What causes PCOS?
Many of the PCOS “experts” in the world do not understand fully the connection between the endocrine system and the reproductive system. Because of this, they miss a very important link between metabolic syndrome and PCOS. I have read maybe a dozen books about PCOS that recommend nothing but taking birth control pills in response. This puts a patch on a problem that is, in the authors’ views, a simple result of genetics. Some authors go so far as to recommend a low fat, low carbohydrate, moderate protein diet. If a woman tries to eat that way, what is possibly left?
Others—the real doctors, not the one’s publishing books—understand that PCOS is a disorder of the endocrine system. It is not just an ovarian problem, but is rather a problem of hormone signaling to and within the ovaries. This means that ovarian hormone production, pituitary action, and even hypothalamic action are all crucial for proper reproductive health. Check out the Journal of Endocrinology’s 681 articles on PCOS if you want to know more about that.
What makes PCOS so hard for doctors to figure out is not just 1) the grab bag of symptoms but also 2) the heterogeneity of its population. There are two primary groups of PCOS patients. In the first group are about 60 percent of the patients, all of whom are overweight. More importantly, they are insulin resistant. High levels of insulin in these patients shift hormonal balances away from estrogen and towards testosterone. Insulin directly stimulates testosterone production. It’s pretty clear to endocrinologists how to fix this problem. Lose weight, and create better insulin sensitivity. Low carbohydrate (specifically low fructose) diets, exercise, and intermittent fasting are all excellent means by which to do this. The issue is much more complicated than this–really, it is, and many overweight women still have some issues when they lose weight–but it can more or less be boiled down to these steps. On the other hand, the problem is a fair bit more complicated for the other 40 percent, the “thin cysters.” If it’s not overt insulin resistance causing their issue, what is it?
Things that give people PCOS and why
Overweight, metabolic derangement and/or insulin resistance
Like I just mentioned, metabolic derangement is the single greatest cause of reproductive derangement in women. Insulin makes ovaries produce testosterone. This is bad news. We all need testosterone—it’s the crucial hormone for generating sensation in the clitoris!—but too much can entirely derail that.
Dramatic weight loss
Fat cells are major players in endocrine systems. This means that any kind of weight fluctuation can significantly disrupt endocrine function. Primarily, this is an estrogen problem. Estrogen is produced in fat cells. When people gain weight, their estrogen levels increase (obese PCOS patients might have elevated testosterone AND estrogen). When they lose weight, they decrease. Having high androgen levels is the most universal element in diagnosing PCOS, but having appropriate estrogen levels is also crucial for proper reproductive signalling. Moreover, higher levels of estrogen can block harmful effects of androgens and even reduce circulating androgen levels. For these reasons, it may be more important to have proper balance between testosterone and estrogen rather than having good absolute value of either hormone. For example, in my own case, when I was first tested for PCOS, my testosterone was slightly elevated and my estrogen was slightly depressed. These weren’t alarming numbers in either case, but combined they spelled serious issues.
The jury is still out in the world of science, weight loss, and eating disorders on the long term impact of weight loss. Can someone lose weight slowly and maintain reproductive health? Does the speed with which she loses weight matter? If someone loses a significant amount of weight, will her ovaries ever “learn” to make up for the estrogenic load her fat cells used to give her?
From what I can, the answer to each of those questions is “sort of.” I will use a personal example again to demonstrate. I used to weight 137 pounds. In three months I dropped to approximately 105 and today sit fairly solidly at 120 pounds. At 120 pounds, my estrogen levels have increased. They have not reached the same level I experienced at 137 pounds, when my fat cells were pumping out a lot of estrogen, but it is still much more significant than it was at 105. My testosterone has also dropped, at least minimally, and my LH and FSH have remained “normal.” It seems as though it was not the speed of the weight loss, but the simple fact of having a lower body weight that was hurting me so much. I have been experiencing irregular periods and symptoms of low estrogen such as insomnia and hot flashes since I was a young girl, and I have also been amenhorreic at 137 pounds. The issue goes deeper than simple weight loss and weight gain. Achieving 120 pounds has been helpful, but it has not solved everything.
Excessive exercise or low body fat– or even just weight loss in sensitive individuals
This issue is virtually the same as the one above, except the literature on it is more extensive, and it relies less on the actual production of estrogen in fat cells and more on being in starvation mode. When a woman burns calories at a high rate, and when she consumes a low calorie diet (and also if she consumes a lot of fructose) her leptin response is minimal. This means that less satiety is reaching your hypothalamus. The hypothalamus is in charge of telling the rest of the body how nourished it is, and whether or not it should be running on “conserve” mode and shutting down peripheral systems such as reproduction. To do this, it releases Gonadotropin Releasing Hormone, which signals to the Pituitary to release FS and LSH, the hormones that tell the ovaries to produce sex hormones. Without leptin, GRH is impeded, and the entire neuronal cascade is impeded. No proper balance of pituitary hormones is produced.
It is absolutely crucial to convince the body that it is not starving in order to mitigate PCOS. The problem comes with how exactly to do that. There’s no formula. Exercise less, eat more. Eat different foods. Not fruit. Seems as though other carbohydrates — glucose — have the highest of all leptin responses. Put on weight, achieving at least 22 per cent body fat.
Sex hormones are produced in our bodies via two axes: the first is the specifically reproductive axis which includes the pituitary gland and the ovaries, and the second is the adrenal system. If a body has fatigued adrenals in any significant fashion, it’s hormone cascade can be seriously disrupted. Cushing’s disease, an adrenal disorder that causes abnormal cortisol production, often causes PCOS in its patients.
Literature seems to show, interestingly, that cortisol promotes estrogen production. When women present to evolutionary medicine folks (and regular medicine folks) with symptoms of estrogen dominance, such as PMS or abdominal fat, they are advised to reduce stress. High stress often puts women into states of hyper-estrogenism. This has to do with HPA axis dysregulation in general. A woman can have HPA axis hyperactivity, or HPA axis hypoactivity. In either case, reducing stress will serve to restore natural hormone signalling. It may take some time, but it is the only cure.
Metabolic derangement during puberty
Check out the book Ancient Bodies, Modern Lives by Wenda Trevathan for an excellent book on fertility in general. It’s where I first read this theory, that whatever physiological state a girl is in in when she begins menstruating can affect her cycle for the rest of her life. Trevathan proposes that conditions of famine and bounty are determined by this metabolic state, such that deviating from the start-of-puberty norm triggers famine or bounty responses in a woman’s body. For example, many rail thin women in the world, particularly in developing countries, menstruate their entire lives. But when someone who has a BMI of 25 loses 15 pounds, or maybe has less of certain micronutrients in her system, and also has some metabolic derangement from other sources, her hypothalamus might think this is a period of starvation and turn off her reproductive response.
A lot of evidence in the pathogenesis of PCOS, specifically in thin women, points to problems during puberty, childhood, and even the womb (if someone’s mother’s hormones are messed up, hers will be, too.) Menstruation is kicking into gear earlier and earlier in young girls. The middle teen (~14-16 years old) menarche that used to be the norm is now considered “late,” and the average age of menarche in American girls is 11 years old. Evolutionarily, this is quite young. This is partly because young girls are heavier than they used to be. Menstruation starts when a certain estrogen level is reached in the body, and estrogen is not just produced in the ovaries but also in fat cells. The problem therefore is that the ovaries sometimes start out with a handicap, as I touched on above. They are dependent on the fat cells. So any time weight fluctuates, ovaries necessarily have to adjust, and often do so poorly.
Another factor is related: childhood insulin resistance. Having high testosterone levels at a young age primes the body to always act in that fashion. This spells trouble for the entire endocrine system.
I explored the link between hypothyroid and PCOS for a while last year, and I wrote about it here at my other blog. I abandoned my quest when I didn’t see much improvement and may have overdosed on iodine, unknowingly taking upwards of 2000 percent of the daily allowance for a significant amount of time, but I have remained aware of how important the thyroid hormone is for reproductive function.
Thyroid hormone is made in the thyroid gland. First, however, thyroid stimulating hormone, TSH, is produced by the pituitary (after being signaled by the hypothalamus) and sent to the thyroid gland. This instructs it to make T4. T4, though it accounts for 99 percent of the thyroid hormone in the bloodstream, is inactive, and rather just floats around in until the body needs more of it. T4 is converted to T3 in the liver, and the T3 is then used by every cell in the body. In this way, T3 is the hormone of primary interest. But since it is at the end of the chain, things can go wrong at any step in this process. TSH can be underproduced, and either or both of thyroid hormones can go missing. T4 can be underconverted to T3. Someone can be dealing with an inflamed system, menopause, or Hashimoto’s thyroiditis (accounting for approximately 90 percent of hypothyroid cases), and in each case the functioning of every cell in the entire body is impaired. T3 is as crucial for cellular function perhaps as ATP, so you had best have your thyroid health in mind no matter what your presenting condition. This can be bolstered by proper iodine intake, high dose iodine in the form of iodoral, or supplementation with T3 or T4. Whichever step one takes depends on where her endocrinologist sees the problem occurring.
Because every cell is dependent on T3, and because bodies try to optimize its T3 resources, peripheral systems such as reproduction can be shut down in favor of protecting other systems. If the thyroid is malfunctioning, the hypothalamus may reduce signalling to the pituitary gland in order to protect the thyroid system as much as possible. This is analogous to the phenomena of starvation. Another possible point at which hypothyroidism influences PCOS is at the level of cellular functioning. If there isn’t enough thyroid hormone in a cell, it will shut down or become sluggish independently. Reproductive tissues, such as those in the ovaries, might therefore not have enough energy or resources to produce estrogen at the proper rates.
PCOS patients who present with subclinical levels of thyroid hormone begin ovulating once regular thyroid functioning is achieved. One of my favorite articles reports that thyroid hormone replacement therapy achieves a “significant reduction in total as well as free testosterone,” and also states that “ovarian volumes of patients with hypothyroidism were significantly great compared with controls, and their magnitudes diminished significantly during thyroid hormone replacement therapy.”
BPA, environmental toxins, and endocrine disruptors
I mentioned before that thin women with PCOS present with greater gland and endocrine dysfunction than overweight women. What is the root of this malfunction?
One plausible answer is environmental toxins. One of the most concerning ones is environmental toxins. Almost all fruits and vegetables are covered in chemicals that act as phytoestrogens in the body. Over time, specifically when young, these can have a major impact on reproductive physiology. Some foods are worse than others. The way to mitigate this is to eat organic, to peel vegetables, or to wash them with organic soap. A great way to wash vegetables is to soak them in vinegar for several minutes. Vinegar binds with some of these toxins and will help chelate them off of the skin of the vegetables.
A second endocrine disruptor, perhaps the most prevalent one in American lives today, is BPA. BPA is a polymer leached from plastics that disrupts endocrine function in a way not entirely yet understood, but appears to have estrogenic effects.
When rats are exposed to BPA, their male offspring have decreased fertility, and only after exposure to small doses. Of the male rats, one study concludes:
“The BPA exposed males had a suite of reproductive deficiencies that collectively created subfertility in the rats. Some of these included lower sperm counts, poor sperm motility and cellular defects within the testes. Circulating levels of testosterone, estrogen and other reproductive hormones were also significantly lower.
The BPA exposed males were also significantly heavier than unexposed controls.
Mating behavior was also negatively impacted. The BPA-exposed males took longer to copulate with females and a few failed to copulate at all. These observations suggest that the males had lower sexual motivation.
Potentially most concerning, is that the sons and grandsons of the exposed males were also subfertile, indicating that the germ line itself was damaged by the initial exposure to BPA. The mechanism for this transgenerational effect is unclear.”
Female rats are affected just as strongly, if not worse. THEY GET PCOS. Not only do they present with cystic ovaries, but they have increased testosterone and estrogen levels, and also decreased progesterone. Recall that progesterone is THE crucial hormone for menstruation. They also have lowered fertility and higher BMIs than non-exposed rats.
If that doesn’t convince you BPA is bad, note that this result has also been reported in human females. A high correlation has also been shown between mothers with high levels of BPA having children with mood, behavior, and personality disorders.
Moreover, women with PCOS, both lean and overweight women, have 40 percent higher levels of BPA in their blood than those without. Notably, the levels are even more markedly increased in thin women with PCOS. In thin women, PCOS patients had 1.6 times ordinary BPA levels, and in overweight women the ratio was just 1.3. Some researchers speculate that this is because BPA is being stored in fat cells, while other posit that BPA causes brain-related hormone signaling dysfunction, which could explain why thin people end up having PCOS at all. The question of causation rather than just correlation remains, however: does BPA cause increased testosterone levels or do increased testosterone levels inhibits the body’s ability to clear BPA out of its system? The research is inconclusive.
Hard plastics, the polycarbonate plastics such as #7, are worse than soft plastics. Plastics 1, 2, and 4 seem to be BPA free. Heated plastics leach at much higher rates than cold ones (such that buying frozen vegetables is not as scary as one might originally imagine.) However, just because a plastic is free of BPA does not mean it is free of estrogenic activity. All plastics have EA–Estrogenic Activity–just from different chemicals and in different amounts, with not any of them yet measured significantly. Finally, research has shown that BPA gets into bodies in even higher doses from eating out of aluminum cans than out of plastic. Cans are lined with BPA on the inside, so virtually everything eaten out of a can is swimming in BPA. Here’s a list of consumer tips if you’re interested.
Another source of environmental estrogens is body applications. Parabens are phytoestrogens and are one of the most common elements in lotions and soaps. Consume organic here, or check labels, or, even better, stop washing altogether. Also importantly, there is a lot of BPA in receipts. So if you are a cashier, you can ask your boss to let you wear gloves and she had best say okay. Many people actually already do this.
Glands get hormones pupming into the bloodstream, but the liver filters them. I’ll talk more about what one can do with a liver below.
Pituitary or hippocampal tumors
If LH, FSH, TSH, or Gonadotropin Releasing Hormone levels are significantly impaired, and if all other causes have been ruled, this is an indicator that an MRI should be performed.
1) A high insulin diet – that is, one that is full of carbohydrates, particularly refined carbohydrates and fructose-containing carbohydrates — is particularly bad for women with PCOS. It is not clear what the cause of metabolic syndrome is. Chronically high insulin levels may be the cause, but micronutrient deficiencies, inflammation, and leaky gut may also contribute. For this reason, insulin-minimizing foods such as fat and protein should be eaten in sufficient quantities. Inflammatory foods should also be limited. These include, most notably, grains, sugars, and omega 6 vegetable oils.
2) Soy and phytoestrogens. Soy is a phytoestrogen. Phytoestrogens resemble– but are not chemically the same as–estrogen in the body. This leads to confusion in the endocrine system (and, significantly, breast cancer.) Remarkably, soy may play a greater role in endocrine disruption than BPA.
Phytoestrogens can help mitigate some side effects of low estrogen levels such as hot flashes, but they cannot perform the proper signaling functions of true estrogen. This means that exposure to BPA results in a body totally devoid of proper estrogen. When the body detects “estrogen” in its bloodstream, it stops producing it on its own. In this way, phytoestrogen consumption decrease estrogen levels at the time of ingestion. Perhaps more importantly, however, it might also impair the body’s ability to produce estrogen, since the ovaries essentially get out of practice. This is similar to the issue of gaining or losing weight. Soy, like excess weight, is a “crutch” for the ovaries. But it goes beyond that simple role in that it is a malfunctioning crutch, only working in certain circumstances.
One study measured phytoestrogen levels of different foods, and while some vegetables had an order of magnitude greater than others, soy itself has 10,000 units per gram, rather than 4 or 5 hundred like other potent vegetables.
4) Dairy. Pregnant cows produce a protein that inhibits testosterone binding mechanisms, such that dairy is the most androgenic category of foods. This spans butter, milk, yogurt, cream, and any product from a pregnant cow. Moreover, dairy also has a significant insulin response, which can irritate acne and PCOS.
Other foods have less dramatic impacts but may be important to consider for hypersensitive PCOS patients.
5) Factory farmed meat is injected with Bovine Growth Hormone, which can increase insulin-like growth factor 1 in humans. This is bad. Other hormones such as estrogen and testosterone are approved by the FDA for injection into the animals via an earpiece each animal is implanted with at birth. The FDA claims that even with supplementation the animal’s hormonal profile falls within normal ranges, but I’m skeptical. As a personal example, aside from noticing that my acne gets worse whenever I eat meat, chicken, or any other farmed animal (not fish), I also noticed that while in Taiwan I rarely got new cysts, except for one day I ate hamburger meat from Costco.
6) Cruciferous vegetables. These veggies not only act as goitrogens and can decrease thyroid functioning when eaten raw, but they also promote the activity of cytochrome P450 enzyme CYP1A2. This enzyme resides mostly in the liver and is responsible for clearing estrogen out of the system. This is not an issue in regular individuals, and in moderate doses. It is only an issue for seriously dysregulated women who over-consume cruciferous vegetables.
The one food that has been found to reverse this “on” effect on cytochrome P450 enzyme CYP1A2 of cruciferous vegetables in the liver is grapefruit. This is well documented in the medical literature. Grapefruit is the only food that promotes estrogenic activity without acting as a phytoestrogen. But women who eat a lot of grapefruit should be careful: this enzyme also inhibits the processing of a wide variety of drugs.
What can somebody with PCOS eat? The trick is, first, to experiment with one’s own body. The second trick is honestly not to worry about it too much. There are important things that women should always avoid, such as soy, but what’s most important is making sure all the foods are natural and whole.
The extent to which foods influence the production of hormones can be great in a hyper sensitive person, yet phytoestrogens are thousands of times less potent than endogenously produced estrogens. What this means is that foods might serve as a tool to help women achieve better holistic health and hormone balance, but absolute values of certain chemicals in the body from ingesting certain foods might not ever make a difference. There is no reason to become obsessive about micro changes in the diet. PCOS is a bigger problem than that, and what it requires first and foremost is natural foods, proper body weight, and stress reduction.
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.