Polycystic ovary syndrome (PCOS) is one of the most common endocrine (hormone) and metabolic disorders faced in pre-menopausal women. Affecting approximately one in five women (based on the new, more inclusive diagnostic criteria), it is a shame that, although the body of research surrounding the condition is growing within the scientific community, little appears to be being done internationally and or by local health authorities to adequately identify and address the issue.
PCOS is frequently associated with abdominal adiposity, insulin resistance, obesity, metabolic disorders and cardiovascular risk factors. There is also some suggestion it can leave women more susceptible to autoimmune diseases. It can be a truly debilitating disorder, one that we've helped people with but seen many more women suffer from.
In this article we're going to briefly cover;
What is PCOS?
Identifying PCOS
The underlying causes of PCOS
How we can address them through dietary, supplementation and lifestyle means
What is PCOS?
PCOS is a condition defined by a combination of signs and symptoms of androgen excess (hirsutism (male pattern hair growth in women) and/or hyperandrogenaemia), ovarian dysfunction (oligo-ovulation (irregular ovulation) and/or polycystic ovarian morphology (PCOM) i.e. excessive amounts of follicles within the ovaries (currently defined as greater than 25).
To note, the term androgen simply refers to the group of hormones which have an important role in defining male characteristics and traits.
Contrary to the term, PCOS can be anything but "polycystic". Not every patient with PCOS necessarily has the "cysts" which the name suggests and, to make things even more confusing, the cysts aren't even cysts; they incorrectly refer to the accumulation of the egg cell containing follicles which create a "cyst" like appearence.
The name PCOS is confusing for many. Not just those who suffer from the condition but also those healthcare professionals whose job it is to diagnose and treat the condition. Many suggestions for alternative titles have been proposed but, due to lack of consensus agreement, none have been adopted (at least in a widespread and or recognized capacity).
Identifying PCOS
So, by far the easiest and most straight-forward diagnostic criteria in identifying an individual that may be suffering from PCOS (or however you'd like to call it, but for the sake of this article we'll be sticking with PCOS) is that... they're female.
After that it's a bit of a crap shoot.
You see, PCOS is non-heterogenous both in terms of it's diagnostic phenotype and the severity of it's health consequences / disorders. Not all individuals with PCOS have all the possible manifestations of the disorder nor are they exposed to the same health risk factors. If you can imagine it, instead of appearing as a definite black and white diagnoses (like a broken leg would for example), it appears along a spectrum from mild to the most severe symptoms.
There are different classifications of PCOS (in terms of clinical diagnoses) based on diagnostic criteria. There are three major groups of diagnostic criteria; hyperandrogenism, oligo-ovulation and PCOM, of which we'll discuss too. These will be important as if we can address the underlying causes of the diagnostic criteria, we can then improve the symptoms of the condition.
Let's first look at the clinical phenotypes (i.e. how the condition is expressed in relation to characteristics/traits in an individual). As a rule of thumb, the more diagnostic criteria met by an individual the more severe her particular phenotype is (in terms of health consequences and again thinking more so along the lines of a spectrum rather than "black and white" diagnoses).
"Classic" PCOS
The most "severe" of the clinical diagnoses, "classic" PCOS, presents with both hyperandrogenism and ovarian dysfunction (with or without PCOM). It is the phenotype most commonly associated with metabolic disorders and insulin resistance and likely the most well known / common iteration of the syndrome.
Ovulatory PCOS
The next most severe of the phenotypes is ovulatory PCOS, which presents with both hyperandrogenism and PCOM (but may not necessarily present with ovarian dysfunction). Those who fall under this phenotype suffer from similar metabolic issues and other symptoms of the PCOS condition.
Non-hyperandrogenic Phenotype
Considered the least severe of the three primary phenotypes, and often not even clinically recognized as PCOS, is the non-hyperandrogenic phenotype. This form of the disorder presents itself with ovarian dysfunction and PCOM. It should be noted that insulin resistance is not commonly associated with this form of the condition, however there may be lower levels of sex binding hormone globulin (SHBG is a carrier protein which helps to transport sex hormones around the body).
When SHBG levels are lower it leaves more free sex hormones that can potentially be used by the body resulting in PMS like symptoms, weight gain, mood changes and irregular menstrual cycles.
Primary causes underlying the three major groups of diagnostic criteria
Hyperandrogenism
Hyperandrogenism is arguably the most well known of the diagnostic criteria associated with PCOS and the central "driver" of the conditions symptoms in the majority of cases (PCOS is considered a predominantly hyperandrogenic disorder).
Hyperandrogenism may be the primary mechanism contributing to the development of oligo-ovulation (one of the other major diagnostic criteria groups) as well as increased fat deposition around the midsection (visceral adiposity) and associated issues effecting the skin (acne). There is some suggestion that it may be contribute to PCOM too, but we'll discuss this in more depth later on.
So, what causes hyperandrogenism in the first place? Well it appears to be a biproduct of hyperinsulemia which in turn is caused by insulin resistance.
Essentially insulin acts as a co-gonadotropin. A gonadotropin stimulates the ovary (in this case) which in turn leads to increased production and secretion of androgenic hormones (which then results in the undesirable symptoms of hyperandrogenism).
With PCOS being considered a hyperandrogenic disorder, it has been suggested that hyperinsulemia and therefore insulin resistance are the major underlying pathways leading to the development of PCOS.
It's important to note at this stage that not all women with insulin resistance will develop PCOS and not all women with PCOS will necessarily have insulin resistance, it's just fairly common that the two go hand in hand. insulin resistance and the compensatory hyperinsulinemia affects some 65–70% of women with PCOS with 70–80% of obese (BMI >30) and 20–25% of lean (BMI<25) women exhibiting these characteristics.
This shows that, whilst insulin resistance is commonly found in women who would be classified as obese (and generally you become more insulin resistant with the more body fat you have), not all women who are obese will have insulin resistance and or PCOS and those who would fall into a healthier body mass criteria may still be insulin resistant and or develop PCOS.
Researchers have proposed a progressively worsening "loop" of PCOS progression. Insulin resistance leads to hyperandrogenism which in turn leads to increased visceral adiposity. Increased visceral adiposity will in turn lead to increased insulin resistance (and the cycle repeats). I appreciate that this is getting a bit "science-y" at this stage so I thought I'd throw in a quick illustration to show you what I mean and why addressing insulin resistance (in most cases) could be of huge benefit to yourself personally and or the clients you may work with.
How do we tackle insulin resistance?
To clarify before we go any further the approaches we discuss in this article will be purely lifestyle, diet and supplement focused, not clinical intervention using medication. If you want to dig deeper into that, metformin is the primary medicine used in the treatment of PCOS and is relatively safe and effective. Worth checking out but certainly wouldn't advise that being the first "port of call" on the road to restorative health.
Insulin resistance and increasing body fatness go hand in hand, so the primary intervention would be reducing body fat through a calorie controlled diet (preferably higher in protein, achieving adequate fibre intake, lower in added / free sugars and rich in anti-inflammatory foods) combined with increased activity (exercise has been shown to improve insulin sensitivity acutely and long term). There should also be a focus on achieving adequate sleep quality and quantity (at least seven if not eight hours of sleep a night) consistently. Poor sleep health can also contribute to insulin resistance and I'd advise checking out "Why we Sleep" by Matthew Walker for more on the subject.
Essentially, we should look to instill habits and strategies more conducive to our body operating correctly. I believe this would be of utmost benefit in women who would fall into the overweight / obese classifications as lean women may not have to necessarily lose any body fat (however the other lifestyle interventions would still be of some benefit).
Now, with those women who are overweight / obese the question "Did the chicken come before the egg?" may arise. Which, in this scenario, would be; "Was the person insulin resistance before the weight gain or did the weight gain cause the insulin resistance?". However, in lean women a different question must be asked; "What has caused the insulin resistance in the first place?"
Now, whilst it could be in theory related to their lifestyle (if they chronically under sleep or have poor sleep, live a sedentary lifestyle etc.) there is another possible reason that, when addressed, has been shown to lead to significant improvements in health outcomes (from quality of life, to restoring menstrual cycle, attenuating hyperandrogenism etc.).
Inositol, or myo-inositol to refer to it in the form it typically appears in and whose metabolites appear to have the relevant health benefits, could be the key to solving many PCOS women's woes.
Reduced and or deficient levels of inositol have been observed in PCOS women. Inositol deficiency may arise through a plethora of different mechanisms including; reduced food-dependent intake, increased catabolism, and excretion, decreased biosynthesis and inhibition of intestinal and cellular uptake. Each one of these is a Pandora's box in of itself but a great review to read on the subject can be found here (click me!)
When investigated, systematic reviews and meta-analyses (which we'd deem to be the highest level of evidence we can produce on a given subject) have heralded inositol supplementation (predominantly in the myo-inositol form) as improving the metabolic profile of women with PCOS and attenuating hyperandrogenism. Anecdotally, clients of mine have found that they're able to achieve greater weight loss, have reduced PMS symptoms, improved mood control and even restore their menstrual cycle.
I don't affiliate with them but BulkPowders do a relatively cheap, great quality option that I'd advise virtually all women who have (or believe they have) PCOS to supplement with. Between 2 - 4g would be an ideal serving (testing first at 2g to gauge gastrointestinal comfort before scaling up to 4g). Click on this link to find it (me, click me!)
In conclusion, hyperandrogenism appears to be the primary driver of symptoms in most cases of PCOS. This issue should be addressed by improving insulin sensitivity (and therefore attenuating hyperinsulemia) through lifestyle interventions (which will be listed in a table at the end and our techniques we employ with our clientele). Supplementation of myo-inositol is another possible option and is recommend (it may not be necessary in clients with greater body fatness but could be of added benefit and has no real detriment even in excess of 10g a day).
Oligo-Ovulation
Oligo-ovulation (or oligoamenorrhea) is when ovulation occurs infrequently or irregularly, and usually, is classified as having 8 or fewer periods in a year.
This section itself could be summarized quite quickly (at least in relation to PCOS). Generally speaking, if we can address hypoandrogenism, menstrual regularity should resume.
However, that's not much of a read, and I wanted to draw attention to how complex treating women can be and why they deserve a greater level of care than that they are currently receiving. It's my article, I'll write what I want. I'm just a guy, standing here, writing about menses (well, irregular menses).
It's important to note that at this stage ovulatory dysfunction may appear in women who do not have PCOS. Although the majority of cases could be attributed to PCOS there are other contributors that can result in ovulatory dysfunction. We'll soon find out why this matters, particularly in relation to treatment strategies.
One such contributor that can result in ovulatory dysfunction is relative energy deficiency; one of the diagnostic criteria of the "female athlete triad". The triad isn't unique to athletes (who we'll assume for the sake of this refers to women engaging in some form of high-performance sport), and is now being seen more universally among women (particularly younger women and likely as a result from media and social pressures driving them to look a certain way).
This contributing factor falls under the umbrella of functional hypothalmic amenorrhea (FHA), a form of amenorrhea often incorrectly diagnosed as PCOS. FHA is a form of amenorrhea (irregular menstruation) which differentiates from PCOS menstrual dysfunction due to it's specific pathophysiology i.e. how it's caused. FHA is a product of; excessive, chronic stress, excessive exercise and or eating disorders / aggressive weight loss. These can lead to low gonadotrophins and oestrogen deficiency, which then results in FHA.
So, FHA presents in the face of low gonadotrophins and oestrogen deficiency, whearas PCOS mediated amenorrhea presents as a result of hyperinsulemia. Clinicians not trained in ovulatory health may incorrectly diagnose one for the other. This is important as those with FHA are at a greater risk of early onset osteoperosis, bone fracture and infertility and, ultimately, require different treatment strategies.
It's important to note at this stage that many will freely interchange between oligo-ovulation (also referred to as oligomenorrhea) and amenorrhea. This lack of terminology clarity also causes a lot of confusion in diagnoses. Stricly speaking, oligo-ovulation refers to menstrual periods occurring at intervals of greater than 35 days, with only four to nine periods in a year. Amenorrhea refers to the complete absence of menstruation.
As mentioned, we shouldn't treat both forms of amenorrhea the same as each requires specific, tailored solutions. The medical industry generally fails to identify and treat amenorrhea adequately.
One example of this is, in dietary related FHA, oral contraceptives may be recommended. Although oral contraceptives can cause menses to return, oral contraceptives should not be the initial treatment. They can mask the underlying problem and allow other effects of the disorder, like osteoperosis, to continue to develop.
On a side note, it's important to understand that contraception can also cause ammenorhea as well as act as a "masking agent" of sorts. Not hugely relevant to this article, but further highlights how poorly managed and understood women's reproductive and overall health is (despite all the medical and technological advancements we are blessed with in our current time).
In a roundabout way, I think we've managed to show how complex it is to treat PCOS (even in relation to one segment of the diagnostic criteria). Not only is there a general lack of awareness surrounding PCOS itself, we also aren't doing a good enough job in identifying and treating it correctly.
Amenorrhea is just one example but I hope it shows A) how complex female physiology can be B) how vulnerable it can be when mismanaged C) the added level of care/attention we need to give to women (particular when it is in relation to their hormonal balance/health).
I've seen it, far too many times for me to count; women being treated like "smaller men" and or being offered incorrect / inadequate solutions / strategies when it comes to their nutrition, exercise, lifestyle recommendations etc.
The dynamic nature of their physiology demands that we, as coaches (be it self-coaching and or coaching clients) or healthcare practitioners, are adequately equipped to handle the challenges that can be presented, but also be mindful and sympathetic to them when they present.
In summary, oligo-ovulation, in the case of PCOS at least, may be best addressed by first tackling hypoandrogenism (through improving hyperinsulemia and insulin resistance). It is also important that we treat the right conditions with the right approach, diagnosing the correct issue for which we're being / have been presented with.
PCOM
The last of the three primary diagnostic criteria of PCOS; PCOM. We know that if we can address hyperinsulemia that we can attenuate hyperandrogenism. This, in turn, will benefit menstrual cycle irregularities / dysfunction. But what about PCOM? What causes it and how do we go about addressing it?
Well, thankfully, this final section will be quite short. Not that the condition itself isn't wildly complex but, for the sake of this article, our focus is predominantly on improving symptoms of PCOS through lifestyle factors. Why is this section going to be short you ask? Well, it appears hyperandrogenism is, once again, the primary driver in most cases. So, we address hyperandrogenism, we then in turn may attenuate PCOM.
It should be noted that not all cases of PCOM can be attributed to hyperandrogenism or insulin resistance (the data is varied and inconclusive). Identical ovarian morphology has been documented in 16–25% of normal women who do not have PCOS or at least have PCOS at the mildest end of it's respective spectrum. PCOM (and PCOS) may also resort from hypothyroidism however the pathophysiological pathway and contributing factors behind this association are yet to be fully understood / defined.
PCOM may result due to subclinical (not severe enough to present symptoms) hyperandrogenism and or dysregulated levels of a hormone called anti-Müllerian hormone (AMH). We aren't going to go down this rabbit hole however as I feel it'd just be further complicating a condition which is already extremely complex (and quite frankly this article is long enough).
Ok, so should we be worried if we have PCOM? Well, that we aren't quite sure of yet. Some would think that having PCOM may predispose a woman to PCOS. However, recent data would contradict this thought and actually shows that PCOM changes over time (so much so that almost 50% of the subjects in this study which I'm referring to Murphy et al., 2006 failed to meet the PCOM critera over time) so becoming overly concerned with addressing the issue may be irrelevant altogether (thanks for being so clear science!).
Conclusion
Instead of a prototypical summary, I'm going to give a quick sentence or two (denoted by speech marks) to wrap up this subject. I thought I'd then design a table that you can use as a kind of "check list". This check list will comprise of approaches you can trial and gauge their effectiveness for your own personal situation and or your clients. This is a fairly wordy article, so I figured a bit of respite in the form of a "try this" table would be welcome by most.
"PCOS is a grossly misunderstood condition. Not only are we still unsure as to what causes PCOS to appear in some women and not others, but general awareness of the condition and how to adequately treat it remain sub par. In most cases PCOS appears to be driven by hyperandrogenism. Hyperandrogenism and insulin resistance / hyperinsulemia go hand in hand. Addressing insulin issues should in turn attenuate hyperandrogenism which, should then, subsequently improve the symptoms of PCOS (in most cases).
A lot more work has to be done in this field to better understand the condition. We need to elucidate that drivers of the condition; are they genetic (which, at the moment research would say is unlikley) or are they a product of lifestyle and environment?
Are some groups more prone than others?
We know certain ethnicities are more prone to insulin resistance so does that mean our approach has to change to optimize outcomes in these groups?
These are just a few of the questions which we have yet to answer conclusively but, trust us, there are many, many more questions that we didn't include. We hope that this article will provide some interesting and helpful information that you can employ in your own daily life and or use with your clients. As always, any questions about the article feel free to send us a message!
Book your free consultation today to work with one of our expert team coaches!
*Bare in mind this isn't an exhausted list of strategies nor are they in any particular order (e.g. the first noted may not necessarily be the most effective and the last the least effective). It covers the main options which you should focus on that should provide some immediate benefit. Many of these can also be done simultaneously but we ask you just be mindful of the sustainability and practicality based on your lifestyle. These are all referenced based but it's a Saturday morning and we'd rather watch the rugby than spend several hours referencing studies no one will look at.
References
Azziz, R., Carmina, E., Dewailly, D., Diamanti-Kandarakis, E., Escobar-Morreale, H., Futterweit, W., Janssen, O., Legro, R., Norman, R., Taylor, A. and Witchel, S. (2006). Criteria for Defining Polycystic Ovary Syndrome as a Predominantly Hyperandrogenic Syndrome: An Androgen Excess Society Guideline. The Journal of Clinical Endocrinology & Metabolism, 91(11), pp.4237-4245.
Dewailly, D., Lujan, M., Carmina, E., Cedars, M., Laven, J., Norman, R. and Escobar-Morreale, H. (2013). Definition and significance of polycystic ovarian morphology: a task force report from the Androgen Excess and Polycystic Ovary Syndrome Society. Human Reproduction Update, 20(3), pp.334-352.
Escobar-Morreale, H. (2018). Polycystic ovary syndrome: definition, aetiology, diagnosis and treatment. Nature Reviews Endocrinology, 14(5), pp.270-284.
Escobar-Morreale, H. and Millán, J. (2007). Abdominal adiposity and the polycystic ovary syndrome. Trends in Endocrinology & Metabolism, 18(7), pp.266-272.
Kataoka, J., Tassone, E., Misso, M., Joham, A., Stener-Victorin, E., Teede, H. and Moran, L. (2017). Weight Management Interventions in Women with and without PCOS: A Systematic Review. Nutrients, 9(9), p.996.
Keski-Rahkonen, A. and Mustelin, L. (2016). Epidemiology of eating disorders in Europe. Current Opinion in Psychiatry, 29(6), pp.340-345.
Marshall, J. and Dunaif, A. (2012). Should all women with PCOS be treated for insulin resistance?. Fertility and Sterility, 97(1), pp.18-22.
Murphy, M., Hall, J., Adams, J., Lee, H. and Welt, C. (2006). Polycystic Ovarian Morphology in Normal Women Does Not Predict the Development of Polycystic Ovary Syndrome. The Journal of Clinical Endocrinology & Metabolism, 91(10), pp.3878-3884.
Nestler, J., Jakubowicz, D., Reamer, P., Gunn, R. and Allan, G. (1999). Ovulatory and Metabolic Effects of D-chiro-inositol in the Polycystic Ovary Syndrome. Obstetrical & Gynecological Survey, 54(9), pp.573-574.
Rosenfield, R. (2015). The Polycystic Ovary Morphology-Polycystic Ovary Syndrome Spectrum. Journal of Pediatric and Adolescent Gynecology, 28(6), pp.412-419.
Singla, R., Gupta, Y., Khemani, M. and Aggarwal, S. (2015). Thyroid disorders and polycystic ovary syndrome: An emerging relationship. Indian Journal of Endocrinology and Metabolism, 19(1), p.25.
Unfer, V., Carlomagno, G., Dante, G. and Facchinetti, F. (2012). Effects of myo-inositol in women with PCOS: a systematic review of randomized controlled trials. Gynecological Endocrinology, 28(7), pp.509-515.
Unfer, V., Facchinetti, F., Orrù, B., Giordani, B. and Nestler, J. (2017). Myo-inositol effects in women with PCOS: a meta-analysis of randomized controlled trials. Endocrine Connections, 6(8), pp.647-658.
Yildiz, B., Bozdag, G., Yapici, Z., Esinler, I. and Yarali, H. (2012). Prevalence, phenotype and cardiometabolic risk of polycystic ovary syndrome under different diagnostic criteria. Human Reproduction, 27(10), pp.3067-3073.
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