PCOS & Insulin resistance
It is estimated that about 75% of women with PCOS have some degree of insulin resistance (Moghetti and Tosi 2021). From my own experiences, I have a working hypothesis that this is an underestimate of the incidence, and that perhaps all women with PCOS have some degree of insulin resistance, during at least some portion of their cycle. I say this because for about 75% of my cycle, my blood work looks amazing. And indeed, whenever I’ve had blood drawn, it’s (not surprisingly) fallen in this larger portion of my cycle. Wearing a continuous glucose monitor for the duration of my cycle, however, tells a very different story.
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Given my hypothesis that insulin resistance underpins pretty much every woman’s experience with PCOS, I’m devoting a few posts on different aspects of the problem (and there will surely be plenty more coming in the future).
This first post provides an overview of the basic problem of insulin resistance.
Part II will cover the relationship between hormones and insulin resistance, both across the menstrual cycle and across a woman’s life. This will be applicable to all women, both with and without PCOS.
Lastly (for this series), Part III will give an overview of ways to improve insulin sensitivity. Future individual posts will dig deeper into the research on specific individual practices.
carbohydrate digestion & The Role of insulin
To understand insulin resistance, we first need to understand a bit about how the body handles carbohydrates.
The simplest forms of carbohydrates are glucose, fructose, and galactose. All carbohydrates (regardless of whether they came from potatoes, whole grains, candy, vegetables, etc.) must be broken down into these simplest forms in the digestive tract in order to be absorbed. Common table sugar is a compound with only one fructose molecule and one sucrose molecule. It is quickly broken down into fructose and glucose to be absorbed by the body. When we consume large amounts of sugar (or other sweeteners like honey, coconut sugar, maple syrup, high fructose corn syrup, etc.), our body quickly absorbs the sugars, raising our blood glucose levels sharply.
More complex carbohydrates contain long chains of carbon, hydrogen, and oxygen atoms, requiring more time to be broken down fully into the simplest sugars for absorption. This leads to a slower increase in blood sugar spread out over a longer duration of time. Hence the idea that complex carbohydrates provide sustained energy.
Our bodies tightly regulate the concentrations of various substances in our blood, including glucose. Glucose is the easiest source of fuel for our cells to use, so we ideally have a stable concentration of glucose at the ready for all of our bodily energy needs. Our body can even convert protein and some fats to glucose to use as fuel when needed. When our blood glucose dips too low, we experience extreme fatigue because our cells don’t have the energy they need to carry out the millions of reactions and processes going on in our bodies at any given time.
But too much glucose is also a problem.
As blood glucose levels rise past what your body needs in that moment, your pancreas secretes insulin, which is used to signal cells, both muscle and fat cells, to let glucose enter. In muscle cells, glucose is stored as glycogen, prime fuel for your future squats, running, or basic body movements like lifting a fork or typing on your computer. Once your muscle cells are at capacity, the remaining glucose is stored as fat in fat cells for longer term storage.
When you have repeatedly elevated blood sugar from consuming fast-absorbing carbohydrates regularly, insulin is constantly being secreted. We all know someone who talks too much or maybe nags too much, who we eventually just tune out over time or perhaps we just walk away from them when they start nagging. Well, our cells in the face of ever-present insulin are much the same way; our cells lose some of their insulin receptors (akin to those who walk away from the incessant talker) and the receptors that stick around are less sensitive to glucose (those that ignore the talker). Without sensitive receptors on the cells, the cells don’t create the transporters needed to let glucose into the cell. Excess glucose then remains in our blood.
Your body’s only mechanism for controlling blood glucose is to secrete insulin, and so in response to your cells tuning out insulin, your body pumps out even more insulin in its struggling attempt to lower blood glucose levels. This vicious cycle is what leads to insulin resistance and eventually type II diabetes and chronically elevated blood sugar levels.
The common story is that insulin resistance and type II diabetes are “lifestyle” diseases. While they are the result of lifestyle choices for some people, many people, including women with PCOS, have a genetic tendency towards insulin resistance.
As such, it’s a bit unfair to just point fingers, and say, “Well, you did this to yourself.”
Actually, you didn’t.
But you DO have control over how the problem evolves.
Blood sugar regulation and pcos
There is a debate in the literature about whether the excessive androgens, like testosterone, that are present in women with PCOS result in insulin resistance (excess androgens can contribute to insulin resistance), or whether insulin resistance causes the excess androgens (high insulin can cause secretion of androgens). It is a true chicken and egg debate, with substantial consequences for women with PCOS.
However, there is some evidence that at least for some women with PCOS, genetic abnormalities in insulin signalling and/or insulin receptors exist (Moghetti and Tosi 2021), and studies have shown that women with PCOS have a harder time clearing insulin from their systems than women without PCOS (Peppard et al. 2001). The chronic presence of insulin from poor insulin clearance would lead to insulin resistance, just as the chronic presence of insulin from eating too many carbs would do. Other studies have demonstrated that treatment of insulin resistance with Merformin improves fertility outcomes (Morley et al. 2017). These findings suggest that genetic tendencies towards insulin resistance drive excess androgens and impaired reproductive function, for at least some portion of women with PCOS.
My own experiences suggest that my insulin resistance also drives excess androgens. Reducing my carbohydrate intake during my late luteal phase has reduced my hirsutism and also shifted my cycle from a 34 to 38 day cycle to a 30 to 32 day cycle. For reference, 35 days is considered the upper limit on a “normal” cycle length.
Signs of insulin resistance
Most people with insulin resistance do not show obvious signs. Some people will developed dark patches of skin in their armpits or on the back or sides of their neck, known as acanthosis nigricans. Skin tags may also be present in these areas (NIH 2018).
Blood tests can also be used to identify prediabetes. Fasting plasma glucose (FPG) tests and A1C tests are most commonly used.
An FPG test measures blood glucose after fasting for at least 8 hours (usually done overnight). Per the American Diabetes Association, a measurement of 100 to 125 mg/dL is used to determine the presence of prediabetes. Readings of 126 mg/dL or higher are classified as diabetes.
For reference, this morning, in the insulin sensitive phase of my cycle, my continuous glucose monitor said I was at 77 mg/dL, an excellent level. During the insulin resistant phase of my cycle, I am usually between 100 and 115 mg/dL first thing in the morning, putting me in the prediabetic range. (More on this phenomenon in post II!)
A1C measures the average presence of glucose in the blood stream over three months. A result of 5.7 to 6.4% is given the diagnosis of prediabetes. I have not had this test done, but I am curious if this would pick up the variation in my insulin sensitivity better than a one-time fasting glucose test.
Consequences of insulin resistance
While many people may be aware that insulin resistance is a precursor to type 2 diabetes, I think fewer people are aware of its more far-reaching consequences. Insulin resistance, even in the absence of type 2 diabetes, also increases the risk of high blood pressure, atherosclerosis, and cardiovascular disease (Abel et al. 2012). And indeed, women with PCOS are at higher risk for all of these health complications.
When I learned that I had insulin resistance, at least part of the time, a part of me felt quite discouraged. A part of me wanted to stomp my feet and complain that it wasn’t fair that I had to deal with this.
And it’s not fair. But alas, these are the cards I have been dealt.
There is a quote by Cheryl Strayed that I just love:
“You don’t have a right to the cards you believe you should have been dealt. You have an obligation to play the hell out of the ones you’re holding.”
So I’m learning all that I can about insulin resistance, how my hormones impact it, and how my nutrition and lifestyle choices impact it, so that I can play the hell out of the cards I have been dealt.
Stick around for more to come! Let’s play our hands together.
References
Abel ED, O’Shea KM, and Ramasamy R. 2012. Insulin resistance: Metabolic mechanisms and consequences in the heart. Arteriosclerosis, Thrombosis, and Vascular Biology 32(9):2068-2076.
Moghetti P and F Tosi. 2021. Insulin Resistance and PCOS: Chicken or Egg? Journal of Endocrinological Investigation 44:233-244.
Morley LC, Tang T, Yasmin E, Norman RJ, and Balen AH. 2017. Insulin-sensitising drugs (metformin, rosiglitazone, pioglita- zone, d-chiro-inositol) for women with polycystic ovary syn- drome, oligo amenorrhoea and subfertility. Cochrane Database Syst Rev 11:CD003053
National Institutes of Health. 2018. Insulin Resistance and Prediabetes. Available: https://www.niddk.nih.gov/health-information/diabetes/overview/what-is-diabetes/prediabetes-insulin-resistance#diagnose
Peppard HR, Marfori J, Iuorno MJ, Nestler JE. 2001. Prevalence of polycystic ovary syndrome among premenopausal women with type 2 diabetes. Diabetes Care 24:1050–1052.
Tosi F, Bonora E, Moghetti P. 2017. Insulin resistance in a large cohort of women with polycystic ovary syndrome: a comparison between euglycaemic-hyperinsulinaemic clamp and surrogate indexes. Hum Reprod 32:2515–2521.
Disclaimer: This post is not intended to diagnose or treat any medical issues. It is intended for informational purposes only. I am not a medical practitioner. Always consult a trusted healthcare provider with any questions you may have about a medical condition or treatment and before starting any new health care regimen.