Last Friday I spoke on Facebook Live about food triggers and Hashimoto’s.  I thought the presentation went well, but I decided to put together a different presentation on the same topic.  You can watch the video by clicking here, or if you prefer to read the information I also will give a summary in this blog post.  By the way, I plan on appearing on Facebook live every Friday at 1:30pm EST up until the release of my new book, and then even after the release I hope to continue doing them on a regular basis.  Although I’ll be focusing on Hashimoto’s the next few weeks due to my book release, a lot of the information discussed will also benefit those who have Graves’ Disease.

For those who prefer to read rather than watch videos, here is a summary of what I discussed in the video:

I started off by talking about the triad of autoimmunity, which involves 1) a genetic predisposition, 2) an environmental trigger, and 3) an increase in intestinal permeability, which is also known as a leaky gut.  I then briefly mentioned a few of the common triggers of Hashimoto’s.  Besides food allergens such as gluten and dairy, other common triggers include stress, infections, and environmental toxins.  In my upcoming book “Hashimoto’s Triggers” I discuss all of the different triggers in detail, along with how to detect and remove your specific triggers.

Why Is Food A Trigger In Some People?

I then briefly explained the difference between IgE food allergies and IgG food sensitivities.  IgE allergies usually elicit an immediate response, whereas food sensitivities don’t always produce symptoms, and when symptoms do appear they can sometimes take place a few days after eating the food you’re sensitive to.  I also mentioned how having an IgE allergy or IgG food sensitivity doesn’t necessarily mean this food is a direct trigger of your autoimmune thyroid condition.

For example, some people have an IgE peanut allergy, but this doesn’t mean that this is the trigger in someone with Hashimoto’s.  In fact, in all likelihood the person with such an allergy will avoid peanuts.  As for food sensitivities, just because you’re sensitive to a certain food also doesn’t mean it’s an autoimmune trigger.  For example, I just consulted with someone who has digestive symptoms whenever she eats Brussels sprouts.  This doesn’t mean that Brussels sprouts are a direct trigger in her situation, although if she has a sensitivity to Brussels sprouts and continues to eat them, this probably will cause gut inflammation, and thus it would be a good idea to avoid this food.

I briefly spoke about molecular mimicry and food triggers.  According to one theory, gliadin has an amino acid sequence that resembles the thyroid gland, which in turn causes the immune system to attack it.  And so essentially this is a case of mistaken identity, as the immune system attacks the thyroid gland because it looks like gluten.  I do want to add that as of now this is still a theory, although in the research there is a molecular mimicry mechanism involving certain pathogens.

Food Isn’t a Trigger In Everyone

I then spoke about how food isn’t a trigger in everyone with Hashimoto’s, and this is one reason why some people don’t feel better when eliminating common allergens such as gluten.  This is also a reason why some people don’t feel better when following an autoimmune Paleo diet.  However, I also mentioned how the lack of symptoms when eating certain foods doesn’t mean it’s not a trigger.  I discussed how when gluten isn’t a “direct” trigger it can cause a leaky gut.  In fact, there is strong evidence that gluten causes a leaky gut in everyone.

I then discussed “direct” triggers vs. “leaky gut” triggers.  This is discussed further in my book on Hashimoto’s.  I also mentioned how it’s possible to have multiple triggers.  In fact, I will add that it’s common to have more than one trigger.

The Problem With Gluten, Dairy, and Corn

I’ve spoken about gluten in numerous other blog posts, and during this presentation I spent a few minutes on this.  I started by discussing how many people are sensitive to gluten.  I then differentiated between celiac disease and a non-celiac gluten sensitivity.  In both cases you ideally want to avoid gluten on a permanent basis, and if you test for gluten, please keep in mind that you need to be eating gluten for the test to be positive.  And the reason for this is because if you don’t eat gluten, your body won’t produce antibodies to the proteins of gluten, even if you have a gluten sensitivity.  I then reinforced how the research shows that gluten causes a leaky gut in everyone.

Some question whether the problem isn’t with gluten or wheat, but instead is with glyphosate.  I dedicated an entire chapter to glyphosate in my book, and while this is a big problem, the truth is that both gluten and glyphosate are problematic.  Sure, there might be some cases where someone is reacting more to the glyphosate than the gluten, and vice versa.

Dairy is another common allergen, and it also cross-reacts with gluten.  In other words, consuming dairy products can lead to the production of gliadin antibodies.  And while some people do fine eating healthier forms of dairy (i.e. raw dairy), this isn’t the case with everyone.  In other words, some people have problems with dairy, regardless of the source.

Let’s not forget about corn, as this also is a common allergen, and, like dairy, corn also cross-reacts with gluten.  In addition, most corn is genetically modified.  There of course are other food allergens, and in my book I discuss food triggers in much greater detail.

Should You Follow An Autoimmune Paleo Diet?

I also have had plenty of articles and blog posts that focused on an autoimmune Paleo (AIP) diet.  In the video I explained the difference between an AIP diet and a “standard” Paleo diet, and if you want to learn more about this you can either watch the video or read a blog post I wrote entitled “Should Everyone With Graves’ Disease and Hashimoto’s Thyroiditis Follow an Autoimmune Paleo Diet?“.  But essentially an AIP diet eliminates the most common allergens AND foods that can interfere with gut healing.

As for who should follow an AIP diet, in the video I mentioned two specific categories:

Category #1: Those with an autoimmune condition.  This not only includes those with Hashimoto’s, but Graves’ Disease and other autoimmune conditions as well.

Category #2: Anyone who has a leaky gut.  As I mentioned earlier when discussing the triad of autoimmunity, everyone with an autoimmune condition has a leaky gut.  However, it of course is also possible to have a leaky gut in the absence of an autoimmune condition.

How long should someone with Hashimoto’s (or a different autoimmune condition) follow an AIP diet for?  I recommend to follow an AIP diet for at least 30 days, and if someone is thriving after 30 days then it makes sense for them to continue following it for a few additional months.  On the other hand, if they don’t feel better and are struggling with the diet then I’m open to them reintroducing some of the excluded foods.

I finished up the video by listing the following action steps you can take:

• Consider avoiding gluten, dairy, and corn
• Avoid refined foods and sugars
• If you want to go a step further, follow an AIP diet for at least 30 days
• Also try to avoid genetically modified foods
• Reminder: a lack of symptoms when eating a certain food doesn’t mean it’s fine to eat that food
• Should you consider food sensitivity testing?
• Many times following an elimination/reintroduction diet can help identify foods you’re reacting to

Most of these are self-explanatory, although if you read through these steps you might wonder what my thoughts are on food sensitivity testing.  I’m definitely not opposed to such testing, although I will say that most of my patients don’t obtain this type of testing.  And the main reason for this is because false results are common.  I usually recommend an elimination diet to my patients, and while I’ve written about both the elimination diet and food sensitivity testing in past blog posts, I go deeper in my book.

That essentially is a summary of the video.  Speaking of which, I hope you found this information to be valuable.  If so please let me know in the comments below, and if the feedback is positive I’ll try to write a summary with future videos as well.  I realize that while some people love watching videos, others prefer reading information, and so I think it would be a good idea to do both.  But of course what I think doesn’t matter, as my goal is to serve you, which is why I want to get your opinion.

One thing that was in the video that I didn’t mention here (until now) was the opportunity to get a free chapter of my book, Hashimoto’s Triggers.  You can get this chapter by clicking here.

Most people with Hashimoto’s thyroiditis are told to take thyroid hormone replacement, and nothing is ever done to address the cause of the problem.  Endocrinologists know that Hashimoto’s is an immune system condition, but we need to keep in mind that they aren’t immune system specialists.  This is one reason why they don’t do anything to improve the health of your immune system.  But the main reason why endocrinologists ignore the immune system is because they simply aren’t trained in medical school to address the cause of Hashimoto’s.

For someone who does well on thyroid hormone this might not seem like a concern, and the truth is that many people who are diagnosed with Hashimoto’s simply follow the advice of their medical doctor.  And for those reading this who are taking thyroid hormone replacement due to the advice of an endocrinologist, or another type of medical doctor, I’m not suggesting that you shouldn’t take it.  But I am here to say that there are risks of taking thyroid hormone without improving the health of your immune system.  Here are two of these risks:

Risk #1: Many people take Synthroid, which has numerous fillers, as well as artificial ingredients.  While I’m not opposed to someone taking synthetic thyroid hormone, there are better options available than Synthroid.  An example is Tirosint, which is a hypoallergenic form of synthetic T4.  Taking natural desiccated thyroid such as Armour, Nature-Throid, or WP Thyroid is also something to consider, as many people do better on these than synthetic thyroid hormone.

I realize that Synthroid is probably a less expensive option, and perhaps even covered by your health insurance, but we all know that you usually get what you pay for.  For example, purchasing organic food is more expensive than non-organic food, but the reason why many people are willing to pay extra money for organic food is to minimize their exposure to the chemicals that are present in non-organic food.  One problem is that many people who take Synthroid don’t read the ingredients, while others don’t realize that there are hypoallergenic forms of synthetic thyroid hormone available (for those who can’t take or prefer not to take desiccated thyroid).

Risk #2: People with Hashimoto’s have an increased risk of developing other autoimmune conditions in the future.  This is in the research, and it’s a big reason why EVERYONE with Hashimoto’s needs to be proactive and try to detect and remove their autoimmune triggers.  While nobody wants to be diagnosed with Hashimoto’s, and some people with this condition have extreme fatigue, brain fog, and other symptoms, keep in mind that some other autoimmune conditions are arguably worse to have.  For example, while many people are able to function normally when taking thyroid hormone, this might not be the case for someone who has been diagnosed with multiple sclerosis, rheumatoid arthritis, or other autoimmune conditions.

Just to be clear, I’m not advising anyone to stop taking their thyroid hormone replacement.  But for those who do this without improving their immune system health, you are at risk of developing other autoimmune conditions in the future.

What Does It Mean To “Reverse” Hashimoto’s?

The headline of this blog post is “Can Hashimoto’s Be Reversed?”  The answer to this question is “yes”, it is possible to reverse Hashimoto’s.  But what exactly does this mean?  Well, when I use the word “reverse” I’m suggesting that the autoimmune component can be reversed.  In other words, it’s possible to detect and remove the autoimmune triggers and normalize the thyroid antibodies.  I’m not suggesting that this is easy to accomplish, as without question some cases of Hashimoto’s are more challenging than others.  And then even when the autoimmune component has been reversed, for some people it is challenging to maintain a state of remission.

This is true with all autoimmune conditions.  As many reading this know, I was diagnosed with Graves’ Disease in the past, and I have been in remission since 2009.  Since then, I have helped many people with Graves’ Disease and Hashimoto’s achieve a state of remission.  The primary key to helping people with these autoimmune thyroid conditions achieve a state of remission is to find and remove the person’s triggers.  I’ve written about this in past articles and blog posts, have conducted webinars on this topic, and soon I will be releasing a new book that focuses on helping you find and remove your specific autoimmune triggers.

Yes, I know there are currently books on Hashimoto’s that focus on natural treatment methods.  In fact, I’m friends with many of the authors of these books.  But I promise you that my upcoming book is going to be the most comprehensive book to date with regards to discussing the different triggers of Hashimoto’s, along with helping those with this condition detect and remove their triggers.

As for when the book will be released, I don’t have an exact date yet, but I’m 99% certain that it will be released in the first quarter of this year.  In fact, the editing process has been completed, and it’s now in the hands of the formatter.  I’ll add that the first week it’s released there will be a huge discount, along with a few special bonuses for those who purchase the book.  In a couple of weeks I’ll have another update, and I’ll also include a copy of the cover.

In past articles and blog posts I have discussed some of the different conventional medical treatment options for hyperthyroid conditions, but I haven’t discussed something called block and replace therapy.  One of the main reasons for this is because this is rarely recommended to those with hyperthyroidism and Graves’ Disease, although every now and then I’ll work with someone who was recommended to receive this treatment by their endocrinologist.  As a result, I figured it was time to put together a brief post on this topic.

So what exactly is block and replace therapy?  Well, many people with hyperthyroid conditions are told to take antithyroid medication, which includes Methimazole, Carbimazole, and PTU.  These are given to “block” the production of thyroid hormone, and antithyroid medication accomplishes this by inhibiting an enzyme called thyroid peroxidase.  What it specifically does is inhibit the metabolism of iodide and the iodination of tyrosine residues in the thyroid hormone precursor thyroglobulin by thyroid peroxidase (1).

One problem with antithyroid medication is that people who take it commonly become hypothyroid.  So for example, it’s common for someone with elevated thyroid hormone levels to get a prescription for antithyroid medication, and when doing a follow-up thyroid panel their thyroid hormone levels will be low, while their TSH will be on the high side.  When this is the case, the medical doctor will usually lower the dosage of antithyroid medication and hope that the next thyroid panel will show a lower TSH and higher thyroid hormone levels, but at the same time prevent the person from becoming hyperthyroid again.

The “Seesaw” Effect of Antithyroid Medication

Sometimes this can become a frustrating process for the patient, as I’ve worked with people who were told to take a higher dosage of antithyroid medication, and then when the thyroid panel revealed a hypothyroid state the dosage was greatly reduced, and in some cases the patient was told to stop taking the Methimazole, and the person became hyperthyroid again.  So for example, a person with Graves’ Disease or toxic multinodular goiter might be told to take 40mg of Methimazole, and the next thyroid panel presents with hypothyroid numbers (elevated TSH and low thyroid hormone levels), and so the person’s dosage is reduced to 10mg, only to have the person become hyperthyroid again.

With block and replace therapy, the person isn’t only put on antithyroid medication to “block” the production of thyroid hormone, but they are also given thyroid hormone replacement (i.e. levothyroxine).  So it’s almost like a balancing act, as the antithyroid medication will prevent the person from becoming hyperthyroid, but the person is also given some thyroid hormone to prevent them from becoming hypothyroid.  Block and replace therapy is usually reserved for moderate to severe cases of hyperthyroidism, as with this treatment higher doses of antithyroid medication are usually taken by the patient.

Why Is Block and Replace Therapy Seldom Used?

Rarely does an endocrinologist in the United States recommend block and replace therapy, and it also isn’t commonly recommended by medical doctors in other countries.  One reason for this is because the relapse rates are comparable to someone who is taking antithyroid medication alone, but another reason is because side effects seem to be more common with block and replace therapy (2).  Another thing to keep in mind is that most endocrinologists are far more concerned about managing hyperthyroidism, which is why many will recommend radioactive iodine or thyroid surgery as the first line of treatment.  In other words, many aren’t concerned if their hyperthyroid patients become hypothyroid by taking antithyroid medication.

This doesn’t mean that there aren’t times when block and replace therapy can be beneficial.  For example, pregnant women with hyperthyroidism are usually told to take antithyroid medication.  While many people are understandably concerned about the effects of these medications on the liver, another concern during pregnancy is that antithyroid medication can lead to hypothyroidism.  And of course thyroid hormone is very important for the developing fetus.  Block and replace therapy during pregnancy was discussed in a case study involving a 36-year old woman, as the authors explained how it is challenging to keep the free T4 in the upper range of normal with antithyroid medication alone, and that block and replace therapy can prevent fetal hypothyroidism from developing (3).

Graves’ orbitopathy might be another situation where block and replace therapy is indicated, as a study showed that using long-term block and replacement therapy until Graves’ orbitopathy becomes inactive might be a good option (4).  One thing to keep in mind was that the patients in this study were treated with block and replace therapy for an average of 41 months, and many endocrinologists would refuse to have their patients take antithyroid medication for that long, even if the liver enzymes were fine during treatment.

The truth is that block and replace therapy might be beneficial in certain situations, but most endocrinologists are trained to prescribe antithyroid medication alone, which is why they commonly recommend this to their patients with hyperthyroidism and Graves’ Disease.  In fact, some endocrinologists aren’t even familiar with block and replace therapy, and one reason for this is because only a small percentage of their patients have hyperthyroidism and Graves’ Disease.  It is far more common for endocrinologists to deal with patients who have Hashimoto’s thyroiditis.  As a result, those with a hyperthyroid condition can expect to be advised to take antithyroid medication by their endocrinologist, or to receive radioactive iodine or thyroid surgery.

In summary, block and replace therapy involves taking both antithyroid medication and thyroid hormone.  So essentially the goal is to block the production of thyroid hormone, but at the same time have the patient take thyroid hormone replacement to prevent them from becoming hypothyroid.  Block and replace therapy is rarely recommended by endocrinologists, and two reasons for this are because 1) the relapse rate is comparable to taking antithyroid medication alone, and 2) side effects are more common.  However, pregnancy and Graves’ orbitopathy are two situations when this type of treatment might offer some benefits.

It’s common for people with hypothyroidism and Hashimoto’s Thyroiditis to have low levels of triiodothyronine, also known as T3.  Sometimes the T3 levels will be within the lab reference range, but less than optimal.  On the other hand, sometimes they will be outside of the lab reference range.  Either way, the goal is to try to bring the T3 to an optimal level, and in this blog post I’ll discuss seven ways to increase low T3 levels.

Before I discuss the seven ways to increase low T3 levels, you might wonder why I’m not talking about T4 in this post.  In 2016 I did release a blog post entitled “7 Causes of Low T4 Levels”, and while some of the same factors will cause low T3 levels, there are different causes as well.  In addition, I usually recommend to test for the free T3 levels, and from an optimal perspective you want to see these levels between 3.0 and 3.5 pg/ml, although some sources will suggest a tighter range (i.e. between 3.2 and 3.5 pg/ml).

It’s also important to mention that not all medical doctors will test the T3 levels.  Many will only test the TSH and T4, while some will test the TSH alone.  The reason for this is because in most cases the T3 isn’t going to change their recommendations, as most medical doctors will 1) base their recommendations off of the TSH, and 2) prescribe synthetic thyroid hormone to just about all of their patients with a hypothyroid condition. If this describes your doctor then you might want to consider switching to a different doctor, or another option is to try to order free T3 on your own.

With that being said, let’s go ahead and look at the seven ways to increase low T3 levels.  Please keep in mind that I’m not listing these in the order I recommend.

1. Take synthetic T4.  Although I’m starting with synthetic T4 because this is the most common recommendation by medical doctors to address both low T4 and low T3 levels, this isn’t my first preference.  And the reason for this is because while taking thyroid hormone replacement is necessary at times, this doesn’t do anything to address the underlying cause of the problem.  In addition, Synthroid is the most common brand of synthetic thyroid hormone medication recommended, and it has a lot of fillers, along with artificial ingredients.  As a result, if someone absolutely needs to take synthetic T4, they should look into a more hypoallergenic form, such as Tirosint.

Some reading this might wonder how taking synthetic T4 will increase low or depressed T3 levels.  Well, T4 converts into T3, and so if someone has healthy levels of T4, then they should be able to convert the T4 into T3.  However, if someone has a problem converting T4 to T3 then taking synthetic T4 won’t be effective in raising T3 levels.

2. Synthetic T3.  If someone has low or depressed T3 levels, then it might make more sense to take synthetic T3 rather than synthetic T4.  Synthetic T3 is also known as liothyronine, with Cytomel being a common brand.  A recommended starting dosage is 25 mcg per day, although some will start with lower doses (i.e. 5 mcg).  While some medical doctors will recommend synthetic T3 if someone has low T3 levels, since T3 is the active form of thyroid hormone, many are cautious about doing this out of fear that the person will develop hyperthyroid symptoms.

Earlier I mentioned that it might make more sense for someone who has low or depressed T3 levels to take synthetic T3 instead of synthetic T4, although it depends on the situation.  For example, if someone has depressed levels of both T4 and T3, then it wouldn’t make sense to only have the person take synthetic T3.  In fact, as I mentioned previously, if the person is able to convert T4 to T3 then in this scenario they might be fine just taking synthetic T4, although in some cases taking both synthetic T4 and T3 might be warranted.  On the other hand, if someone has normal levels of T4 and low or depressed levels of T3, then this might be a good indication that synthetic T3 is needed.

However, just as is the case with taking synthetic T4, synthetic T3 doesn’t do anything to address the cause of the problem.  And so while taking synthetic T3 might be necessary in some cases, the obvious goal should be to fix the conversion problem and/or address the autoimmune component (for those who have Hashimoto’s), which I’ll discuss later in this post.

3. Natural thyroid hormone.  If someone needs to take thyroid hormone replacement, desiccated thyroid hormone should be considered.  Brand names include Armour, Nature-Throid, and WP Thyroid.  These all include T3 and T4, along with other thyroid cofactors (T1, T2, and calcitonin).  This type of thyroid hormone replacement can especially be helpful if someone has low or depressed levels of both T4 and T3.  Although over the years I have had many patients take Armour and do fine, I prefer Nature-Throid and WP Thyroid because they are hypoallergenic.  And while many people do fine taking synthetic thyroid hormone, some people don’t do well on this, yet thrive when taking desiccated thyroid hormone.  On the other hand, a small percentage of people don’t do well on natural thyroid hormone, and actually do better when taking synthetic thyroid hormone replacement.

4. Thyroid glandular supplements.  For those who are unable to get a prescription for Armour, Nature-Throid, WP Thyroid, or a different brand of natural thyroid hormone, there are thyroid glandular supplements that contain desiccated thyroid hormone, and don’t require a prescription.  Some of these thyroid glandular only include T3, while others have both T4 and T3.  It’s common for these thyroid glandular supplements to also include nutrients and/or herbs that support thyroid gland function.  Common nutrients included include selenium, tyrosine, and zinc, and ashwagandha is an adaptogenic herb that is added to some thyroid glandular supplements.

5. Compounded thyroid hormone medication.  Compounded T4/T3 is made by a compounding pharmacist, and is another option to consider.  One advantage of compounded T4/T3 is that the doses can be customized.  Another advantage is that the product can be formulated to be hypoallergenic.  Some compounding pharmacists can also put together a custom formulation using desiccated thyroid.  However, getting T4/T3 through a compounding pharmacy can be considerably more expensive.

6. Correct the conversion problem.  So far I have focused on different types of thyroid hormone replacement.  But even if you need to take thyroid hormone, it makes sense to address the cause of the problem.  I mentioned earlier that ideally T4 should convert into T3, but many people have problems converting T4 to T3.   If someone’s thyroid panel reveals normal T4 levels and low or depressed T3 levels, then this is a pretty good indication of a conversion problem.  However, it’s also possible for BOTH T4 and T3 to be low and to have a conversion problem.  When this is the case it can be more challenging to determine if the person has a problem converting T4 to T3, although reverse T3 may be elevated in this situation.

There are numerous factors that can interfere with the conversion process, but three of the more common reasons why people have a problem converting T4 to T3 include 1) liver problems, 2) gut dysbiosis, and 3) elevated cortisol levels.  As a result, these are the primary areas I focus on, and while most of the time doing so will correct the conversion problem, in some cases this can be challenging.  For more information I would read my blog post entitled “6 Factors Which Can Affect The Conversion of T4 to T3”.

Should Someone Take Thyroid Hormone Replacement While Fixing The Conversion Problem?

As for whether someone who has a conversion problem should take thyroid hormone, this depends on the person.  While the cause of the problem needs to be addressed, we also need to remember that T3 is the active form of thyroid hormone.  As a result, if someone has very low or depressed thyroid hormone levels then we don’t want these to be low for too long.  The reason for this is because thyroid hormone affects every cell and tissue in the body.

In addition, while sometimes the T3 levels will increase relatively quickly while addressing the cause of the problem, this isn’t always the case.  Sometimes it can take many months to correct the conversion problem.  There can be a few reasons for this.  One reason is because it can take time to address the liver, gut, or adrenal imbalance which are responsible for the conversion problem.  Another reason is because sometimes we greatly improve the health of these areas, only to find another factor is responsible for the poor conversion of T4 to T3.

7. Detect and remove the autoimmune trigger.  Most people with hypothyroidism have Hashimoto’s Thyroiditis, which is the reason behind their low or depressed T4 levels, and low or depressed T3 levels are common as well.  So when someone has low T3 (and T4) levels as a result of Hashimoto’s, the goal is to do everything necessary to detect and then remove the autoimmune trigger.  This is easier said than done, and over the years I’ve written many articles and blog posts on some of the different triggers, and I also talk about this during my free webinars.  In my upcoming book on Hashimoto’s I’ll go into even more greater detail about triggers, including an entire section dedicated to how to detect all of the different triggers, and another section that focuses on removing your triggers.

While some people with Hashimoto’s don’t need to take thyroid hormone replacement, others need to take it while addressing the cause of the problem.  And there are those who need to take it on a permanent basis.  It depends on how much damage to the thyroid gland has taken place.

Can There Be Other Factors Responsible For Low T3 Levels?

Although having Hashimoto’s and/or a conversion problem are the most common reasons why someone has low T3 levels, there can be other factors.  I’m not going to get into great detail about these here, and ideally you want to work with a natural healthcare professional to address this.  But here are some other potential causes of low T3 levels:

Dysregulation of the hypothalamic-pituitary-thyroid (HPT) axis.  Although T3 is produced during the conversion process, some T3 is also produced in the thyroid gland.  TSH is a pituitary hormone, and it is responsible for signaling to the thyroid gland to release T4 and T3.  The hypothalamus communicates with the pituitary gland.  As a result, if there are problems with the communication between the hypothalamus and pituitary gland, this in turn can affect the communication between the pituitary gland and thyroid gland, which can result in low T4 and/or T3 levels.

Direct inhibition of the thyroid gland.  Although most cases of hypothyroidism are a result of Hashimoto’s, some factors can directly inhibit thyroid hormone production.  For example, certain environmental toxins such as mercury can inhibit thyroid hormone production, although sometimes environmental chemicals can cause an immune system response.  Either way, in this situation the goal should be to reduce your toxic load.

Some people are concerned about goitrogenic foods inhibiting thyroid hormone production.  Although I would be cautious about eating soy, eating cruciferous vegetables usually won’t cause any problems.  I spoke more about this in a blog post entitled “5 Things To Know About Goitrogenic Foods”.

Problems with T3 binding to the carrier proteins.  Both T3 and T4 are carried through the bloodstream bound to certain proteins.  Thyroxine-binding globulin (TBG) is one of these, although it has a higher affinity for T4 than for T3.  Both T4 and T3 bind to serum albumin, although these hormones have a higher affinity for TBG.  So for example, if the TBG level is low due to a person taking corticosteroids, this will result in lower levels of thyroid hormone in the blood.

In summary, many people with hypothyroidism and Hashimoto’s have low or depressed levels of T3.  Unfortunately many medical doctors don’t test the T3 levels, as they will only test for the TSH, and perhaps T4.  Ideally you want to increase T3 levels by addressing the cause of the problem, which is usually either damage to the thyroid gland caused by the immune system, or a problem converting T4 to T3.  However, thyroid hormone replacement can also increase the T3 levels, and some of the different options include synthetic T4, synthetic T3, desiccated thyroid hormone, thyroid glandular supplements, and compounded T4/T3.

It’s common for people with thyroid and autoimmune thyroid conditions to have thyroid nodules.  It’s also common for people to be concerned about them, and to wonder whether their nodules are malignant, if there is a way to shrink nodules, etc.  While I have written a few articles in the past on this topic, I figured I’d put together an updated post that discusses five things anyone with thyroid nodules should know.

1. Many people have thyroid nodules.  As I mentioned in the opening paragraph, it is very common for people to have thyroid nodules.  One journal article mentioned that while 4 to 7% of the population have palpable thyroid nodules, ultrasonography reveals that up to 67% of the population has them (1).  Another study mentioned that up to 35% of the population have thyroid nodules show up on an ultrasound (2).  Even if we go with the lower number, 35% is quite high, as this means that roughly one third of the population has thyroid nodules.  The incidence of thyroid nodules increases as we age, and the prevalence is higher in women (2), although they are more likely to be malignant in men, especially those over 70 years of age (3).

2. Most thyroid nodules are benign.  Only around 5% of thyroid nodules that are detected through palpation are malignant (1).  But most thyroid nodules are not detected through palpation.  And for those thyroid nodules evaluated by a biopsy, the prevalence of malignancy ranges from 4% to 6.5% (4).  So while at least one third of people reading this will test positive for thyroid nodules, only a very small percent of these nodules will be malignant.

With that being said, the incidence of thyroid cancer has increased substantially in the United States over the last four decades (5), as the American Cancer Society estimated that 62,450 people in the United States were diagnosed with thyroid cancer in 2015 (6).  Most people with thyroid cancer are diagnosed with papillary thyroid cancer.  According to the American Cancer Society, both stage one and stage two papillary thyroid cancer have a 5-year relative survival rate of nearly 100%, and in stage three it’s 93% (7).  In stage four, the 5-year relative survival rate drops down to 51%.

Follicular thyroid cancer also has a near 100% 5-year relative survival rate in stage one and two, with a 71% 5-year relative survival rate in stage three, and a 50% 5-year relative survival rate in stage four (7).  Medullary thyroid cancer has a pretty good 5-year relative survival rate in stages one through three, but only a 28% survival rate in stage four.  Anaplastic thyroid cancer has a 5-year relative survival rate of only 7%, but fortunately only 1-2% of all thyroid cancers are anaplastic.

The reason why I’m talking about these statistics is to show you that while there without question is a risk of untreated thyroid cancer, the progression is much slower when compared to other cancers, and overall the 5-year relative survival rate is pretty good.  By comparison, the 5-year relative survival rate for the four most common malignancies in developed countries is 73-89% for breast cancer, 50-99% for prostate cancer, 43-63% for colorectal cancer, and only 12-18% for lung cancer (8).

If you’re wondering when a biopsy is necessary, please read an article I wrote in the past entitled “Is It Necessary To Get A Biopsy For Thyroid Nodules?”

3. A radioactive iodine uptake test won’t confirm or rule out malignant nodules.  For those are diagnosed with hyperthyroidism, a radioactive iodine uptake test is commonly recommended.  One reason is to confirm or rule out Graves’ Disease, as most people with this condition will have a high uptake of radioactive iodine, although I’ll add that testing positive for thyroid stimulating immunoglobulins is not only a better way of diagnosing Graves’ Disease, but is less invasive.

Besides trying to confirm a diagnosis of Graves’ Disease, another reason why endocrinologists will recommend this test is to detect thyroid nodules, as well as to differentiate between benign and malignant nodules.  And the way it tries to accomplish this is by looking at “hot” and “cold” nodules.  About 80 to 85% of thyroid nodules show up as being cold on the uptake test, and about 10% of these nodules are malignant (9).  Hot nodules account for only 5% of nodules, although the likelihood of these being malignant is less than 1%.  So essentially you’re hoping to see a hot nodule, but are far more likely to see a cold nodule, and 90% of these will be benign.

I’m not suggesting that the radioactive iodine uptake test has no value, but in my opinion it makes more sense to first get a thyroid ultrasound.  First of all, this is less invasive than the radioactive iodine uptake test.  Second, it can provide an accurate measurement of the size of the nodule, which isn’t the case with the uptake test.  And third, other characteristics of the nodule on an ultrasound can give an indication if it is potentially malignant, and thus warrants a biopsy.  It’s also worth mentioning that for those who don’t have health insurance, a thyroid ultrasound usually costs a lot less than a radioactive iodine uptake test.

The truth is that neither an uptake test or a thyroid ultrasound are perfect methods for confirming or ruling out malignant nodules.  But since the uptake test is more invasive and costs more, it makes sense to start with the thyroid ultrasound.

4. Problems with estrogen metabolism is a common cause of thyroid nodules.  According to the research, estrogen is a potent growth factor both for benign and malignant thyroid cells (10) (11).  Estrogen is also a factor with uterine fibroids, and one study involving 1144 participants looked at the relationship between thyroid nodules and uterine fibroids (12).  The authors concluded that uterine fibroids in women were definitely associated with the presence of thyroid nodules, and that estrogen might play a pivotal role in the occurrence of both of these.

As a result, if you have one or more thyroid nodules, doing things to support estrogen metabolism is a good idea.  One of the best ways to accomplish this is by eating plenty of cruciferous vegetables, as these help to support estrogen metabolism due to the compounds Indole-3-Carbinol and 3,3′-diindolylmethane (DIM) (13) (14).  Another option is to take DIM in supplement form.

For those women who are taking estrogen, I came across one study involving 33 women who received estrogen therapy for one year, and it did not seem to increase the growth of thyroid nodules (15).  While I can’t say that I’m a big fan of estrogen therapy, I realize that some women can benefit from taking estrogen (preferably bioidentical estrogen).

5. There are no specific herbs or supplements to shrink thyroid nodules.  Although supporting estrogen metabolism can help to shrink thyroid nodules, the truth is that this isn’t always effective.  Shrinking thyroid nodules can be challenging, but here are a few other factors to consider:

An iodine deficiency can cause thyroid nodules.  A few studies show a relationship between iodine deficiency and thyroid nodules (16) (17) (18).  Of course iodine is very controversial in the world of thyroid health, which I have discussed in past articles and blog posts.  Although many people with thyroid and autoimmune thyroid conditions don’t do well with iodine, at the same time we can’t ignore an iodine deficiency.  This doesn’t mean that everyone with thyroid nodules should supplement with iodine, but it probably would be wise for those with thyroid nodules to do a urinary iodine spot test, and if they are iodine deficient they should work with a healthcare practitioner who can help them correct this deficiency over time.

The main reason some people don’t do well with iodine, even when they have an iodine deficiency, is because they are also deficient in antioxidants.  While some doctors will recommend for their patients to take antioxidants while administering iodine supplementation simultaneously, I have found that a safer approach is to first increase the person’s antioxidant status over the course of a few months before having them supplement with iodine.  And when the person starts supplementing with iodine they should start with smaller doses.

Thyroxine may help to suppress thyroid nodules.  It is thought that levothyroxine-induced suppression of TSH secretion can shrink thyroid nodules, as it prevents the growth-promoting effect of TSH on thyroid cells (19).  Of course this would only be an option for those people with hypothyroidism and Hashimoto’s Thyroiditis, as you wouldn’t want a person with hyperthyroidism to take thyroid hormone.  I’ll also add that this treatment isn’t always effective, as a study involving 40 patients with confirmed benign nodules showed that suppressive therapy with levothyroxine didn’t decrease the size of benign nodules (20).

Ethanol ablation.  Percutaneous ethanol ablation for cystic thyroid nodules was introduced in 1989.  Yes, injecting ethanol into thyroid nodules can actually shrink thyroid nodules (21) (22).  This wouldn’t be my first option if I had thyroid nodules, but I would probably consider this procedure before surgery.  Ethanol ablation has been reported to have a success rate of 82-85% reduction after an average of two sessions in the management of thyroid cysts (23) (24).  However, it doesn’t seem to be as effective in shrinking solid thyroid nodules.

Laser thermal ablation.  This is a relatively new treatment option, and it can be effective with minimal complications (25).  In addition, while ethanol ablation seems to be more effective for shrinking cystic nodules, laser ablation can help with solid nodules.  It also seems to be less costly than other procedures.

I came across a journal article on laser therapy (26) which discussed a study involving 1531 patients who underwent laser ablation for 1534 nodules.  According to the study, 83% of the nodules were treated with a single session of laser ablation, and the average reduction in nodule volume at 12 months was 72% (26).  There were 17 complications, with 8 of them being major, although all of them recovered completely after they were treated with steroids.  So there are some risks, but of course this is also the case with the surgical removal of the thyroid gland, which is what many doctors recommend when someone has nodules.  A more recent meta-analysis from 2017 showed that percutaneous laser ablation was safe and useful in shrinking benign thyroid nodules, improving thyroid function, and relieving symptoms related to pressure (27).

While laser ablation for thyroid nodules seems promising, I’m not sure where someone would go to get this procedure done.  Not surprisingly, it doesn’t seem like there are many of practitioners who offer this type of treatment.  In addition, we need to keep in mind that this treatment doesn’t do anything to address the cause of the problem.  On the other hand, if someone takes a natural treatment approach but the thyroid nodules don’t shrink, then they might want to consider this procedure.

So hopefully you learned a few new things you didn’t already know about thyroid nodules.  Although many people have thyroid nodules, the good news is that most of these are benign.  Problems with estrogen metabolism and an iodine deficiency are common causes of thyroid nodules, and while addressing these imbalances is essential, there are other treatment options to consider.  Thyroid surgery is an option, but should be the last resort.  Other options include thyroxine therapy, ethanol ablation, and laser ablation.