PCOS is complicated. It’s an easy diagnosis, but the causes of it are rarely understood. This is because cysts crop up under a wide variety of hormonal circumstances. We might think that this would mean that the medical community recognizes the need for diverse treatment among PCOS patients, but actually it does not. Instead of considering the wide variety of PCOS needs, many doctors (especially those who are not endocrinologists) use blanket diagnoses and treatments for all of their PCOS patients. This is not wholly unreasonable. There is a majority PCOS condition, and the biochemistry of this condition is both simple and compelling. However, there remain other causes and problems. Failing to address them means that thousands of women end up falling through the cracks.
The current understanding of PCOS is flawed in two major ways. First is what I just described above, the fact that the wide array of different hormonal issues that might cause PCOS has not really been explored or emphasized. Instead, PCOS is broadly regarded as a direct effect of being insulin resistant and overweight. However, this only accounts for between 60-80 percent of PCOS patients. The second flaw is a corollary of that nearsightedness: most members of the medical community (though there is a real debate getting off the ground) believe that it is impossible to have both PCOS and hypothalamic amenorrhea at the same time.
The belief in problem number two, ie, that HA and PCOS are incompatible, derives from the first problem, ie– the lack of a nuanced understanding of PCOS. PCOS is widely regarded as a problem of insulin resistance and being overweight. These are two significant factors that generate cystic ovaries. But they are not the only ones. Only 60 percent of PCOS patients are overweight. Some normal weight PCOS patients are also insulin resistant. Yet others still are not. What causes normal weight women to develop cystic ovaries? And what about insulin-sensitive women?
Recommendations for overcoming PCOS are directed at this insulin-resistant. PCOS patients are advised by the National Institute of Health to “drop 5 percent of their body weight” in order to become fertile. This is, again, great for the majority of PCOS patients, who usually do well and recover reproductive function with the simple implementation of an insulin-sensitized lifestyle. This is why the paleo diet kicks ass for overweight women with PCOS. When they exercise, eat low-ish carbohydrate diets and eliminate refined foods…. these women correct their insulin resistance, reduce their testosterone load, and as such watch their hormone balance fall elegantly in line. It is worth noting that there are different nuances within this population– that some of them have vastly different estrogen and progesterone levels and varying degrees of hormonal imbalance. This is another reason that a nuanced understanding of PCOS is necessary for the health of each women. Nonetheless, however, overweight PCOS patients generally recover well on weight-loss and insulin-sensitizing programs.
This does not really do the trick, however, for the rest of the women out there with PCOS.
Below, I discuss the typical and some atypical causes of PCOS, which will hopefully shed light on a) the variety of ways in which hormones can be disrupted, but also in particular b) how hypothalamic amenorrhea (and hypothyroidism) can play a powerful role in causing cystic ovaries.
There are three characteristics necessary for a PCOS diagnosis for all women:
-Cystic ovaries, as detected via ultrasound
-Elevated androgen (male sex hormone) levels
-Irregular or absent menstruation
Overweight and insulin resistance are two important ways these characteristics can be brought about, yet other ways are equally powerful. The thing is– having cystic ovaries means that the process of menstruation is not completed properly. It does not mean necessarily that one universal step (such as insulin resistance) goes wrong. Instead, it means that at some point along the chain throughout the four menstrual weeks, one or more factors misfires. A signal is missed, one hormone floods the rest of them, or one hormone isn’t properly produced, for example. Androgens usually end up at dominating the reproductive scene, and cysts usually develop. But the mechanisms by which this occurs are not as simple as many PCOS practitioners would have us believe.
The dominant pathway by which women develop poly cystic ovaries is, again, that of the overweight woman. It is a fairly simple process:
1) insulin stimulates testosterone production in the ovary, and
2) testosterone production throws off estrogen levels and inhibits estrogen signalling.
In PCOS, testosterone and estrogen become improperly balanced, and the rest of the menstrual cycle, which takes its cues from the rise and fall of estrogen levels, suffers. LH and FSH, two pituitary hormones that tell the ovaries what to do and when, are of particular concern. LH and FSH levels become dysregulated with dysregulated estrogen because they take their cue from blood estrogen concentrations. This is why the vast majority of PCOS patients have a reversed and high LH and FSH ratio compared to healthy women. The pituitary gland keeps trying to make the body ovulate, but it does not read estrogen signals properly, and the ovaries do not hear the pituitary properly. So these are the markers of the typical PCOS diagnosis: inverted LH and FSH, insulin resistance, overweight, and elevated testosterone levels.
Yet there are other means by which a woman’s hormonal profile can create cysts.
First is a simple case, and this one is thankfully recognized by many in the medical community: that of hypothyroidism. Having low T3 (the active form of thyroid hormone) in the blood is strongly correlated with cystic ovaries. When women with subclinical hypothyroidism correct their condition (this is normally done in medical studies by taking T3 pills), the majority of cases begin menstruating again. This is presumably because low T3 levels decrease the activity of cells and hormonal signalling, which means that the menstrual cycle proceeds with fits and starts, rather than powerful, holistic health. Three common causes of lower thyroid function are poor sleep, restricted calorie intake, and a long-term carbohydrate limited diet (since glucose is necessary for the conversion of T4 to T3 in the liver).
Second is the important and powerful case of hypothalamic amneorrhea. HA is known by many to be exactly the opposite of PCOS. In PCOS, hormone levels often skyrocket. High testosterone, high and uneven LH to FSH ratio, high estrogen levels (though not always). In HA, hormone levels plummet. Low LH, low FSH, low estrogen, low testosterone. PCOS is a problem of being overweight; HA is a problem of being underweight. In PCOS, women over-produce hormones. In HA, women under-produce hormones.
Or so the story goes. However, women can present with cystic ovaries and still have low levels of hormones. The problem– the real, truly universal problem that creates cysts–is a hormone imbalance. Absolute levels of the hormones are important, but even more important is the balance between testosterone, estrogen, progesterone, and leptin, even. The other factors– insulin resistance, LH and FSH inversion, and being overweight– they are not the only thing that can create an androgen-dominant cystic profile.
Hypothalamic amenorrhea is a problem of being too stressed, eating too few calories, exercising too much, and having too little body fat. In essence, it is a condition caused by hypothalamic stress and down-regulation. Hence the name.
The ways in which these four problems typically classed under a diagnosis of hypothalamic amenorrhea– the eating, the exercising, the stress, and the body fat– can cause cysts and/or co-occur with more classically PCOS-type symptoms are vast. Here are a couple of examples:
-A woman is really stressed out by work and life. While most of her hormone production plummets, her DHEA-S production (the top-of-the-food-chain hormone produced by the adrenal gland) skyrockets in response to HPA axis dysregulation. DHEA-S is an androgen, and it influences the development of cystic ovaries if estrogen levels are not equally as high.
-A woman is fairly healthy but has slept poorly throughout her entire life. This pushes her towards insulin resistance, but more than that it dys- and up-regulates her cortisol production. Cortisol signals to the HPA axis to decrease pituitary activity, and it does so. Her hormone levels all decrease. This woman’s predisposition to insulin resistance coupled with adrenally-induced fluctuations triggers the development of ovarian cysts.
-A woman is stressed out via the typical HA pathways–caloric restriction, excess exercise, and stress–so her pituitary hormones decrease in potency. Testosterone and estrogen levels are low but okay, and the woman is probably thin but may also be larger, depending on the degree of stress. Nevertheless, this time it is progesterone that takes the largest hit from the stress (taking it’s cue from both estrogen and LH), and menstruation can never occur without sufficient progesterone levels.
-A woman has a tendency towards insulin resistance, and is overweight, and then loses weight. While this corrects the insulin problem, the drop in estrogen levels she experiences from the weight loss (since estrogen is produced in fat cells) causes an imbalance in her predisposed-to-testosterone-production ovaries.
- Or a similar phenomenon occurs with leptin: In this case, a woman may be a bit insulin resistant, and therefore have a predisposition to testosterone production, but she does not test into a “dangerous” testosterone zone. Instead, her problem lies in the fact that she lost weight, and with it, she lost the potency of her leptin stores. During puberty, each woman’s body adapts to whatever levels of estrogen and leptin she has circulating in her blood at the time (creating a bit of a leptin “set point”). Later in life, one of these women loses weight. As she loses weight, and, significantly, if she is restricting calories or exercising excessively, her leptin (and estrogen) levels drop. The hypothalamus perceives this drop as an indication of a time of famine, and initiates a starvation response, primarily by decreasing the production of sex hormones. In this woman’s case, therefore, estrogen is low, and testosterone may be low to high, depending on the degree of insulin resistance and ovarian malfunction, but LH and FSH are both also low. She does not present with typical PCOS. She is not over-producing hormones, but is, instead, under-producing.
All that said, these are some examples of how typical HA problems can cause the cystic condition that is typically associated solely with PCOS. Stress, excess exercise, restricted macronutrient intake, restricted calories, and weight fluctuation can all contribute to cyst development. Many of these situations can co-occur, and that totally depends on a woman’s genetics, epigenetics, lifestyle, and diet.
The problem with having a poorly-nuanced understanding of PCOS lies in the way in which blanket recommendations are made for women with PCOS or HA. As a result of this mindset, I have been criticized for recommending that thin women with PCOS eat carbohdyrates. This is because those who are criticizing me believe that PCOS is solely a result of insulin resistance. I do not believe so. I believe that many women with PCOS do not necessarily have a problem with insulin resistance, and even if they do, it can be compounded by factors that lie outside of that typical diagnosis.
I would, then, tentatively recommend that women who are overweight and insulin resistant follow the typical PCOS protocol and under-take insulin sensitizing steps. On the other hand, I would tentatively recommend that potentially under-weight and overly-stressed women with PCOS consider eating more, possibly upping their carbohydrate intake, and exercising less. Women with low thyroid would do well to correct that problem however they see fit. This is, however, particular to the individual, so please do not take my musings about PCOS etiology and treatment as prescriptions. At all.
The real recommendation, therefore, is to get a blood test (!), and to have discussions with your doctor about all of the possibilities that could be affecting your hormone levels. With PCOS it is crucial to order blood tests. While it is a near certainty that androgen levels are elevated relative to the rest of the hormones, that is not the case 100 percent of the time. All of the hormone levels– testosterone, estrogen, progesterone, LH, FSH, and T3 levels may be all over the map and still cause a woman to present with PCOS. An adequate picture of what is happening in the body is crucial for moving forward. This then enables women to undertake dietary and lifestyle changes appropriate to their own holistic health and well-being needs.
For more information on PCOS, why you have it, and how to overcome it, check out PCOS Unlocked: The Manual, the multi-media resource I created in order to share all the PCOS information and experience I’ve amassed in my brain, and apply it to solving the unique case of your PCOS.