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What You Need To Know About PCOS

Jul 13, 2020


Are you experiencing cycle, skin, weight and/ or unwanted hair growth symptoms? Has Dr Google has lead you to Polycystic Ovarian Syndrome (PCOS) as a possibility? Or perhaps you've been given a diagnosis of PCOS by your GP, but you really don't know where to go from here?

Read on to gain an understanding of what PCOS is, the signs, symptoms, causes, consequences of and how you can get a diagnosis, so you can seek the guidance you need to support your hormones, cycle and body back to balance. 

What is PCOS

Polycystic ovarian syndrome (PCOS) is a hormone disorder with increasing prevalence and now affecting 1 in 5 Australian women of a child bearing age and 1 in 7 world wide.1 It is one of the leading drivers for female infertility and alarmingly 71% of women with PCOS remain undiagnosed.2

Having PCOS means that your ovaries aren’t getting the right hormone signals from the pituitary gland in your brain, resulting in an overall increased level of androgen production.

The heightened androgen production is contributed by an elevated Luteinising Hormone (LH) to Follicle Stimulating hormone ratio (produced from your pituitary gland, in the brain), and often an increased production of insulin from the pancreas. This incidence of abnormal insulin activity associated with PCOS further contributes to androgenic activity and the symptoms of PCOS.3

How Androgens Play A Role In PCOS

Androgens are a group of hormones that are made in the ovaries and adrenal glands, including DHEA Sulphate (DHEAS), DHEA, androstenedione and testosterone.

Your adrenals produce all of your body’s DHEA Sulphate (DHEA-S), 80% of DHEA levels, 50% of androstenedione and 25% of testosterone. High adrenocorticotropic hormone (ACTH), secreted from your pituitary gland in response to stress contributes to this adrenal androgen production.

The health of your adrenal glands is therefore paramount for balanced hormones.

These hormone imbalances prevent a normal (short term) LH surge required for ovulation each month. Without ovulation, periods are irregular and the hormonal imbalances can (but not in all cases), contribute to growth of benign masses on your ovaries, called ovarian cysts.

Constant increased luteinising hormone (LH), from your pituitary gland, as seen in PCOS is another contributing factor for excess androgen production. 

Other Causes of PCOS

Early menarche, a family history of PCOS, together with a preexisting irregular cycle can increase your chance of developing PCOS. Other contributing factors include:

Obesity, Insulin resistance & Leptin Resistance

A staggering 40-80% of women with PCOS will show have insulin resistance.4 When your blood sugar levels are erratic over the day, this creates stress on your insulin producing organ, the pancreas. A diet high in glucose and fructose containing foods contribute to a condition of insulin resistance and can lead to weight gain and type 2 diabetes.

Insulin resistance is also a known driver for adrenal, thyroid and sex hormone imbalance. The condition up regulates an enzyme called 17, 20-Lyase, which results in excessive testosterone production from the ovaries and contributes to the condition of PCOS. Heightened insulin also reduces circulating sex hormone binding globulin (SHBG) which increases the availability of your body to use and respond to testosterone.1 It may also help the production of androgens from the ovaries and adrenals.5

Insulin resistance also has the potential to increase oestrogen (testosterone is still higher proportionally) and this increased oestrogen suppresses FSH, heading to a state of infertility.

Interestingly in men, insulin resistance encourages an enzyme called aromatase, which converts testosterone into oestrogen. Higher oestrogen levels in men contributes to loss of head hair.

In Leptin resistance, the message from your fat cells to the brain is no longer sensitive to your leptin signal, leading to constant hunger. Over time, insulin and leptin resistance can contribute to PCOS. 


Central obesity is common in PCOS and has shown to be a factor of fertility issues.This central fat distribution contributes to disturbed ovarian function and is associated with higher levels of fasting insulin, LH, oestrone and androstenedione than if you have PCOS lacking central fat distribution. Elevated leptin levels are also common with this obesity, where it  decreases aromatase activity (an enzyme allowing the conversion of androgens into oestrogens).6


In response to stress, DHEA/ DHEA-S and androstenidione levels are produced from your adrenal glands (via the HPA Axis). These hormones are then converted into testosterone in the peripheral tissues of the body, contributing to higher androgens levels and the symptoms of PCOS. The more chronic the stress, the higher the production of DHEA and testosterone levels.

The adrenal hormone cortisol has a feedback loop when produced at high levels to tell the pituitary gland to slow the production of ACTH. Unfortunately, androgens don’t send this same message and if stress continues, levels of DHEA, androstenedione and testosterone continue to rise, compounding the symptoms of PCOS. This can happen even with normal insulin sensitivity and in the absence of ovarian cysts, indicating that stress alone is a powerful driver of hormonal imbalance.

Included in the contributors of PCOS is the stress of over-exercise. If you are working out daily and pushing your body to the limits but struggling with hormonal imbalance symptoms such as irregular cycles or hirsutism, listen to your body. It may be time to change your exercise routine. 

Other sources of stress to explore, may include:

  • Work
  • Financial
  • Relationships
  • Travel
  • Alcohol
  • Caffeine intake eg. over one cup of coffee per day
  • Processed foods (trans fats, sugar, artificial sweeteners, additives, preservatives)
  • Electromagnetic (wi-fi, phones, i-pad, laptop and computer screens)
  • Toxic exposures
  • Poor sleep quantity and quality


In the state of an under active thyroid, phase II elimination of sex hormones in your liver, including testosterone, is slowed and a buildup effect can occur.7

Inflammation & Gut health

Inflammation can impact your gut health and encourage beta-glucuronidase enzyme activity.8 Just as it does with oestrogen, beta-glucuronidase contributes to a recycling effect of your detoxified testosterone, leading to higher overall levels in your body.


Studies have shown higher levels of toxins including per fluorinated compounds, bisphenol A (BPA), pesticides and polycyclic aromatic hydrocarbons showing in women with PCOS, over control groups. Yet this as a direct cause is still not confirmed. BPA exposure can contribute to increased androgen and insulin levels, which has an association with PCOS development. Most shockingly, a mothers exposure to BPA during pregnancy has been linked to PCOS development in female children.9,10,11

Luteal Phase Defect 

The luteal phase of a cycle can vary from woman to woman but is generally the same time frame during each of your cycles. This can vary from 11-16 days, but must be at least 11 days for the cycle to be considered fertile. A short luteal phase indicates an issue at ovulation leading to inadequate progesterone production or an early drop in progesterone levels. As progesterone is the hormone required to ripen and preserve the tissue and blood of your uterus, a deficiency causes premature shedding of the uterus lining and results in an infertile cycle called a luteal phase defect.

The absence of a LH surge required to bring on ovulation, can also cause a luteal phase defect. This is a common occurrence in the condition of PCOS.

Signs & Symptoms of PCOS

It is important to firstly note that not all cases of PCOS include polycystic ovaries, which show up on an internal (transvaginal) ultrasound. 

Other important diagnostic factors for the condition of PCOS, include: 

  • High androgen levels through blood tests (hyperandrogenism)
  • Growth of body and facial hair
  • Signs of male pattern baldness
  • Absence of ovulation
  • Together with an increase in androgen levels, PCOS is often also driven by oestrogen dominance and deficient progesterone levels.

The full list of PCOS signs & symptoms, include:

Clinical Signs

  • Menstrual abnormalities
  • Facial and body hair growth including the chest, abdomen and upper thighs occurs in 60-70% of women with PCOS.12 This is referred to as hirsutism.
  • Oily skin and acne
  • Thinning of head hair
  • Irregular or absent menstrual cycles. Less than 8 cycles per year is referred to oligomenorrhoea and amenorrhoea is an absence of a period for 3 months of more- both of which are signs of PCOS.
  • Fertility challenges
  • Reoccurring miscarriages

Endocrine Signs

  • Elevated androgens
  • Elevated luteinising hormone (LH)
  • Highened oestrogen 
  • High prolactin
  • Other symptoms of progesterone deficiency, as the lack of ovulation prevents progesterone levels from peaking

Metablic Signs

  • Insulin resistance occurs in 50-70% of women with PCOS.12 The high level of circulating androgens causes a release of inflammation producing cytokines, TNF-alpha and IL-6 into the bloodstream and overtime they contribute to insulin resistance.
  • Impaired glucose tolerance and type 2 diabetes mellitus13
  • Difficulty shifting weight. 30-75% of women with PCOS are also obese.14  It is important to note however, that women who are a healthy weight range can still develop PCOS

Complications Of PCOS

Living with the high insulin, luteinising hormone, androgen levels and weight challenges of PCOS, increases the chance of developing health conditions. These include:14,15,16,17

  • Impaired glucose tolerance and Type 2 diabetes prevalence is much higher amongst women with PCOS.18 This develops more so with obesity and alongside cases of insulin resistance.
  • Midsection weight gain. As insulin resistance and fatty liver increase, weight management often presents as a challenge
  • High free fatty acid levels in the bloodstream. Insulin resistance contributes to fatty liver and an increase in blood lipids.
  • Other cardiovascular risk factors including hypertension, abnormal blood coagulation (increasing risk of blood clots) and markers of inflammation.19
  • Inflammatory based diseases, due to the high insulin levels causing an increased level of inflammatory cytokines.
  • Oxidative stress and decreased antioxidant activity.
  • Formation of advanced glycation end products (AGE’s). This happens when fructose or glucose attaches itself (without an enzyme) to amino acids and fats. The glycation process leads to a greater production of damaging inflammation. Another reason to be mindful of refined carbohydrate intake with PCOS. 
  • Stressed detoxification organs, due to the higher androgen levels. The result is an accumulation of endocrine disrupting chemicals, such as BPA, or pesticides20
  • Progesterone Insufficiency. Conditions that promote either irregular or anovulatory (no ovulation) cycles, such as high stress and PCOS will contribute to progesterone deficiency. Ovulation needs to occur for a corpus luteum to be produced and therefore progesterone to be manufactured at higher levels.
  • Increased risk for abnormal endometrial growth. With lack of ovulation (anovulation) there is no corpus luteum development to increase progesterone levels, leading to unopposed oestrogen - a known contributor to abnormal endometrial growth 
  • Abnormal uterine bleeding. Lack of ovulation contributes to low progesterone levels and the subsequent unopposed oestrogen, can lead to breakthrough bleeding
  • Thyroid imbalances, including autoimmune thyroiditis21
  • Mood disturbances, anxiety, depression and eating disorders22 may be present, possibly contributed by the common physical manifestations of PCOS as well as the existing hormone imbalances.
  • Fertility challenges. This is caused by high androgen levels impairing oocyte development and contributing to higher miscarriage rates. Gestational diabetes or pregnancy induced high blood pressure.

Steps To Get A PCOS Diagnosis

In order to gain a PCOS diagnosis, you will need to make an appointment with your GP / Integrative GP to have a referral for the following tests:

1) Blood test for your androgen levels (DHEAS, testosterone, sex hormone binding globulin, free androgen index) as well as your day 3 LH/FSH ratio. A ratio of 2:1 or 3:1 is evident in PCOS.

Oestrogen, progesterone and thyroid function tests will give you additional hormone health information.

2) Metabolic profile testing, including a blood test for fasting glucose tolerance test with insulin, HbA1c, as well as a detailed lipid profile is recommended. With a diagnosis of PCOS, these should be repeated regularly.23

2) Referral for an internal (transvaginal) ultrasound. They will be looking for the presence of 12 or more follicles 2-9mm in diameter, or increased ovarian volume >10mL in the follicular phase of your cycle.18

3) Your GP will want to discuss symptoms of high androgen levels, such as hirsutism, acne and head hair thinning.

4) Your personal cycle charting will provide great information for you and your health practitioners to identify signs of ovulation issues and/or luteal phase defect. Learn more about cycle charting in my Instagram live with Naturopath Kirsty King, here.  

Take Control Of PCOS

Once you have the awareness of a PCOS diagnosis and your personal contributing factors, be empowered to balance your whole body and hormones within Balanced, The Natural Way To Healthy Hormones. This will give you the tools you need to begin dietary, lifestyle and supplementation support for PCOS, including:

  • Balance your blood sugar levels, increase insulin and leptin sensitivity
  • Control your androgen production
  • Reduce and build resilience to stress
  • Control inflammation
  • Reduce toxin exposure and enhance detoxification
  • Improve your thyroid health

If you are seeing a health practitioner, this book will also give you an understanding of your holistic health treatment. You can pick up your eBook or physical copy of Balanced, The Natural Way To Healthy Hormones here




1) Norman RJ, Dewailly D, Legro RS, et al. Polycystic ovarian syndrome. Lancet 2007;370:685-97.

 2) Boyle J, Teede HJ. Polycystic ovarian system. An update. Aust Fam Physician 2012;41(10):752-756.3) van der Spuy ZM, Dyer SJ. The pathogenesis of infertility and early pregnancy loss in polycystic ovarian syndrome. Best Pract Res Clinger's Obstet Gynaecol 2004;18(5):755-71.

3) Carmina E, Rosato F, Janni A, et al. Extensive clinical experience: relative prevalence of different androgen excess in 950 women referred because of clinical hyperandrogegism. J Clinger's Endocrinol Metab 2006;91:2-6.

4) Norman RJ, Hickey T, Moran L, et al. Polycystic ovarian syndrome-diagnosis and ethology. Int congres Ser 2004;1266;225-32.

5) Willis D, Mason H, Gilling Smith C, et al. Modulation by insulin of follicle stimulating hormone and Luteinising Hormone actions in human granulose cells of normal and polycystic ovaries. J Clin Endocrinol Metab 1996;81:302-9.

6) van der Spuy ZM, Dyer SJ. The pathogenesis of infertility and early pregnancy loss in polycystic ovary syndrome. Best Pract Res Clin Obstet Gynaecol 2004;18(5):755-71. 

Merkin SS, Phy JL, Sites CK, et al. Environmental determinants of polycystic ovary syndrome. Fertil Steril 2016;106(1):16-24.

7) van der Heide SM, Joosten BJ, Everts ME, Klaren PH. Activities of UDP-glucuronyltransferase, beta-glucuronidase and deiodinase types I and II in hyper-and hypothyroid rats. J Endocrinol. 2004 Jun;181(3):393-400.

8) Shimoi K, Nakayama T. Glucuronidase deconjugation in inflammation. Methods Enzymol. 2005;400:263-72. 

9) Palioura E, Kandaraki E, Diamanti-Kandarakis E. Endocrine disruptors and polycystic ovary syndrome: a focus on bisphenol A and its potential pathophysiological aspects. Horm Mol Biol Clin Investig 2014;17(3):137-44. 

10) Rutkowska A, Rachon D. Bisphenol A (BPA) and its potential role in the pathogenesis of the polycystic ovary syndrome (PCOS). Gynecol Endocrinol 2014;30(4):260-5.

11) Merkin SS, Phy JL, Sites CK, et al. Environmental determinants of polycystic ovary syndrome. Fertil Steril 2016;106(1):16-24.12) Sgarlata C. PCOS Natural Fertility Masterclass Program. Viewed March 2016,

13) Durant E, Leslie NS. Polycystic ovarian syndrome: loss of the apoptotic mechanism in the ovarian follicles? J Clin Endocrinol Metab 1998;21:552-7.

14) Boyle J, Teede HJ. Polycystic ovarian system. An update. Aust Fam Physician 2012;41(10):752-756.

15) Rotstein A. Polycystic ovarian syndrome (PCOS). McMaster Pathophysiol Rev 2015. Viewed December 2015,

16) Attaran M. Polycystic ovarian syndrome. Cleveland Medical Clinic. Viewed December 2015, http://www.

17) Rojas J, Chavez M, OlicarL, et al. Polycystic ovary syndrome, insulin resistance, and obesity: navigating the pathophysiologic labyrinth. Int J ReproMed 2014;article ID 719050

18) Norman RJ, Dewailly D, Legro RS, et al. Polycystic ovarian syndrome. Lancet 2007;370:685-97.

19) Orio F, Palomba S, Colao A. Cardiovascular risk in women with polycystic ovary syndrome. Fertil Steril 2006;86(Suppler. 1):S20-1.

20) Takeuchi T, et al. Elevated serum bisphenol A levels uner hyperandrogenic conditions may be caused by decreased UDP-glucuronosyltransferase activity. Endocr J. 2006 Aug;53(4):485-91.

21) Arora S1, Sinha K1, Kolte S1, Mandal A1. Endocrinal and autoimmune linkage: Evidences from a controlled study of subjects with polycystic ovarian syndrome. J Hum Reprod Sci. 2016 Jan-Mar;9(1):18-22.

22) Kerchner A, Lester W, Stuart SP, et al. Risk of depression and other mental health disorders in women with polycystic ovary syndrome: a longitudinal study. Fertilities Steril 2009;91(1):207-11.

23) Ehrmann DA, Barnes RB, Rosenfield RL, et al. Prevalence of impaired glucose tolerance and diabetes in women with polycystic ovary syndrome. Diabetes Care 1999;22:141-6.

Chang WY, Knochenhaut ES, Bartolucci AA, et al. Phenotypic spectrum of polycystic ovarian syndrome: clinical and biochemical characterisation of the three major subgroups. Fertilities Steril 2005;83:1717-23.

 Gilling-Smith C, Willis DS, Beard RW, et al. Hypersecretion of androstenedione by isolated thecal cells from polycystic ovaries. J Clin Endocrinol Metab 1994;79(4):1158-65. 



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