Hashimoto’s and polycystic ovary syndrome (PCOS)

Illustration by Kelly Dern.

Illustration by Kelly Dern.

What’s the connection?

Hashimoto’s and PCOS are connected by more than one molecular mechanism, and they share certain genetic components.

As they have not been extensively studied together, not much is known how their combination can impact your overall health. One condition might trigger the other, and besides genes, they can be triggered by the environment. There’s more research needed on how or why Hashimoto’s and PCOS codevelop, and what can we do to prevent it.

Thyroid disorders may cause irregular menstrual cycles, problems with ovulation, and fertility issues (1–3).

PCOS affects up to 12 in 100 females of reproductive age (4-7). It is characterised by irregular menstrual cycles, either multiple ovulations in one cycle or no ovulation at all, hyperandrogenism (excessive levels of testosterone), and insulin resistance (6, 8, 9). PCOS can be very different from person to person, and can also cause different grades of metabolic or menstrual cycle irregularities (10, 11).

High levels of anti-TPO or anti-Tg antibodies—a hallmark of an autoimmune thyroid condition—are found in 1 in 3 of PCOS patients (12). If a person has either Hashimoto’s or PCOS, the chance to be diagnosed with the second condition increases up to a ten fold (12, 13).

Five most commonly mutated genes or molecules in Hashimoto’s and PCOS

Hashimoto’s is the most common autoimmune disorder in adults, causing a wide range of health complications (14). Similar to PCOS, it’s caused by mutations in a specific set of genes (15- 19).

Several of these genes are common for both Hashimoto’s and PCOS: fibrillin 3 gene (FBN3), vitamin D receptor gene (VDR) (20- 22), TGFβ (23, 24), gonadotropin-releasing hormone receptor (GnRHR) (25) and CYP1B1 (26).

Some of these molecules regulate each other, like FBN3, which regulates TGFβ (27, 28), a molecule important for many bodily processes, including regulation of the immune response (28- 31). Low levels of TGFβ are found in both Hashimoto’s and PCOS, making it hard for our body to naturally control own immune system (23, 24, 28).

Gonadotropin-releasing hormone receptor (GnRHR) regulates how much luteinizing hormone (LH) and follicle stimulating hormone (FSH) your body produces. It also regulates insulin balance and its function depends on TSH levels (25).

CYP1B1 is an enzyme that metabolizes estrogens, regulates thyroxine (T4), free triiodothyronine (fT3), and free T4 (fT4) levels in the body (26).

Vitamin D deficiency and high estrogen-to-progesterone ratio is often found in PCOS—this can trigger or exacerbate the autoimmune response (32, 33). To have an effect on different cells and tissues in your body, vitamin D needs a functional vitamin D receptor (VDR), and a non-functional VDR makes people more likely to develop Hashimoto’s (34, 35).

Vitamin D supplementation is supposed to improve menstrual cycle and metabolic disturbances in women with PCOS (36), but this likely only helps people who have a functional vitamin D receptor.

The thymus connection

The connection between the cycle of Hashimoto’s and PCOS goes beyond genes—it might be caused by changes in the function of the entire organ, just like the case with the thymus.

The thymus is an organ involved in regulating and preventing the autoimmune response, and it does so even before your birth (14, 37, 38). High estrogen exposure before birth prevents thymus activity, and in many cases triggers the development of autoimmune diseases (39- 41).

The role of sex hormones

Autoimmune disease problems start when sex hormone levels rise in your body for the first time (during puberty) and this continues through all life stages (42).

Increased estrogen-to-progesterone ratio, as seen in PCOS causes an autoimmune response, and a rise in anti-TPO and anti-Tg antibody levels (42- 44). Transient and reversible changes in the level of autoimmune response and antibody levels even happen in non-PCOS people during distinct phases of menstrual cycle (such as ovulation; 45). However, in the case of a high and a prolonged estrogen exposure, as is the case with PCOS, the chance of developing an autoimmune disease increases significantly (12, 44).

Common health issues in Hashimoto’s and PCOS

Hashimoto’s and PCOS go beyond complex hormone and autoimmune issues. Some shared health issues are:

  • Higher body mass index (BMI, 46)

  • Changes in glucose and lipid metabolism: an increase in LDL-cholesterol and triglycerides; and a decrease in HDL-cholesterol (47, 48)

  • Insulin resistance and a higher chance of developing type 2 diabetes (8, 49)

What can help?

Metformin—a diabetes medicine that helps control blood sugar levels—is frequently prescribed to patients with PCOS. One study found that a six month metformin treatment in PCOS and Hashimoto’s patients normalized TSH blood values, but it didn’t do much for fT3 and fT4 levels (50). More research is needed, but perhaps it can be a helpful treatment strategy for some people

High estrogen levels seem to be the main culprit for development of Hashimoto’s thyroiditis in people diagnosed with PCOS.

What can you do to improve your health?

You might want to avoid estrogen rich foods (soy and/or flax seeds).

Ask your doctor if it makes sense to check your vitamin D, estrogen, progesterone, and SBGH blood serum levels. It can give both of you an indication if there is an estrogen-driven cause to your Hashimoto’s, and it might help with finding better treatment strategies.

What are your experiences? We would love to hear more


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