Did scientists just find the cause of PCOS?

By Clare Goodwin

Last updated: September 3, 2020

‘New Scientist’ publication released an article titled “Cause of PCOS discovered at last”. But while this new research from Tata et al. (1) published in Nature is amazing and offers great new insights…. the bottom line is we’re not all cured yet.  The New Scientist journalists have been overzealous with their title and conclusions here, and while I’m sure Tata et al. are stoked with the publicity, they would not agree that they’ve found the ONE cause, because their research didn’t reverse any weight gain, therefore if it is relevant, it’s only relevant to those with LEAN PCOS>

The research looked at a hormone called Anti-Mullerian Hormone (AMH).  This is a hormone that your egg cases (called follicles) release.  In very simple terms, the more follicles you have the more AMH you release, the less the less AMH you release.

PCOS women don’t ovulate (get our period as regularly), so we have more of these egg houses, and therefore AMH.  In fact, those of us with PCOS can produce levels of AMH up to 75 times higher than women without PCOS (2).

But, and this is a BIG but, the researchers of this study found that there was “no difference in AMH levels of obese pregnant women with PCOS and obese pregnant women without PCOS”- only for lean PCOS women. And given that this accounts for up to 80% of women with PCOS (3), it’s a fairly big but (no pun intended).

The researchers of this study thought if the AMH levels were high in women with PCOS, then maybe the high levels of AMH in pregnant women was causing PCOS in their daughters.

They took a bunch of pregnant mice and they injected them with AMH and tested the daughter mice.  What they found was that the daughter mice did develop PCOS. They developed high testosterone, late onset of puberty and disrupted periods. This is incredible information as it shows it might not only be a genes that influence our predisposition to develop PCOS but also the hormone levels of our mother. But we already knew that fetal exposure to endocrine disrupting chemicals and hormones can
stimulate the offspring to develop PCOS. We’ve seen this not only with testosterone (4) but also with the plastic chemical BPA (5).

Interestingly, when they injected the daughter mice with a drug called Cetrorelix (which is not a new drug, it’s used in IVF treatments), they could reverse this.  The daughter mice’s testosterone normalised, they got their cycles back and could conceive. This is promising for lean PCOS women who have high AMH, however given that this drug has been used in IVF I struggle to believe that no ‘lean PCOS’ have already been given this, and I think we would have noticed if it cured them of their symptoms.

The Big FAT Missing Piece(s)

What the journalists at New Scientist failed to understand from the study is:

a) This only pertains to those with LEAN PCOS.

Considering 80% of women with PCOS are overweight (3), this leaves only 20% as lean. As I mentioned above, the scientists found that it was only lean women with PCOS that had elevated AMH. The graph below I’ve taken from the study and the second column is the women with lean PCOS.  You’ll see that only they have higher AMH than those without PCOS.  The fourth column is the majority of us:  overweight/ obese and high levels of testosterone.

b) The daughter mice didn’t gain weight.

This is a huge point to understand. In this study the mice, although having increased testosterone, disrupted cycles and infertility did not gain weight.

This lead the researchers to conclude:

“However, PAMH animals (the daughter mice or mothers injected with AMH) did not present weight alterations, indicating that this model is most representative of the lean PCOS phenotype.”

So as the mice didn’t gain weight, the drug Cetrorelix isn’t likely to help reverse that symptom 80% of us have .  They also doesn’t account for the insulin resistance which 80%(6) of women  with PCOS suffer from.  We know from previous studies that high levels of insulin in our bodies can cause our ovaries to overproduce testosterone.  Insulin levels was not something that the researchers looked into in this study.

c) Not all women that have PCOS had mothers with high AMH or PCOS.

This shows that there are likely other causes, and while this might be one, it doesn’t account for all of us.

We are all different. PCOS is a syndrome NOT a disease (like, say, cancer is).  The definition of a syndrome (7) is that we have similar symptoms that the medical profession group together to make sense of us (like Irritable Bowel Syndrome IBS, or Pre-menstrual Tension Syndrome PMS). The key is that it doesn’t progress the same way in all of us, and we don’t have all the same symptoms so it’s very likely that there are many causes (and therefore treatments).

d) Not all of us develop high androgens at a young age or puberty.

If high AMH in the mothers is the only way of developing PCOS, then we’d all have high testosterone and irregular periods from puberty.  But this isn’t the case for all of us.

I didn’t develop irregular periods and high androgens until my 20s.  Before then, I’d had regular periods and no other signs or symptoms of PCOS.  I’ve also seen this similar pattern in many of my patients. They started out having normal periods, which then only became irregular later in their teens or twenties when they developed other symptoms.

e) It’s a mouse model- which isn’t often replicated in human studies.

Humans and animals can process drugs can be very, very different. If you’re wondering how that can be the case, then just think about how your dog processes chocolate.  If you’re a dog owner, you’ll know chocolate can kill a dog, but we can process it fine.  Although chocolate is (arguably) not a drug, the same difference occurs in how we vs mice process drugs.

A 2006 review looked at studies how well mouse studies were replicated in human trials.  It found that only 37% were replicated in human randomised controlled trials (8). 

We always need to replicate this in human trials, and multiple times at that before we can know whether it will work for humans.

What can you do, right now to help your PCOS symptoms?

My biggest fear from this research being popularised by New Scientist is that you’re now going to again going back to feeling hopeless because your doctor won’t prescribe the Cetrorelix drug, and you’re counting on that for a miracle. Or worse, you are given it and then its back to square one.

As you saw above, this likely won’t work for you, especially if you’re insulin resistant and/or overweight (up to 80% of us).

While this study has been groundbreaking in showing one mechanism for developing PCOS, and a possible way to reverse it, its only one mechanism.

There are many things you can do to reverse your symptoms, for example treat your insulin resistance!

Up to 80% of us with PCOS (myself included) have insulin resistance.  We know from studies that increased insulin stimulates our ovaries to over produce testosterone- so this is one known mechanism for developing our symptoms.

You can read my full article on insulin resistance to find out if that is you, but one classic sign you have insulin resistance, is if you gain weight especially around your middle.

Many doctors will just put you on the drug Metformin.  But while Metformin. might be helpful, it isn’t the only way to treat insulin resistance.  Changing your diet, the way you exercise, increasing your sleep and supplementing wisely are all as effective, if not more effective for treating insulin resistance than Metformin.  If we use these together then we are likely to have a much better outcome.  My method is to use these natural methods first and use the potentially damaging Metformin as a last resort (9).


2) https://www.ncbi.nlm.nih.gov/pubmed/17062765

3) https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5672719/

4) https://www.ncbi.nlm.nih.gov/pubmed/22076147

5) http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0036129

6) https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3277302/

7)  https://en.wikipedia.org/wiki/Syndrome

8) https://jamanetwork.com/journals/jama/article-abstract/203577