Inositol and Polycystic Ovary Syndrome (PCOS): The Definitive Guide

The topic we’re going to discuss in this post is a woman-related pathology you may have heard about. I’m referring to Polycystic Ovary Syndrome, known by the acronym PCOS, but what does it consist of?

Increasingly common among young and reproductive-age girls, it is a syndrome that significantly decreases their quality of life. And somewhat surprisingly, PCOS affects between 5-21% of women of reproductive age!

What are the criteria to define PCOS?

When establishing what PCOS is, we have to make use of the so-called Rotterdam criteria and conclude that, to speak of Polycystic Ovary Syndrome, at least three criteria must be considered:

1. Oligomenorrhoea or amenorrhea, or what’s the same, a menstrual alteration that conditions the appearance of fewer periods than would be expected and even the absence of them, circumstances that would be justified by a lower number of ovulatory cycles. In other words, many of these girls or women aren’t ovulating properly.
2. Clinical or biochemical symptoms of hyperandrogegism. Among them, acne or hirsutism stand out, as we’ll see later.
3. A characteristic ultrasound image corresponding to a microfollicular ovary, the presence of 10-12 cysts or ovarian enlargement above a certain volume.

Although these have been (and will continue to be) the classic criteria that doctors use, we’ve also found that these girls often have problems at the metabolic level.

Not surprisingly, most of them, in particular 80% of the girls suffering from obesity/being overweight with PCOS, and between 15-30% of lesser-weight girls with PCOS, presented a certain degree of Insulin Resistance, which results in a higher cardiometabolic risk.

How are my hormones if I have PCOS?

At this point, let’s look at the endocrine profile of a Polycystic Ovary Syndrome patient. This information is relevant in order to properly understand both its manifestations and the syndromes that such pathology produces.

Its hormonal alterations can be summarised as follows:

Why does Polycystic Ovary Syndrome occur?

To this day, the origin of Polycystic Ovary Syndrome remains unclear to researchers, causing them more than one headache.

The most strongly backed hypothesis is that it’s a hypothalamic-pituitary abnormality that would produce abnormal LH and FSH pulses, resulting in a higher than normal LH/FSH (gonadotropins) ratio.

It is the aforementioned excess LH and deficiency of FSH that leads to an overstimulation of ovarian cells called theca cells, which produce an increased amount of ovarian androgens such as testosterone and androstenedione.

In addition, as we have already seen, androgens circulate free in greater quantities, due to the fact that the transporter hormone (SHBG) is diminished.

However, there is one definite fact that we’ve not yet looked at, and that’s that excess circulating androgens facilitate insulin resistance, which is exacerbated in the case of overweight/obese girls.

Furthermore, it appears that insulin resistance facilitates excess androgens, causing patients to enter a loop it’s difficult to get out of (although it is possible to do so).

Insulin resistance makes everything worse

Insulin resistance is a condition based on an alteration of peripheral tissues, primarily muscle and liver, but also others such as the CNS, to the action of insulin.

Insulin reaches the cells in abundance, that is, in sufficient quantities, but affected by a defect in the receptor, perhaps by excessive phosphorylation of Serine residues, although it could also be due to a defect at the post-receptor level, making it impossible for insulin exerts its action.

This causes the pancreas to secrete more insulin for compensatory purposes. It seems that the mechanism would be that, as this organ is not functioning at those levels to exert the necessary action, it secretes more in order to get the tissues to react.

The problem is that this insulin resistance (IR) worsens both ovarian function and androgen production, amplifying LH hyperstimulation.

And those spots on your face?

At the beginning of this post, we alluded to the fact that one of the cornerstones of PCOS is hyperandrogegism, a condition that in the traditional medical context has been treated with:

These drugs work well for many girls and markedly improve their symptoms.

However, the main problem behind hyperandrogegism is insulin resistance and as long as it remains high, hyperandrogegism will resist going away, no matter how many patches we put on the situation.

Why do slim women also suffer from insulin resistance and PCOS?

When we learned that insulin resistance was one of the causes of Polycystic Ovary Syndrome, doubts did not take long to appear.

The hypothesis then arose that the problem not only had to do with weight loss, but that these women had a defect in insulin signalling, at the post-receptor level, and of molecules such as Inositol phosphoglycan (IPG), crucial in hormone signalling.

IPG is produced by the hydrolysis of Glycosyl-phosphatidyl-inositol in the inner cell membrane and, as we’ve been saying, it’s a key factor in the complicated insulin signalling cascade, which exerts a direct and indirect control of the oxidative and non-oxidative metabolism of glucose, as well as the translocation of GLUT4 receptors to the cell membrane.

In short, inositols and their derived molecules, such as IPG, are necessary for the proper functioning of the insulin system.

This has to be especially taken into account for the effects of PCOS and the functioning of Inositol as a supplement.

Administration of Inositols in patients with PCOS

Inositol is a substance present in cell membranes, similar at the molecular level to a sugar, of which we have up to 9 isomers (which MyoInositol is the most abundant) and that occurs in a multitude of cell signalling processes.

This is the reason why Inositol and its derivative products (such as the aforementioned IPG) are relevant both in PCOS and in other pathologies that cause insulin resistance.

We have scientific evidence that both myoinositol (MI) and D-Chiro-Inositol (DCI) are excreted in greater amounts by the kidney of diabetic patients. In this respect, it could be said that these patients do not make adequate use of inositols, discarding them in a higher proportion.

On the other hand, the conversion of myoinositol to INN takes place in our body, a conversion that is also reduced in diabetic patients and those with Polycystic Ovary Syndrome due to the fact that the action of the epimerase enzyme is reduced.

Inositol supplementation, why?

It was under this hypothesis that the first clinical studies on Inositol and health were carried out, with Nestler being the first by selecting a group of 24 obese women suffering from Polycystic Ovary Syndrome and offering them 1200 mg of ICD.

The result? The study concluded by verifying a decrease in insulin resistance, a total restoration of ovulation and a lower free testosterone (Ivorno, 2002).

Later, Chiu had the opportunity to verify that the MI content in the follicular fluid, a substance found inside the ovarian follicles, correlates with the quality of the oocyte.

RawSeries Inositol Powder.

The results of most of the studies agreed on:

The mechanism of action appears to be to enhance the bioavailability of the 2nd messenger in the insulin-IPG signaling cascade.

Is it good to combine DCI and MYO?

It is possible to distinguish between the metabolic characteristics of the ovary and the rest of the tissues in women with Polycystic Ovary Syndrome.

Carlomagno is credited with demonstrating that myoinositol epimerises under normal circumstances to DCI in the ovary because it is a more insulin-sensitive tissue than other tissues, thus justifying the importance of adequate MI  supply for reproductive health.

Along these lines, and in accordance with what’s been said, IM epimerises (transforms) to DCI in tissues, with the DCI being the one ultimately in charge of carrying out the biological action. On the other hand, it was Genazzani who found that the administration of DCI to patients predisposed to DM restores the decreased levels of DCI, with the end result of improving insulin sensitivity.

In addition, and in the opinion of LaMarca, a daily intake of 1-1.5 g of ICD modulates the concentration of anti-Müllerian hormone in patients with PCOS.

Does this mean that MI and DCI should be combined in the same compound to improve its effectiveness?

PCOS Care from EssentialSeries.

To clarify, Facchinetti points out that, at least from a theoretical point of view, a treatment based on the combination of MI+DCI in the most physiological ratio (which is usually 40:1) could be the best way to achieve the improvement/correction of the metabolic alterations underlying PCOS.

What’s the relationship between diabetes and PCOS?

How should you view this information? Well, to the extent that you should put all your efforts into the prevention of these pathologies from the moment of diagnosis. And we’re talking about prevention because, although it’s about increased risks, they are pathologies that can be widely prevented by adopting a suitable lifestyle.

What you can’t ignore if you have PCOS

Continuing with what was explained in the previous section, we’re collecting some tips on the the aforementioned lifestyle changes that you should implement.

Implement strength training in your routine

Muscle is the tissue that most conditions insulin resistance. That’s why you need to look at muscle as a major endocrinometabolic organ. If you have insulin resistance, your muscle is also insulin resistant.

What does this mean? Well, your muscle has trouble using energy.

Paradoxically, you can improve this situation by using muscle, contrary to what you might think …

Increase the intensity

Strength training is a great idea, but if you go to the gym, do three sets of biceps curls and when you finish you’re still full of energy, you’re training well below the right intensity threshold.

For the improvements we’re talking about to happen, you’ll need to bring intensity to your training.

And this isn’t just about strength training, as cardiovascular training is another great option you can consider for cardiometabolic improvement, but as long as you go for intensity.

HIIT

Again, make sure you go with intensity!

Be careful with ultra-processed foods!

One of the most frequent questions I get asked is what foods increase insulin resistance. And to tell you the truth, there’s no single food that increases insulin resistance.

So what’s this going to depend on? Well, on the context, but if I had to question one food group, ultra-processed food would be the one I’d pick, as well as its daily and indiscriminate intake.

Of course, we can all treat ourselves to a sweet treat, like a doughnut from time to time. It would be another matter if we were to engage in regular ingestion of such foods, as this is associated with cardiometabolic worsening, weight gain and an increased risk of metabolic syndrome and the onset of diabetes.

Inositol

We invite you to check out our complete article about this supplement that, according to what we’ve been explaining, is one of the best candidates for the improvement of your PCOS.

EssentialSeries Inositol.

Be sure to read the conclusions

Fortunately, if there’s one thing we can safely say about this pathology, it’s that we’re learning more and more about its physiological and pathophysiological aspects.

As an all-embracing entity, the metabolic disturbance affects, the functioning of the reproductive system, and more.

Bibliographic Sources:

• Wang R, Mol BWJ. The Rotterdam criteria for polycystic ovary syndrome: Evidence-based criteria? Hum Reprod. 2017.
• Unfer V, Carlomagno G, Dante G, Facchinetti F. Effects of myo-inositol in women with PCOS: A systematic review of randomized controlled trials. Gynecological Endocrinology. 2012.
• Genazzani AD, Ricchieri F, Lanzoni C. Use of metformin in the treatment of polycystic ovary syndrome. Women’s Health. 2010.
• Unfer V, Facchinetti F, Orrù B, Giordani B, Nestler J. Myo-inositol effects in women with PCOS: a meta-analysis of randomized controlled trials. Endocr Connect. 2017.
• Ortmeyer HK, Bodkin NL, Lilley K, Larner J, Hansen BC. Chiroinositol deficiency and insulin resistance. I. urinary excretion rate of chiroinositol is directly associated with insulin resistance in spontaneously diabetic rhesus monkeys. Endocrinology. 1993.