PCOS and Thyroid Autoimmunity: The 4 Major Links Between Hashimoto’s and PCOS Inflammation

PCOS and thyroid disorders are two of the most common endocrine, or hormone, disorders in women.

PCOS, or polycystic ovary syndrome, is a condition involving both metabolic and reproductive hormone imbalance. Many women with PCOS experience irregular periods, lack of ovulation, fertility challenges, acne, unwanted facial hair growth, hair loss, as well as insulin resistance and difficulty losing weight.

PCOS can be classified into 4 different types – insulin-resistant, inflammatory, post-birth control, and adrenal PCOS. These classifications correspond to the primary drivers of the condition, although there certainly can be overlap. With inflammatory PCOS (PCOS-I), autoimmune thyroid conditions like Hashimoto’s are often present, in addition to other sources of inflammation that may stem from the gut, for example.

The most common cause of hypothyroidism in women is Hashimoto’s thyroiditis, an autoimmune thyroid condition marked by elevated thyroid antibodies. Thyroid autoimmunity, namely Hashimoto’s, is more prevalent in those with PCOS, with thyroid peroxidase (TPO) antibodies present in 27% of PCOS patients, according to one study! 

Below we will walk through why PCOS and Hashimoto’s are often connected. Let’s dive in!

 

Link #1 – Hormonal Shifts

Women in particular experience significant hormonal transitions – just think about all that goes on during puberty, pregnancy, and menopause! These transitions have a significant effect on both our innate and adaptive immune systems. This is one reason why women have a much higher prevalence of autoimmune diseases compared to men.

Thyroid autoimmunity has been called the “window into autoimmune states.” It’s very common for individuals to have multiple autoimmune conditions, with thyroid autoimmunity often being one of them. Again, women are much more susceptible to this, with 85% or more individuals with multiple autoimmune disease being female.

It’s thought that these hormonal transitions women undergo may trigger downstream effects that negatively impact the balance between immune regulation and our inflammatory response. This opens the door to the development of autoimmune conditions, and conditions such as PCOS-I. 

 

Link #2 – Low Thyroid Hormones or Hypothyroidism

Hypothyroidism occurs when thyroid function is downregulated. Clinically, this could look like an increase in thyroid stimulating hormone (TSH), or a decrease in free thyroid hormones, specifically free T3 and free T4. Subclinical hypothyroidism, in which these hormone irregularities are mild, may go undiagnosed for many years!

Not everyone who has Hashimoto’s also has hypothyroidism. However, Hashimoto’s as an autoimmune condition develops into hypothyroidism in most individuals. 

This can happen because of glutathione depletion or because TPO and TG antibodies produced with Hashimoto’s affect the thyroid cells’ ability to utilize nutrients and produce thyroid hormones. The constant attack on thyroid tissues from these antibodies can cause fibrosis, or scarring, of the thyroid gland, which can result in hypothyroidism down the road. 

If the thyroid does become damaged, the thyroid gland is not able to produce enough thyroid hormone. This is called primary hypothyroidism, and can lead to a rise in a hormone called thyrotropin-releasing hormone (TRH) from the hypothalamus of the brain. 

A rise in TRH causes an increase in the hormones prolactin and TSH. These hormones are produced by the pituitary gland in the brain and work within a feedback loop to help regulate other important hormones such as follicle stimulating hormone (FSH) and luteinizing hormone (LH).

Prolactin inhibits ovulation by altering the ratio of FSH to LH, increasing adrenal DHEA production, and can actually lead to ovarian cyst development! High prolactin levels are implicated in both amenorrhea (irregular menstrual cycles) as well as infertility. As TSH increases, so can FSH, which further alters the FSH:LH ratio and promotes polycystic activity in the ovaries.

A rise in TSH and a decrease in thyroid hormones affects our metabolism, particularly our carbohydrate metabolism. When carbohydrate metabolism is impaired, this drives elevated insulin levels, which in turn promotes androgen production. Androgens are a class of hormones that include hormones like testosterone, DHEA and DHEA-S. Elevated androgens are one of the diagnostic criteria for PCOS, and a factor that causes a number of classic PCOS symptoms!

Because of this phenomenon, it’s important to explore any potential thyroid disorders, especially Hashimoto’s, when facing PCOS symptoms or a PCOS diagnosis. Unfortunately, this is not common practice among many practitioners. Many women are left with a (sometimes false) PCOS diagnosis and zero guidance as to how to address the root cause of their symptoms.

 

Link #3 – Insulin Resistance and Blood Sugar Imbalances

Just as thyroid dysfunction can lead to PCOS symptoms, PCOS can also in turn affect the thyroid. Thyroid disorders are more common among women with PCOS. While about 10% of the general population have subclinical hypothyroidism, prevalence shoots up to 22.5% among women with PCOS.

Insulin resistance and blood sugar dysregulation are common factors at play in PCOS. Both can fuel inflammation by triggering a stress response in the body. We know that inflammation and a heightened stress response can promote immune system activation, and thus worsen autoimmunity, such as in Hashimoto’s.

A common symptom of PCOS is difficulty losing weight due to underlying insulin resistance and elevated androgens. This can lead to difficulties with management of body composition such as regulating healthy amounts of adipose or fat tissue storage. However, this can also impact thyroid function, making the issue of weight loss resistance even more challenging for women. 

In one study, excess adipose tissue was shown to secrete proinflammatory molecules and increase insulin resistance. This can decrease the activity of an enzyme in the pituitary gland called deiodinase-2. This enzyme is responsible for converting inactive thyroid hormone (T4) into the active form (T3). T3 is the metabolically active form of thyroid hormone responsible for supporting metabolism, weight management, energy, and many other systems in the body.

 

 

Link #4 – Leptin – The Fuel Gauge Hormone

Another theory behind the PCOS-thyroid connection is via leptin. Leptin is one of our appetite-regulating hormones that is produced by adipose or fat tissue. Leptin levels can increase when there is excess adipose tissue in the body. This can lead to more production of TRH (thyroid releasing hormone) by the hypothalamus. And again, the cycle continues given the downstream effects of excess TSH levels, which can result in hypothyroidism.

Something else can happen when leptin levels increase, and that is a shift in immune cell activity. Leptin triggers the activity of effector T cells, which are recruited to fight whatever the immune system is fighting and promote inflammation. At the same time, leptin also downregulates our regulatory T cells, which work to dampen or control our inflammatory response. This alteration to the immune system can promote autoimmunity!

It is worth reiterating that women with PCOS have higher antibody levels, with  TPO antibodies present in 27% of PCOS patients. This is likely related to the complex interplay between PCOS, insulin resistance, adipose tissue, thyroid dysfunction, and autoimmunity.

 

Getting to the Bottom of Your PCOS & Hashimoto’s Link(s)

We’ve already talked in depth about how the immune system is involved in the development of Hashimoto’s and thyroid dysfunction, and how that can in turn impact the ovaries and the development of PCOS, particularly inflammatory PCOS. 

There are a variety of ways that the immune system can be triggered, and how this immune dysregulation can develop. One way that has already been discussed is simply from the hormone transitions that make up puberty, pregnancy, and menopause. There are also biologic, dietary, and genetic factors that can cause this dysregulation.

From a biologic or environmental perspective, mycotoxins from mold, viral or parasitic infections such as Epstein-Barr Virus (EBV), endocrine-disrupting chemicals, and heavy metal exposure, are all factors that can throw our immune system for a loop and lead to immune dysfunction. Especially if you’ve identified Hashimoto’s as an underlying driver of your PCOS, we can dig even deeper into understanding your immune trigger or triggers. 

This is a critical first step in order to regulate thyroid hormone production and improve your ovarian function to ultimately control your PCOS. We utilize advanced lab testing to investigate this. Having a complete thyroid workup is an important first step. Check out our Complete Thyroid Hormone Testing Package if you’re unsure where to start!

Once we understand your thyroid antibody and hormone levels, we can then look into the biologic and environmental factors listed above, as well as any underlying infections, in order to look deeper into the root causes of immune dysfunction. We do this by way of options like stool testing to see what’s going on in your gut microbiome, and immune testing to understand immune system triggers in our 1:1 coaching program. Let’s get to the bottom of your symptoms!

 

Written by Romana Brennan, MS, RD