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Two Peas In A Pod: PCOS & Hypothyroidism

Polycystic Ovarian Syndrome (PCOS) is one of the most common endocrine disorders impacting roughly 6-10% of reproductive aged women [1]. Unfortunately, this number does not encompass a large percentage of women who are undiagnosed or misdiagnosed as the symptoms of PCOS can overlap with symptoms of other conditions such as hypothyroidism. But did you know 1 in 4 women with PCOS also have hypothyroidism? [2,3] If you have been feeling misheard or unsettled in the diagnosis you have received, it could be because maybe you don’t simply fit into one box. It could be in order to achieve your goals it is imperative to consider you may not be able to be defined to one diagnosis.

As PCOS and hypothyroidism have been so commonly diagnosed together, the ongoing debated question persists: does PCOS cause hypothyroidism, does hypothyroidism cause PCOS or are they so intertwined they ironically coexist?

According to the Rotterdam criteria, which most physicians use to diagnose, a female is diagnosed with PCOS if she has 2 out of 3 of the following criteria [1]:

1. Hyperandrogenism: high levels of androgen hormones such as testosterone

2. Oligo/Anovulation: lack of ovulation or inconsistent ovulation which commonly leads to irregular or absent menstruation

3. Cystic ovaries: ovaries contain ‘cyst-like’ appearances

*As we discuss further, keeping these in the back of your mind will help to piece together the connection between PCOS and hypothyroidism.

Foremost before we proceed, it is also important to understand the function of the thyroid gland. Most associate the thyroid gland with weight as it is commonly recognized in hypothyroidism most experience weight gain and in hyperthyroidism the opposite is true. But the thyroid gland is actually a pivotal part of how your entire body functions via its control of your metabolism. Metabolism is an umbrella term for the countless areas the thyroid gland helps to regulate: breathing, heart rate, digestion, reproductive system, brain development, bone and muscle strength, glucose regulation, lipid levels such as cholesterol and so much more [4]. Every single cell in your body has a receptor for thyroid hormone meaning the presence of thyroid hormone helps every cell in your body to function optimally. As with other hormones throughout the body, thyroid hormones are messengers. The production and secretion of one hormone sends a message to another part of the body to produce and secrete more hormones or send reverse messaging to slow down production to keep all organs, glands, cells, tissues and structures functioning optimally. The messaging never ends; it is a constant forward and reversal communication network to keep your body in a state of homeostasis.

Through this vast messaging network, communication of thyroid hormones in conjunction with other hormones throughout the body lead some to speculate the potential that hypothyroidism can cause PCOS.

Thyrotropin Releasing Hormone(TRH) is considered the master regulator of your thyroid gland. It is released from an area of your brain called the hypothalamus and controls how much thyroid hormone is produced and secreted from the thyroid gland [5]. In hypothyroidism, this hormone is decreased which causes an increase in TSH (Thyroid Stimulating Hormone) in an attempt to create more thyroid hormone [3,6]. This alteration in hormones also increases a hormone called Prolactin which is responsible for hundreds of functions throughout the body but most notably for milk production (stress, inflammation and tumors also have the potential to raise prolactin levels) [7]. High prolactin levels alter and decrease the production of FSH and LH: hormones required for ovulation and a normal menstrual cycle [3,6]. Remember, hormones are a large network of communication of constant forward and reversal messaging so you can imagine this as a long telephone chain of one hormone impacting the function of another (Figure 1 below displays this cascade of hormone messaging in hypothyroid states). Follicle Stimulating Hormone (FSH) and Luteinizing Hormone (LH) function by sending messages to the ovaries to develop a follicle. Through this follicle, an egg is matured and released every month in what is known as ovulation. When FSH and LH are decreased, the growth of this follicle does not develop appropriately and an egg cannot efficiently be released for ovulation to occur. The result of this are ‘cyst-like’ structures on the ovaries which in reality are actually immature follicles that were unable to release an egg; coining the term polycystic ovaries, a hallmark feature of PCOS. Furthermore, if an egg were released the location becomes a ‘gland-like’ structure called the Corpus Luteum on the surface of the ovary. This is responsible for Progesterone production but when ovulation does not occur, progesterone is never produced leading to irregular or absent menstrual cycles [6].

Low levels of thyroid hormone, as seen in hypothyroidism, also leads to a decrease in a hormone called the Sex-Hormone Binding Globulin (SHBG) [8]. The function of this hormone is exactly like it sounds: to bind to sex hormones and transport them throughout your body. When hormones are not bound to SHBG they are free and active to influence other hormones, tissues and cells. This contributes to a risk factor for PCOS by creating an increase in free, unbound, active Testosterone leading to hyperandrogenism (a defining feature of PCOS) [8]. High androgens, or testosterone levels, can act directly on the ovaries to further disrupt ovulation and a normal menstrual cycle by altering levels of estrogen and progesterone production. This can also contribute to common symptoms associated with PCOS related to high levels of androgens such as unwanted hair growth, acne and an oily scalp.

We could continue on forever about the potential mechanisms the thyroid may cause in PCOS but the last, clearly studied mechanism to mention is the role the thyroid gland plays in glucose regulation.

As mentioned, every cell in the body has a receptor for thyroid hormone and, among many things, this receptor helps thyroid hormone to bind and contributes to the movement of glucose inside of the cell for utilization and energy. Lower levels of thyroid hormone throughout the body are associated with lower sensitivity of cells to insulin. [2,3,6] Insulin often gets a bad rep, but it is not a bad hormone. Naturally, after you eat a meal glucose levels will rise and insulin levels will follow as its presence is required to move glucose inside of your cells. T3 (the active form of thyroid hormone) controls and regulates the release of insulin but in order for T3 to be present it has to first be converted from T4 [2,3]. When levels of T3 are low whether due to primary hypothyroidism, subclinical hypothyroidism, Hashimoto’s Thyroiditis or conversion complications, the incidence of insulin resistance is high [2,3,6,9,10].

If you have been diagnosed with PCOS you are most likely extremely familiar with the term insulin resistance but maybe have not fully comprehended what it actually means. For simplicity, in insulin sensitive states after a meal glucose rises, insulin rises, insulin binds to your cell and opens up the gates to allow glucose to flow inside. In insulin resistance, when your cells see insulin in the bloodstream they do not allow insulin to easily bind and therefore glucose cannot be moved inside the cell as efficiently as it should. When this occurs, levels of circulating blood glucose and insulin generally remain high rather than returning to a resting, fasting state as it should once a meal has been digested.

While the presence of thyroid hormone is one obstacle to ensure its sensitivity, there are other factors that can decrease insulin sensitivity involving a combination of genetics and lifestyle factors: dietary choices, physical activity, smoking, mineral deficiencies, stress, and inflammation [2]. However, in hypothyroidism, it has been found that even if insulin resistance is not present, fasting insulin levels remain high showing there is still some degree of decreased sensitivity [3].

High levels of insulin in the bloodstream can directly stimulate the production of more androgens (testosterone) and cause a further decrease in the Sex-Hormone Binding Globulin which as mentioned allows even more free, unbound testosterone to circulate [10]. Among many other impacts, high insulin also increases fat storage which can lead to weight gain as commonly, but not always, seen in women with PCOS.

Bare with us as we bring this full circle. We’ve mentioned a few ways hypothyroidism may be causing PCOS, but now let’s look at the potential of the presence of PCOS in causing hypothyroidism.

Insulin resistance (IR) has been identified as a primary root cause of PCOS and when addressed countless women have been able to put their diagnosis into remission. As we mentioned, IR has the potential to be caused by hypothyroidism but there are other factors that can cause insulin resistance signifying insulin resistance could be present first and therefore in a reverse messaging pattern cause or exacerbate hypothyroidism.

It is also well known that PCOS is associated as a pro-inflammatory condition meaning women with PCOS have some degree of chronic inflammation either systemically or locally [11]. Inflammation is an immune response created by the body as a protective mechanism when the body is exposed to something which threatens the safety or homeostatic status of the body. In healthy responses, this can be a positive aspect but when excess, chronic or repeated inflammation is present it poses a problem. Chronic exposure to the ‘markers’ released from the immune system which creates inflammation interfere with various vital functions throughout the body. In relation, they interrupt the activity of an enzyme known as deiodinase [3,6]. Referring back, we mentioned T3 regulates insulin but has to be converted from T4 to be active. In order to be converted, it requires the enzyme deiodinase. Without proper functioning of this enzyme most of your thyroid hormone may be stuck in an inactive form. Therefore when chronic inflammation is present, as often seen with PCOS or caused by PCOS, there is less active thyroid hormone impairing optimal functioning of the cells and body while contributing to insulin resistance.

Additionally, as previously discussed, insulin resistance (whether caused by hypothyroidism or other external factors) generally leads to the development of fat storage. These ‘fat cells’ are formally termed adipocytes which have the ability to create and release these inflammatory markers all on their own. Estrogen, commonly seen elevated or elevated in relation to levels of progesterone in women with PCOS, also has the capability to increase these inflammatory markers [12]. Therefore, it has been well studied that high estrogen levels associated with PCOS are often attributed to an increase in autoimmune conditions such as Hashimoto’s Hypothyroidism.

Autoimmune hypothyroidism, as in the case with Hashimoto’s, occurs when the body mounts an immune response against the thyroid gland. Essentially, the body has created antibodies (TPO) and these antibodies will attack and destroy the thyroid gland due to a dysregulated immune system or response. In women with PCOS, Hashimoto’s has been found to be three times more likely than in women without PCOS and can be strongly correlated to its exacerbation from elevated estrogen levels and inflammation [12,13].

It has also been established that a statistically significant amount of women with PCOS have been found to have a goiter (an increased thyroid gland size) or nodules present on their thyroid gland [13]. A goiter or nodules can occur despite normal levels of TSH and T3/T4 but still has been found to impact levels of Prolactin and therefore ovarian function as well being associated with higher levels of the TPO antibody present in Hashimoto’s [6,13].

With so much of the focus on hypothyroidism, it would be remiss to not briefly mention hyperthyroidism and its potential role in insulin resistance and PCOS.

In 50% of cases of individuals with hyperthyroidism, altered glucose metabolism and insulin resistance has also been found [3]. Where hypothyroidism mostly causes insulin resistance peripherally at the level of tissues and muscles, hyperthyroidism has been found to cause insulin resistance at the level of the liver [3]. When your body has a higher demand for glucose than what you have consumed through your diet, it has the ability to create its own glucose from stores and other sources in the liver in a process known as gluconeogenesis. This process is regulated by your thyroid hormones and in individuals who have elevated thyroid hormones this process is increased [3]. Therefore your body is creating and being exposed to higher levels of blood glucose despite what you may have consumed through your diet and consequently, more insulin is produced.

Additionally, in hyperthyroidism the rate at which your stomach empties and digests is abnormally increased [3]. Therefore your body is able to break down carbohydrates more quickly leading to higher levels of blood glucose after a meal which in turn also increases the demand for insulin. The link between hyperthyroidism and PCOS has not been as readily established but with the predisposition for insulin resistance and its role in menstrual abnormalities it should not be completely overlooked and may provide some insight into individuals labeled as ‘lean PCOS’.

If you are someone diagnosed with PCOS or diagnosed with hypothyroidism and you’ve made it this far and are wondering: so, what caused what? Truthfully, we may never know. It’s a chicken or the egg situation and the evidence could go around and around showing how PCOS may have caused hypothyroidism and how hypothyroidism may have caused PCOS. But one thing is for certain: the co-occurence of the two is extremely common and the tightly intertwined network of hormone communication proves it is not by coincidence.


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