When digging further into the root causes of polycystic ovary syndrome (PCOS) in my attempts to manage my PCOS holistically (see previous blog post), I quickly came across literature on insulin resistance. The literature seemed split between thinking that the hormone imbalances characteristic of PCOS caused insulin resistance and thinking that the reverse was true - insulin resistance caused hormone imbalances. While many women regain regular cycles by reducing insulin resistance through either a low-carb diet and/or through intermittent fasting, other women (like myself) tend to experience more hormonal derangement when trying a keto diet or intermittent fasting.

Knowing the connection between PCOS and insulin resistance, I was particularly excited when I received blood test results about a year ago showing that my fasting blood glucose was excellent and that my fasting insulin levels were actually a bit below the normal, healthy level. My doctor exclaimed that I had the lowest fasting insulin she had ever seen among women with PCOS! I breathed a huge sigh of relief.

At the same time, I had some symptoms that suggested I was experiencing insulin resistance including cravings for sweet and salty foods, needing frequent bathroom breaks, having bouts of “hangriness,” and lower belly fat that never budges even at my leanest of times.

Then a few months ago, I started having extreme fatigue an hour or two after eating breakfast on training days. On work-from-home days, the most I could manage to do was curl up with Manny (my greyhound) in his giant beanbag chair, and just wait until I felt better. On days I had to go onto campus, I relied heavily on caffeine to try to bolster my energy. This was usually not very effective, and I’d spend a good half hour or so just blankly staring at my computer screen.

Suspecting that I was having blood sugar crashes, I decided to try using a continuous glucose monitor. For the first week or so, I noticed that my energy crashes were, indeed, associated with blood sugar crashes or reactive hypoglycemia, to be specific. I was crashing so low that the pre-programmed low blood sugar alerts on the sensor were being triggered to warn me of impending blood sugar doom. I was a bit confused though because my blood sugar was relatively stable. Even after consuming high carbohydrate loads, when composed of complex carbs, my blood sugar did not increase beyond normal levels and quickly returned to baseline. (There is a discussion of carbohydrate digestion and blood sugar regulation at the end of this post if that sort of thing interests you…)

I didn’t understand why my pancreas was sending out too much insulin in the mornings.

And then… I entered the late luteal phase of my cycle. The late luteal phase is what most of us colloquially refer to as PMS. It usually begins a week or so before the start of your period.

This phase started for me on a day when my dog and I were competing in a nosework trial, so I suspected that my spiking and soaring blood sugar levels were just a result of my competition nerves. I knew that stress could spike blood sugar, so that must have been it. Then the following day, I had to replace the sensor (they are replaced every 10 days). Sensors can take a couple days to calibrate correctly, so I assumed my erratic readings were the sensor. But after the 48-hour calibration period, my blood sugar levels were still spiking easily and staying high. Even small amounts of carbohydrates, like a handful of blueberries, were causing these sharp and long-lasting spikes.

It wasn’t stress. It wasn’t a new sensor. My blood sugar levels indicated that I had insulin resistance.

Additionally, my fasting blood sugar levels were now in the range that would get me diagnosed with pre-diabetes.

Confused about what had caused this sharp change in blood sugar patterns, I turned to google. As it turns out, the hormones prevalent during the late luteal phase can cause insulin resistance, and this is especially common in women with PCOS and in women with diabetes, particularly type I diabetes. My below-normal fasting insulin levels are potentially consistent with type I diabetes, so this finding was particularly interesting (and mildly alarming) to me. Future testing might be in my future.

That said, I’m fairly certain that this almost monthly bout of insulin resistance explains why my pancreas is secreting too much insulin during the rest of my cycle. And this is particularly problematic on days when I train early in the morning. Exercising makes cells extra insulin sensitive. Combining this sensitivity with too much insulin means my cells are sucking in too much sugar, too fast. Hence, the energy-zapping blood sugar crashes.

Armed with this information, I’m trying to make changes to mitigate my bouts of insulin insensitivity and get my pancreas back on track with its insulin production.

My plan going forward will largely focus on changing eating habits during that late luteal phase. While I haven’t loved it previously, I think trying to follow a low-carbohydrate diet for that week or so when my insulin sensitivity plummets will help to re-calibrate my pancreas’s production of insulin. If it doesn’t have to work much during this phase, it will hopefully stop over-producing insulin outside of this phase.

For the time being, I am also minimizing my consumption of added sugar. While I didn’t consume much, I do love the occasional dark chocolate bar, bowl of ice cream, or macaron. Even outside of the late luteal phase, these treats were causing sharp increases in blood sugar. My body was just able to bring that blood sugar back down quickly. Ideally, I will still be able to enjoy the occasional treat outside of my late luteal phase. But for now, the primary goal is to minimize blood sugar spikes and minimize the need for my pancreas to dump out large amounts of insulin. Complex carbs, though they also get broken down into glucose eventually to be absorbed, do not appear to cause significant blood sugar spikes for me, and so, I will still happily enjoy such carbs for the majority of my cycle.

It will take another 35 or so days to test out my theories, and then I will use my new data to make changes as needed. I’d love to have a medical practitioner to help with my experiment, but I am pretty certain that my primary care physician, with visits that average about 5 minutes, will not have time for blood sugar sleuthing. My gynecologist might be interested in talking with me further, but she’s not trained in insulin resistance or nutrition. In fact, the only nutrition advice she has given me with regards to my thyroid hormone levels, I now know, were incorrect. So, I’ll continue investigating on my own and learning all that I can. And someday soon, I’ll be able to use what I’ve learned to help others do their own blood sugar sleuthing as well.

Stay tuned for Part II of this post after my first chance to experiment with lowering my carbohydrate intake in my late luteal phase.

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A primer on carbohydrate digestion for those who want to know more…

The simplest forms of carbohydrates are glucose, fructose, and galactose. All carbohydrates 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 fasting 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. Well, our cells in the face of ever-present insulin are much the same way; they stop responding to insulin and stop letting glucose in.

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 good news is that diet and exercise can help you restore insulin sensitivity, especially when insulin resistance is caught early.