By Kim Crawford, M.D.
Last updated: April 7, 2021
Before we start discussing Hashimoto’s thyroiditis, let’s just touch on the traditional treatment you are probably getting. You are not on a special diet to heal or protect your gut. You have elevated antibodies and are told “don’t worry about them.” You are simply placed on a synthetic version of T4, not a combination of the inactive T4 and the active T3, tailored to your physiology. You are told that your thyroid will “just burn out” if you aren’t yet on thyroid replacement, and that, at that point, you will be treated with synthetic T4. There are many disease processes; notably autoimmune diseases, where the traditional medicine I used to practice really seems dead wrong. One of these instances is Hashimoto’s thyroiditis treatment. You’ll see why after you read this article.
Introduction
Hashimoto Thyroid Disease, AKA Hashimoto’s thyroiditis, is the most common autoimmune disorder in the U.S., affecting between seven and eight percent of the population. While not all people with Hashimoto’s have hypothyroid symptoms, thyroid antibodies are a marker for future thyroid disease. When we talk about hyperthyroidism vs. hypothyroidism, the majority of “Hashi’s” patients are diagnosed after TPO antibodies have destroyed enough of their thyroid gland, so they have low (hypo) thyroid function. Hypothyroidism is characterized by weight gain, loss of the outer 1/3 of the eyebrows, brain fog, dry skin, fatigue, constipation and more. The sad state of medical treatment is such that doctors fail to treat the autoimmune disease and then, simply replace the lost thyroid hormone with synthetic hormones. Standard treatment fails to address many concerns including the underlying cause or the necessary Hashimoto diet. In this article, I’ll discuss Hashimoto Thyroid Disease and treatment including:
Necessary Laboratory Tests
I (personally) find it shocking that the new patients I see who tell me they have “thyroid issues” have never had proper bloodwork done. It’s not hard to order the correct tests, and now I’m going to teach you what to ask your doctor to order. To begin, start with the “usual and customary labwork” including a complete blood count, liver and kidney function tests, a complete chemistry profile, urine analysis and so on. Then for the thyroid specifics, here’s what you want to have done.
Ask your your doctor to order a TSH, a Free T3, Free T4, CRP, r (reverse) T3, TPO antibodies, and anti-thyroglobulin antibodies. Rarely are TSH-stimulation blocking antibody (TSBAb) positive but get those done, too. TPO antibodies are much more apt to be the positive antibodies you find in Hashimoto’s thyroiditis, but why not be thorough? Reverse T3 is a test that has been criticized as being “useless” by Endocrinologists who all tend to ignore an elevated rT3. What is rT3? It’s a metabolite of the inactive form of thyroid hormone- T4. The problem with an elevated rT3 level, is that it means it is clogging up the actual T3 receptor sites. When the receptor sites are clogged, the converted and functional Free T3 cannot bind to the receptors and you are therefore “functionally hypothyroid.” Let’s discuss what that means.
If your lab work shows a high reverse T3 level- you are converting most of your T4 into reverse T3. Reverse T3 is simply an isomer of T3. If you recall-Free T3 is the active form of thyroid hormone and it is converted from T4 as needed by two enzymes called deiodinases. The problem with rT3 is that it binds to T3 receptors but it has no metabolic activity-meaning-high rT3 levels can give you signs of being hypothyroid even though your Free T4 and Free T3 are the “normal range”.
Medical issues that will results in increased rT3 levels are any sort of severe illness, starvation, excessive nutritional deficiencies and high cortisol levels-generally caused by stress. This is why you have likely heard that adrenal and thyroid function are linked. Those with adrenal fatigue or adrenal stress tend to be functionally hypothyroid. It is also more common in hypothyroid patients who have SIBO-more to come on this topic. rT3 obviously will then slow down metabolism and is therefore theorized to aid in survival. A quick fun fact: hibernating bears have high rT3 levels.
We treat high rT3 with T3 for 2 or 3 months. The negative feedback to the pituitary slows down the production of T4- that then slows the production of rT3.
Most physicians don’t analyze why they often see a normal Free T4 and a sub-par Free T3 on a typical patient’s lab work. Here’s the answer: for proper enzymatic (deiodinase) function, these enzymes require quite a few minerals for optimal function. While most people think of iodine and some are aware of selenium as being important for thyroid function, I’ll bet you didn’t know that you also need zinc, molybdenum, boron, copper, chromium, manganese, and the proper balance of calcium and magnesium, did you? Well, neither do your doctors! They also don’t know about the iodine to selenium balance that needs to occur, which we’ll discuss in the next section.
Endocrinologists continue to use the typical thyroid replacement—a synthetic hormone: Levothyroxine (Synthroid). However, if you don’t have a “high enough” Free T3 which is defined as being more than 2.9 pg/ml, you are going to be clinically hypothyroid. And this a totally separate issue from having a high rT3. Now let’s get into the selenium/iodine issue.
Selenium (not iodine!) deficiency is one of the main reasons for clinical hypothyroidism. It’s crucial for the production of thyroxine (T4). It is also needed for the deiodinase to convert T4 to the active T3. But, there’s more: a total of 11 selenium-dependent enzymes have been identified as necessary for thyroid function. If you take iodine without selenium, you can cause selenium deficiency. Conversely; if you take selenium without iodine, you can cause iodine deficiency. Since all regular salt is iodized, you are much more likely to have selenium deficiency if you use iodized salt. Use Himalayan pink salt instead, and it will be less likely to contain plastics, too.
The current recommended dietary intake of selenium in adults is between 55 and 75 mcg daily. Foods rich in selenium are brazil nuts, mushrooms, oysters, most types of meat, and sunflower seeds.
Many people are under the impression that too little iodine is the issue when it comes to any type of thyroid disease. This probably dates back to the days when “goiter” was linked to the lack of iodine; hence the subsequent iodization of our salt supply. However, our national over-consumption of iodized salt now usually causes the opposite problem. Many clinical (epidemiologic) studies demonstrate the presence of more autoimmune hypothyroidism in iodine-replete demographic areas than in iodine-deficient areas.
A number of studies even indicate that mild or moderate iodine excess (meaning a urinary iodine excretion of 220µg per 24 hours) is associated with hypothyroidism. To make matters worse, other studies show that low-dose iodine supplementation may even be associated with increased thyroid autoimmunity. Regardless of the “mechanism”, now will you ditch the iodized salt shaker in exchange for some pink Himalayan salt?
Conventional medicine simply does not have safe, effective treatments for any autoimmune disease. In fact, steroids and even more toxic drugs such as “biologics” are often used to suppress the immune system. If you have Hashimoto’s, it’s even worse, as the autoimmune condition is left to simmer like a boiling pot on a stove. Let me explain.
If you have elevated-let’s say- TPO antibodies, it means your thyroid gland is under attack. Often, the CRP (a biomarker for inflammation) is elevated. If you don’t address (and then lower) these antibodies being made, the thyroid gland will continue to be under attack, and systemic inflammation will continue. Symptoms such as fatigue, sleep disruptions, hair loss, dry skin and more will just continue until the thyroid gland is burned out, at which point you will be deemed “hypothyroid” and placed on thyroid hormone for life. But there’s even more to this story of autoantibodies and inflammation.
All autoimmune disease starts with leaky gut: we’ll cover this topic next. Anyway, since Hashimoto’s thyroiditis also starts with leaky gut, causing systemic inflammation, if you don’t repair the gut, you can’t reduce the antibodies. You’ll also need to change your diet to reduce the antibodies. Here’s why. It is clear that there is thyroid gland tissue and gluten biomimicry—and there are likely also IGG food allergies to things like milk, grains, eggs, and more. Therefore, to get rid of “possible food offenders” and start getting antibody levels and inflammation down, you need to eat an “autoimmune protocol diet” (phase 1-a bit strict) while your gut is healing: the first two months of treatment. A benefit most people love is that they effortlessly drop some unwanted pounds.
Leaky gut (AKA gut hyper-permeability syndrome) is an extremely common condition. It can be caused by antibiotics, anti-inflammatory medications, antibiotics, stress (leading to high cortisol which wrecks your gut and brain), mold and mycotoxins or just “typical American food.” If you have leaky gut, you may or may not have gastrointestinal symptoms. If you are already hypothyroid from your Hashimoto’s thyroiditis you will probably be constipated and possibly have some bloating after meals.
Getting you into remission from any autoimmune disease starts with fixing your leaky gut. Changing your diet to my autoimmune diet is the first step towards healing your gut and reducing your auto-antibody production. Functional doctors use gut-healing peptides and supplements such as collagen powder and l-glutamine. Vitamin D levels need to be normalized, and sporulating probiotics with their “fertilizer”-prebiotics, should be added when the symptoms start to subside. We’ll discuss all of this in upcoming sections.
As you heal your gut over two months, your (probable) food sensitivities and, therefore, your bloating will diminish. If it doesn’t, it often means you have SIBO, which is quite common in those diagnosed with Hashimoto’s thyroiditis.
First, let’s posit that a fair number of those diagnosed with Hashimoto’s thyroiditis have actual or functional hypothyroidism. Since gut motility decreases when someone is hypothyroid, constipation is a common symptom of Hashimoto’s. This constipation, decreased gut motility, as well as the leaky gut, often leads to small intestinal bacterial overgrowth (SIBO.) Small intestinal bacterial overgrowth is an increased number and/or abnormal type of bacteria growing in the small intestine section called the jejunum, a part of the bowel that is supposed to be sterile. It’s estimated in numerous studies that a minimum of half of those with Hashimoto’s have untreated SIBO.
The symptoms of SIBO symptoms are often confused with those of other GI disorders. The most common symptoms are bloating and flatulence and bloating after meals. Other symptoms include abdominal discomfort, constipation; but often- diarrhea, too. This causes many patients to be labelled as having irritable bowel syndrome and never having their symptoms clear up. Multiple food intolerances are also common. If symptoms are mild, they are often “blamed” on the hypothyroid state. Those with SIBO are more likely to have T4 to rT3 conversion issues, causing even more gut issues.
To diagnose this condition, the lactulose hydrogen breath test (LHBT) is often used. However, because breath tests are not very sensitive or specific (up to 60% false negatives), many experienced Functional doctors will treat a patient if they exhibit classic symptoms associated with typical underlying conditions.
Treatment in the non-Functional GI world is typically a long course of Rifaximin-an antibiotic which is not absorbed by the gut. Herbal therapies are at least as effective as rifaximin for curing small intestinal bacterial overgrowth in comparison clinical trials. Some effective herbals include oregano oil, barberry, berberine, olive leaf extract, and wormwood.
The Hashimoto Diet
You can actually get creative with this limited list. As mentioned, you’ll drop the pounds you wanted to lose while you’re at it. You’ll feel great on this diet which is naturally the most anti-inflammatory diet you can eat. To help you: there are many social media groups, pages and websites that contain creative recipes. If you’re my patient, I’ll be communicating with you about your food preferences, and sending you links for food services, alternative bakeries and so on. I’ll help you transition to month 3, 4 and onward, adding as many foods as your Hashi’s can tolerate.
There is firm evidence of a correlation between Vitamin D deficiency and several autoimmune diseases. Notably examples include systemic lupus erythematosus, multiple sclerosis, mixed connective tissue disease, rheumatoid arthritis, type 1 diabetes mellitus, celiac disease, and more.
In general, Vitamin D tends to activate the innate immune response and to regulate the adaptive immune response. This improved adaptive immune response, in the presence of higher levels of vitamin D appears to hold true in autoimmune thyroid disease as well.
Most data on Vitamin D and autoimmune thyroid diseases have come from cross-sectional studies and tend to support the existence of an association. There is additional evidence supporting a relationship between vitamin D and Hashimoto’s thyroiditis in particular. Approximately ten recent studies identify lower 25(OH)D levels in individuals with Hashimoto’s thyroiditis versus control subjects, with a tendency for a higher prevalence of (vitamin D) deficiency in patients with hypothyroidism than those with normal thyroid function tests.
The relationship with antibody titers is characterized by more inconsistent data.
Vitamin D may also affect disease manifestations. There have been several reports of a significant correlation between mild cognitive impairment and 25(OH)D deficiency in adult patients with Hashimoto’s thyroiditis. This complication will be covered in the last section of this article.
Approximately one third of patients with Ulcerative colitis or Crohn’s disease are resistant to all currently available “drug” pharmaceuticals, or they relapse over time. Therefore, when the doctor who first realized that LDN (low dose naltrexone) was helping his patients with multiple sclerosis, he turned the researchers of IBD onto the concept of looking closely at LDN. And, indeed the studies have been remarkable for inflammatory bowel disease and a host of other autoimmune disorders. It works by increasing endorphin levels, secreted by the posterior pituitary gland, and by yet another mechanism which also bolsters the part of the immune system responsible for autoimmunity.
There have been a paucity of controlled, clinical trials using LDN in patients with Hashimoto’s thyroiditis simply because there has been “no will” to do so. If you take a patient with IBD that flares, they have serious gastrointestinal issues such as explosive, non-stop diarrhea, rectal bleeding, awful abdominal cramps and more. If you have a patient with either multiple sclerosis or ALS, the neurological effects can be drastic and are readily observed.
When someone with Hashimoto’s thyroiditis “flares” it may be nothing more than some fatigue, sleeplessness and mild “tummy” upset. Of course, these symptoms are quite bothersome to the patient with Hashi’s, but I strongly believe this is why the research is sorely lacking. Meanwhile, everyone who treats autoimmune disease functionally uses LDN, and patients report that they feel considerably better taking it. I am not one to treat patients based on “anecdotes” but until we get some better research done on Hashimoto’s thyroiditis patients, that’s really what we’re all doing. As an addendum: we all see that it decreases antibody levels and there is one great study showing that pregnant women with Hashi’s who tend to miscarry in the first trimester, not only have significantly less miscarriages when they are taking LDN, but the babies all have better outcomes. That’s a great start, right? Now, let’s talk about something we know is good for everyone’s immune system: having a well balanced microbiome.
In recent years, numerous studies have elucidated the crucial role of gut microbiota on multiple metabolic as well as autoimmune diseases, such as diabetes mellitus, obesity, systemic lupus, Alzheimer’s disease, and inflammatory bowel disease. The active form of thyroid hormone can influence the gastrointestinal structure and function, especially motility of the gut. And on the flip side, a healthy gut microbiota also has quite a beneficial effect on thyroid function.
Numerous studies show that the gut microbiota composition in Hashimoto’s thyroiditis patients are considerably less diverse than in any control group. Interestingly, among the factors that influence the stability and variety of gut microbiota, T3 is thought to be one of the most important.
A healthy gut microbiome is not only beneficial for the function of the immune system, but also for proper thyroid function. It’s not well known, but the prevalence of co-existence of thyroid and intestinal diseases are far larger than mere coincidence. For example, Hashimoto’s thyroiditis is the most common autoimmune thyroid disease and often co-occurs with both Celiac Disease and Non-celiac wheat sensitivity. This can be explained by the damaged intestinal barrier (leaky gut) and the subsequent increase in intestinal permeability, which then allows antigens to pass more easily and activate the immune system or cross-react with extra-intestinal tissues such as the thyroid gland.
Finally, the composition of the gut microbiota influences the availability of essential micronutrients for the thyroid gland we’ve discussed earlier. Iodine and copper are crucial for thyroid hormone synthesis, selenium and zinc are necessary for converting T4 to T3, and vitamin D assists in regulating the immune response. Those micronutrients (and more) are often found to be deficient in Hashi’s patients, resulting in malfunctioning thyroid glands. Supplementation with sporulating probiotics have repeatedly shown beneficial effects on thyroid hormones and thyroid function in general.
Additional Factors Affected by Hashimoto’s Thyroiditis
There are many considerations, when treating someone with Hashimoto’s thyroiditis. Your Endocrinologist will tell you to take your Synthroid, not worry about your antibody levels, not inquire about gut function, and tell you to rest if you’re fatigued. That’s all you’re going to get. You probably won’t even get other important female hormones measured (if you’re a woman).
In functional medicine, we recognize that patients prefer not to have ongoing leaky gut, inflammation, brain inflammation, brain fog, hair loss, skin dryness, sleeping issues and so on. So we treat each and every issue separately and completely. We also take it very very seriously regarding the amount of first term miscarriages that Hashi patients have due to high antibody levels. It’s just not acceptable to us to give someone a T4 synthetic product, and do nothing about the rest of the syndrome. I would hope you would agree.
We can treat the brain issues with designated peptides: Oral or intra-nasal, with two of my favorites being dihexa and semax. We address sleep issues because sleep is when everything repairs, and with inadequate sleep, people feel just awful all day. We address mitochondrial dysfunction; often a product of autoimmune issues, and “fix the energy issues”. We repair the dry skin and the hair loss; even the eyebrow loss. Yes, there are peptides for this, too.
Lastly, since this is yet another disease where we see TNF-alpha elevation, and drugs which lower TNF-alpha are commonly used, It’s certainly worth trying natural supplements which lower TNF-alpha: resveratrol, curcumin and PQQ. They all have a host of other benefits, too! Meanwhile, a whole host of research continues.
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