The PCOS Post: Hormonal Havoc From Hyperinsulinemia

As I mentioned in the previous post, I’ve been plugging away this blog since 2012. It’s hard to believe it’s been seven years, but even harder to believe that in all that time, I’ve completely neglected the topic of polycystic ovarian syndrome (PCOS). I’ve written a ton about insulin, glucagon, thyroid hormones, digestion, cancer, and more, but not one word about PCOS, except for a brief mention in this post. This is a glaring omission, because PCOS is a huge issue for reproductive aged women these days, and, no surprise if I’m writing about it here, it’s intimately tied to chronic hyperinsulinemia and metabolic dysregulation.

A while back I wrote about the effect of elevated insulin on men’s hormones, explaining the concept of a “male equivalent to PCOS,” and I didn’t realize that I hadn’t even yet written about actual PCOS. I don’t know how such a huge gap has existed on my blog for so long, but this is being corrected right now. Whew!

I’ve seen online in various places women saying that they’re at increased risk for type 2 diabetes or metabolic syndrome because they have PCOS. It’s actually the other way around: chronically high insulin (basically metabolic syndrome, whether you know you have it or not) is the main driver of PCOS. The reason so few women who have PCOS are aware of this is … surprise, surprise … most doctors are clueless about insulin’s many functions unrelated to blood sugar and they never bother measuring insulin levels.

Women with PCOS are often given unhelpful and condescending advice.  There is a lot of "blame the victim" that goes on with this condition. I sincerely hope this post does not come off that way. That is the very last thing I intend. I have only one goal here: to provide information. Information that can be empowering to women who have PCOS. If you are living with this condition and you feel disappointed by the help you've gotten from healthcare professionals so far, please know that you can take control. You have more power than you might realize. I hope what follows here is helpful.   

This is a long post (some of you are rejoicing now and others are groaning), so grab yourself a beverage of choice, a bag of pork rinds or some string cheese, and happy reading!

PCOS is a major cause of infertility, menstrual irregularity, and reduced quality of life in reproductive age women. One study notes that PCOS “is the most common endocrinopathy of reproductive aged women affecting 6-10% of the population,” with this going as high as 18% among certain cohorts when different diagnostic criteria are used. The PCOS Awareness Association (PCOSAA) puts the numbers at 10 million women affected worldwide. If you know a lot of women, chances are one of them, and likely more than one, is living with PCOS.

The condition results from a cluster of hormonal abnormalities, namely, elevated insulin, elevated androgens (male characteristic sex hormones), and often, reduced progesterone. These hormonal irregularities are responsible for the signs and symptoms of PCOS, which are no joke and can seriously reduce quality of life, not to mention be a roadblock to conception for those looking to have children.

The main signs & symptoms include: 

• Weight gain; obesity
• Acne; oily skin
• Infertility or difficulty getting pregnant
• Mood swings
• Pelvic pain
• Irregular or absent periods
• Excess androgens (male-characteristic hormones, e.g., testosterone)
• Anovulatory menstrual periods (bleeding without ovulation)
• Hair loss on the head or thinning of hair on the head
• Hirsutism (particularly facial hair, but may also include hair on the chest, back, abdomen, and arms) – what a bummer: you lose hair from where you want it and grow hair where you don’t want it!

Despite the name of the syndrome—polycystic ovarian syndrome—many women diagnosed with PCOS don’t actually have cysts on their ovaries, so it’s a bit of a misnomer. That’s right: you don’t have to have cystic ovaries to be diagnosed with PCOS. (Oh, that kooky conventional medicine…gets me every time!) According to PCOSAA, “In 2013, an independent panel of experts recommended to the National Institutes of Health that the name be changed because the name is confusing and hinders patient care and research efforts.” This change has yet to occur, however. In fact, diagnostic criteria for PCOS vary, including no requirement whatsoever for cysts in the ovaries. The reason it’s called a “syndrome” – kind of like “metabolic syndrome” – is that there’s no single, silver-bullet definitive diagnostic test like there are for certain bacterial and viral infections. You get diagnosed with PCOS based on a constellation of signs & symptoms, although this is usually accompanied by blood tests for some of the hormonal imbalances mentioned earlier.

There is no doubt, however, that chronic hyperinsulinemia is at the heart of this condition:

“Hyperinsulinemia associated with insulin resistance has been causally linked to all features of the syndrome, such as hyperandrogenism, reproductive disorders, acne, hirsutism and metabolic disturbances.”

Did you see that part in bold? This is a bold statement (no pun intended, hehheh). Most of the time, researchers say something is “associated” with something else, because they’re too timid to come right out and say that something is the cause of something else. Here, however, they’re saying with no reservations that hyperinsulinemia is the cause of PCOS.

Insulin Resistance in PCOS: “Diabetes in Bearded Women”

PCOS has become a catch-all diagnosis for otherwise idiopathic female reproductive abnormalities. (Idiopathic means something has no known cause. I prefer to say “idiotpathic,” because things always have causes, even if we haven’t yet identified them.) Meaning, if a woman goes to the doctor with weird period issues, if she’s having trouble conceiving, and if she also happens to be overweight or obese, she will likely be diagnosed with PCOS without a whole lot of questions asked. This does a disservice to women because anovulation and amenorrhea (lack of a period) have many causes, including undernutrition and/or excessive exercise, particularly among adolescent girls and young women. It’s also a disservice to all the thin women with PCOS who won’t receive a proper diagnosis because the “stereotypical” PCOS patient is overweight. (More on this in a minute, but the bottom line is, a heavyset woman is probably more likely to be suspected of having PCOS than a thinner woman who presents with the same signs and symptoms.)

While PCOS could easily be considered an endocrine problem, it’s really more of a metabolic disorder. It has long been known that PCOS was associated with—if not outright caused by—blood sugar and insulin dysregulation. A phenomenon of “diabetes in bearded women” was recognized as early as the 1960s, when doctors observed a clustering of blood sugar abnormalities or overt type 2 diabetes, hirsutism, and virilization or hyper-androgenism in women. It was originally called Achard-Thiers syndrome (after the physicians who identified it) prior to its renaming as PCOS. (As an aside, think to back a long time ago when they had circus sideshows. Remember the bearded lady? Illustrations or photographs usually showed her as being on the heavy side, right? I suspect “bearded ladies” from back in the day were simply women with PCOS due to hyperinsulinemia, long before anyone knew this was simply a hormonal imbalance—and an easily treated one, at that. And to think they were considered sideshow freaks. This breaks my heart. I guess maybe back then, they were such a rarity that they were considered “freaks,” while today, all of us probably know at least one gal dealing with PCOS. How sad that they didn’t know more about this back then, because it is entirely treatable. It’s even sadder, however, that so many doctors right now still have zero clue about the connection to insulin.)

Chronic hyperinsulinemia is the primary driver of PCOS, and while many people who have chronic hyperinsulinemia are overweight or obese, not everyone with PCOS is carrying extra weight. As much as 50% of women with PCOS are at a normal body weight. (Setting aside for now that there's really no such thing as a "normal" weight.) PCOS should not be discounted when a lean woman presents with other indicators of the condition even in the absence of excess body weight. Researchers have identified “profound insulin resistance” in PCOS patients who are obese as well as those who aren’t. (Yes, major metabolic dysregulations, including metabolic syndrome and/or type 2 diabetes, can occur in people of any body weight. I wrote about this here if you’d like to learn more.)

Women with PCOS are more likely than non-PCOS women to receive a future diagnosis of hypertension, pre-diabetes, or type-2 diabetes, which should come as a shock to no one who’s read my blog for a while. They also typically have higher insulin levels and higher HOMA-IR than women without PCOS. “PCO women have significant insulin resistance that is independent of obesity, changes in body composition, and impairment of glucose tolerance.” It is not obesity or hyperglycemia that results in PCOS, but rather, hyperinsulinemia that drives the hormonal aberrations in PCOS, with or without excess body fat, and with or without elevated glucose. This is a point I’ve harped on in several blog posts in the past and will continue to point out in the future. It’s a huge sticking point for me – that excess weight is so often blamed for every health problem under the sun, when the truth is, for most people, excess body fat is the result of metabolic dysregulation rather than the cause. (Here’s a snarky but educational post I wrote about this awhile back.) It’s a sticking point because of the bias and stigma heavy people face while simply trying to exist in the world and be treated with the same human dignity thinner people are afforded as a matter of course.

Remember when I wrote about the work of Dr. Joseph Kraft, who uncovered the huge scope of high insulin even in people with normal glucose? (Details here if you’re new to the blog and missed that.) In an perfect demonstration of Dr. Kraft’s findings regarding “diabetes in-situ,” even among those with normal glucose tolerance, compared to healthy controls matched for age and BMI, women with PCOS had higher values for post-load 2-hour glucose, fasting insulin, post-load 2-hour insulin, and HOMA-IR. “Women with PCOS and normal glucose tolerance showed higher IR than controls matched for age, BMI, and β-cell function.” In plain English: even in women with normal glucose responses to an oral glucose tolerance test, those with PCOS had higher insulin (both fasting and in response to the oral glucose load) compared to women who don’t have PCOS but were the same age and BMI. So you can see here again that it’s not about body weight, because two women at the same BMI can have wildly different insulin levels in response to the same amount of glucose. Can we please, please stop blaming everything on weight?

In performing hyperinsulinemic-euglycemic clamp studies, researchers have observed “that both obese and lean women with PCOS have some degree of insulin resistance. Insulin resistance is implicated in the ovulatory dysfunction of PCOS by disrupting the hypothalamic-pituitary-ovarian axis.”

The actions of insulin influence a cascade of effects in other hormones, and this has profound ramifications for the menstrual cycle, fertility, and overall quality of life for women with PCOS.

Hyperinsulinemia Drives Hormonal Abnormalities in PCOS

Chronically elevated insulin stimulates ovarian and adrenal androgen production and decreases levels of sex hormone binding globulin (SHBG). Hyperinsulinemia contributes to elevated androgens through multiple mechanisms: it augments luteinizing hormone-stimulated androgen production by the ovaries, it stimulates adrenal androgen production, and inhibits hepatic synthesis of SHBG, resulting in increased free testosterone levels. SHBG is important: certain hormones don’t travel through the bloodstream on their own all the time. A portion of them is “free” (think “free T3” or “free T4” if you’ve ever had a thyroid panel done), and a portion is bound to a binding protein: if hormones traveled in the blood always free, they might have unwanted effects in tissues they weren’t supposed to affect. The binding protein keeps them from latching onto cells willy-nilly. SHBG keeps a portion of estrogen, testosterone, and dihydrotestosterone bound, protecting the body from adverse effects of the full amount of hormone being free/unbound in the bloodstream. Women with PCOS produce less SHBG, so less testosterone (and the other hormones) are bound and more is free: more free testosterone and more free estrogen are responsible for some of the issues women experience with PCOS.

Various hormone feedback loops are altered in PCOS: production of luteinizing hormone (LH) is increased and production of follicle-stimulating hormone (FSH) is decreased. This results in increased androgen synthesis and interferes with normal follicle development and ovulation.

All women normally produce ovarian testosterone from LH stimulating predominant follicles. (Yes, ladies, your ovaries produce testosterone! And this is totally normal. The issue in PCOS is that the ovaries make more testosterone than normal.) In PCOS, abnormally elevated LH influences excessive ovarian testosterone production. A dominant follicle does not develop properly. In a healthy menstrual cycle, a dominant follicle would lead to ovulation. Rather than being ovulated, however, this follicle becomes cystic. Insulin in the brain could possibly drive abnormal LH hypersecretion, which then drives the ovarian testosterone hyperproduction. Interventions that reduce insulin levels may help normalize these other hormones and allows the cycle to operate normally.

The image below is taken from a very informative paper: Polycystic Ovary Syndrome. I’ve circled “Hyperinsulinemia” in red for your convenience (in the panel on the right). See how it spurs all the other hormonal changes? (I have to say, though, that I disagree with them depicting “obesity” as the driver of hyperinsulinemia. Again, what about all the people—women and men—with hyperinsulinemia at a “normal” weight? I know I’m a broken record here, but as someone who struggled with weight most of her life, and still does to some extent, you can see why this is such a sore point for me. There are thin people with all the same metabolic problems we overweight folks have!)

Hormonal and metabolic feedback loops in PCOS.

Source: McCartney CR, Marshall JC. Polycystic Ovary Syndrome. The New England journal of medicine. 2016;375(1):54-64. doi:10.1056/NEJMcp1514916.

 (Click here for a larger version of the image above.)

Dietary Influences on PCOS

Ketogenic and low carb diets as therapeutic interventions for PCOS are underrepresented in the medical literature. Considering how effective low carb/keto is for lowering insulin levels, there should be a zillion studies on this. Instead, there’s a distinct paucity. Weight loss is cited as frontline therapy, but do doctors ever advise patients about how effective low carb/keto is for fat loss? And one more time for the people in the back: what about PCOS patients who aren’t overweight? What are they supposed to do? Lose 50 pounds they don’t have to lose?

What women with PCOS should be informed of is that their condition is coming from chronically high insulin, and whether or not they’re carrying excess body fat, a low carb or ketogenic diet is a dynamite way to bring down insulin levels.

A review of “nutritional management” in women with PCOS mentioned a low-calorie diet, with limited intake of simple sugars and refined carbs and increased intake of low-glycemic foods. It was also suggested to reduce saturated fat and trans fats. I can get behind decreasing consumption of simple sugars, refined carbs, and trans fats, but the low calories and restricted saturated fat? Not necessary. Again, should a woman with PCOS who’s at a “normal” weight be advised to follow a low-calorie diet? If so, why? She’s not looking to lose weight. And if not, what’s the alternative? If weight loss is not an issue, what’s a woman with PCOS supposed to do when “lose weight” is the go-to recommendation? (*Banging my head against the desk.*)

Low carb/keto diets promote fat loss partly through lower insulin, but they can normalize insulin levels even in people who are not overweight. For this reason—normalization of insulin—low carb diets are ideal for restoration of normal hormone signaling and healthy reproductive function regardless of body weight or BMI.

In a systematic review of low carb diets on fertility hormones and outcomes in overweight and obese women (not all with PCOS, though), the individual studies examined had mixed findings, but on balance, the evidence was stacked in low carb’s favor. The authors wrote, “reducing carbohydrate load can reduce circulating insulin levels, improve hormonal imbalance and resume ovulation to improve pregnancy rates compared to usual diet.” Color me shocked. And the kicker is, they defined “low carb” as less than 45% of calories from carbs… ell-oh-ell. So some of the studies they included had subjects consuming less carbohydrate than their usual diet, but way more than you and I would consider truly low carb. Imagine how much more compelling the results would have been if all the diets were actually low carb or ketogenic.

Studies employing food recall and food frequency questionnaires—which, admittedly, are almost worthless (if you can’t remember what you had for lunch on Wednesday three weeks ago, imagine trying to account for what you’ve eaten over the past few years)—suggest a correlation between greater intake of foods with high glycemic indexes and loads and incidence of PCOS. One case/control study showed that compared to subjects without PCOS, subjects with PCOS had the same approximate total energy (calorie) and macronutrient intakes, but the women with PCOS had higher intakes of high-glycemic index foods and lower intakes of vegetables and legumes than the controls. Studies like this can’t establish a causal relationship, but considering the undeniable driving role of hyperinsulinemia/insulin resistance in the condition, it seems reasonable to speculate that diets high in high-glycemic carbs and low in fiber could potentially contribute to the etiology of PCOS.

I have to say, though, that I really dislike the concept of glycemic index (GI) and glycemic load (GL). They’re helpful as a basic—very basic—framework. Things like maple syrup or blueberry muffins are probably going to affect most people’s blood sugar and insulin levels much more than, say, spinach or mushrooms. BUT: things get a bit murkier when comparing foods that are both relatively high in carbohydrate. For example, a cookie versus a banana. Experiments have been done looking at glucose responses in many people in response to many different foods, and the researchers were surprised to see radical differences in glucose responses. One person’s high-fiber, whole-grain bread is another’s white bread with grape jelly. In the authors’ own words: “Here, we continuously monitored week-long glucose levels in an 800-person cohort, measured responses to 46,898 meals, and found high variability in the response to identical meals, suggesting that universal dietary recommendations may have limited utility.”

“Universal dietary recommendations may have limited utility” … um, YA THINK?! So much for across-the-board low fat, vegan, DASH, and whatever other diets they’re trying to shove down our throats, literally and figuratively.

With regard to glycemic responses after consuming the same foods, Eran Segal, one of the authors of the study cited above, noted: “There are profound differences between individuals—in some cases individuals have opposite response to one another and this is really a big hole in the literature.” Talk about an understatement. Segal also noted: “After seeing this data I think about the possibility that maybe we’re really conceptually wrong in our thinking about the obesity and diabetes epidemic. The intuition of people is that we know how to treat these conditions and it’s just that people are not listening and are eating out of control--but maybe people are actually compliant but in many cases we were giving them wrong advice.” (Emphasis added.) 

Hallelujah and pass the bacon!

  

Low Carb and Ketogenic Diets for PCOS

The interwebs abound with “anecdotes” from women successfully managing (or reversing, really) PCOS with a low carb or ketogenic diet, but published clinical trials are scarce. The great Dr. Eric Westman (who's been researching low carb and keto diets for over 20 years) was behind one of the only ones out there, and it’sa damn good one. It was very small – only five subjects, so that’s a bummer, but it’s not a reason to ignore the findings, especially when you see how powerful those findings were. Subjects were overweight or obese women with PCOS who were instructed to limit their carbohydrate intake to 20 grams or less per day for 6 months. 20 total grams or fewer is the strict approach Dr. Westman uses in his clinic at Duke University (the famous “page 4 diet”) and here’s what happened in the women: 

• Body weight: -12%
• Percent free testosterone: -22%
• LH/FHS ratio: -36%
• Fasting insulin: -54%

Check out that drop in fasting insulin – a FIFTY PERCENT DECREASE! That’s your smoking PCOS gun right there, dear readers.

And the best part? Two of the subjects got pregnant!! TAKE THAT, PCOS! As I mentioned at the very start of this post, PCOS is a major cause of infertility. It accounts for as much as 80% of anovulatory infertility cases and 70% – 80% of women with PCOS have infertility. And two out of five women in this study conceived after a few weeks on a low carb diet—despite previous failed attempts. Granted, these are very small numbers, and correlation is not causation, but come on. If you’ve understood anything about the role of insulin in affecting multiple reproductive hormones, it’s not a huge logical leap to suggest that lowering insulin levels via the very low carb study diet probably played a role in these conceptions.

Let’s talk a bit more about infertility for a sec here. Getting pregnant should be easy. It’s darn near the most natural thing in the world. When I was a kid, our junior high health classes were basically nothing but lessons in how not to get pregnant, because teenage pregnancy was such a big concern and it seemed like unless you took heroic measures to protect yourself, odds were that you would get pregnant. Things have changed a lot in the decades since then. Now, couples trying to conceive struggle like never before. They pay tens of thousands of dollars (or more) for advanced testing, fertility treatments, hormone injections, in vitro fertilization (IVF), and other interventions in the hope of having a child. Getting pregnant should not be this difficult.

Of course, there are approximately four zillion different reasons why attempting to conceive can be unsuccessful. PCOS is only one thing on a long list of issues that can interfere with a woman’s fertility, and goodness knows men can have difficulty fathering a child for an endless list of their own reasons. I mean absolutely no offense to anyone who desires to have a child and has experienced the devastation of that not happening. I’m only trying to point out that PCOS is a major cause of infertility for women, and it’s an issue that was very rare until recently. It existed awhile back, yes (remember that “diabetes of the bearded woman” thing from the 1960s), but it was rare—just like type 2 diabetes, obesity, and metabolic syndrome were once rare. All of these conditions have exploded in incidence in the past few decades, and it’s really no mystery why: they all come from the same underlying problem.  

A systematic review that looked at the effects of different diets for the management of PCOS found:

“…greater weight loss for a monounsaturated fat-enriched diet; improved menstrual regularity for a low-glycemic index diet; increased free androgen index for a high-carbohydrate diet; greater reductions in insulin resistance, fibrinogen, total, and high-density lipoprotein cholesterol for a low-carbohydrate or low-glycemic index diet; improved quality of life for a low-glycemic index diet; and improved depression and self-esteem for a high-protein diet.” (Source)

A study of 60 overweight or obese women with PCOS compared the effects of a “conventional hypocaloric diet” (15% of energy from protein) and a modified hypocaloric diet (30% of energy from protein, plus low-glycemic-load foods selected from a list) after 12 weeks. Weight loss was similar in the two groups, and mean testosterone level decreased in both groups. FSH and LH were unchanged by either diet, but compared to the conventional diet, only the higher protein, low-glycemic diet resulted in significant decreases in insulin, HOMA-IR, and C-reactive protein (a marker of inflammation). The higher-protein lower glycemic approach improved insulin and HOMA-IR while the conventional low-calorie diet didn’t? YOU DON’T SAY!

In a crossover study of obese women with PCOS comparing three weeks of a conventional diet (60% carbs; 25% fat) to an isocaloric higher fat diet (40% carbs; 45% fat), both with 15% of total energy from protein, the higher fat diet resulted in an impressive 30% decrease in daylong insulin levels along with improvements in the lipid profile. Both diets were relatively low in saturated fat (<7% of total energy), with the increased fat in the higher fat diet coming predominantly from mono- and polyunsaturated sources. The study authors concluded, “Replacement of dietary CHO [carbohydrate] with mono/polyunsaturated fat yields clinically important reductions in daylong insulin concentrations, without adversely affecting lipid profile in obese, insulin-resistant women with PCOS. This simple and safe dietary intervention may constitute an important treatment for PCOS.”

What? Say WHAT? Replacing carbohydrate with fat reduced insulin levels without wacky effects on the lipid profile? And cutting back on carbs and eating more fat is a simple and safe dietary intervention that may be an important treatment for PCOS? *Insert my shocked face.* (Not.) This study was published in 2017. Since the increased fat was specifically from mono- and polyunsaturated sources, I guess the authors must’ve missed the 2010 meta-analysis from the American Journal of Clinical Nutrition looking at the association of saturated fat with cardiovascular disease. This analysis concluded “that there is no significant evidence for concluding that dietary saturated fat is associated with an increased risk of CHD or CVD.” (CHD is coronary heart disease; CVD is cardiovascular disease.) So yeah, being that pretty much the only reason we’ve ever been advised to reduce saturated fat is to reduce risk for these issues, and there’s no evidence that this reduced risk actually occurs, there’s basically zero reason to cut back on saturated fat, whether you have PCOS or not. 

The same researchers published a separate paper in 2010 in which they wrote that replacing saturated fat “with a higher carbohydrate intake, particularly refined carbohydrate, can exacerbate the atherogenic dyslipidemia associated with insulin resistance and obesity that includes increased triglycerides, small LDL particles, and reduced HDL cholesterol.” So yeah: higher carb intake (not higher fat intake) worsens the lipid profile associated with insulin resistance…like the insulin resistance women with PCOS have.

Another study found that after 8 weeks of a low-starch, low-dairy, higher-fat diet, overweight and obese women with PCOS had significant increases in fat oxidation and decreases in carbohydrate oxidation—that is, they were burning more fat and less carbohydrate—deriving more of their energy from fat. The diet also resulted in a substantial reduction in fasting insulin: a mean decrease of 19.5μg/mL (± 8.9), which is pretty huge, as well as impressive weight loss: subjects lost an average of about 8 kg (17.6 lbs) – in just 8 weeks. That is a damn fine rate of weight loss!

And no surprise whatsoever, the composition of the diet sounds very much like a well-formulated low-carb diet:

“The diet included ad libitum consumption of lean animal protein (meat, chicken, turkey, other fowl, fish, shellfish, and eggs), non-starchy vegetables, fruits (including fatty fruits, such as avocado and olives), nuts, seeds, and oils. Subjects older than 21 years were allowed one 6 oz (177.44 mL) glass of red wine per day, and all subjects were allowed up to 1 oz (28.35 g) of prepared or fresh, full-fat cheese per day. Cheese has not been found to be as insulinemic as other dairy products because of its low whey content and was allowed in restricted amounts to aid in dietary compliance. The diet excluded all grains (refined and whole), beans, pulses, dairy products (low-fat and whole milk and milk products), and sugar (including fruit juice from concentrate, cane sugar, beet sugar, raw turbinado sugar, evaporated cane juice, brown rice syrup, high-fructose corn syrup, corn sugar, honey, or a gave nectar) because of their insulinemic properties. Non-nutritive sugar substitutes were allowed for participants that wished to use them. Participants were not advised to count calories or CHOs and were encouraged to eat until they were satisfied, but not to overeat. Participants were instructed not to change their level of physical activity throughout the intervention.” (Source)

It’s noteworthy that artificial sweeteners were permitted, as some people claim that these affect insulin levels and blood glucose, but many physicians who use low carb interventions with their patients have not found these substances to be problematic. (In fact, for some people, including them makes it much easier to stick to low carb/keto for the long term because it expands the food and beverage options. Be a purist if you want to [I’m definitely not], but some of us like to drink things other than plain water now and then. I’ve used artificial sweeteners for over 20 years, and I have not found them to interfere with fat loss, nor with my metabolic markers, including fasting insulin, fasting glucose, HbA1c, and my lipid profile. But you do you! I’m not your food police!)

It’s also noteworthy that the weight loss and lower insulin levels in this study were achieved without changes to subjects’ usual exercise habits, and without them specifically being told to cut back on calories—or to count calories at all. You know what that means? It means that the dietary change alone was effective. No “eat less, move more.” Just a low carb diet. Period. (If subjects did end up eating less, it was because low carb/keto tends to be more satiating and regulates appetite to the point that people spontaneously reduce their total energy intake without having to count and track everything. They eat less naturally, because once blood sugar and insulin levels are stable and people are off the blood sugar rollercoaster, they don’t need to eat several meals a day plus snacks in between.)

This is especially interesting because regarding PCOS, the prestigious Mayo Clinic in the US states:

“Your doctor may recommend weight loss through a low-calorie diet combined with moderate exercise activities. Even a modest reduction in your weight — for example, losing 5 percent of your body weight — might improve your condition.”

Right. Or, you could do a low-carb diet, not count calories, not exercise more than you already do, and somehow lower your insulin levels substantially and lose an impressive amount of weight. This isn’t rocket science, ladies.  

Inositol for PCOS

As an adjunct to carbohydrate restriction, certain supplements might be helpful for aiding with insulin sensitivity and blood glucose management. Two that come to mind are chromium and berberine. For PCOS, specifically, inositol appears to be a biggie, in the forms myo-inositol (MI) and D-chiro-inositol (DCI). These compounds have an impressive record of efficacy for reducing fasting insulin, HOMA-IR, total and free testosterone, and for restoring normal ovulation and menstrual cycles (sources: 1, 2, 3).  In a randomized trial in women with PCOS, 6 months of treatment with myo-inositol (4g/day) was shown to have similar effects as metformin (1500mg/day) for improving insulin sensitivity and restoring the menstrual cycle.  A systematic review of randomized controlled trials evaluating the effects of inositols as therapy for PCOS concluded that myo- and D-chiro-inositol have “a pivotal role […] as a safe and effective therapy for PCOS. Combined with inositol, alpha-lipoic acid is another compound that might be helpful to supplement with for PCOS, mainly owing to beneficial effects on insulin sensitivity and glucose tolerance. (See here and here.)

(See here for the brand of supplements I use, myself. Sensitol is the mixed myo- and D-chiro-inositol product I suggest for PCOS. This is an affiliate link; I make a small commission from sales.)

However: if you have PCOS, you can do just fine on low carb/keto without these supplements. The diet alone is powerful enough to bring down insulin and have a beneficial cascading impact on the other hormonal abnormalities responsible for your signs & symptoms. Supplements might give you a little extra edge, but honestly, the diet will be responsible for the vast majority of improvement.)

Diabetes Drugs for PCOS

It is telling that metformin and other diabetes drugs top the list of pharmaceutical interventions for women with PCOS. If PCOS had nothing to do with insulin and/or blood sugar, why would anyone ever have bothered to research this, let alone have physicians actually prescribe these drugs for this condition as a regular course of action? They know this is the issue, and yet…

And yet, how many women actually living with this condition are told it’s the insulin?

Findings from studies looking at diabetes drugs for PCOS have been mixed, but overall, the evidence indicates these drugs are effective for improving insulin sensitivity, reducing androgen levels, and restoring normal menstruation. (See here, here, and here for examples, and there are many more such studies and reviews.)

In one study, lean and obese women with PCOS were treated with either metformin (850mg twice a day) or rosiglitazone (4mg/day) for 12 weeks. In all groups, HOMA-IR, fasting insulin, area under the curve for insulin, and C-peptide levels decreased. (C-peptide is a measure of insulin production.) Metformin therapy resulted in regular menstruation in nearly 42% of lean and 36% of obese patients who had menstrual disturbance at baseline. Rosiglitazone therapy improved menstrual disturbance in 61.5% of lean and 53.8% of obese patients.

If you’re dealing with PCOS, you could take these drugs if you’d like to, or…

Or, you could reverse your PCOS eating juicy steaks, bacon, fatty pork chops, grilled asparagus, roast chicken with crispy skin, mushrooms sautéed in butter, and all other manner of extremely delicious very low-carb foods. You do you, but I know which one I’d choose. And these are not mutually exclusive. You can do a keto diet and start on some of these medications or the supplements I mentioned, with an eye toward weaning off of them as your metabolic condition improves.

It boggles my mind why low-carb or ketogenic diets are not standard of care for women with PCOS. It is a slam dunk, and I can only speculate that the reason it’s not the first, immediate go-to strategy is simply that most doctors just don’t know. The main piece of advice they give is probably to lose weight (if the perspective is that PCOS is caused by being overweight), but what do doctors tell thin women with PCOS? I have no idea. “Take your metformin and see you in six months” would be my guess. This is an absolute travesty, and we should be furious over it.

If you know someone living with PCOS, consider sending them a link to this post. It’s my hope that they’ll see they are most definitely not helpless, and the situation is not hopeless. They’re not at the mercy of inexplicable imbalances in hormones. There’s one hormone that’s influencing all the others, and it’s insulin. Regulate insulin, regulate the others – and control PCOS with food. No need for starvation, deprivation, rabbit food, or innumerable hours on treadmills or elliptical machines. 

If someone needs help getting started with keto, I’m available for consultations, or you can simply point them toward the good ol’ Atkins diet, which, other than the page 4 diet (which is basically Atkins induction), is still the simplest, most straightforward and effective way to start keto. (See here for a post I wrote about this.)

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Disclaimer: Amy Berger, MS, CNS, NTP, is not a physician and Tuit Nutrition, LLC, is not a medical practice. The information contained on this site is not intended to diagnose, treat, cure, or prevent any medical condition and is not to be used as a substitute for the care and guidance of a physician. Links in this post and all others may direct you to amazon.com, where I will receive a small amount of the purchase price of any items you buy through my affiliate links.