensitivity.
- NAC 1800-3000 mg daily. NAC has insulin-sensitizing properties and is great in non-responders undergoing IVF treatment
- Omega 3 fatty acids– protective against the progression from insulin resitance to glucose tolerance. Increase insulin secretion from beta-cells and assist with blood sugar regulation (Ajiro et al 2000)
- Vitamin C up to 5 g daily to support adrenal & ovarian function (Vit C is stored in adrenal glands so beneficial for stress
So, thats your quick 101 in PCOS, what is it and what to do about it. This is by no means meant to replace medical advice and I implore you to please seek help from your integrative, functional, complementary health care practitioner in the recognition, diagnosis and management of PCOS. Your fertility will love you for it.
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