Thyroid and rheumatoid arthritis


Does Rheumatoid Arthritis Impact Thyroid Function?

Autoimmune diseases can join forces. If you have one, you’re at risk for developing others.

For example, people with rheumatoid arthritis are also more likely to develop an underactive thyroid disease, hypothyroidism or Hashimoto’s thyroiditis. And people living with Hashimoto’s thyroiditis are also at higher risk for developing rheumatoid arthritis.

According to the Arthritis Foundation, about 1.5 million Americans are affected by rheumatoid arthritis (RA), which occurs when the body’s immune system misfires against its own joints and connective tissues, causing pain and inflammation.

Similarly, Hashimoto’s occurs when the immune system mistakenly attacks thyroid cells, interfering with their ability to make thyroid hormone. Hypothyroid symptoms such as fatigue, joint and muscle pain, and depression can also mimic RA symptoms, making it tricky to sort out which condition is responsible for which symptoms.

Exactly how the two conditions are linked is not yet fully understood, but shared genes may play a role in susceptibility to autoimmune diseases, experts say.

Eric L. Matteson, MD, rheumatologist and professor of medicine at Mayo Clinic in Rochester, Minnesota says heart disease is also more prevalent among individuals with both hypothyroidism and RA, or more than one autoimmune condition.

“It’s the trifecta,” said Dr. Matteson. “When you have an under-active thyroid, it can make you feel quite tired, just like RA. Everyone assumes it is the RA, so nobody thinks to look for alternate causes.”

Plus, he says, when a patient has both autoimmune hypothyroidism and RA, it can be difficult to determine which condition is causing which symptoms.


Objective: Rheumatoid arthritis (RA) patients have an increased risk of developing cardiovascular diseases (CVD). Other autoimmune diseases such as hypothyroidism are also associated with an enhanced risk for CVD. Our objective was to determine first, the prevalence of hypothyroid disorders in RA patients, and second, the risk of CVD in RA patients with hypothyroid abnormalities.

Methods: Subjects were RA patients who participated in an ongoing prospective cohort study of cardiovascular mortality and morbidity (n = 358) in which hypothyroid abnormalities were assessed. CVD was defined as a verified medical history of coronary, cerebral or peripheral arterial disease.

Results: Clinical hypothyroidism was observed in 16 of 236 female RA patients (6.8%), which is significantly higher than in the general population of The Netherlands. Subclinical hypothyroidism was detected in 6 out of 236 RA women (2.5%). In female RA patients, CVD was present in 6 out of 16 (37.5%) of all hypothyroid women. The odds ratio for CVD comparing female hypothyroid RA patients with female euthyroid RA patients was 4.1 (95% CI 1.2–14.3) after adjustment for sex, age, diabetes, smoking (ever), hypertension and statin use.

Conclusions: Clinical hypothyroidism was observed three times more often in female RA patients than females in the general population. In female RA patients, clinical hypothyroidism was associated with a fourfold higher risk of CVD in comparison with euthyroid female RA patients independently of the traditional risk factors.

Hypothyroidism and RA

Managing hypothyroidism

Generally, my thyroid levels remain quite stable, and I only need to visit the endocrinologist on a yearly basis. On the occasions when he does alter my dosage, I return a few weeks later to repeat level testing to ensure that the new medication strength is appropriate. I was initially diagnosed with autoimmune thyroiditis at the age of eight, and my prescription required frequent adjustment as I proceeded through a series of growth spurts.

Thyroid fluctuations during pregnancy

Since adulthood, my levels have rarely needed to be changed, with the exception of during my two pregnancies. I experienced quite a bit of thyroid fluctuation while pregnant, and therefore my endocrinologist requested that my OBGYN test my thyroid levels and send him the results at each of my monthly prenatal check-ups. Weight gain can impact the body’s need for thyroid, as a larger body mass generally requires a higher dosage of synthetic hormone. At times when my weight has fluctuated, I have needed a corresponding change in medication.

Monitor thyroid levels

As people with RA are more likely to develop autoimmune thyroiditis than the general population, and as the symptom of fatigue can easily be attributed to RA when it may actually be stemming from hypothyroidism, it is recommended that people with rheumatoid arthritis have their thyroid function and hormone levels regularly screened via testing TSH and free thyroxine (T4) levels.4 This ensures that symptoms caused by hypothyroidism are not incorrectly attributed to RA.

Furthermore, hypothyroidism carries an increased risk of cardiovascular disease5, and patients with both autoimmune thyroiditis and rheumatoid arthritis are at an even higher risk for heart problems.6 Therefore, receiving treatment for both conditions is important in limiting the risk of additional complications.

Address gut bacteria for joint pain and Hashimoto’s low thyroid

By Josh Redd, DC on May 4, 2018

Osteoarthritis, or degenerative joint disease affects more than 31 million people and is the number one cause of disability. Treatment has always been aimed at pain relief but not the underlying cause. With Hashimoto’s low thyroid affecting an estimated 25 million people, perhaps you have both. Now however, new research demonstrates improving gut bacteria — or the gut microbiome — through prebiotic fiber can not only reduce osteoarthritic pain but also dampen inflammation. These same benefits will better manage Hashimoto’s low thyroid.

Inflammation drives joint pain and Hashimoto’s low thyroid

Obesity is a risk factor for developing osteoarthritis, but not for the reasons we believe. It has always been thought the extra weight overloading the joints caused the pain, but new findings suggest it’s more likely caused by inflammation from a “obesity-prone” gut microbiome profile. In the study, obese mice with arthritis had less beneficial Bifidobacteria and too much inflammatory bacteria that caused joint deterioration. When researchers gave the mice a prebiotic fiber called oligofructose, an inulin, their gut microbiome signature shifted to reduce inflammation despite still being obese. This research suggests osteoarthritis treatment should focus on gut bacteria and inflammation. This same approach will also help manage your Hashimoto’s low thyroid to prevent autoimmune thyroid flare ups.

Prebiotics improve your gut microbiome

Good gut bacteria not only help alleviate arthritis pain, they also improve your immune function, brain function, mood, and Hashimoto’s low thyroid condition. Chronic inflammation, regardless of obesity, is the root cause of many common chronic health problems, including Hashimoto’s low thyroid, heart disease, cancer, and arthritis. While probiotics are recognized as helping gut bacteria, prebiotics are more recently getting the recognition they deserve. Prebiotics are non-digestible carbohydrates your gut bacteria (probiotics) depend on for sustenance. You can get them from the fruits and vegetables you eat or prebiotic supplements. Once prebiotics make it to the colon, gut bacteria consume them and create byproducts such as vitamins and short chain fatty acids (SCFAs), which are valuable to human health. Good sources of prebiotics include all vegetables but particularly:

  • Garlic
  • Jerusalem artichokes
  • Jicama
  • Dandelion greens
  • Onions
  • Peas
  • Broccoli
  • Brussels sprouts
  • Fruits
  • Beans

Prebiotics and probiotics work together to battle inflammation and lower disease risk.

Support SCFAs to dampen pain and inflammation

The short chain fatty acids (SCFAs) produced by the gut microbiome are necessary to dampen the inflammation of obesity, arthritis, and Hashimoto’s low thyroid. The most important SCFAs is butyrate. To increase butyrate and other SCFAs:

  • Eat abundant and varied fruits and vegetables daily — 7 to 9 servings is recommended.
  • Eat probiotic-rich fermented and cultured foods such as kimchi, sauerkraut, and coconut water kefir.
  • Take SCFA-supporting supplements such as Saccharomyces boulardii, Lactobacillus sporogenes, and DDS-1 Lactobacilli acidophilus.
  • Take arabinogalactan, a compound made up of protein and sugar, which is helpful for immune support and SCFA production.

Intolerance to foods also triggers joint pain and Hashimoto’s low thyroid

Joint pain and Hashimoto’s low thyroid can also be triggered by an immune reation to certain foods. Two of the most common dietary triggers are gluten and dairy. Gluten sensitivity triggers pro-inflammatory immune cells that cause inflammation that damages soft tissue, including the joints and the brain. The same can happen for dairy and other foods. Gluten intolerance has been linked in several studies to Hashimoto’s low thyroid. Many people find nightshade vegetables cause pain and inflammation in their joints. These include eggplant, potatoes (but not sweet potatoes or yams), peppers, tomatoes, tomatillos, hot pepper products (cayenne, Tabasco, etc.), and pepper-based spices. Simply removing nightshades from the diet has helped many people find relief from joint pain, especially those with rheumatoid arthritis. Gluten, dairy, and nightshades are common reactive foods, but there are other common ones, such as corn and soy. An anti-inflammatory diet is a great strategy for dampening pain and inflammation while helping you figure out which foods trigger an immune reaction. Another way to find out which foods are inflammatory is via a food sensitivity panel. Chronic pain creates vicious cycles in the immune system and the brain that perpetuate even more pain. Fortunately, functional medicine strategies can unwind these vicious cycles. Ask my office for more information on alleviating your chronic joint pain and Hashimoto’s low thyroid by addressing the root causes.

How to learn if you have Hashimoto’s low thyroid

Many patients are not diagnosed with hypothyroidism or Hashimoto’s until after several years and going through several doctors. It is a demoralizing journey richly illustrated in my book The Truth About Low Thyroid: Stories of Hope and Healing for Those Suffering With Hashimoto’s Low Thyroid Disease, through real-life stories from patients in my practice. Managing Hashimoto’s goes far beyond using thyroid medication as you must work to stop the immune system from attacking the thyroid. For more information on identifying and managing Hashimoto’s low thyroid, contact my office.

About Dr. Josh Redd, Chiropractic Physician — Utah, Arizona, New Mexico functional medicine

Dr. Joshua J. Redd, DC, MS, DABFM, DAAIM, author of The Truth About Low Thyroid: Stories of Hope and Healing for Those Suffering With Hashimoto’s Low Thyroid Disease, is a chiropractic physician and the founder of RedRiver Health and Wellness Center with practices in Utah, Arizona, and New Mexico. He sees patients from around the world who suffer from challenging thyroid disorders, Hashimoto’s disease, and other autoimmune conditions. In addition to his chiropractic degree, Dr. Redd has a BS in Health and Wellness, a BS in Anatomy, and a MS in Human Nutrition and Functional Medicine. He speaks across the nation, teaching physicians about functional blood chemistry, low thyroid, Hashimoto’s, and autoimmunity. You can join his Facebook page here.

Over the years of working with people with Hashimoto’s, I have learned that most people will experience pain on some level. For some, it may manifest as a chronic condition, such as migraines or joint pain. In other cases, people may experience gastrointestinal pain that comes and goes. When I was first diagnosed with Hashimoto’s in 2010, I struggled with pain in the form of body aches and stiffness, as well as carpal tunnel in both arms. To deal with the pain and get through my workday, I took NSAIDs (painkillers) every day… before eventually getting to the root cause of my thyroid condition and making diet and lifestyle changes. These interventions alleviated my pain within weeks.

As a pharmacist, I certainly understand the value of pain medication and other conventional therapies in the right context. However, I also know that getting to the root cause of why we have pain, and treating the trigger itself — often through natural methods — can be more effective at providing a long-term resolution to pain.

Each pain disorder requires a unique, comprehensive treatment plan, as pain is a complicated and multifaceted issue, with many potential root causes — and therefore, many potential treatments. For example, a person may be in pain because of an injury, migraines, a structural abnormality, nerve damage, fibromyalgia, an autoimmune process, or because of an increased sensitivity to their environment.

In this article, I would like to:

  • Explore the conventional approach to pain management
  • Discuss the Root Cause approach to addressing pain
  • Provide some effective, natural strategies for reducing pain

The Conventional Approach to Pain Management

While pain may have various root causes, and some types of pain may require physical rehabilitation and other incredibly helpful conventional treatments, the most common conventional approach to treating pain is through the use of surgery and pharmaceutical pain medications. While this is not meant to be a complete review of the conventional approach, I’ll mention some of the more common options I’ve seen as a pharmacist.


The use of opiate medications is a constant source of controversy. On one hand, they are overused, and often lead to addiction and health problems. On the other hand, for people who are terminally ill or seriously injured, opiates are often necessary and serve an important purpose in alleviating severe pain.

Opiates work by disconnecting the pain receptors in our brain from the pain signals themselves, making us “forget” that we’re in pain. While these medications are effective “band-aids” for pain relief, they can also be habit-forming for many people. The potential side effects of opiates include sedation, dizziness, nausea, vomiting, constipation, physical dependence, and respiratory depression. Over time, people can build up a tolerance to these drugs and require increasingly large dosages to counteract pain, leading to dependance, increased side effects and even death from overdosing.

Sadly, in 2017, over 47,000 people died in the United States from drug overdoses due to opiates. In some cases, people overdose on prescription drugs, while in other cases, they may turn to street drugs due to addiction and needing a stronger drug. A dear friend from high school became addicted to opiates after a sports injury while playing college football and lost his life to a fentanyl overdose, so this subject hits close to home for me.

Despite their habit-forming potential and potential for serious side effects and even death, a growing number of people are being prescribed opiates. Interestingly, Synthroid was the number one prescribed drug in 2013 and 2014 in the United States. In 2015, Synthroid dropped to number two and was displaced by Vicodin, an opiate painkiller. As a pharmacist, the irony is not lost on me that in many cases, addressing inflammation could prevent the use of both of these medications.


NSAID medications (Non-Steroidal Anti-Inflammatory Drugs) are often a first line treatment for pain disorders. They help with reducing pain and inflammation by preventing an enzyme called cyclooxygenase (COX) from creating hormone-like chemicals called prostaglandins — one of the greatest contributors to inflammation in the body. Unfortunately, they are also associated with numerous side effects, most significantly gut dysfunction, which can lead to an increased likelihood of ulcers. For short-term use, such as the occasional headache or acute injury, NSAIDs can be very helpful. However, the longer we take them, the more likely we are to suffer adverse reactions.

Most medications have their time and place. As a pharmacist who is trained in both medication therapy management and functional medicine, I believe that instead of glorifying or demonizing medications, health professionals and patients need to be educated about appropriate medication use, along with complementary therapies that can eliminate or reduce the need for medications.


Surgical intervention is sometimes necessary in addressing pain. However, it is more likely to be used in the case of acute pain (such as a broken bone) rather than chronic pain. Oftentimes with chronic pain, the source is difficult to identify. A surgeon can’t operate if they don’t know what to “fix.” However, there are some circumstances in which the source of pain is identifiable and surgery is an option, usually as a last resort when other solutions have failed.

An example of this would be a herniated (ruptured) spinal disk that presses on the sciatic nerve and causes chronic sciatica. Surgery to remove part of the offending disk (called a discectomy) may be performed to relieve the pressure and, thereby, the source of chronic pain.

Though surgery might be the best option in certain circumstances, the risks of surgical and invasive procedures are not minor. They include permanent injury to the body, psychological stress, and time, cost, and productivity losses.


In some cases, steroids can be used to reduce pain. Most steroids are synthetic forms of cortisone (a hormone naturally made in your adrenal glands) and include prednisone, methylprednisolone, prednisolone, dexamethasone, and hydrocortisone. These come in many forms, including pills, topical creams, and injections.

Steroids decrease inflammation by reducing the production of inflammatory chemicals in order to minimize tissue damage. This might be particularly helpful in conditions such as rheumatoid arthritis, where chronic inflammation causes painful swelling in the tissue surrounding the joints.

However, as with all medications, steroids do come with negative side effects, and these side effects increase with dosage. In other words, most of the negative consequences that come from using steroids are a result of long-term use for managing chronic pain.

These side effects include adrenal insufficiency (altered response to physical stress), steroid withdrawal syndrome (fever, fatigue, and joint pain), infection (steroids depress the immune system), gastrointestinal ulcers and bleeding, osteoporosis, weight gain, depression, insomnia, elevated blood pressure, blood sugar imbalances, cataracts and glaucoma, elevated risk of heart disease, and even bone death (aseptic necrosis).

While there are some short-term circumstances in which steroids can be very helpful, they don’t address the root cause of pain itself, and may create more health consequences down the road.

What we know is that pain medications, surgery, and other conventional approaches don’t get to the root cause of the pain condition, and thus, we need to take a comprehensive approach to reducing pain in the body.

Addressing the Root Causes of Pain

Inflammation is always a factor with Hashimoto’s, as thyroid disease itself involves inflammation of the thyroid gland. When inflammation occurs, the body’s white blood cells release chemicals into the affected tissues to protect the body from what it sees as foreign substances. In autoimmune disease, the body views part of its own body as a foreign invader and stages an attack, resulting in inflammation. In most cases of Hashimoto’s, where the body attacks its own thyroid cells, the inflammation is not limited to the thyroid gland, but can manifest anywhere in the body.

When we experience pain with Hashimoto’s, inflammation will oftentimes be at the root, and reducing inflammation in our bodies will always help reduce pain and promote healing. While NSAIDs do reduce inflammation in the short term, they won’t get to the root cause, and the pain will return.

Instead, there are several natural approaches that have been shown to be effective without the unwanted side effects. Many of these solutions will target the reason that inflammation occurred in the first place, and may eliminate pain altogether.


Nutrient depletions may be at the root cause of pain in some cases, and supplementing with key nutrients can be very helpful for treating pain and reducing inflammation. Common nutrient deficiencies associated with pain include:

  • Magnesium – People with Hashimoto’s are at risk for being deficient in magnesium, which can lead to a long list of symptoms, including headaches, joint pain, leg and hand cramps, and menstrual pain. In my own case, I noticed a dramatic decrease in menstrual cramps when I began taking a magnesium supplement on a daily basis.
  • Omega-3 Fatty Acids – Omega-3s are a powerful ally against pain, intestinal permeability, and most conditions associated with inflammation. Additionally, omega-3 fatty acids can help manage oxidative stress, which often goes hand-in-hand with chronic inflammation associated with Hashimoto’s. Research has even shown that compared with the over-the-counter NSAID ibuprofen, omega-3 essential fatty acids could equally reduce arthritic pain, and be a much safer alternative for long-term pain reduction.
  • B Vitamins – Various B vitamins can help with different types of pain. B12 can help neuropathic pain, when taken in high doses of 40 mg/day. Vitamin B6 or the active form, P5P, taken at a dose of 100-200 mg/day, can relieve carpal tunnel syndrome, while B1 (thiamine), at high doses of 600–1800 mg/day, can help with pain from fibromyalgia.

Dietary Triggers

In addition to addressing nutrient depletions to reduce pain associated with Hashimoto’s, many symptoms can be helped by making dietary changes. In May of 2015, I conducted a survey of my readers to find the most helpful interventions for those with Hashitmoto’s. The results showed that many people experienced a reduction in pain by finding and eliminating foods that were causing excess inflammation and contributing to leaky gut.

  • Eliminating Nightshades: In my survey, 62 percent of people reported that removing nightshade vegetables from their diet helped to reduce their pain. Nightshades include: tomatoes, potatoes, bell peppers, eggplants, tomatillos, Goji berries, and the herb ashwagandha. (Note: Even if you’re not in pain, hot, capsaicin-containing peppers have the propensity to cause leaky gut, so they too could potentially contribute to autoimmunity.) I recommend trying a nightshade free diet for two weeks, to see if that makes a difference for you.
  • Low FODMAPs Diet: In my survey, 48 percent of readers saw an improvement in pain by following the low FODMAPs diet. This diet, typically used for irritable bowel syndrome (IBS), reduces the consumption of specific fermentable carbohydrates that can contribute to intestinal distress. For more information about the low FODMAP diet, you can visit the Monash University site, and stay tuned for a new article from me about FODMAPs in the very near future!
  • Autoimmune Paleo Diet: 50 percent of people reported a reduction in pain when following the Autoimmune Paleo (AIP) diet, which removes gluten, dairy, soy, grains, nightshades, legumes, nuts, seeds, and eggs — common food sensitivities for those with Hashimoto’s.
  • Low Oxalate Diet: Oxalates are substances that are found in some foods. They are also waste products made by our bodies, and excreted through our kidneys. Studies have shown that oxalates may contribute to Hashimoto’s. Symptoms of oxalate sensitivity include joint pain, pain in the body, and pain with urination, among others. A low-oxalate diet may provide relief from pain for those who have a sensitivity.

Additional diets that were reported to reduce pain, in my May 2015 survey, include the gluten free diet (47 percent), the grain free diet (43 percent), as well as an egg free diet (40 percent).

Hidden Infections

Another factor for many in overcoming pain can be addressed by treating infections, a common root cause of Hashimoto’s. In 2015, 80 percent of my clients who hit a plateau with nutrition and took the gut tests I recommended, tested positive for at least one gut infection.

The infection I have encountered the most in people with chronic pain and migraines is Helicobacter pylori. When combined with the use of NSAIDs, this infection (most commonly known for causing ulcers) creates a double whammy risk for ulcers. Treating this gut infection helped reduce pain for 50 percent of the people I surveyed. Please see my article on H. pylori for information on how to test for and treat this infection.

Small intestinal bacterial overgrowth (SIBO) is another infection that is common in Hashimoto’s. SIBO is an overgrowth of bacteria in the small intestine that leads to a variety of gastrointestinal symptoms and is often times associated with irritable bowel syndrome (IBS). Treating it helped 51 percent of people in my survey reduce their pain.

Additional infections that I often see in people with Hashimoto’s include Candida (yeast) overgrowth, Blastocystis hominis, and reactivated Epstein-Barr virus. Testing for and treating these infections, which are at the root cause of many cases of Hashimoto’s, may eliminate the pain symptoms that result from them.

Supplements for Pain

While these don’t get to the root cause per se, they may be options that are less likely to cause side effects. In my survey, I also asked my readers to identify some of the most helpful supplements specific to reducing their pain. These were the results:

  • Turmeric – Up to 65 percent of people reported a reduction in pain by taking a curcumin or turmeric supplement. Turmeric has a long history of reducing inflammation, and curcumin (its active component) has anti-inflammatory benefits that can be helpful in down-regulating autoimmune conditions. It has been found to reduce joint inflammation in rheumatoid arthritis, and has therapeutic anti-inflammatory effects for a variety of gastrointestinal conditions, including Crohn’s disease, ulcerative colitis, and irritable bowel syndrome. Adding this spice to your cooking, or adding a curcumin supplement to your regimen, may help relieve a variety of pain symptoms associated with Hashimoto’s.
  • Betaine with pepsin – Another 40 percent of people with Hashimoto’s reported a reduction in pain by assisting their digestion with the use of betaine with pepsin. At first, this caught me a bit off guard, but the more I thought about the mechanism of action, it made perfect sense. Betaine (also known as trimethylglycine) and pepsin (naturally occurring components of gastric juice) break down protein bonds in food, thereby aiding digestion, reducing intestinal inflammation, and even leading to reduced systemic inflammation and less pain for many people. Trimethylglycine (betaine) can also be helpful for breaking down homocysteine, which has been associated with inflammation. Furthermore, it can increase the amount of SAMe, a naturally occurring substance with mood-boosting and pain-relieving properties, within the body.

  • Wobenzym – This systemic enzyme has been shown in studies to significantly decrease the levels of both anti-TPO and anti-TG antibodies in Hashimoto’s patients. Some people have found that this led to a reduction in pain associated with their thyroid symptoms.
  • Neurotransmitterlogical Support – Additional supplements that can be helpful for pain include supplements that support the production of neurotransmitters. Some examples include the supplement GABA, which supports the production of GABA (our “chill” neurotransmitter that helps with muscle relaxation) and 5HTP, which supports serotonin production. (Low serotonin has been a long known potential target for pain relief and pharmaceutical agents, including SSRIs like Paxil.)

Pain Relief Tools and Procedures

In recent years, a few new technologies have emerged that may offer relief from pain without many of the negative side effects associated with conventional therapies. Check with your care provider to see if any of these therapies might be of benefit to you.

  • Cold Laser Therapy: Also known as Low Level Laser Therapy (LLLT), cold laser therapy utilizes specific wavelengths of light to interact with tissue, in order to help accelerate the healing process. It can be used to alleviate a variety of acute and chronic conditions, which can help eliminate pain and inflammation. Cold lasers are handheld devices that are placed over the affected area of the body by a clinician. Non-thermal light that emits from the laser passes through the layers of skin and is absorbed by the body’s cells. When our cells absorb this energy, it is theorized that damaged or injured tissue can be normalized, resulting in reduced pain and an increased rate of healing in the damaged area.
  • Platelet-rich plasma injections (PRP): This therapy utilizes a process in which blood is taken from a patient. The platelets are then removed before being reinjected into the affected site of that same patient, to accelerate the healing of injured tendons, ligaments, muscles, and joints. PRP therapy has emerged in recent years as a promising treatment for chronic pain, and has even been used post-surgery to speed up the healing process. PRP may benefit those suffering from arthritis, sciatic pain, tendonitis, carpal tunnel, and musculoskeletal pain.

Using the Healing Arts to Manage Pain

Getting to the root cause of your pain may take some time and experimentation. There are a number of holistic approaches to pain that can help you manage it while you look for your own triggers. They also provide many therapeutic benefits that make them particularly helpful when you are pursuing whole-body health.

  • Massage Therapy: Of the readers I surveyed, 62 percent found that massage helped their pain. As a bonus, 80 percent found it beneficial for mood as well. In fact, one study asked patients in an acute care hospital setting to rate their pain levels on a scale of 1 to 10, before and after receiving massage therapy. The average rating before therapy was 5.81. After therapy, it dropped to 2.33, with patients also reporting improvements in emotional well-being, relaxation, and their ability to sleep. So if you’re in pain and struggling with depression, I urge you to treat yourself to a massage — pharmacist’s order! (I love in-home massages from Zeel on-demand. Massage therapists show up at your house with a massage table! You can use my personal Zeel invite code, 9qa2, and get $25 off your first Zeel Massage!)
  • Acupuncture: Similar to massage, 61 percent of people experienced pain relief with acupuncture treatments (a form of Chinese medicine in which thin needles are inserted at specific points in the body to remove “energy blockages”). I used to have a huge needle phobia — this is one reason why I went to pharmacy school and not medical or nursing school! However, the needles used in acupuncture are extremely tiny and are barely felt by the patient. In fact, most people report acupuncture to be a relaxing and therapeutic experience. The research supports the use of acupuncture for pain relief, and it is becoming more and more common in the West as an alternative to habit-forming opiates. Results from several studies suggest that acupuncture may help ease chronic pain, such as low-back pain, neck pain, and osteoarthritis pain. It has also been shown to reduce the frequency of tension headaches and prevent migraine headaches.
  • Chiropractic Care: Many people think of chiropractic treatment as “cracking the back” or realigning the spine. However, chiropractic care can take on several different forms, and involves looking at the whole body as an interconnected series of systems that all have an impact on each other. As such, finding alignment in one area of the body may release pain and stiffness in another part of the body. While opinions on the efficacy of chiropractic care vary amongst medical professionals, there is research supporting its use as an effective tool for pain relief. One study conducted at a hospital in the United Kingdom followed 30 patients with chronic low-back pain, for eight weeks. Twelve patients received treatment with medications at a hospital pain clinic, while 18 received chiropractic care. At the end of the eight week trial, the patients who received chiropractic care reported a greater reduction in pain compared to those who had received the standard pain medications.
  • Rolfing: Also known as Structural Integration, rolfing is a form of holistic bodywork that uses hands-on manipulation of the body’s soft tissue to create balance and alignment in the body. It is used to relieve chronic pain, improve posture, and reduce stress. Rolfing focuses on fascia, which is the connective tissue that attaches to all of the muscles and organs of the body. The theory is that by releasing tension in this tissue, whole-body wellness can be achieved. Rolfing is performed by a licensed practitioner and is used for a variety of conditions, including chronic back pain, alignment of the spine, and breathing issues (such as asthma).
  • Physical Therapy: The most well-researched and often prescribed treatment for chronic pain, physical therapy works to treat pain at its source through a variety of exercises and movements, as prescribed by a licensed physical therapist. Therapies that may be used include low-impact aerobic exercise, resistance training, and stretching. Additionally, the therapist may use heat or cold therapy to reduce inflammation, warm up the muscles before exercising, and aid in pain relief.

  • Osteopathic Manipulative Treatment: Osteopathic Manipulative Treatment (OMT) is a set of hands-on techniques used by osteopathic physicians to diagnose, treat, and prevent illness or injury. To use OMT, a practitioner uses stretches, gentle pressure, and resistance to move a patient’s muscles and joints. This form of therapy can help treat arthritis, back pain, headaches, tennis elbow, digestive issues, and postural problems.
  • Craniosacral Therapy: Typically used by osteopaths, chiropractors, and massage therapists, craniosacral therapy uses gentle pressure to manipulate the joints in the cranium or skull, parts of the pelvis, and the spine, to treat illness or injury. The light touch of the practitioner is said to release restrictions in the craniosacral system (which affects the pressure and circulation of the fluid around the brain and spinal cord) to improve the functioning of the central nervous system. This process is thought to relieve pain, and is often used in conjunction with other therapies, such as massage or chiropractic treatments.

I have found that all of these forms of holistic treatment can be helpful for many people with pain related to Hashimoto’s. In fact, I have used acupuncture, chiropractic care, B6 supplementation, and nutrition in the past to help recover completely from a severe case of carpal tunnel.


While there can be many sources of pain for those living with Hashimoto’s, finding your root cause can also bring relief from pain once your triggers have been identified and addressed. For many people, this will come in the form of dietary changes that allow the body to heal. However, there are a variety of natural supplements and healing tactics that can bring relief along the way!

Wherever you are on your healing journey, I want you to be encouraged that you are not limited to a life of pain, nor required to suffer the side effects of addictive medications. There are many natural solutions to pain management that can help you feel better and live your life.

In future articles, I will dive deeper into the common sources of pain for those with Hashimoto’s, to provide you with more information on your road to becoming pain free! In the meantime, I’d love to hear how these recommendations help you manage and treat your pain!

P.S. For continued updates and interaction, please become a part of our Facebook community and sign up for my newsletter to have helpful information delivered right to your email inbox. You’ll also receive occasional updates about new research, resources, giveaways, and more!

Note: Originally published in February 2017, this article has been revised and updated for accuracy and thoroughness.

Hypothyroidism and Arthritis: Understanding the Link

Your thyroid is a butterfly-shaped gland located in your neck, just under your Adam’s apple. Its job: to produce and store hormones that help regulate your metabolism (or the rate at which cells perform their duties). Thyroid hormone helps control how fast your heart beats, how quickly you burn calories, and your body temperature. It also helps keep your brain, muscles, and other organs working as they should. Too little hormone production (called hypothyroidism) slows your body down; too much (or hyperthyroidism) sends it into overdrive.

What does a joint condition like arthritis have to do with this tiny gland? Research has shown people with rheumatoid arthritis (RA) are more likely to develop a thyroid condition such as hypothyroidism. “Estimates suggest between 15 percent and 25 percent of patients with RA will develop thyroid disease sometime during their lifetime,” says Eric Matteson, MD, rheumatologist and professor of medicine at Mayo Clinic in Rochester, Minnesota. In comparison, about 10 percent to 12 percent of adults in the general population develop thyroid disease.

The connection appears to go both ways: People living with autoimmune thyroid disease are also at higher risk for developing rheumatoid arthritis. One study published in the American Journal of Medicine found that about 14 percent of people with Hashimoto’s thyroiditis — a condition in which your immune system attacks your thyroid and often leads to hypothyroidism — had another autoimmune disorder, most commonly RA.

What Exactly Is Hypothyroidism?

This condition occurs when your thyroid gland is underactive, which means that it can’t make enough thyroid hormone to keep your body running normally. You have hypothyroidism if you have little thyroid hormone in your blood. When cells can’t get enough of this hormone, the body’s processes slow down.

“Thyroid hormone is a necessary hormone, thus a dysregulation for thyroid hormone changes the whole body,” says Alexa Simon Meara, MD, assistant professor in the division of immunology and rheumatology at The Ohio State University Wexner Medical Center. Signs of hypothyroidism vary, depending on the severity of the hormone deficiency. Symptoms tend to develop slowly, often over several years, and may include:

  • Fatigue
  • Increased sensitivity or intolerance to cold
  • Weight gain
  • Dry skin and hair
  • Constipation
  • Puffy face
  • Muscle aches
  • Forgetfulness
  • Depression
  • Enlarged thyroid gland (goiter)

What Causes Hypothyroidism?

The most common cause of hypothyroidism is the autoimmune disease Hashimoto’s thyroiditis. In this disorder, the immune system mistakenly targets and damages the thyroid, causing inflammation and leading to an underactive thyroid.

Other causes of hypothyroidism include thyroid surgery, radiation therapy to treat certain cancers, thyroiditis (or inflammation of the thyroid gland), and certain medications.

Why Do Rheumatoid Arthritis and Hypothyroidism Often Coexist?

While the link between the two conditions isn’t fully understood, experts do know that having one autoimmune disease raises your risk of developing another. “Patients with rheumatoid arthritis are more likely to develop any number of other autoimmune conditions, including autoimmune thyroid dysfunction,” says Dr. Matteson. “The link relates to the systemic abnormal response of the immune system leading to involvement of other organ systems.”

Another potential connection: There may be shared genetic predispositions to both RA and autoimmune thyroid disease, adds Dr. Matteson.

Does Hypothyroidism Cause Joint Pain?

It can, according to the Mayo Clinic. Hypothyroidism may lead to joint pain and stiffness, as well as muscle aches and tenderness particularly in the shoulders and hips. In RA, however, swelling occurs in affected joints, while hypothyroidism can cause swelling of the soft tissue in the hands, arms, legs and feet, and even puffiness in the face in some people, explains Dr. Matteson.

Both RA and hypothyroidism can also cause carpel tunnel syndrome, a condition that causes numbness, tingling, and other symptoms in the hand and arm.

Increased Cardiovascular Risk for Rheumatoid Arthritis and Hypothyroidism

Just having RA means your heart attack risk is as much as 68 percent higher than it is for someone without RA. An underactive thyroid can further contribute to heart disease risk because it may cause a slow heart rate, a rise in cholesterol, an increase in fluid around the heart, and heart failure.

Research suggests having the two conditions together may drive up cardiovascular risk. According to Dutch research, women with inflammatory arthritis and hypothyroidism had more than three times the risk for cardiovascular disease, compared to people who didn’t have either condition.

How Is Hypothyroidism Diagnosed?

With well-controlled RA, your doctor may suspect thyroid disease if you have unusual swelling in your hands, arms, legs and feet, or even unusual fatigue and weight gain, says Dr. Matteson. “Thyroid tests will help to sort this out,” he says.

Hypothyroidism is diagnosed with a physical exam for symptoms and results from a blood test that measures the levels of thyroid-stimulating hormone (TSH). An abnormally high TSH means hypothyroidism. It indicates the thyroid gland is being asked to make more of the hormone thyroxine (T4) because there isn’t enough T4 in the blood.

Sometimes doctors may run another blood test to measure T4 levels, if needed.

How Is Hypothyroidism Treated if You Have RA?

Hypothyroidism is treated the same whether or not you have RA, explains Dr. Meara. The goal is to get thyroid hormone back to normal levels. It’s also important to continue to manage your RA and keep it under good control to help manage symptoms and for your overall health.

Hypothyroidism can’t be cured, but in most cases, it can be completely controlled. Standard treatment involves a daily dose of the synthetic thyroid hormone levothyroxine (Levo-T, Synthroid). It comes in pill form, works just like your own body’s thyroid hormone, and helps bring hormones back to normal levels, thus reversing hypothyroid symptoms.

“Medications used to replace thyroid hormone do not interfere with RA medications,” adds Dr. Matteson. Your doctor will determine the best dose initially and over time.

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Hashimoto’s Disease

The thyroid gland is a butterfly-shaped gland located in the front of the neck. The thyroid gland produces two hormones that control metabolism (how the body turns food into energy) and keep the body working properly.

What is Hashimoto’s disease?

Hashimoto’s disease is a disease that affects the thyroid gland. It is also called Hashimoto’s thyroiditis, chronic lymphocytic thyroiditis, or autoimmune thyroiditis.

What causes Hashimoto’s disease?

Hashimoto’s disease is an autoimmune disease, which means the body’s immune system is attacking its own cells and organs. Normally, the immune system protects the body against infections caused by bacteria, viruses, and other harmful substances. In Hashimoto’s disease, the immune system makes antibodies that attack and damage the thyroid. As a result, the thyroid gland becomes inflamed and hypothyroidism can develop.

What is hypothyroidism?

Hypothyroidism is a disorder that occurs when the thyroid gland doesn’t make enough thyroid hormones to meet the body’s needs. The thyroid gland isn’t making enough hormones because the body’s immune system has attacked and damaged it.

Thyroid hormones regulate metabolism, which is how the body turns food into energy. Without an adequate amount of energy, the body cannot operate normally and the body’s functions begin to slow down.

Hashimoto’s disease is the most common cause of hypothyroidism in the United States.

What are the symptoms of Hashimoto’s disease?

Some patients may not have any symptoms at first. As the disease slowly progresses, the thyroid gland will become enlarged (a condition called goiter), creating a feeling of fullness in the throat. Goiter is often the first sign of Hashimoto’s disease. Other symptoms that develop over time include:

  • Tiredness (fatigue)
  • Weight gain
  • Feeling cold
  • Joint stiffness and muscle pain
  • Constipation
  • Depression
  • Puffy eyes/face
  • Dry skin
  • Thinning hair/hair loss
  • Heavy or irregular periods
  • Difficulty becoming pregnant
  • Memory problems/difficulty thinking or concentrating
  • Slow heart beat

What are the risk factors for developing Hashimoto’s disease?

Hashimoto’s disease:

  • Is more common in women than men.
  • Commonly appears between the ages of 30 and 50.
  • Tends to run in families (appears to be a heredity link).
  • Is more likely to develop in people who have other autoimmune diseases. For example, certain liver conditions, B12 deficiency, gluten sensitivity, rheumatoid arthritis, type 1 diabetes, Lupus, and Addison’s disease (an adrenal gland condition).

Consuming too much iodine can trigger hypothyroidism in patients who have Hashimoto’s disease but don’t have any symptoms of the disease. High iodine levels could be obtained by consuming iodine-containing supplements or eating large quantities of iodine-containing foods, such as kelp and seaweed.

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Does this patient have thyroid syndrome?

Thyroid disease can be accompanied by a variety of musculoskeletal manifestations ranging from early growth defects during infancy to adult manifestations including myalgias, arthralgias, myopathy, acropachy and frank arthritis.

Musculoskeletal manifestations are most pronounced in extreme states of thyroid dysfunction. A thorough history is essential in evaluating thyroid disease, including medical co-morbidities, radiation exposure, surgeries, family history and medications.


In hypothyroidism, often other non-musculoskeletal manifestations dominate the clinical presentation including fatigue, cold intolerance, constipation, memory/concentration issues, menorrhagia, infertility, weight gain, coarse and brittle hair.

Cretinism, or congenital deficiency of thyroid hormone at birth, is a common treatable birth defect. At birth there rarely are any physical findings. This is due to partial placental transfer of maternal thyroid hormone. The physical exam findings are first seen after the first few weeks of infancy, when maternal hormones are lost. Without treatment; pallor, lethargy, slow movement, feeding problems, constipation, macroglossia, umbilical hernia, enlarged fontanels, hypotonia, dry skin, hypothermia and prolonged jaundice can occur. There is an increased risk of cardiac, renal, urinary tract, and gastrointestinal malformations in utero.

The musculoskeletal effects of cretinism include delays in ossification at the epiphyseal centers. Multiple foci of ossification occur causing growth stunting, bone deformity, and kyphosis predominantly at the thoraco-lumbar junction.

In adults, there are diverse musculoskeletal symptoms resulting from the hypothyroid state. Features include muscle weakness, arthralgias, arthritis, myalgias with and without elevations in creatinine phosphokinases, carpal tunnel syndrome, erosive osteoarthritis, and crystal induced arthritis.

Hypothyroid arthropathy most commonly affects the knees, metacarpophalangeal (MCP) joints, proximal interphalangeal (PIP) joints, metatarsal phalangeal (MTP) joints and wrists. On exam, tenderness, synovial thickening and joint effusions can be present. The joint effusions can be be large and characteristically lack erythema or warmth, unless secondary disease processes are present.

Synovial fluid analysis is characterized as non-inflammatory, with normal protein and cell counts. There is increased hyaluronic acid concentration in the synovial fluid producing the characteristic highly viscous synovium with a strongly positive “string test”.

Neuromuscular symptoms are common in hypothyroidism, estimated to occur in 30-80% with overt disease. The symptoms include weakness, cramping, myalgias, diminished reflexes and myoedema. Symptoms can occur any time during the course.

Weakness is the most common phenomena. Creatine kinase (CK) can be elevated and is associated with a prolonged ankle jerk reflex and muscle enlargement. Cramping can be severe, and myalgias worse after exertion. Electromyography (EMG) and muscle biopsy can be used for further characterization.

Myoedema is the phenomenon of mounding of the muscle tissue after light percussion lasting 30-60 seconds. It is not specific to hypothroidism and is thought to be due to sustained contraction due to decreased calcium uptake from sarcoplasmic reticulum. There is no EMG correlate for myoedema. Reflexes can have prolonged relaxation time, noted to be best seen at the Achilles tendon.

Hoffman’s syndrome, characterized by weakness, cramping and muscular enlargement is a rare complication, and often is accompanied by elevated creatinine phosphokinase. Similarly, in children with cretinism, Kocher-Debre-Semelainge syndrome can occur, characterized by diffuse muscle hypertrophy and proximal muscle weakness.

Carpal tunnel syndrome has been described in case reports to occur frequently in myxedema.

A polymyositis like syndrome due to hypothyroidism, with slowly progressive symmetric proximal muscle weakness at the shoulder and hip girdle has been frequently described, with elevated creatinine phosphokinase and modest elevations in erythrocyte sedimentation rate. The symptoms and myopathy respond rapidly to thyroid replacement.

Statin use can potentiate the musculoskeletal effects of hypothyroidism even in patients on thyroid replacement therapy. Complications include rhabdomyolysis as most statins (except for pravastatin and fluvastatin) are metabolized via the hepatic CYP3A4 system and can accelerate the catabolism of Levo-thyroxine, leading to unexpected hypothyroidism.

Sleep is affected in hypothyroidism and polysomnography performed in hypothyroid patients reveal decreased stage 3 and 4 sleep. This result is similar to findings seen in fibromyalgia.


In hyperthyroid states, non-musculoskeletal features often dominate the clinical presentation. The symptoms include heat intolerance, onycholysis, hair thinning, dermopathy, ophthalmopathy, tachycardia, dyspnea, urinary frequency, psychosis, depression, and in the elderly, apathy. Musculoskeletal symptoms include myopathy, adhesive capsulitis, myxedema, acropachy, and osteoporosis

In hyperthyroidism osteopenia and osteoporosis are the most common complications. Failure to recognize a declining need for thyroid replacement in the elderly is a preventable cause of iatrogenic hyperthyroidism. Bone density can improve after the correction of the hyperthyroid state, although often incompletely. In contrast, osteoporosis and osteopenia is not a complication of hypothyroidism.

In hyperthyroidism, mild proximal muscle stiffness and weakness including the bulbar muscles can occur. Myopathy and loss of muscle mass is a severe complication.

Thyrotoxic periodic paralysis is an extremely rare condition associated hyperthyroid myopathy, characterized by rapidly progressive paralysis of the proximal legs. It is due to intracellular potassium shifts.

Thyroid ophthalmopathy occurs in the setting of Graves’ disease, with symptoms of lid lag, lid retraction, proptosis, corneal irritation and diplopia. If severe, damage to the cornea and optic nerve can lead to permanent vision loss. It is due to an inflammatory infiltrate and enlargement of the ocular muscules is caused by mucopolysaccharide deposition.

Pretibial myxedema is a syndrome of painless nodules varying in size and color from pink to purple can occur in hyperthyroid states. The lesions can have a shiny, purple to pink appearance and can mimic erythema nodosum, scleroderma or morphea. It is due to increased hyaluronic acid in the skin.

Thyroid acropachy is a rare extreme complication of Graves’ disease characterized by insidious onset of swelling at the fingers and toes with digital clubbing. It is painful and can occur after the euthyroid state is achieved. Thyroid acropachy is strongly associated with Graves ophthalmopathy (1%) are pretibial myxedema (4%) and tobacco use.

Adhesive capsulitis is frequently described in the hyperthyroid state. It is often insidious in onset and responds poorly to standard therapy.

There is conflicting evidence that calcium pyrophosphate deposition disease (Pseudogout), is associated with hypothyroidism. Chondrocalcinosis on knee radiographs and calcium pyrophosphate crystals from synovial fluid samples have been reported to occur more frequently although the association with pseudogout has not been consistently reproduced.

Purine metabolism is impaired in thyroid disorders, with an increased incidence of hyperuricemia seen in both hypothyroid and hyperthyroid states. Uric acid levels have been shown to normalize after achievement of the euthyroid state. The incidence of gout is is higher in hypothyroid patients compared to age matched controls.

Differential diagnosis

The differential diagnosis is often case specific due the variety of musculoskeletal presentations. In hand arthropathy, erosive osteoarthritis, rheumatoid arthritis and all inflammatory small joint arthritides should be considered. At the larger joints, such as hips, osteoarthritis, aseptic necrosis, and inflammatory arthritides can mimic the presentation. Additionally, atypical infections such as tuberculosis, sarcoidosis, and malignancy should remain on the differential. The differential for the neuromuscular manifestations include polymyositis, rhabdomyolysis, carpal tunnel syndrome, polymyalgia rheumatica, muscular dystrophy, other causes of myopathy, myasthenia gravis, and motor neuron diseases.

What tests to perform?

Lab Testing

The initial step is to screen with thyroid-stimulating hormone (TSH) and free thyroxine (T4).

To evaluate the various differential diagnoses, Inflammatory markers should be ordered including erythrocyte sedimentation rate (ESR) and C-reactive protein (CRP).

Further evaluation based on history, exam and imaging results could include rheumatoid factor and antinuclear antibodies (ANA). Secondary causes for calcium pyrophosphate deposition disease (CPPD) should be investigated if present, including parathyroid hormone (hyperparathyroidism), calcium, magnesium, and hemochromatosis screening (liver function testing including AST, ALT, transferrin saturation and ferritin).


Initial imaging includes radiographs of the affected joint. Small joints can show periarticular calcific deposits and central erosions of the articular surfaces, predominantly at the MCP and PIP which can mimic erosive osteoarthritis (EOA). Destructive lesions of the tibial plateau similar to compression fractures have been described, possibly due to epiphyseal dysgenesis or aseptic necrosis.

Wormian bones, named after Danish anatomist Ole Worm, are accessory sutures seen within the skull, most often at the lambdoid suture, and are associated with hypothyroidism. It is considered pathologic when there are greater than 10 accessory bones or if they become large. Wormian bones are a normal variant seen in the general population, more frequently in the Asian population.

Imaging findings with thyroid acropachy include periosteal bone formation, described as spiculated or lacy in appearance at the metacarpals, proximal, middle phalanges of the hand and the metatarsals and proximal phalanges of the toes.

Magnetic resonance imaging (MRI) can be further used to evaluate structural damage. Bone scans are useful in thyroid acropachy, showing increased uptake which may predate radiograph findings. Both MRI and bone scans are not routinely used in evaluation.

In cretinism, long bone radiographs will reveal multiple foci of ossification resulting in a stippled appearance of bone referred to as epiphyseal dysgenesis.

In children, delayed bone age and delays in skeletal maturation can cause short stature and dwarfism. Secondary ossification centers are delayed and slipped femoral capital epiphysis is a common complication.

Electromyogram (EMG) can distinguish hypothyroid associated myopathy from other eitiologies, with EMG correlates including myopathic motor units with hyperirritability and increased polyphasic potentials.


Muscle biopsy is useful in long standing hypothyroidism to differentiate inflammatory myositis, showing Type 1 and 2 fiber atrophy, hypertrophy and myofiber necrosis.

How should patients with thyroid syndromes be managed?

  • Treatment involves achieving the euthyroid state. In hypothyroidism, this is commonly achieved with hormone replacement therapy. Replacement levo-thyroxine should be taken on an empty stomach with water in the AM. It is recommended to wait at least 1/2 hour prior to eating.

  • In primary hyperthyroidism, radioactive iodine ablation, medication therapy such as methimazole and propylthiouracil, or surgery are common modalities. Referral to an endocrinologist is recommended. Patients generally recover well with treatment at both extremes.

  • Osteoporosis associated with hyperthyroidism requires treatment to achieve the euthyroid state. Additional treatment with bisphosphonates based on FRAX guidelines is recommended. Calcium and vitamin D supplementation when appropriate is recommended. Bone density should be checked every 2 years and often improves with the correction to the euthyroid state.

  • Treatment of thyroid acropachy often requires systemic corticosteroids for joint manifestations. Tobacco cessation is recommended. In ophthalmopathy, corneal drying and ulceration must be prevented ocular lubricants. Orbital decompression can be used in severe cases.

  • Beta-blockade in hyperthyroid myopathy may assist in muscle function.

What happens to patients with thyroid syndromes?

Natural history and epidemiology

The incidence and prevalence of thyroid related musculoskeletal disease has not been established.

  • It is estimated that 1/3 of the world’s population live in areas of iodine deficiency, defined as having a daily intake of iodine less than 50μg. When the intake falls to less than 25μg per day, congenital hypothyroidism is encountered. In the iodine replete countries, most thyroid disorders have an autoimmune basis, ranging from Hashimoto’s thyroiditis to thyrotoxicosis caused by Graves’ disease. The prevalence of thyroid disease is different between ethnic groups and estimated to be approximately 8% of the US population. Additionally, up to 5% of the population are estimated to have undiagnosed disease.

  • Hypothyroidism, as defined solely by laboratory findings due to the variable clinical presentation, includes elevated serum TSH greater than 3.89mIU/L (controversial due to age discrepancies, accepted values range from 3-6 mIU/L) and low serum free Thyroxine (T4). In iodine replete communities, the prevalence of spontaneous hypothyroidism is estimated between 1-2%, and is 5-10 times more common in females than in men. The mean annual incidence is estimated at 3.6/1000 women and 0.6/1000 males. The most common cause of thyroid disease is due to goiter. The incidence of thyroid cancer, a less common cause of thyroid dysfunction, is estimated at 3.5/100,000 women and 1.3/100,000 men.

  • Congenital hypothyroidism affects approximately 1/4000 births and is the most treatable cause of mental retardation. In iodine replete communities, congenital hypothyroidism is due to developmental defects of the gland. There is a higher incidence seen in Trisomy 21. Newborn thyroid screening is mandated in all US states.

  • Subclinical hypothyroidism is defined as elevated TSH and normal free Thyroxine (T4). The estimated prevalence of subclinical hypothyroidism ranges from 4-10% of the population, with a higher frequency in elderly females.

  • In hypothyroidism, 95% is considered primary, due to direct or antibody mediated destruction of the thyroid gland. There are two forms of destruction – goitrous and atrophic. These differ in the extent of lymphocytic infiltration, fibrosis, and follicular cell hyperplasia. Secondary and tertiary causes are due to pituitary and hypothalamic defects, respectively.

  • Hyperthyroidism is defined as a serum TSH concentration less than 0.1mIU/L and a serum total of T4 greater than 170nmol/l. Hyperthyroidism is estimated to occur in 0.5-2% of the population and is estimated to be 10 times more common in women than men in iodine replete communities. Graves disease is the most common etiology, followed by toxic multinodular goiter.

  • Autoimmune thyroid disease can be caused by multiple autoantibodies. All thyroid antibodies can be seen in all forms of autoimmune thyroid disease, in varying degrees of specificity. This includes anti-thyrotropin receptor antibodies, which are seen in 80-95% of Graves’ disease and 10-20% of autoimmune thyroiditis. Anti-thryroglobulinantibodies, seen in 5-20% of the healthy population, and found in 50-70% of Graves’ disease, and 80-90% of autoimmune thyroiditis. Anti-thyroid peroxidase antibodies are estimated to occur in 8-27% of the healthy population, 50-80% of Graves’ disease, and 90-100% of the autoimmune thyroiditis. Both anti-thyroglobulin and anti-thyroitropin antibodies are seen in varying degrees in relatives with autoimmune thyroiditis, reinforcing a genetic predisposition for antibody development.

  • Bone remodeling consists of cycles of activation and resorption lasting approximately 210 days. In hypothyroidism there is a lengthened bone remodeling cycle, of up to 700 days. Osteoporosis is rare due to prolonged bone formation and decreased active resorption. This can be estimated by measuring bone markers including alkaline phosphatase, osteocalcin activity, and urinary excretion of calcium, all of which would be reduced..

  • In hyperthyroidism, osteopenia and osteoporosis is common, due to the shortened bone remodeling phase, with excessive bone remodeling and subsequent reduced bone density. Histological changes include increased turnover in trabecular bone, increased remodeling and porosity in cortical bone with increased osteoclastic activity.

  • There is debate whether exogenous levothyroxine or low circulating thyroid stimulating hormone is an independent risk factor for development of osteoporosis. When thyroid supplementation is given in suppressive doses (i.e.. during thyroid cancer treatment) with a target thyroid stimulating hormone less than 0.4mU/L, there is an increased risk of osteoporosis and fracture. When given at doses for physiological maintenance, there has not been an observed increase of risk for bone disease.

  • Associated rheumatic conditions include an increased incidence of positive ANAs in patients with autoimmune thyroid disease. Many have Anti-DS DNA Ab. In cross sectional analysis, there is an increased prevalence and relative risk in developing systemic lupus erythematosus (SLE) and rheumatoid arthritis (RA) in patients with Graves’ disease and/or Hashimoto’s thyroiditis.

  • Psoriatic arthritis and limited scleroderma both have an observed increased incidence with thyroid peroxidase Ab positivity.

  • Scleroderma can directly induce hypothyroidism due to fibrosis of the gland.

  • SLE patients with thyroid disease have an increased risk of preterm delivery.

  • TNF-alpha receptors are found in thyroid follicular cells. In Graves’ disease serum levels of TNF-alpha are elevated. In a small study of hyperthyroid patients, achievement of the euthyroid state led to normalization of TNF-alpha levels. The same was not observed in hypothyroid patients.

Pharmacologic considerations
  • There are numerous medications used in thyroid and rheumatic diseases that have unintentional adverse crossover effects. Propylthiouracil has been shown to be the culprit for ANCA-positive drug-induced vasculitis. Methimazole can cause SLE-like syndromes. Aspirin and non steroidal anti-inflammatory drugs (NSAIDS ) lower serum total thyroid hormone by interfering with binding proteins. Glucocorticoids inhibit TSH secretion and reduces serum thyroid hormone concentrations.

What is the evidence?

Bland, JH, Frymoyer, JW, Newberg, AH. “Rheumatic Syndromes of Endocrine Disease”. Seminars in Arthritis and Rheumatism. vol. 9. 1979. (A review of rheumatologic diseases associated with the endocrinopathies)

McLean, RM, Podell, DN. “Bone and Joint Manifestations of Hypothyroidism”. Seminars in Arthritis and Rheumatism. vol. 24. 1995. pp. 282-290. (In depth review of the rheumatic manifestations of thyroid disease)

Vanderpump, MP. “The Epidemiology of Thyroid Disease”. British Medical Bulletin. vol. 99. 2011. pp. 39-51. (A review on the epidemiology of thyroid disorders including incidence and prevalence, from data taken from multiple studies from the US and Europe)

Boelaert, K, Newby, PR, Simmonds, MJ. “Prevalence and relative risk of other autoimmune disease in subjects with autoimmune thyroid disease”. The American Journal of Medicine. vol. 123. 2010. pp. 183.e1-183.e9. (A cross sectional multicenter study of patients with Graves’ disease or Hashimoto’s thyroiditis and the prevalence of coexisting autoimmune disorders)

Schumacher, RH, Dorwart, BB. “Joint effusions, chondrocalcinosis and other rheumatic manifestations in hypothyroidism”. The American Journal of Medicine. vol. 59. 1975. pp. 780-798. (Small study of 12 patients evaluating the clinical and histological findings of joint effusions)

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