Melanoma and Hypothyroidism
My grandmother was diagnosed with a rare type of melanoma in 2016. By that time, I’d already been researching skin physiology and effects of skincare ingredients on skin for a number of years. Still, her diagnosis made me reconsider everything I thought I knew about skin health and I began digging back into the research with fresh eyes.
What I discovered was just how much skin reflects our internal state of health. And, how nothing within the body exists in isolation.
Hiding in Plain Sight
She’d jabbed a section of laminate flooring under her nail bed and it never healed properly. My grandma was an extra special sort of stubborn and over the next few years her treatments reminded me so much of the mantra from a popular movie “put some Windex® on it!”
Meanwhile, the wound festered. When she allowed them to, doctors chased infection until one finally had the right idea to biopsy it. I don’t think any of us were expecting melanoma. While her finger had a growth now, which honestly looked more like a deformity on her index finger something she might have been born with instead of a separate entity, all of it was flesh colored, just as light as the rest of her.
The biopsy results revealed something else though, a rare and extremely aggressive type of melanoma known as amelanotic melanoma.
This type of melanoma is flesh colored.
For amelanotic melanoma, the typical metrics employed by healthcare professionals suspicious of melanoma don’t apply because there’s no color to evaluate. Being flesh-colored, it’s harder to assess asymmetry, border irregularity, and even diameter. Alternative metrics include whether the spot itches or bleeds.
As my grandmother began receiving treatment for melanoma, I meandered onto a new path in my own personal health journey. Little did I know at the time how intertwined each of our paths were.
Weight Gain, Rashes, and Hashimoto’s Thyroiditis
After my gallbladder was removed, I thought my appetite would return. It didn’t. I’d been gaining weight for a little while even as my appetite was diminishing, and I just assumed it was due to my body not processing fats very well as gall sludge built up. I’d also gotten used to feeling bad after meals so suspected there was a psychological component to it too.
To support breakdown of fats, I tried lots of different digestive enzymes and one morning after taking one with ox bile salts, I experienced extreme GI distress. In addition, both of my earlobes swelled and a rash broke out on both shins. The GI distress subsided over the next few days along with the swollen earlobes. The rash on both shins? It persisted for two years. In that time, I had biopsies, I tried a variety of prescription and non-prescription products. None of which worked.
It took a diagnosis of Hashimoto’s thyroiditis and treatment for this autoimmune condition for the rash to disappear.
Pretibial Myxedema and Autoimmune Thyroiditis
The orange peel like rash on both of my shins was actually pretibial myxedema, a symptom more commonly seen in Graves’ disease even though it’s not unknown in Hashimoto’s thyroiditis.
Graves’ disease is an autoimmune thyroid condition where too much thyroid hormone is made (hyperthyroidism). I was diagnosed with Hashimoto’s thyroiditis, an autoimmune thyroid condition where too little thyroid hormone is made (hypothyroidism).
While pretibial myxedema is a more common symptom of Graves’ disease, myxedema (swelling and fluid retention of the skin caused by low levels of thyroid hormone) is a common symptom of hypothyroidism (regardless of etiology). Myxedema of any sort (pretibial or otherwise) is caused by a build-up of hyaluronic acid in the skin.
Hyaluronic acid (HA) belongs to the group of molecules known as glucosaminoglycans (GAGs). These molecules are main components of the extracellular matrix (ECM) providing structure to the body and a medium through which signaling molecules travel from one cell to another through the interstitial spaces. These molecules also help maintain sufficient hydration in the extracellular spaces because of their ability to bind water.
As GAGs (including hyaluronic acid) build-up in the extracellular matrix, more water is drawn into these spaces resulting in edema (swelling) due to fluid retention. In a healthy state, the body regulates both HA expression and also HA breakdown by controlling synthesis of both HA and hyaluronidase, the enzyme that breaks down HA.
Autoimmune thyroid states (both with Graves’ disease and Hashimoto’s thyroiditis) alter the body’s expression and break-down of hyaluronic acid. Low levels of thyroid hormone (like in Hashimoto’s and other non-autoimmune hypothyroid states) also impact hyaluronic acid expression and breakdown. In both hypothyroid states and in autoimmune thyroid conditions, HA expression and breakdown is altered in a way that allows for build-up of hyaluronic acid in tissues.
This goes beyond the skin and is one of the reasons for thyroid goiter and fibrinogenic build-up within the body in people who are struggling with poorly maintained autoimmune thyroid conditions and hypothyroidism. Build-up of HA is also associated with a variety of other autoimmune conditions including: Rheumatoid Arthritis, Type I Diabetes, Primary Sclerosing Cholangitis, and Multiple Sclerosis.
Going back to look at melanoma again, hypothyroidism is linked to an increased risk of developing melanoma. The thyroid makes 3 different hormones: T3, T4, and calcitonin. Typically, T3 and T4 are given the most focus.
There are several theories on why and how sufficient levels of both T3 and T4 act to reduce the development and progression of melanoma. Both T3 and T4 regulate cell differentiation, growth, and metabolism and also modulate immune response. It’s believed that the immune modulating effects of these two hormones alters migration of melanocytes (the melanin producing cells of skin). Melanocyte migration is important to development and spread of melanoma.
This gives rise to another question… is sun exposure to blame for melanoma?
It turns out there are many different types of melanoma. The World Health Organization (WHO) now classifies melanoma into nine different categories with only three related to cumulative sun damage. If it’s possible that other factors like low thyroid also increase the risk of melanoma and reduce patient survival rates, why are we overlooking this connection?
Undiagnosed low thyroid is a common cause of many health symptoms and unfortunately, our medical establishment has been trained to test TSH (thyroid stimulating hormone), a hormone produced by the pituitary as the end-all-be-all for determining healthy thyroid function.
I myself struggled for years to find a practitioner who knew to test for anti-thyroid antibodies to rule out autoimmune thyroid condition, and it was years after discovering I in fact had Hashimoto’s thyroiditis before I found a doctor who knew how to treat the condition properly.
In her early 40s, my grandmother was diagnosed with thyroid cancer. At this point, I’m not sure anyone remembers which type of thyroid cancer she had, but certain thyroid cancers are associated with an increased risk of melanoma and for as long as I knew her, she was treated with T4 only after her thyroidectomy. In my heart of hearts, I believe my grandmother’s melanoma started because of long-standing inflammation due to that jab with the piece of laminate flooring. I also wonder… would she have been spared progression of that melanoma if her doctors factored in the thyroid piece? Would cutting edge therapy have failed if she’d been receiving T3 and T4 replacement therapy or natural desiccated thyroid? I don’t know the answer to those questions, but it seems to me that we ought to be considering these possibilities.
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