thyroid

Is This Why PCOS and Autoimmune Thyroid Disease Often Occur Together?

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I went hot, then cold, then started cursing my doctor. Not that it was his fault. Just another case of the blind leading the desperate.

In the podcast I was listening to, Dr. Jorge Flechas was explaining new research that showed the ovaries contain two enzymes responsible for the creation of thyroid hormone, thyroid peroxidase (TPO) and thyroglobulin (Tg) (also here).

These enzymes were expressed in granulosa cells in the ovaries and endometrial cells in the uterus.

Why this is important, to anybody with a thyroid condition and anyone taking thyroid hormone medication is this implies:

  • The ovaries are capable of creating thyroid hormone.
  • If you have an autoimmune thyroid condition with high antibodies for either TPO or Tg, your immune system is likely attacking your ovaries and endometrial tissue along with your thyroid.

Compensating for Autoimmune Thyroid: Hashimoto’s Thyroiditis

Being at a point in the Hashimoto’s disease stage where my body does not have enough healthy thyroid tissue to meet demands for thyroid hormone, I was struggling to get my thyroid hormone dosage right.

It had taken years (6 to be exact) from diagnosis to finding a thyroid literate doctor. In that 6 years, I was grossly undertreated, prescribed a mere 25 micrograms of levothyroxine (T4) to compensate for the gap between where I was and where I should be for levels of triiodothyronine (T3) and T4, the two thyroid hormones typically replaced in a treatment plan for people in my stage of the disease.

When I found that doctor, I was self-dosing with bovine desiccated thyroid because it was the only thing I could get over-the-counter without a prescription and because I knew I was under-medicated.

The problem with bovine desiccated thyroid is that the ratio of thyroid hormones do not mimic those found in man. When T4 is converted by deiodinase enzymes in the body, there are two possible pathways. Conversion by Type 3 deiodinase to rT3 and conversion by Type 1 deiodinase to T3. rT3 (reverse T3) binds to thyroid hormone receptors on cell membranes blocking the uptake of T3 and T4 by the cell, which slows metabolism.

Cows are known to produce more rT3 in the euthyroid state than people and even though I knew this, I was doing what I could with what was available to me, which meant by the time I found a thyroid literate doctor, my rT3 levels were so high he considered that most of the thyroid hormone receptors in my body (receptors on every cell of the body) were blocked.

A result like that would prompt most thyroid literate doctors to start T3 only therapy.

Normal ratio of T3 to T4 and why TSH doesn’t indicate thyroid function

The thyroid gland produces about 85 to 100 micrograms of T4 daily and only about 5 to 6.5 micrograms of the ~30 to 40 micrograms of T3 made by the body daily. The remaining T3 is made locally by cells within each tissue when T4 is converted into T3 by deiodinase enzymes. Three of these enzymes are known and expressed at different rates in different cell types.

  • Deiodinase Type 1: converts T4 to T3
  • Deiodinase Type 2: converts T4 to T3
  • Deiodinase Type 3: converts T4 to reverse T3 (rT3)

Reverse T3 (rT3) is considered an anti-metabolic hormone because it binds to thyroid hormone receptors making them unavailable for either T3 or T4 to bind and enter the cell.

NOTE: This is why it’s impossible to diagnose thyroid dysfunction using TSH alone. The pituitary, which secretes TSH, maintains a different ratio of T4 to T3 than the rest of the body because of its unique ratio of deiodinase enzymes compared with the rest of the body. The pituitary secretes TSH based on the local levels of T3 in the pituitary, so it’s possible to be grossly hypothyroid before TSH values ever suggest there’s a problem.

Fat cells have different ratios of deiodinase enzymes compared to muscle cells. Liver cells have different ratios compared to cells in the reproductive tract and each cell type of the body expresses different ratios of deiodinase enzymes.

It’s known that people in various disease states (and on calorie restricted diets) have altered expression of deiodinase enzymes and can express more Type 3 deiodinase, the enzyme that preferentially makes rT3 from T4. In patients with high rT3, thyroid literate doctors frequently prescribe T3 only therapy.

Impact of Too Much Thyroid Replacement Hormone

I was up to 45 micrograms T3 per day and not only was I still struggling with symptoms, I started seeing cycles consistent with PCOS (polycystic ovarian syndrome). PCOS cycles showed up for me once before when I was actively struggling with chronic UTI symptoms. In the years since I had broken free of those symptoms, I had also seen a return to healthy cycling.

My suspicion was I was getting too much T3 and not enough T4, a suspicion that bloodwork confirmed by low free T4 values. Even though my doctor assured me this was fine (T3 is the active form of thyroid hormone after all), I asked if we could test combo therapy with both T3 and T4. He agreed. Once the doses of each were titrated, I was still taking about 45 micrograms T3 each day and about 100 micrograms of T4 and my hypothyroid symptoms had gotten worse (weight gain, swollen lymph nodes, frequent headache).

While it’s common to prescribe super physiological doses of thyroid hormone to hypothyroid patients, I wasn’t sold on my dosage. My estrogen levels were tanked and I was barely ovulating. And, I knew I was too young to be menopausal regardless of what my doctor said.

Dogs, Radiation, and Iodine

A chance conversation that week with a co-worker who was treating her dog with radiation therapy for cancer brought up the topic of iodine. Back when I was first diagnosed with Hashimoto’s, the endocrinologist I was referred to recommended I stop all iodine intake to try to reduce the anti-TPO antibody level and thereby the autoimmune attack on my thyroid.

Within 1 month of following her advice, I’d developed a breast cyst. This was abnormal for me, so I started researching the connection between iodine and fibrocystic breast disease, reincorporated iodine into my diet, and voila, that breast cyst went away. Iodine has continued to pop up on my radar more than once since then and here we were in the middle of another conversation that turned to iodine (because of its effectiveness in improving the outcomes of cancer treatment among many cancers… and I don’t mean radioactive iodine, we’re talking naturally occurring iodine).

I bring this up because this seemingly unrelated lunch chat catapulted me right back into the iodine research rabbit hole, which led me to the discovery of several papers discussing the presence of thyroid peroxidase, the enzyme that converts T4 to T3, in the ovaries. This suggests that the ovaries don’t just create T3 with deiodinase enzymes, they’re far more involved in thyroid hormone synthesis than that and if the ovaries contain the very same enzyme that’s attacked in about 80% of Hashimoto’s patients, well… it’s no wonder that PCOS and infertility struggles are so prevalent among women with Hashimoto’s. The body isn’t just attacking the thyroid. It’s attacking the ovaries too.

Is This Worth Altering Treatment for Hypothyroidism?

Why would this information make me piping mad? Well, I have long believed that the body makes T4 for a reason (even if doctors will argue T4 is a storage hormone), that reason being to provide the cells of the body with iodine when one atom of iodine is cleaved from T4 by deiodinase enzymes to make either T3 or reverse T3. Iodine is profoundly important for many essential processes in various tissues and organs of the body and again is closely linked with positive outcomes for a number of cancers (which in my mind makes this theory even more likely).

This was my main reason for requesting my doctor add T4 therapy back into my treatment plan. And, while I am glad to have a doctor who is agreeable enough to concede to my request on that point, shouldn’t it be expected for a thyroid literate doctor to be up on his research and know that the ovaries also appear to be equipped to make thyroid hormone on their own by the same mechanism used in the thyroid?

It would have saved some bitter debates over ovarian function. And, it would have been a great metric for adjusting my replacement hormone levels on the fly. Had I known the ovaries might also be making part of the body’s daily T3 and T4 rations, as soon as I started experiencing PCOS cycles while titrating up on T3 therapy, I would have backed off because that was an indication I was overdosing T3.

In the moment I started pulling up research papers showing this finding about the presence of thyroglobulin (Tg) and thyroid peroxidase (TPO) in the ovaries, observations I’d been flummoxed by suddenly made sense. It now made sense why women with hyperthyroidism also struggle with cycle disturbances. It made sense why my estrogen levels were through the floor recently. It made sense why my FSH levels were higher than they “should” be and still I wasn’t in menopause.

I backed off on my T3 dosage immediately. And, within a week’s time my estrogen levels were finally climbing consistent with follicular recruitment in preparation for ovulation. I felt better, less inflamed, less responsive to some of my known dietary triggers. I was struggling less with headaches. Is this everything I need to know about hypothyroidism? Probably not. But in the words of Bono, I’m one step closer to knowing.

We Need Your Help

More people than ever are reading Hormones Matter, a testament to the need for independent voices in health and medicine. We are not funded and accept limited advertising. Unlike many health sites, we don’t force you to purchase a subscription. We believe health information should be open to all. If you read Hormones Matter, and like it, please help support it. Contribute now.

Yes, I would like to support Hormones Matter. 

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I Will Not Go Gentle Into That Good Night: An Alternative Approach For Hyperactive Thyroid

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A Thyroid Revolution

Who would have thought my favorite poem would end up being my fight song, but I will not go gentle into that good night. The last time I wrote about my wellness journey, it ended with the comment to stay tuned to find out what happens next. That was in December 2021. I was looking forward to an appointment with a doctor of Chinese Medicine and hoping for more improvement regarding my health situation. This article will detail my progress with Traditional Chinese Medicine (TCM) and other alternative methods to treat the thyrotoxicosis associated with Grave’s disease.

Limited Medical Solutions for Hyperthyroidism

It will be 7 years in September 2024 since I walked into the emergency room thinking I was having a heart attack. In my previous article for Hormones Matter, “I’ll Sleep when I’m Dead”, the official diagnosis was thyrotoxicosis with nodule. My heart was reacting to a hyperactive thyroid, which was being fueled by an autoimmune condition called Graves’ disease. The recommendations were to utilize a radioiodine scan and uptake test to determine the breadth of the damage and to take a variety of medications to treat the associated symptoms of a hyperactive thyroid. I refused the radioiodine scan, due to its potential to increase cancer, and while I initially utilized the prescribed medications, ultimately, the negative side effects forced me to investigate more holistic options.

Medications and Medication Reactions

Initially, I was prescribed a medication called methimazole, along with blockers to combat the heart-related effects of a hyperactive thyroid. Neither of these medications affected thyroid hormone levels. They are intended to lessen symptoms of hyperthyroidism, such as a tremor, rapid heart rate and heart palpitations. Sometimes, health care providers prescribe them to ease symptoms until thyroid hormones decrease sufficiently.

I struggled with the prescribed medications. I took the beta blocker for one night, but I slept for only two hours and decided against it. I took the methimazole for three months because my T3 was extremely high, and then my liver enzymes became alarmingly high as well. Liver damage is a reported side effect of this medication but when I expressed my concern that this medication had caused the liver problems, my doctor became combative. She argued that my liver enzymes were high, not because of the methimazole, but because there was an unidentified cancer lurking that had now spread to the liver. She said that this was a result of my refusal to do the radioactive iodine test.  With a family history of cancer, cancer is a huge concern for me, and it is exactly why I refused the radioiodine test, as it can increase the risk of cancer.

Taming the Sympathetic Overdrive: The Non-traditional Route

With a hyperactive thyroid, I live in a constant state of fight, flight or freeze. The automatic threat response in order to evade danger and return to a calm state is compromised repeatedly. My sympathetic system was in overdrive. I have compared this to a nightmarish roller-coaster ride that doesn’t end. Since the options for treatment offered by conventional medicine were fraught with problems, I sought a variety of non-traditional options that included nutrient support and TCM/acupuncture.

Nutrition

During this time, I supplemented with a number of vitamins and minerals. With a hyperactive thyroid, my body was running on a continuous loop and that was depleting me of vital nutrients to maintain mitochondrial function and energy production. The ultimate goal with the extra nutrition was to provide my body with what it needed during this hyperactive state, so that ultimately, my nervous system could settle down and switch over to the rest and digest portion of autonomic function.

I relied on a modality called muscle testing, scanning, or what is best known as the Feldenkrais Method to identify what my body was missing or lacking. I had been using muscling testing since 2003 and so this was not new. After my diagnosis though, it became more important and evolved while I studied Pranic Healing. The muscle testing made the task of figuring out which of the 90 essential minerals and vitamins I would need to replenish daily much easier. Some of the supplements I utilized included grass fed liver to give my body the basic minerals such as copper, iron, zinc, phosphorus, and selenium, B vitamins, along with additional B1 and Vitamins A, D, E, K. I also cooked mostly from scratch and avoided gluten. This seemed to help, but by the end of the day my energy gas tank was still empty.

Potassium Iodide

Perhaps, if I could slow the thyroid output, I might be able to recover. For that, I learned that potassium iodide could be used to treat hyperthyroid, this was in 2018. The effectiveness of potassium iodide (KI) was evaluated in hyperthyroid patients who experienced side effects to thioamides, i.e. methimazole. Since my liver enzymes were significantly elevated after taking methimazole, I decided to try to potassium iodide. A high dose of potassium iodine would be an integral piece to remission of the Grave’s disease.

Traditional Chinese Medicine

As I mentioned above, the impact of hyperthyroidism on the autonomic nervous system (ANS) is destructive and while the potassium iodide and other nutrients were helping, I wasn’t fully recovered. After more research, I found Traditional Chinese Medicine (TCM). Studies show that acupuncture positively influences autonomic nervous system functions.

I began TCM in January 2022. Traditional Chinese Medicine dates back to over 3,000 years ago. It was influenced by Taoism and Buddhism, which orients towards a holistic goal in order to achieve wellness. To my surprise and benefit, research shows that the benefits of acupuncture plus herbal medicine with drug therapy for the treatment of hyperthyroidism, more effective than the typical medication approach using propranolol and methimazole.

When I began with TCM, the first order of business was to balance the kidney and liver energy. According to TCM: “The liver affects the thyroid by receiving signals from the thyroid to produce glycogen. The pituitary produces TSH, which tells the thyroid to make T4; T4 then goes to the peripheral tissues (mostly the liver, kidneys, and muscles) and turns into the much more active T3. The liver also makes proteins that bind and carry thyroid hormone in blood and helps the body break down thyroid hormone.”

To that end, with acupuncture and TCM herbal remedies, my health began to improve slowly. Unfortunately, my eye sight was worsening.

To See or Not To See, That Is the Question

In March of 2022, issues with eyes became problematic. Grave’s disease, it turns out, can lead to something called Thyroid Eye Disease (TED). The excessive thyroid hormone negatively affects the muscle and fatty tissue behind the eyes, increasing intraocular pressure and reducing eye sight. It makes the eyes feel dry and gritty, which also reduces vision. Since traditional ophthalmology seemed reticent to treat and offered little help, I once again turned to TCM. Studies have shown promising results using TCM to reduce the thyroid-related eye symptoms.

In November 2023, I decided to try a drastic approach to alleviate eye pressure. I began using Sananga eye drops. Sanaga is a plant medicine, which is made from the roots of the Tabernaemontana undulata tree in the Amazon rainforest. I was given a referral to a website called Four Visions. It was not an easy decision. After reading that there would be some pain involved and it is known to cause a burning sensation to the eyes. They warn that it may be uncomfortable for certain people.

At one point, I had to stop using it due to extreme headaches. I wasn’t sure if it was from the eye drops, but I suspected so. Although the Sananga eye drops were painful, my recent appointment with my eye doctor March 2024 showed that the pressure had reduced in my eyes. The bad news is, I now had the beginnings of cataracts in both eyes. Back to the drawing board.

I found a Chinese formula that addresses eye pressure as well as hypertension. Because of my hyperactive thyroid, my heart rate and blood pressure are elevated. We had already implemented the Chinese formula Zhi Can Cao to lower my heart rate. Remember, conventional treatment uses the drug Propranolol for this purpose, but I could not take it. After a month on this remedy my blood pressure began to decrease. I also implemented a liver cleanse recommended by my acupuncturist. It is made by a former chemist. The ingredients include: Milk Thistle, Burdock, Yellow Dock, Dandelion, and Licorice. In TCM, the eyes are the sense organ relating to the liver. The liver supports our eye health and is vital in governing the capacity for vision in our lives.

Luo Bu Ma Formula was added in September of 2024, and after only one day of taking it, I noticed an increase in energy. I am looking forward (pun intended) to seeing (another pun) how this new formula can reduce pressure as well as continuing with the Sananga.

Electrostim Acupuncture For Thyroid Health

In addition to the herbs, I was pleasantly surprised to find an article about applying electromagnetic frequencies to increase telomere length. Telomere length is a major determinant of health and as we age telomeres shrink. At 66 years old, I am on the downward slope of telomere length, but I wondered if adding electromagnetic frequencies to acupuncture points would improve my health and ultimately help my waning eyesight. There is some research to suggest that that using transcutaneous electrical stimulation or TENS on acupuncture points helps with pain, but it is not clear whether it would help with hyperthyroidism more generally or the associated eye issues more specifically. Nevertheless, I thought it was worth a try.

According to my acupuncturist, the best area to set this up would be on the liver points. Hyperthyroidism and liver dysfunction are not uncommon. Autoimmune conditions especially with Graves’ Disease set the stage for preexisting liver disease and my goal is to avoid, prevent, or minimize liver dysfunction. This protocol would enlist the help of a Transcutaneous electrical nerve stimulation (TENS unit.)  I’m in my second month but can’t wait to see my results.

Progress So Far

To summarize, here are my observations thus far adding acupuncture, minerals and vitamins in order to treat the thyrotoxicosis associated with Grave’s disease and restore my health. First and foremost, pain management improved significantly. Prior to the TCM, my pain levels could reach a 10, but now, I have zero pain.

My body is now producing energy, not just using energy reserves. I can now walk every day and still accomplish daily tasks of grocery shopping, household chores and even attend family events. Whereas before, I would struggle to do just basic everyday tasks.

The double vision is better to where I can drive now. The pressure in the eyes has greatly diminished, they are no longer gritty or dry, and they don’t get as tired.

My blood pressure and my heart rate have gone down.

All in all, I am doing much better. It was a long road, as TCM is not a quick fix, but gradually and over time, I have begun to regain my health. I still have a ways to go, but I am confident that I made the right decision to pursue an alternative approach to restoring my health.

We Need Your Help

More people than ever are reading Hormones Matter, a testament to the need for independent voices in health and medicine. We are not funded and accept limited advertising. Unlike many health sites, we don’t force you to purchase a subscription. We believe health information should be open to all. If you read Hormones Matter, like it, please help support it. Contribute now.

Yes, I would like to support Hormones Matter. 

Photo by Johannes Plenio on Unsplash.

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Are You More at Risk of Melanoma When You Have a Thyroid Problem?

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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.

And, altered expression of hyaluronic acid, which allows reforming of the ECM, is also a way that cancer cells proliferate and spread.

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.

We Need Your Help

More people than ever are reading Hormones Matter, a testament to the need for independent voices in health and medicine. We are not funded and accept limited advertising. Unlike many health sites, we don’t force you to purchase a subscription. We believe health information should be open to all. If you read Hormones Matter and like it, please help support it. Contribute now.

Yes, I would like to support Hormones Matter. 

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Vitamin D3 and Thyroid Health

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The benefits of vitamin D3 garner a plethora of glowing press these days but little information has been reported about how this essential nutrient may be associated with thyroid disorders. An alarming number of Americans—over 25 million—suffer from thyroid disease. Women are four times more likely than men to develop a thyroid disorder. The thyroid, a butterfly-shaped gland located in your neck, regulates your metabolism and affects every cell in your body. When your thyroid is not working properly, your body becomes unbalanced, potentially causing symptoms including weight gain or loss and chronic fatigue as well as autoimmune disease and cancer. Let’s look at how vitamin D3 may affect thyroid health:

Thyroid Hormonal Balance

Vitamin D receptors (VDR) are present in the cells of the pituitary, the pea-sized gland located at the base of the brain that controls your thyroid. The pituitary produces a hormone called thyroid stimulating hormone (TSH) that signals your thyroid gland to make thyroid hormone (T3 and T4). Thyroid hormone constantly circulates throughout your body, regulating metabolism. Either inadequate or excessive thyroid hormone can wreak havoc to your health, culminating in hypo- or hyperthyroidism. Understanding the regulating effects of VDR in our cells, I surmise that the amount of activated vitamin D3 in the pituitary’s VDR may be connected to the balance of thyroid hormone.

Autoimmune Thyroid Diseases

Adequate levels of vitamin D3 may protect the immune system from attacking itself. Low vitamin D3 levels have been linked to autoimmune thyroid diseases including Hashimoto’s and Graves’ thyroiditis.

Discovered one hundred years ago by a Japanese physician, Hashimoto’s disease is caused by abnormal blood cells and white blood cells constantly attacking and damaging the thyroid. About 95 per cent of Hashimoto’s disease patients are women. A study published in a 2011 issue of the journal Thyroid revealed that 92 per cent of Hashimoto’s thyroiditis cases had insufficient circulating vitamin D3 levels.

Ten times more likely to develop in women than men, Graves’ disease is caused by antibodies that overstimulate thyroid hormone production, causing hyperthyroidism. Researchers, who investigated Japanese female and male patients with Graves’ disease over a one-year period, found a high prevalence of woefully low circulating vitamin D3 in the female patients compared to the male subjects.

Thyroid Cancer

Incidences of thyroid cancer have doubled over the past four decades. The likelihood of women developing thyroid cancer is three times greater than for men. Activated vitamin D3 regulates cell differentiation, cell proliferation, and cell death. If these vital functions go awry, cancer may develop. Epidemiological studies indicate a link between vitamin D3 and thyroid cancer. Vitamin D researcher W.B. Grant, Ph.D. published a paper in a 2012 issue of the journal Anticancer Research that indicated an association between solar ultraviolet B, vitamin D3, and cancers including thyroid.

A relatively rare form of thyroid cancer—medullary thyroid cancer—originates in the thyroid C cells where a hormone called calcitonin is secreted. Calcitonin’s functions include stimulation of vitamin D3 production in the kidneys. The measurement of calcitonin is a diagnostic screening tool for medullary thyroid cancer. VDR are present in the thyroid C cells. Understanding the powerful effect of activated VDR on cell regulation, I hypothesize that activated VDR in the C cells may possibly prevent the development of medullary thyroid cancer.

In conclusion, recent medical literature suggests a connection between vitamin D3 and thyroid health. However, additional research is required to determine if thyroid dysfunction may cause vitamin D3 deficiency, or low vitamin D3 status may contribute to thyroid disorders.

Copyright ©2012 by Susan Rex Ryan, all rights reserved.

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Thyroid Disease and Testing During Pregnancy

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One in five women of reproductive age suffers from some form of thyroid disease, mostly hypothyroidism (Gharib et al. 2005; Hollowell et al. 2002). In adult women, 95% of clinical hypothyroidism results from primary disease of the thyroid gland, generally, the autoimmune condition Hashimoto thyroiditis (Wartofsky et al., 2006). Autoimmune thyroid disease is also common among women with Type 1 diabetes mellitus, Sjogren syndrome, Addison disease, or pernicious anemia. Up to 25% of patients with Type 1 diabetes will develop postpartum thyroid disease (Alvarez-Marfany et al., 1994).

Hypothyroidism During Pregnancy

What happens when a woman with untreated thyroid disease gets pregnant? Depending upon the diagnostic criteria, hypothyroidism affects 0.3% (Casey & Leveno, 2006) to 5% (Gharib et al. 2005) of pregnancies. The symptoms are vague and are similar to other pregnancy concerns making diagnoses based on clinical symptoms alone difficult. Hypothyroid symptoms include fatigue, constipation, cold intolerance, muscle cramps, insomnia, weight gain, carpal tunnel syndrome, hair loss, voice changes, and slowed thinking.

The consequences of undiagnosed hypothyroidism during pregnancy are significant. Hypothyroidism is associated with premature birth, pre-eclampsia, abruption, low birth weight (LBW), postpartum hemorrhage, and impaired neuropsychological development in childhood (Burman, 2009). Research found that fetal loss was higher in untreated hypothyroid women (29%) vs hypothyroid women taking levothyroxine (6%), highlighting the need for early detection (Hallengren 2009).

Hyperthyroidism During Pregnancy

Hyperthyroidism, the result of an excess of thyroid hormones, complicates less than 1% of pregnancies (ACOG Practice Bulletin, 2002). Symptoms of hyperthyroidism are uncommon in normal pregnancy and thus somewhat easier to identify clinically. Maternal symptoms include weight loss or failed weight gain despite increased dietary intake, resting tachycardia, hypertension, tremor, eye stare, eyelid lag, proptosis, and thyroid enlargement or nodule.

Graves’ disease, an autoimmune disorder occurring in 0.5% of the population, accounts for more than 90% of the hyperthyroidism associated with pregnancy. Complications associated with undiagnosed or poorly managed hyperthyroidism during pregnancy include pre-term labor, pre-eclampsia and maternal thyroid storm, fetal tachycardia, low birth weight, congenital abnormalities, and stillbirth.

Should Pregnant Women Be Tested for Thyroid Disease?

Yes, but there is little consensus among the major medical associations regarding who, when, and how to test for thyroid function during pregnancy. It is argued that by the time TSH (the gold standard in thyroid diagnostics) becomes hyper-elevated and the clinical symptoms emerge, the damage to fetal neurodevelopment related to insufficient maternal T4 stores, has already been done (Calvo et al. 2002).  Emerging evidence suggests that maternal T4 levels may not track directly with elevated TSH levels especially in the first trimester when the demands for maternal T4 are greatest (Morreale de Escobar et al. 2000), making the need for more advanced testing techniques even more important.

Iodine Deficiency and Hypothyroidism: One More Factor to Consider

Complicating matters even further, in iodine-deficient populations, neither TSH, T4 nor T3 denote the underlying deficiency, which as it progresses, inevitably elicits the range of fetal developmental issues and maternal complications associated with hypothyroidism. In the US, approximately 10% of the population is iodine deficient while 50% of Europe is iodine deficient (Zimmerman 2009). In recent years, iodine deficiency has increased in the US in women of reproductive age with 14.9% percent potentially iodine deficient (Hollowell et al. 1998). Similarly, the incidence of congenital hypothyroidism in newborns has also increased in the US over the last two decades (Parks et al. 2010).

Iodine deficiency in women can lead to overt hypothyroidism and consequent anovulation, infertility, gestational hypertension, spontaneous first-trimester abortion, and stillbirth (DeLong et al., 1997). Iodine deficiency is also associated with an increased risk for thyroid carcinoma in animal models and humans (Mellemgaard et al., 1998). In the Bryansk region of Russia, an area of known radioactive I-131 exposure following the Chernobyl disaster, the risk of all types of thyroid cancer was inversely associated with urinary iodine excretion levels (WHO Health Risk Assessment).

What Constitutes Hypothyroidism in Pregnant Women?

In addition to the debate over whether to test pregnant moms routinely for thyroid disease, especially hypothyroid moms, there is much debate regarding what constitutes elevated TSH and whether to include subclinical hypothyroidism (SCH) or mild hypothyroid cases in the testing matrix (Fatourechi 2009; Surks et al. 2004). SCH or mild hypothyroidism is suggested by only slightly elevated TSH concentrations without the normally accompanying changes in T4.  Arguments against testing for SCH include the enormous increase in cases; up to 28 million more people could be diagnosed with hypothyroidism, and the conflicting data regarding treatment benefits and disease progression. Moreover, recent evidence suggests significant age and race-based differences in TSH reference ranges across the non-pregnant population complicating diagnoses even further (Surks & Boucai 2010).

Given the dire consequences of untreated thyroid dysfunction during pregnancy, there is a need for more accurate, non-invasive and less expensive thyroid function tests with reference ranges specifically identified for this population of women. Screening for thyroid function in women of reproductive age and in pregnant women could reduce maternal and fetal complications.

Our view on thyroid disorders during pregnancy can be summarized as follows:

  • Thyroid disease is common in pregnancy.
  • Hypothyroidism and hyperthyroidism are associated with adverse pregnancy outcomes, and treatment may improve these outcomes.
  • Untreated hypothyroidism during pregnancy is associated with impaired intellectual development in childhood.
  • Routine, universal screening for thyroid function in women of reproductive age and in pregnant women could reduce could reduce maternal and fetal complications
  • Normal reference ranges for thyroid function tests in pregnancy must be established

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Postscript: This article was originally published on February 21, 2012 and updated on July 11, 2014. If I were to rewrite this post now, I would attribute much of the thyroid dysfunction to nutrient deficiencies. 

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Vitamin D Plays an Integral Role in Adaptive Immunity

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Severe Adverse Reactions Include Vitamin D Deficiency and Autoimmunity

Hormones Matter researchers discovered that, inter alia, severe adverse reactions to any of the surveyed drugs trigger significant but varying autoimmune responses. Moreover, the research revealed an underlying consistency involving all reviewed drugs: vitamin D deficiency.

Vitamin D Helps Regulate the Adaptive Immune System

The adaptive immune system comprises the body’s intricate network of antibodies and special types of white blood cells (called sensitized lymphocytes ) to thwart new and previous invaders including viruses, bacteria, and drugs. When the adaptive immune system is not strong enough to endure external disruptions such as severe side effects of drugs, it can go awry by signaling antibodies and sensitized lymphocytes to attack healthy cells. This response is called autoimmunity—when the adaptive immune system’s cells do not recognize previous invaders and designate healthy cells as those invaders. In other words, the body’s immune cells attack its own healthy cells.

Scientific research over the past three decades solidifies the connection between vitamin D and autoimmunity. Vitamin D plays an integral role in the regulation of the adaptive immune system. Adequate vitamin D in our bodies can protect us from autoimmunity because adaptive immune cells contain vitamin D receptors (VDRs). These receptors are attached to the surface of the adaptive immune system’s antibodies and sensitized lymphocytes. The VDRs act as “gate keepers” by signaling what external substances, e.g., components of medications, can enter a cell. The VDRs must be replete with vitamin D to effectively regulate adaptive immunity. When the VDRs receive adequate amounts of vitamin D, they enable the adaptive immune system to function properly by attacking new and previous invaders.

When the VDRs attached to the adaptive immune system’s cells do not contain sufficient vitamin D to attack invaders, autoimmunity may kick in, causing the death of healthy immune cells. Thus, low vitamin D levels can lead to autoimmune diseases including thyroid disorders such as Hashimoto’s and demyelinating diseases including multiple sclerosis (MS).

Vitamin D and Hashimoto’s Autoimmune Thyroid Disease

The Real Women, Real Data research also uncovered another consistency among severe adverse reactions to the reviewed drugs: Hashimoto’s thyroiditis, an autoimmune disease caused by abnormal cells constantly assaulting the thyroid gland
.
Vitamin D receptors are present in the thyroid as well as the pituitary, the pea-shaped gland that controls the thyroid. Not surprisingly, low levels of serum vitamin D have been linked to Hashimoto’s thyroiditis, according to recent Turkish medical research:

Published in a 2013 issue of the journal Endocrine Practice, a study conducted at a training and research hospital in Ankara demonstrated that serum vitamin D levels of female chronic Hashimoto’s patients were significantly lower than healthy subjects. Furthermore, the researchers discovered a direct correlation between serum vitamin D levels and thyroid volume as well as an inverse correlation to the antibodies involved in the thyroid.

Researchers at Medeniyet University’s Goztepe Education and Research Hospital in Istanbul learned that 92 per cent of their 161 Hashimoto’s thyroiditis cases had serum vitamin D levels lower than 30 ng/mL (12 nmol/L), a value characterized as “insufficient.” Published in a 2011 issue of the journal Thyroid, the study reports an association between vitamin D insufficiency and Hashimoto’s thyroiditis.

Vitamin D and Demyelinating Disorders

Another disturbing outcome of the Real Woman, Real Data research is the reporting of neurological and neuromuscular symptoms, many which of are consistent with demyelinating disorders such as MS, an autoimmune disease. The development of MS occurs when a poorly functioning, adaptive immune system gradually attacks the protective covering of the nerve cells (called the myelin sheath) of the brain and spinal cord. This potentially debilitating process is called demyelination.

Scientific—primarily epidemiological—research indicates an association between vitamin D levels and the risk of developing a demyelinating disorder such as MS. VDRs exist on nerve cells and the myelin sheath. When the VDRs receive adequate amounts of vitamin D, they help protect the integrity of the myelin sheath. However, when the VDRs do not contain sufficient vitamin D, autoimmunity may occur, resulting in the death of healthy nerve cells. Numerous clinical trials are underway to assess the connection between vitamin D status and the likelihood of developing demyelinating disorders.

Low Vitamin D: The Chicken or the Egg?

The connection between low vitamin D status and the development of autoimmune disease is genuine. However, medical research has not yet determined if vitamin D deficiency plays a role in the development of autoimmune disease, if low vitamin D levels are a consequence of the disease itself, or if vitamin D deficiency acts as both a cause and effect. The authors of the aforementioned 2013 Hashimoto’s study concluded,

“Finally, our results suggested that there may be a causal relation between vitamin D deficiency and development of Hashimoto’s thyroiditis. On the other hand, there might be a possible relation between severity of vitamin D deficiency and progression of thyroid damage. However, further studies are needed especially about the effects of vitamin D supplementation on prevention and/or progression of autoimmune thyroid disease.”

Proactive Protection against Severe Adverse Reactions

We could wait years (or decades) to garner the results of further scientific studies and clinical trials to define the exact relationship between vitamin status and severe adverse reactions to vaccines and medications that culminate in autoimmune disorders. Or we could be proactive by taking daily vitamin supplements and enjoying moderate sunlight exposure to increase our vitamin D levels.

It is imperative to take enough vitamin D3 so this essential nutrient will be stored in your cells to help regulate your immune system. The greater your serum vitamin D level (easily obtained from a simple blood test called 25(OH) D, the more likely you will benefit from a stronger immune system that protects your body’s cells from attacking one another.

No one wants to endure severe adverse reactions to drugs such as Gardasil and Lupron, let alone an autoimmune disease. Attaining and maintaining adequate supplementation provides a safe, easy, and inexpensive approach to improved preventive health. By empowering yourself with adequate vitamin D, you may reap the benefits of avoiding disease and enjoying better quality of life.

Copyright © 2013 by Susan Rex Ryan. All rights reserved.

This article was published previously on Hormone Matter in September 2013.

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Why Fatigue Matters in Thyroid Disease

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The notion that unremitting fatigue is a core clinical symptom is difficult for many physicians and patients to reconcile with its ubiquitous nature in illness. Here is yet another example of the importance of recognizing fatigue and the constellation of other clinical signs that manifest concurrently in thyroid disease. Here we see that fatigue represents a loss of mitochondrial function that, if left untreated, has some subtle and not so subtle effects on central nervous system functioning.

Some Background: Fatigue and the Mitochondrial Connection

Fatigue is one of the most common signs of mitochondrial dysfunction or deficit. Mitochondria, the energy factories within our cells, produce the ATP or cellular energy, that our bodies require to function. This process is called oxidative metabolism. As Dr. Lonsdale wrote about in How can Something as Simple as Thiamine Cause So Many Problems, consider each mitochondrion as a mini, combustion engine.

 Fuel + Oxygen + Catalyst = Energy

 Each of our one hundred trillion body/brain cells is kept alive and functioning because of this reaction. It all takes place in micro “fireplaces” known as mitochondria. Oxygen combines with fuel (food) to cause burning or the combustion – think fuel combustion engine. We need fuel, or gasoline, to burn and spark plugs to ignite in order for the engines to run.

In our body/brain cells it is called oxidation. The catalysts are the naturally occurring chemicals we call vitamins (vital to life). Like a spark plug, they “ignite” the food (fuel). Absence of ANY of the three components spells death.

Antioxidants like vitamin C protect us from the predictable “sparks” (as a normal effect of combustion) known as “oxidative stress”.  Vitamin B1, is the spark plug, the catalyst for these reactions.

 

When there is dysfunction within this pathway, which is also called the OXPHOS or oxidative phosphorylation, when the engine doesn’t get the fuel it needs or the spark plugs don’t work, fatigue and other symptoms arise. Fatigue is an important clinical sign that something is amiss in our cellular combustion engines.

Mitochondria and Hypothyroidism – Beyond One Test One Drug

In chronic hypothyroidism, chronic mitochondrial deficits are clinical signs that can be recognized, if one is looking for them. They present as fatigue, and when chronic, as balance and gait disorders. Recall our discussion and videos on Hashimoto’s disease associated with walking and balance difficulties: Adverse Reactions, Hashimoto’s Thyroiditis, Gait Balance and Tremors –  those examples pointed to mitochondrial dysfunction. Here is yet another example of the importance of recognizing subtle clinical signs of mitochondrial damage.

Watch and listen for the clinical signs. How many do you have?

Notice, he speaks of the importance of proper nutrition, of reducing inflammation, and of exercise and other modalities to correct the functional deficits of hypothyroidism and mitochondrial dysfunction. Notice also, the improvement in functioning after only eight weeks of treatment.

Datis Kharrazian: Developing the Clinical Eye to Discover the Causes of Fatigue from The Institute for Functional Med on Vimeo.

If you or a loved one suffers from chronic and unremitting fatigue rule out thyroid dysfunction and its sister condition mitochondrial damage. A simple TSH test, as is commonly considered, is not sufficient to find thyroid dysfunction. A full panel must given. Once a diagnosis is reached, remember thyroid medications, though they may be necessary, are not enough to correct mitochondrial damage. Diet and nutrients must considered. Put it all together and live healthier.

We Need Your Help

Hormones Matter needs funding now. Our research funding was cut recently and because of our commitment to independent health research and journalism unbiased by commercial interests we allow minimal advertising on the site. That means all funding must come from you, our readers. Don’t let Hormones Matter die.

Yes, I’d like to support Hormones Matter.

Image created in Canva AI.

This article was published originally on Hormones Matter on November 7, 2013. 

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Hormones Matter Top 100 Articles of 2015

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Hormones Matter 2015 Top 100 Articles

Happy New Year, everyone. We have another remarkable year under our belts. Hormones Matter continues to grow month after month. This year, despite the site being down for a month in September, we had over 815,000 visitors, most staying quite a while to read our articles.

Since inception, we’ve published close to 900 articles, many are read by thousands of readers every month. The hysterectomy and endometriosis articles continue to draw large crowds, demonstrating the great need for information in these areas of women’s health.

Our success is thanks to a fantastic crew of volunteer writers who spend countless hours researching complex medical topics, making connections, identifying unconventional therapeutic opportunities, and bringing to light, what are often, invisible illnesses. Without these incredibly talented and compassionate individuals, Hormones Matter would not exist.

Before we begin the new year in earnest, let us take a moment to thank all of the writers of Hormones Matter.

Thank You Hormones Matter Writers!

 

Below are the articles and authors who made the top 100 list for 2015. If you haven’t read these articles, it’s time to do so. If you like them, share them and share our site so we can continue to grow. If you were helped by any of our articles, take a moment and send the writer a thank you note.

This year, we thought we’d do something a little different and include the 25 all-time favorite articles on Hormones Matter. Be sure to scroll down to the second table and take a look. The numbers are quite impressive.

Since we are run by volunteers and unfunded, feel free contribute a few dollars to cover the costs of maintaining operations. Crowdfund Hormones Matter. Every dollar helps.

If you’d like to share your health story or join our team of writers: Write for Us.

Hormones Matter Top 100 Articles of 2015

Article Title and Author

Reads
1. Post Hysterectomy Skeletal and Anatomical Changes -WS 50,814
2. Sex in a Bottle: the Latest Drugs for Female Sexual Desire – Chandler Marrs 47,910
3. Sexual Function after Hysterectomy – WS 28,898
4. In the ER Again – Heavy Menstrual Bleeding -Lisbeth Prifogle 25,326
5. Endometrial Ablation – Hysterectomy Alternative or Trap? -WS 25,048
7.  Adhesions: Cause, Consequence and Collateral Damage – David Wiseman 22, 868
8. Is Sciatic Endometriosis Possible? – Center for Endometriosis Care 11,701
9. Endometriosis: A Husband’s Perspective – Jeremy Bridge Cook 11,626
10. A Connection between Hypothyroidism and PCOS – Sergei Avdiushko 11,024
11. Often Injured, Rarely Treated: Tailbone Misalignment – Leslie Wakefield 10,580
12. Hysterectomy: Impact on Pelvic Floor and Organ Function – WS 8,494
13. Pill Bleeds are not Periods – Lara Briden 8,440
14. Silent Death – Serotonin Syndrome – Angela Stanton 8,408
15.  An Often Overlooked Cause of Fatigue: Low Ferritin – Philippa Bridge-Cook 8,374
16. Wide Awake: A Hysterectomy Story – Robin Karr 7,733
17. How Hair Loss Changed My Life – Suki Eleuterio
18. The High Cost of Endometriosis – Philippa Bridge-Cook 7,170
19. Skin Disorders post Gardasil – Chandler Marrs 6,891
20. Essure Sterilization: The Good, the Bad and the Ugly – Margaret Aranda 6,820
21. Love Hurts – Sex with Endometriosis – Rachel Cohen 6,779
22. Dehydration and Salt Deficiency Migraines – Angela Stanton 6,638
23.  Adverse Reactions, Hashimoto’s Thyroiditis, Gait, Balance and Tremors – Chandler Marrs 6,445
24.  Stop the Metformin Madness – Chandler Marrs 6,400
25. Lupron, Estradiol and the Mitochondria: A Pathway to Adverse Reactions – Chandler Marrs 6,110
26. Endometriosis after Hysterectomy – Rosemary Finnegan 6,093
27. The Reality of Endometriosis in the ER – Rachel Cohen 5,962
28. Mittelschmerz – what should you know – Sergei Avdiushko 5,780
29.  Red Raspberry Leaf Tea to Relieve Menstrual Pain – Lisbeth Prifogle 5,586
30. Mommy Brain: Pregnancy and Postpartum Memory Deficits – Chandler Marrs 5,437
31. Parasites: A Possible Cause of Endometriosis, PCOS, and Other Chronic, Degenerative Illnesses – Dorothy Harpley-Garcia 5,414
32.  Endometriosis and Risk of Suicide – Philippa Bridge-Cook 5,413
33.  Fluoroquinolone Antibiotics and Thyroid Problems: Is there a Connection? – JMR 5, 228
34. Adenomyosis – Philippa Bridge-Cook 5,022
35.  Gardasil: The Controversy Continues – Lisbeth Prifogle 4,809
36.  Hyperemesis Gravidarum – Severe Morning Sickness: Are Mitochondria Involved? – Chandler Marrs 4,801
37.  Oral Contraceptives, Epigenetics, and Autism – Kim Elizabeth Strifert 4,452
38.  High Blood Pressure in Women: Could Progesterone be to Blame? – Chandler Marrs 4,446
39. My Battle with Endometriosis: Hysterectomy at 23 – Samantha Bowick 4,288
40. Thiamine Deficiency Testing: Understanding the Labs – Derrick Lonsdale 4,045
41. My Battle with Endometriosis and Migraines – Angela Kawakami 3,839
42. Tampons with Glyphosate: Underpinnings of Modern Period Problems? – Chandler Marrs 3,835
43. Cipro, Levaquin and Avelox are Chemo Drugs – Lisa Bloomquist 3,792
44. Hysterectomy or Not – Angela’s Endometriosis Update – Angela Kawakami 3,750
45. Warning to Floxies: Beware of New Med for Psoriatic Arthritis – Debra Anderson 3,691
46.  DES – The Drug to Prevent Miscarriage Ruins Lives of Millions – DES Daughter 3,655
47.   Sphincter of Oddi Dysfunction (SOD) – Brooke Keefer 3,540
48. Progesterone for Peripheral Neuropathy – Chandler Marrs 3,278
49. The Fluoroquinolone Time Bomb – Answers in the Mitochondria – Lisa Bloomquist 3,251
50. Why is PCOS so Common? – Lara Briden 3,211
51.  Pregnancy Toes – What Sugar does to Feet – Angela Stanton 2,971
52.  Five Half-truths of Hormonal Contraceptives – The Pill, Patch and Ring – Joe Malone 2,834
53.  Five Years After Gardasil – Ashley Adair 2,831
54. Bleeding Disorders Overlooked in Women with Heavy Periods – Philippa Bridge Cook 2,826
55.  Is Gardasil Mandated in Your State? – Lisbeth Prifogle 2,814
56.  Is Prenatal Dexamethasone Safe: The Baby Makers’ Hubris – Chandler Marrs 2,808
57. Porn Brain – A Leading Cause of Erectile Dysfunction – Chandler Marrs 2,792
58. Lupron and Endometriosis – Jordan Davidson 2,752
59.  Endometriosis, Adhesions and Physical Therapy – Philippa Bridge-Cook 2,746
60.  Glabrata – A Deadly Post Fluoroquinolone Risk You’ve Never Heard About – Debra Anderson 2,703
61. Are You Vitamin B12 Deficient? – Chandler Marrs 2,635
62. Topamax: The Drug with 9 Lives – Angela Stanton 2,635
63.  Cyclic Vomiting Syndrome – Philippa Bridge-Cook 2,622
64.  The Endo Diet: Part 1 – Kelsey Chin 2,614
65.  Endometriosis and Adhesions –  Angela Kawakami 2,544
66.  Thyroid Disease Plus Migraines – Nancy Bonk 2,530
67.  Is it Endometriosis? – Rosalie Miletich 2,414
68. Hysterectomy, Hormones, and Suicide – Robin Karr 2,412
69.  Why I am Backing the Sweetening the Pill Documentary – Laura Wershler 2,321
70.  I Wanted to Die Last Night: Endometriosis and Suicide – Rachel Cohen 2,271
71.  How Can Something As Simple As Thiamine Cause So Many Problems? – Derrick Lonsdale 2,456
72.  Thyroid Dysfunction with Medication or Vaccine Induced Demyelinating Diseases – Chandler Marrs 2,034
73. Angela’s Endometriosis Post Operative Update –  Angela Kawakami 2,017
74.  Fluoroquinolone Antibiotics Damage Mitochondria – FDA Does Little – Lisa Bloomquist 1,993
75.  Endometriosis and Pregnancy at a Glance – Center for Endometriosis Care 1,969
76.  Don’t Take Cipro, Levaquin or Avelox If…. – Lisa Bloomquist 1,960
77.  Gardasil Injured – Dollie Duckworth 1,898
78. Fear of Childbirth Prolongs Labor – Elena Perez 1,888
79. Fluoroquinolone Poisoning: A Tale from the Twilight Zone – Kristen Weber 1,883
80. Personal Story: Thyroid Cancer – Myrna Wooders 1,880
81. Recurrent Miscarriage – Philippa Bridge-Cook 1,873
82. Recovering from the Gardasil Vaccine: A Long and Complicated Process – Charlotte Nielsen 1,842
83. Pelvic Therapy for Endometriosis, Adhesions and Sexual Pain – Belinda Wurn 1,818
84. Hormones, Hysterectomy and the Hippocampus – Chandler Marrs 1,777
85. Why Fatigue Matters in Thyroid Disease – Chandler Marrs 1,718
86. How Do You Deal with the Lasting Effects of Endometriosis? – Samantha Bowick 1,697
87. Depression with Endometriosis – Samantha Bowick 1,678
88. Easing Endometriosis Pain and Inflammation with Nutrition –  Erin Luyendyk 1,648
89. Anti-NMDAR Encephalitis and Ovarian Teratomas – Chandler Marrs 1,634
90. Autoinflammatory Syndromes Induced by Adjuvants: A Case for PFAPA – Sarah Flynn 1,595
91. Endometriosis Awareness Month: A Wish Noted – Philippa Bridge-Cook 1,513
92. The Role of Androgens in Postmenopausal Women – Sergei Avdiushko 1,477
93. It Wasn’t by Choice: Dysautonomia – Margaret Aranda 1,454
94. Fluoroquinolone Antibiotics Associated with Nervous System Damage – Lisa Bloomquist 1,453
95.  Vitamin D3 and Thyroid Health – Susan Rex Ryan 1,439
96. Dealing with Doctors When You Have Undiagnosed Endometriosis -Angela Kawakami 1,439
97. Endometriosis and Being a Trans Person: Beyond Gendered Reproductive Health – Luke Fox 1,436
98. Cyclic Vomiting Syndrome and Mitochondrial Dysfunction: Research and Treatments – Philippa Bridge-Cook 1,430
99. Living with Ehlers Danlos is Hell – Debra Anderson 1,420
100. What is Fluoroquinolone Toxicity? – Lisa Bloomquist 1,415

Hormones Matter All-Time Top 25 Articles

Article Title and Author

Reads
1. Post Hysterectomy Skeletal and Anatomical Changes -WS 105,336
2. Sex in a Bottle: the Latest Drugs for Female Sexual Desire – Chandler Marrs 99,098
3. Endometrial Ablation – Hysterectomy Alternative or Trap? -WS 70,999
4. Adhesions: Cause, Consequence and Collateral Damage – David Wiseman 40,299
5. In the ER Again – Heavy Menstrual Bleeding -Lisbeth Prifogle 39,821
7.  Sexual Function after Hysterectomy – WS 35,188
8. A Connection between Hypothyroidism and PCOS – Sergei Avdiushko 31,193
9. Is Sciatic Endometriosis Possible? – Center for Endometriosis Care 24,691
10. Endometriosis: A Husband’s Perspective – Jeremy Bridge-Cook 23,251
11. Skin Disorders post Gardasil – Chandler Marrs 18,105
12.  Gardasil: The Controversy Continues – Lisbeth Prifogle 14,174
13.  Wide Awake: A Hysterectomy Story – Robin Karr 14,134
14.  Endometriosis and Risk of Suicide – Philippa Bridge-Cook 13,836
15.  Love Hurts – Sex with Endometriosis – Rachel Cohen 13,782
16. Endometriosis after Hysterectomy – Rosemary Finnegan 13,294
17. Hysterectomy: Impact on Pelvic Floor and Organ Function – WS 13,056
18.  Adverse Reactions, Hashimoto’s Thyroiditis, Gait, Balance and Tremors – Chandler Marrs 12,901
19.  How Hair Loss Changed My Life – Suki Eleuterio 12,835
20. Mittelschmerz – what should you know – Sergei Avdiushko 11,919
21.  Often Injured, Rarely Treated: Tailbone Misalignment – Leslie Wakefield 11,521
22.  An Often Overlooked Cause of Fatigue: Low Ferritin – Philippa Bridge-Cook 10,821
23.  Mommy Brain: Pregnancy and Postpartum Memory Deficits – Chandler Marrs 10,591
24. Adenomyosis – Philippa Bridge-Cook 10,249
25.  I Wanted to Die Last Night: Endometriosis and Suicide – Rachel Cohen 9,826

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