Many patients with Graves’ disease experience hair loss, and while this might not be the most concerning symptom someone with this condition has, it is still very distressing for many people.  This is especially true since Graves’ disease (as well as most other autoimmune conditions) is more common in women, and I can tell you that over the years I have worked with many women with Graves’ disease who were stressed out the most over their hair loss.  I’ve written other blog posts and articles on hair loss, but I wanted to put together an updated post that focuses on Graves’ disease and hair loss, because while I do see hair loss in people with hypothyroidism and Hashimoto’s thyroiditis, it is more common in those with hyperthyroid conditions.

When I begin working with someone who has Graves’ disease, of course I want to address the underlying cause of their condition, but initially I want to make sure the person is safe since it’s quite common to have an elevated resting heart rate.  Many endocrinologists will try to lower the person’s resting heart rate through the use of antithyroid medication (i.e. methimazole, PTU) and/or beta blockers (i.e. propranolol, atenolol).  Natural antithyroid agents such as bugleweed and high doses of L-carnitine are also an option to lower the thyroid hormone levels, while herbs such as motherwort and hawthorn can act as natural beta blockers.

It’s worth mentioning that sometimes taking antithyroid medication or herbs will help to decrease the person’s hair loss, while other times the person will experience more hair loss upon taking these.  I’ll talk more about this later in this post, but before we specifically discuss Graves’ disease and hair loss I want to make sure you have taken the necessary steps to start lowering your thyroid hormone levels.  So if you have uncontrolled hyperthyroidism then this needs to be addressed first.

Why Do People With Graves’ Disease Commonly Experience Hair Loss?

The main reason why people with Graves’ disease experience hair loss is due to the thyroid hormone imbalance.  While either high or low thyroid hormone levels can result in hair loss, as I mentioned earlier, it seems that high thyroid hormone levels more commonly result in hair loss.  Based on what I just said here, it might seem obvious that in order to stop the hair loss you simply need to lower the thyroid hormone levels.  While normalizing the thyroid hormone levels will usually cause the hair loss to stop, it frequently will take a good amount of time for this to happen.

The Impact of Antithyroid Medication and Herbs on Hair Loss

I’ll add that taking antithyroid medication such as methimazole or PTU can either improve or exacerbate the hair loss.  I’ve worked with Graves’ disease patients who took methimazole and had an improvement in their hair loss, while others had their hair loss worsen upon taking antithyroid medication.  Some people with Graves’ disease don’t experience any hair loss until they start taking antithyroid medication.  Frequently what happens is that the person takes too high of a dosage of methimazole, which can make them hypothyroid, and this can also cause hair loss.

Bugleweed is an antithyroid herb that can also help to lower thyroid hormone levels.  Because this herb isn’t as potent as antithyroid medication it’s less likely to cause a huge “swing” in thyroid hormone levels over a short period of time.  As a result, taking bugleweed usually doesn’t cause hair loss as much as antithyroid medication does, although you also need to keep in mind that bugleweed isn’t effective in everyone with hyperthyroidism.  In other words, taking bugleweed doesn’t always lower thyroid hormone levels.  Antithyroid medication is more effective, but there is also a greater risk of side effects.

As I’m sure you know, antithyroid drugs and herbs don’t do anything to address the cause of the problem, and so while they might help with hair loss by lowering the thyroid hormone levels, it’s still important to address the underlying cause of the condition.  In other words, if all you do is take antithyroid medication or herbs, this might temporarily help with hair loss associated with Graves’ disease, but once you stop taking these thyroid hormone-lowering agents the hyperthyroidism is likely to return, along with the hair loss.

What Are Other Causes of Hair Loss?

Although elevated thyroid hormone levels are the most common cause of hair loss in people with Graves’ disease, this doesn’t mean that there can’t be other causes as well.  Let’s look at some of the other common causes of hair loss in people with Graves’ disease:

• Nutrient deficiencies.  Nutrient deficiencies are common in those with Graves’ disease, and nutrient deficiencies can cause hair loss in general.  In fact, many people who are suffering from hair loss will take nutritional supplements on their own to see if they will help.  Some of the nutrient deficiencies that can cause or contribute to hair loss include zinc, iron, selenium, biotin, and gamma-linolenic acid (1).  When looking to address nutrient deficiencies, it’s important to look into factors that can cause these deficiencies.  Remember that Graves’ disease is an autoimmune condition, and since most of the immune system cells are located within the gastrointestinal tract, having a healthy gut is necessary for optimal immune system health.  But many people with Graves’ disease have an unhealthy gut, which in turn can affect nutrient absorption.  For example, H. pylori is a potential trigger of Graves’ disease, and numerous studies show that H. pylori can affect iron absorption (2) (3), which can result in hair loss.  Other causes of malabsorption (i.e. Celiac disease, inflammatory bowel disease) can also affect the absorption of nutrients that play a role in hair loss.  It’s also important to mention that overdosing with certain nutrients can cause hair loss.  This includes selenium, vitamin E, and vitamin A (4).  So while it’s important to correct nutrient deficiencies, you want to make sure not to take very high doses of certain nutrients, especially over a prolonged period of time, as this can lead to a toxicity that results in hair loss.
• Sex hormone imbalances.  Imbalances of the sex hormones (estrogen, progesterone, testosterone) can cause hair loss.  Elevated thyroid hormone levels will commonly cause sex hormone imbalances.  Frequently correcting the hyperthyroidism will resolve the sex hormone imbalance, although sometimes additional action will be required to balance the hormones.
• Alopecia areata.  Alopecia areata is an autoimmune condition that causes hair loss on the scalp, face, and sometimes on other areas of the body.  A 2018 study showed that alopecia areata is significantly associated with Graves’ disease and Hashimoto’s thyroiditis (5).  However, it’s important to mention that frequently alopecia areata will develop first, many times in childhood, although it’s also possible for thyroid autoimmunity to precede alopecia areata.

Please keep in mind that it’s very possible for those with Graves’ disease to have more than one factor causing hair loss.  For example, while hyperthyroidism is the most likely cause, the person might also have nutrient deficiencies that are a factor.  In this situation not only will the thyroid hormone levels need to be balanced, but the nutrient deficiencies need to be addressed as well.  As I mentioned earlier, if someone has hyperthyroidism that leads to sex hormone imbalances, lowering the thyroid hormone levels may resolve the sex hormone imbalances, although this isn’t always the case.

Can Diet Alone Help With Hair Loss?

I mentioned how nutrient deficiencies are a potential cause of hair loss.  Because of this you may wonder if eating a nutrient dense diet can correct such nutrient deficiencies, and thus resolve the hair loss problem.  Although it’s important to eat nutrient dense foods, many times supplementation is necessary to correct nutritional deficiencies, and then once this has been accomplished the goal should be to maintain healthy nutritional levels through diet (although I’ll add that sometimes supplementation is still necessary).  Just remember that having a healthy gut is necessary for the optimal absorption of nutrients.

How Long Does It Take To Reverse Hair Loss?

As for how long it takes to reverse hair loss, this of course depends on the person, as well as the cause of the hair loss.  If hyperthyroidism is the sole cause of the person’s hair loss it can take a few weeks to a few months before the hair loss stops.  The same thing applies to sex hormone imbalances.  Moderate to severe nutrient deficiencies will take time to correct, and so if this is responsible for the hair loss then it will usually take longer for the hair loss to stop and grow back.  Based on what I’ve said here, while some people start noticing their hair loss improving within a few weeks of taking measures to correct their hyperthyroidism, for some people it will take a few months before they notice a significant improvement.

What Can You Do To Help With Graves’ Disease Hair Loss?

After reading this post you probably have a pretty good idea what you can do to help with your hair loss, but I’ll list them below in bullet point format:

• Correct the hyperthyroidism.  This is the most common cause of hair loss in those with Graves’ disease, but of course even if someone isn’t experiencing hair loss it’s important to lower the thyroid hormone levels.
• Balance the sex hormones.  Once again, correcting the hyperthyroidism many times will help to balance the sex hormones.  But when this isn’t the case you might need to do other things.  One thing I didn’t mention earlier when discussing sex hormones is that having healthy adrenals is important in order to have healthy sex hormones.  And many people with Graves’ disease have adrenal problems.  So while many doctors will resort to giving bioidentical hormones to their patients with sex hormone imbalances, evaluating the adrenals is a good first step before doing this.
• Correct nutrient deficiencies.  I’ve also discussed how many people with Graves’ disease have nutrient deficiencies, and certain nutrient deficiencies can cause hair loss.  I also explained how it’s important to address the cause of the nutrient deficiencies, and how overdosing with selenium, vitamin A, and/or vitamin E can cause hair loss.

What’s Your Experience With Hair Loss?

If you have Graves’ disease and have dealt with hair loss please feel free to share your experience in the comments section below.  Are you still experiencing hair loss, and if not, how long did it take for your hair loss to stop and grow back?  If you took antithyroid medication, did this improve or worsen your hair loss?  Did you take any nutritional supplements, or do anything else naturally that helped?  Thank you so much for sharing your experience with everyone.

Most people reading this understand the importance of the thyroid gland, as it produces the thyroid hormones, which of course I’ll be discussing in this blog post.  The truth is that all of these markers I’ll be discussing either directly or indirectly affect the thyroid hormones, which play an important role in regulating metabolism, gene expression, brain development, reproductive health, bone health, and wound healing.

For most of the markers I’ll list the lab reference ranges according to Labcorp and Quest Diagnostics, which are two of the most well known labs in the United States.  Just keep in mind that different labs will have different reference ranges, which is why you usually want to pay attention to the optimal reference ranges I have listed below.  For some markers I haven’t listed optimal reference ranges, simply because I don’t know what the optimal reference range is for every single marker.

It’s also important to mention that some markers will have different ranges for males and females, as well as different ranges based on the age of the patient.  For example, according to Quest Diagnostics, the lab reference range for free T4 for those 2 to 12 years in age is 0.9-1.4 ng/dL, but those people over 20 years old should have a reference range between 0.8-1.8 ng/dL.  For simplicity sake I only listed the reference ranges for adult females.

THYROID STIMULATING HORMONE (TSH)

The production of thyroid hormones is regulated by thyroid stimulating hormone (TSH), which is made by the anterior pituitary gland.  TSH also influences the size of the thyroid gland.  While TSH stimulates the production of thyroid hormones, these same thyroid hormones will inhibit the production of TSH.  So it’s a negative feedback mechanism, as if the thyroid hormone levels get too high then the TSH will stop signaling the thyroid gland to produce thyroid hormone, and if the thyroid hormone levels get too low the TSH will increase in an effort to tell the thyroid gland to produce more thyroid hormone.

TSH during hypothyroidism.  High TSH levels typically are associated with an underactive thyroid gland.  In other words, if someone has depressed or less than optimal thyroid hormone levels then the TSH will typically increase.  As mentioned above, what happens is that when the thyroid hormone levels become too low the pituitary gland will produce more TSH in order to stimulate the thyroid gland to produce more thyroid hormones.  Sometimes the TSH will be quite elevated, where it is obvious to any doctor that the person has a thyroid problem (or possibly a pituitary issue).  But what happens more frequently is that the TSH is within the lab reference range, but outside of the “optimal” reference range.  Unfortunately many medical doctors don’t look at the “optimal” reference range, but will only pay attention to a marker if it is out of range.

TSH during hyperthyroidism.  On the other hand, someone with an overactive thyroid (hyperthyroidism) will usually have a low or depressed TSH.  The reason for this is because when someone has elevated thyroid hormone levels this will cause the pituitary gland to produce less TSH so that the thyroid gland will stop or slow down thyroid hormone production.  It’s important to understand that in most cases of hyperthyroidism where someone is taking antithyroid medication (i.e. methimazole) or antithyroid herbs (i.e. bugleweed) the thyroid hormone levels will start decreasing before the TSH starts increasing.  In fact, it’s very common to see someone take antithyroid medication or bugleweed who has normal thyroid hormone levels, but their TSH is still depressed.  In most cases the TSH will eventually increase and normalize.

Reference ranges:

Labcorp: 0.450-4.50 uIU/ml

Quest: 0.40-4.50 uIU/ml

Optimal reference range: 1.0 to 2.0 uIU/ml

TOTAL THYROXINE (TOTAL T4)

Thyroxine, also known as T4, is a type of thyroid hormone.  Approximately 85% of thyroid hormone released by the thyroid gland is T4, with approximately 15% being T3.  When looking at total T4, you need to keep in mind that most of the T4 is protein-bound.  In other words, most of the T4 produced by the thyroid gland (as well as T3) binds to a protein, which is then transported around the bloodstream.  I’ll discuss this in greater detail when I talk about thyroid-binding globulin below.

Total T4 during hypothyroidism.  Hypothyroidism is characterized by low thyroid hormone levels, including total T4.  It’s important to mention that many people with Hashimoto’s thyroiditis have subclinical hypothyroidism, which is characterized by an elevated TSH and normal thyroid hormone levels.  Many times in those with Hashimoto’s the total T4 will be within the lab reference range, but below the optimal reference range.

Total T4 during hyperthyroidism.  Those with overt hyperthyroidism will usually have elevated total T4 levels, although there are times when I see the free T4 elevated and the total T4 on the high side, but within the lab reference range.

Labcorp: 4.5−12.0 mcg/dL

Quest: 5.1-11.9 mcg/dL

Optimal reference range: 6.0 to 11.0 pg/ml

FREE THYROXINE (FREE T4)

Free T4 represents the free form of thyroxine in the blood.  When discussing total T4 I mentioned that most of the T4 is bound to a protein, with a very small percentage being free.  So just to clarify the difference between total T4 and free T4, the total T4 looks at the BOTH the T4 that’s bound to a protein and the free T4 in circulation, whereas when testing the free T4 by itself this obviously is only looking at the free form of the hormone.

Free T4 during hypothyroidism.  Hypothyroidism is characterized by low thyroid hormone levels, including free T4.  As is the case with the total T4, if someone has subclinical hypothyroidism then they will have an elevated TSH and free T4 levels that fall within the lab reference range, although they might be less than the optimal reference range.

Free T4 during hyperthyroidism.  Those with overt hyperthyroidism will have elevated free T4 levels.  If someone has subclinical hyperthyroidism they will have a depressed TSH and free T4 levels that fall within the lab reference range, although sometimes they will be on the high end of the range.   If someone with hyperthyroidism is receiving treatment with antithyroid medication (or antithyroid herbs), free T4 is the test of choice to determine whether the treatment is working since the TSH may remain low for weeks to months.  So as I mentioned earlier, for those with a depressed TSH and elevated thyroid hormone levels who are taking antithyroid medication, it’s common to see the TSH remain depressed for quite awhile, even when the thyroid hormone levels are decreasing in response to the antithyroid medication.

Labcorp: 0.82-1.77 ng/dL

Quest: 0.8-1.8 ng/dL

Optimal reference range: 1.1 to 1.5 ng/dL

TOTAL TRIIODOTHYRONINE (TOTAL T3)

Total T3 consists of both the bound form of T3 and the free T3 in circulation.  So just as is the case with total T4, with total T3 you’ll have most of the T3 bound to a protein, and a small percentage of the hormone is free, and can therefore bind to the thyroid hormone receptors.  When you think about it this makes sense, as you wouldn’t want all of your thyroid hormones to bind to thyroid receptors simultaneously, and so most of them are attached to proteins, and when needed they are released and become the free form, which will bind to the thyroid hormone receptors and have physiological effects.

Total T3 during hypothyroidism.  If someone has overt hypothyroidism then they will see total T3 levels below the reference range, but in subclinical hypothyroidism the total T3 will be within the lab reference range, although it might be below the optimal reference range listed below.

Total T3 during hyperthyroidism.  Those with overt hyperthyroidism will usually have elevated total T3 levels.

Labcorp: 71−180 ng/dL

Quest: 76-181 ng/dL

Optimal reference range: 100-160 ng/dL

FREE TRIIODOTHYRONINE (FREE T3)

Triiodothyronine is the active form of thyroid hormone, and the free form of the hormone (free T3) is what binds to the thyroid hormone receptors.

Free T3 during hypothyroidism.  If someone has overt hypothyroidism then they will have a free T3 below the lab reference range.  If someone has subclinical hypothyroidism then they will have an elevated TSH and free T3 levels that fall within the lab reference range, although they might be less than the optimal reference range.  It’s also important to know that many people have problems converting T4 to T3, which will show up on a lab as a normal free T4 with a low or depressed free T3, and I’ll discuss some of the common causes of conversion problems when discussing reverse T3.

Free T3 during hyperthyroidism.  Those with overt hyperthyroidism will have elevated free T3 levels.  If someone has subclinical hyperthyroidism they will have a depressed TSH and free T3 levels that fall within the lab reference range, although sometimes they will be on the high end of the range.   It’s also worth mentioning that some patients with hyperthyroidism have “T3 toxicosis” where the T4 is normal but there is an elevation of T3 (1).

Labcorp: 2.0-4.4 pg/ml

Quest: 2.3-4.2 pg/ml

Optimal reference range: 3.0 to 3.7 pg/ml

REVERSE T3

The number “4” in T4 means that it has 4 iodine molecules, and if it loses one of them it will yield either T3 or reverse T3, depending on which iodine molecule it loses.  So reverse T3 is manufactured from T4, and the role of reverse T3 is to block the action of T3.  When testing the reverse T3 the main concern is having elevated levels.

Reverse T3 during hypothyroidism.  One of the most common problems I see with patients is a problem converting T4 to T3.  There can be numerous causes of this, but regardless of the cause, when this occurs it’s common to see an elevated reverse T3.  Since most of the conversion of T4 to T3 takes place in the liver, having a liver problem can affect the conversion of T4 to T3, and thus cause an elevated reverse T3.  Some of this conversion also takes place in the gut, and thus an unhealthy gut microbiome can be a factor in an elevated reverse T3.  Elevated cortisol levels can also affect the conversion of T4 to T3, and even inflammation can be a factor.  Anything that results in a decrease of T4 to T3 conversion can cause an elevated reverse T3.

Reverse T3 during hyperthyroidism.  Most people with hyperthyroidism and Graves’ disease will have an elevated reverse T3.  The reason is because with hyperthyroidism there is an excessive amount of T4, and while a lot of this will convert to T3, a good amount of reverse T3 will also be manufactured from the high levels of T4.

Labcorp: 9.2-24.1 ng/dL

Quest: 8-25 ng/dL

Optimal reference range: 10-18 ng/dL

FREE THYROXINE INDEX (FTI)

Most doctors order the free T4 instead of the free thyroxine index (FTI), although every now and then I’ll still see this on a report.  The FTI is determined by the following calculation: Thyroxine (T4)/Thyroid Binding Capacity.

Hyperthyroidism usually causes increased FTI and hypothyroidism causes decreased values.  The FTI isn’t something I specifically recommend for my patients to order, although some thyroid panels will include this marker.

Labcorp: 1.2-4.9 mg/dL

Quest: 1.4-3.8 mg/dL

Optimal reference range: 1.5-3.7 mg/dL

T3 UPTAKE

The T3 uptake measures the amount of receptor sites available on thyroxine-binding globulin (TBG).  So essentially it is an indirect measurement of TBG binding capacity.  The more binding sites that are available on TBG, the lower the T3 uptake will be.  So for example, if someone has hyperthyroidism and has a high total T4, they will have less available binding sites since there is an excessive amount of thyroid hormone bound to those proteins, and this will usually result in a high T3 uptake.  On the other hand, if someone has low total T4 levels, they will have more binding sites available on TBG, and this will have a lower T3 uptake.

Labcorp: 24-39%

Quest: 22-35%

Optimal reference range: 25-33%

THYROXINE-BINDING GLOBULIN (TBG)

Thyroxine-binding globulin (TBG) is manufactured by the liver, and is one of the proteins responsible for transporting thyroid hormones from blood to tissues.  So both T4 and T3 bind to TBG and are transported to the target tissues.  As a result, an increase or decrease of TBG can alter the total concentrations of T4 and T3 in the blood.  For example, estrogen therapy (or taking oral contraceptives) can increase TBG, which means that TBG will bind to more thyroid hormones, which will decrease the free hormone available in the blood.  So in this case we commonly would see a high total T4 and a low free T4.

On the other hand, corticosteroids will lower TBG levels, and so TBG will bind to less thyroid hormone levels.  This will result in low total and free thyroid hormones.  I know this might be a little confusing to some reading this, but the truth is that TBG is a marker that most people don’t need to test for.

Labcorp: 13−39 mcg/mL

Quest: males (12.7-25.1 mcg/mL); females (13.5-30.9 mcg/mL)

Optimal reference range: 18-27 mcg/mL

THYROID PEROXIDASE (TPO) ANTIBODIES

Thyroid peroxidase (TPO) is an enzyme involved in the synthesis of T3 and T4, as it converts iodide to iodine, and the iodine combines with tyrosine on thyroglobulin.  This in turn forms T4 and T3.  Anti-TPO antibodies are the most common type of thyroid autoantibody, as it is present in most people with Hashimoto’s thyroiditis, and many people with Graves’ disease also have elevated anti-TPO antibodies.  Since TPO is involved in the synthesis of T3 and T4, having elevated anti-TPO antibodies can lead to the decreased enzymatic production of thyroid hormone.  Anti-TPO antibodies are also frequently seen in the general population and are 5-fold more common in women than in men.

Labcorp: 0-34 IU/ml

Quest: <9 IU/ml

Optimal reference range: <9 IU/ml

THYROGLOBULIN

Thyroglobulin is a glycoprotein that is produced by thyroid follicular cells. T4 and T3 are synthesized on thyroglobulin within the lumen of thyroid follicles.  Conventional medical doctors use thyroglobulin as a tumor marker, although research shows that elevated levels can also indicate an iodine deficiency (2) (3).  Because thyroglobulin is only produced by thyroid follicular cells, if someone has a total thyroidectomy they should have an undetectable thyroglobulin level, and the same is true for many people who receive radioactive iodine treatment.

Labcorp: 1.4-29.2 ng/mL

Quest: unable to find reference range

Other Lab: 1.7-56.0 ng/mL

Optimal reference range: 2.0-29.2 ng/mL

THYROGLOBULIN ANTIBODIES

I just discussed what thyroglobulin is, and so when someone has elevated anti-thyroglobulin antibodies, this means that the immune system is damaging thyroglobulin, which over time can lead to hypothyroidism.  These anti-thyroglobulin antibodies are associated with Hashimoto’s thyroiditis.  When looking at the lab reference ranges from Labcorp and Quest Diagnostics you’ll see that both ranges suggest that there should be almost no anti-thyroglobulin antibodies, whereas some labs will have much higher ranges, even though they are using the same units.

Labcorp: 0.0-0.9 IU/ml

Quest: <1 or = 1 IU/ml

Other Lab: <20 IU/ml

Optimal reference range: <1 IU/ml

TSH RECEPTOR ANTIBODIES (TRAB)

There are two types of TSH receptor antibodies. Thyroid stimulating antibodies (TSAb), also known as thyroid stimulating immunoglobulins (TSI), are the main antibodies associated with Graves’ Disease.  These antibodies bind to the TSH receptor, which causes thyroid growth, increases the vascularity of the thyroid gland, and causes an excessive production of thyroid hormone.

There are also blocking TRABs, also known as thyrotropin-binding inhibiting immunoglobulins, which can be found in approximately 15% of patients with thyroid autoimmunity (4).

Regarding the reference ranges, I’m going to specifically list the ranges for the thyroid stimulating immunoglobulins below, since this is the most common antibody associated with Graves’ disease.  However, it’s important to know that recently some of the labs (including Labcorp) changed the units associated with this marker.  As a result, when retesting this marker it would be a good idea to use the same lab for comparison purposes.

Labcorp: 0.00-0.55 IU/L

Quest: <140% Baseline

Optimal reference range: <0.55 IU/L or <80%

CALCITONIN

Calcitonin is usually measured if someone is suspected to have medullary thyroid cancer, which is a rare form of thyroid cancer that usually causes an increase in calcitonin.  As a result, it’s not something I commonly test for in my practice.

Labcorp: Male: 0.0−8.4 pg/mL; female: 0.0−5.0 pg/mL

Quest: unable to find reference range

Two Other Thyroid-Specific Diagnostic Tests Worth Mentioning:

THYROID ULTRASOUND

An ultrasound uses sound waves to develop images, and many endocrinologists will recommend a thyroid ultrasound to their patients with Graves’ disease and Hashimoto’s.  There are a few benefits of thyroid ultrasounds, as they are non-invasive, they don’t use ionizing radiation, and they’re not as costly as other imaging techniques (i.e. CT scan, MRI).  But does this mean that everyone with a thyroid or autoimmune thyroid condition should receive a thyroid ultrasound?

I discussed this in detail in a past blog post I wrote entitled “Should You Get a Thyroid Ultrasound?”  In the post I discussed the indications of a thyroid ultrasound according to the American Association of Clinical Endocrinologists.  If you haven’t had a thyroid ultrasound done and are wondering if you need one I would recommend to check out this blog post.

RADIOACTIVE IODINE UPTAKE TEST

This test involves either swallowing or injecting a small amount of radioactive iodine, which allows practitioners to see how active the thyroid tissue is.  The way this test works is that the thyroid gland absorbs the small dosage of radioactive iodine, and is evaluated after six hours and 24 hours.  Graves’ disease is typically characterized by a high uptake of radioactive iodine.

While many endocrinologists will recommend the radioactive iodine uptake test to confirm or rule out Graves’ disease, most of the time this test is unnecessary.  In fact, if someone has hyperthyroidism in the presence of elevated TSH receptor antibodies then this confirms Graves’ disease.  While some doctors will recommend the radioactive iodine uptake test to see if someone has “hot” or “cold” nodules, you can’t confirm or rule out a malignant thyroid nodule with the radioactive iodine uptake test alone.

Which Of These Markers Have You Tested For?

I’d love to hear which of these markers you have tested for. I assume most reading this have had some of the basic thyroid markers (TSH, free T3, free T4), and many have also had the thyroid antibodies tested. If there are any other blood test markers and/or other thyroid-specific tests you think I should have included in this blog post please let me know!

When I was dealing with Graves’ disease, one of the most prominent symptoms I experienced was heart palpitations.  The same is true with many of my patients with hyperthyroidism and Graves’ disease, although occasionally I’ll also have people with hypothyroidism and Hashimoto’s tell me that they’re experiencing palpitations.  While thyroid hormone imbalances can cause heart palpitations, there can be numerous other causes.  In this blog post I’ll discuss many of these causes, when you should be concerned about heart palpitations, and towards the end I’ll discuss some natural treatment solutions.

It makes sense to begin by discussing what palpitations are.  Here are some common descriptions of heart palpitations (1):

• An abnormally rapid or irregular beating of the heart
• A skipped beat and/or rapid fluttering in the chest
• A pounding sensation in the chest or neck
• A flip-flopping sensation in the chest

The good news is that the cause of palpitations is usually benign, although sometimes they can be a sign of a life-threatening condition.  Many people get diagnosed with hyperthyroidism because of the heart palpitations they’re experiencing.  In other words, prior to getting diagnosed with hyperthyroidism, many people will decide to get checked by a medical doctor mainly because they’re experiencing heart palpitations, and will then find out that they have hyperthyroidism.

My situation was different, as prior to being diagnosed with hyperthyroidism I was losing a lot of weight and had an increased appetite, but it was an elevated resting heart rate that led me to schedule an appointment with a medical doctor who ended up diagnosing me with hyperthyroidism (and referred me to the endocrinologist who diagnosed me with Graves’ disease).  In the opening paragraph I mentioned how my heart palpitations were prominent, but I really didn’t start noticing them until after I was diagnosed.

What Can Cause Heart Palpitations?

Let’s take a look at some of the different factors that can cause heart palpitations.  You’ll notice that some of these are actual conditions (i.e. hyperthyroidism), but I’ve listed other factors as well, such as consuming too much caffeine.  It’s worth mentioning that these aren’t listed based on the frequency of occurrence.  For example, hyperthyroidism is listed first not because it’s the most common cause of heart palpitations, but because I work with a lot of people with hyperthyroidism.

• Hyperthyroidism.  This is what caused my heart palpitations in the past, and it is the most common cause of palpitations in my practice.
• Hypothyroidism. When someone with hypothyroidism experiences heart palpitations it usually isn’t due to the low thyroid hormone levels, but other factors, such as sex hormone imbalances and/or high cortisol levels.
• Taking too much thyroid hormone replacement.  I could have discussed this under “hyperthyroidism”, but I figured that some people with hypothyroidism and Hashimoto’s who are overdosing would miss it if I didn’t list it separately.  Although overdosing with thyroid hormone replacement isn’t something I commonly see in my practice, it does happen from time to time.  Some practitioners prefer to see the TSH of their hypothyroid patients who are taking thyroid hormone replacement on the low side, but if the person’s thyroid hormone levels are on the high side and/or the person is experiencing heart palpitations and other hyperthyroid symptoms, then the dosage should be reduced.
• Weaning off of beta blockers.  Sometimes weaning off of beta blockers such as Propanolol and Atenolol can cause heart palpitations.  This is especially true when they are abruptly stopped.
• Stress and anxiety.  We all know that stress can cause a lot of symptoms, and heart palpitations are one of these symptoms.  Anxiety can also cause palpitations, and it’s quite common for my patients to experience anxiety, especially those with hyperthyroidism and Graves’ disease.
• Excess caffeine.  Coffee of course is the most common culprit, although other sources of caffeine can also cause heart palpitations, including black tea, green tea, and chocolate.
• Anemia.  This can be confirmed through a complete blood count (CBC) with differential.  Many people associate anemia with an iron deficiency, although it’s important to remember that there can be other causes.
• Hypoglycemia.  This is yet another potential cause of heart palpitations, and sometimes it can be difficult to diagnose.  Having low fasting blood glucose and insulin levels is a sign of hypoglycemia, along with symptoms such as shakiness and/or irritability when skipping meals, dizziness, and fatigue that is relieved by eating.
• Electrolyte imbalances.  Low calcium, high or low potassium, and/or low magnesium levels can cause palpitations.  A comprehensive metabolic panel (CMP) measures the electrolytes, and is something I recommend for everyone to get.
• Certain medications.  I mentioned that too much thyroid hormone replacement can cause heart palpitations, but other medications that can cause them include amphetamines, anticholinergic drugs, and vasodilators.
• Sex hormone fluctuations.  Due to fluctuations in estrogen and progesterone, heart palpitations can occur in women of all ages, including cycling women (i.e.  the luteal phase of the menstrual cycle), during pregnancy, and the perimenopausal period.
• Structural abnormalities.  Examples include cardiomegaly associated with congenital heart disease, aortic aneurysm, and acute left ventricular failure.

When Are Palpitations a Concern?

I mentioned earlier how most heart palpitations are benign.  Many of my patients with hyperthyroidism and Graves’ disease experience heart palpitations, and while I can’t say that there isn’t a concern in these situations, correcting the hyperthyroidism will almost always resolve the heart palpitations.  It’s also worth mentioning that anxiety is very common in people with hyperthyroidism, and so this can also be a factor.  There are times when heart palpitations are related to an underlying cardiac condition, including an arrhythmia.  One should especially be concerned when someone has symptoms such as perspiration, fainting, alternating headaches, and vertigo or chest pain, as these can be indications of weak or irregular heart function which must be seriously examined (2).

Regarding my patients with hyperthyroidism and Graves’ disease, I’m more concerned with the elevated resting heart rate.  After all, it’s the elevated heart rate that is a risk factor for the development of an arrhythmia/atrial fibrillation.  Fortunately, upon decreasing the thyroid hormone levels there usually is a reduction of both the resting heart rate and palpitations.

Evaluation of Heart Palpitations

As I mentioned earlier, I commonly encounter patients with heart palpitations, which isn’t surprising since many of my patients have hyperthyroidism and Graves’ disease.  If someone didn’t experience heart palpitations until they developed hyperthyroidism, then one can usually assume that the heart palpitations were related to the elevated thyroid hormone levels.  However, it still is important to conduct a comprehensive health history and physical examination to rule out other causes or contributing factors.

For example, I mentioned how anemia and electrolyte imbalances can cause heart palpitations.  As a result, in addition to getting a thyroid panel, it is wise for everyone with any health condition to get a complete blood count (with differential) and comprehensive metabolic panel.  It’s also important to find out what medications the person is taking, if they consume caffeine on a regular basis, find out if they’re consuming alcohol, etc.  Adrenal testing can determine if they have elevated cortisol levels that are causing or contributing to the heart palpitations.

There of course are times when further evaluation of the heart is required.  For example, if someone is considered to be a high risk for an arrhythmia then an ambulatory EKG monitoring device might be indicated, such as a Holter monitor.  This is a 24-hour monitoring device worn by the patient.  Echocardiograms are commonly recommended for patients in whom structural heart disease is a concern.

Conventional Treatments for Heart Palpitations

Conventional treatments for heart palpitations depend on the cause.  For example, if someone has hyperthyroidism then the person will usually be told to take antithyroid medication and/or beta blockers, although many endocrinologists will recommend for their hyperthyroid patients to permanently ablate the thyroid gland through radioactive iodine.  If the heart palpitations are caused by something other than hyperthyroidism then this may be addressed by the medical doctor.

Natural Treatment Solutions for Heart Palpitations

While conventional treatment methods are sometimes necessary, of course the goal of a natural treatment approach is to address the underlying cause of the problem.  However, while doing this the person might need to take medication and/or herbs to help manage the symptoms.  For example, when I was dealing with Graves’ disease I took the herb bugleweed to help lower the thyroid hormone levels, and because I still experienced heart palpitations I ended up adding motherwort.  Both of these herbs don’t do anything to address the underlying cause of the condition, but instead manage the symptoms.

What I’d like to do is first list some things you can do to address the cause of heart palpitations, and then I’ll discuss some specific herbs which can help with the symptoms while one is addressing the cause.

• Lower the thyroid hormone levels.  If someone has heart palpitations due to hyperthyroidism, then it makes sense that lowering the thyroid hormone levels will usually help to resolve the heart palpitations.
• Be aware of medications that cause heart palpitations.  I already mentioned some of the medications that can cause heart palpitations, including amphetamines, anticholinergic drugs, and vasodilators.
• Decrease stress and anxiety.  Although I group these two together because there is some overlap, sometimes stress and anxiety need to be dealt with separately.  For example, someone might have a lot of chronic stress in their life which leads to anxiety, and in this situation addressing the stress should help with the anxiety.  Hyperthyroidism itself can cause anxiety, and in this situation, normalizing the thyroid hormone levels should resolve the anxiety.
• Reduce consumption of stimulants.  If you’re consuming caffeine on a regular basis then it makes sense to reduce your consumption, or better yet, take a break from the coffee, chocolate, etc.
• Address anemia.  Many people with anemia don’t take it seriously, but being anemic can lead to numerous health consequences.  In fact, when I see someone with anemia who has heart palpitations, the palpitations are frequently the least of my concerns.
• Balance blood sugar levels.  If someone has hypoglycemia this needs to be addressed.  Sometimes changing one’s diet and eating regularly can make a big difference, although some cases of hypoglycemia can be complex.
• Correct electrolyte imbalances.  If someone has low levels of calcium, potassium, and/or magnesium, then it makes sense to correct these imbalances.

Herbs That Can Help With Heart Palpitations

I just want to let you know that the list of herbs below isn’t all inclusive, as there can be other herbs, as well as nutrients that can potentially help to reduce heart palpitations.

• Hawthorn (Crataegus oxyacantha).  Many healthcare practitioners recommend hawthorn for overall cardiovascular support.  Not only can hawthorn help with heart palpitations, but it exerts a wide range of cardiovascular pharmacological properties, including antioxidant activity, anti-inflammatory effect, anticardiac remodeling effect, antiplatelet aggregation effect, vasodilating effect, endothelial protective effect, reduction of smooth muscle cell migration and proliferation, protective effect against ischemia/reperfusion injury, antiarrhythmic effect, lipid-lowering effect and decrease of arterial blood pressure effect (3).
• Motherwort (Leonurus cardiaca).  As I mentioned earlier, I took motherwort to help with my heart palpitations when I was dealing with Graves’ disease, and I’ve had many others with hyperthyroidism take this herb over the years.  Pharmacological studies have confirmed its effects on the heart and circulatory system, but motherwort also has antibacterial, antioxidant, anti-inflammatory and analgesic activity (4).
• Bugleweed.  This herb doesn’t specifically support the cardiovascular system, but by lowering thyroid hormone levels in those with hyperthyroidism it can help with heart palpitations.  In my situation taking bugleweed alone didn’t completely eliminate my palpitations, as I mentioned a few times in this post that I ended up adding motherwort.  However, some people do fine with bugleweed alone and don’t need to add motherwort.
• Lemon Balm (Melissa officinalis).  This herb has a calming effect and can help with heart palpitations, but also can benefit people with menstrual problems, hypertension, migraines, vertigo, depression, asthma, eczema, and advanced studies have demonstrated neuroprotective, anxiolytic, antispasmodic, antihyperlipidemic, and hepatoprotective effects (5).
• Valerian (Valeriana officinalis).  Since anxiety is a potential cause of heart palpitations, it makes sense that certain herbs that can help to reduce anxiety can also reduce heart palpitation.  These include valerian root (6), St. John’s Wort (7), and passionflower (8).  Just keep in mind that if hyperthyroidism is the cause of the person’s anxiety then the primary goal should be to reduce the thyroid hormone levels.
• Cortisol-lowering herbs.  High cortisol can also cause heart palpitations.  While taking herbs isn’t a substitute for lowering stress levels and improving stress management skills, certain herbs can aid in lowering cortisol levels by helping us to better adapt to the stress.  This includes herbs such as ashwagandha (which is a member of the nightshade family), rhodiola, and relora.

What’s Your Experience With Heart Palpitations?

If you have dealt with heart palpitations (or currently deal with them) please share your experience in the comments section below.  Were your palpitations caused by hyperthyroidism, hypothyroidism, or something else?  What helped to reduce your heart palpitations?  Thank you for sharing your experience!

Autoimmune conditions are characterized by the presence of autoantibodies.  It’s no exception with Graves’ disease and Hashimoto’s thyroiditis.  While most endocrinologists focus on improving the thyroid panel (TSH and thyroid hormones), very few conventional medical doctors will do anything to improve the health of the person’s immune system, and thus normalize thyroid antibodies.  The main reason for this comes down to their training in medical school, as they aren’t taught how to address the autoimmune component of these conditions.  And it admittedly can be very challenging to normalize thyroid antibodies, which I’ll talk more about later this blog post.

Before discussing how to lower autoantibodies, I’d like to briefly discuss what antibodies are.  Antibodies, also known as immunoglobulins, are Y-shaped molecules that help to protect the body against foreign substances called antigens.  Examples of antigens include bacteria, viruses, fungi, chemicals, and there can even be dietary antigens.  Essentially antigens lead to the formation of antibodies, and each antibody is manufactured to match a specific antigen.  In autoimmunity, autoantibodies are produced against self-antigens, or against the cells of your own body.

I mentioned that antibodies are also known as immunoglobulins, and there are five immunoglobulin classes found in the serum:

Immunoglobulin A (IgA)

Immunoglobulin D (IgD)

Immunoglobulin E (IgE)

Immunoglobulin G (IgG)

Immunoglobulin M (IgM)

When discussing autoantibodies, we’re mostly referring to IgG.  This includes the antibodies associated with Graves’ disease and Hashimoto’s. IgG is further divided into four subclasses, and the majority of known antibody-mediated autoimmune diseases are caused by IgG1 and IgG3 autoantibodies, although IgG4 plays a prominent role in the pathogenesis of at least 13 autoimmune diseases. (1).

With Graves’ disease, unique IgG antibodies bind to and activate the TSH receptor on the surface of thyroid follicular cells, which leads to an increased production of thyroid hormones (1).  Antithyroglobulin antibodies and antithyroperoxidase antibodies are also predominantly of the IgG class (2).  It has been reported that Hashimoto’s thyroiditis can be divided into IgG4 and non-IgG4 thyroiditis (2).

The 3 Main Types of Thyroid Antibodies

Let’s briefly take a look at the three most common types of thyroid antibodies:

Thyroid peroxidase (TPO) antibodies.  Thyroid peroxidase (TPO) is an enzyme that plays a role in the production of thyroid hormone.  TPO antibodies are the most common type of thyroid antibody.  Although they are more closely associated with Hashimoto’s thyroiditis, many people with Graves’ disease have elevated TPO antibodies.

Thyroglobulin antibodies.  Thyroglobulin is a glycoprotein that is secreted by thyroid follicular cells, and when someone has anti-thyroglobulin antibodies this means that the immune system is attacking and damaging thyroglobulin.  These antibodies are associated with Hashimoto’s.

Thyroid stimulating immunoglobulins.  Thyroid stimulating immunoglobulins are associated with Graves’ disease, and they bind to the thyroid stimulating hormone receptor, which causes the excess production of thyroid hormone.

As I’ve discussed in other blog posts, it’s common for people to have multiple types of thyroid antibodies.  So for example, some people will have both TPO antibodies and thyroid stimulating immunoglobulins, while some will have all three of these autoantibodies.  And since people with Graves’ disease and Hashimoto’s commonly develop other autoimmune conditions it’s also possible to have other types of autoantibodies as well.

What Causes Elevated Thyroid Antibodies?

I’ve spoken about the triad of autoimmunity in the past, as there are three factors which are necessary for autoimmunity to develop, and thus lead to elevated autoantibodies.  These three factors include 1) a genetic predisposition, 2) an environmental trigger, and 3) a leaky gut.  The triad of autoimmunity applies to all autoimmune conditions, and not just Graves’ disease and Hashimoto’s.

A loss of self tolerance is also necessary, and this is when the immune system doesn’t recognize our tissues and organs as being “self”.  I discussed how people develop a loss of self tolerance in a past article, but I’ll list some of the different ways below:

1. Exposure to an environmental trigger
2. Having certain genetic polymorphisms
3. Decrease in regulatory T cells
4. Low selenium levels
5. Low vitamin A levels
6. Intestinal dysbiosis (imbalance of the gut flora)

Can Thyroid Antibodies Be Normalized?

It is possible to normalize thyroid autoantibodies.  However, there are a few things you need to understand.  First of all, different labs will commonly have different reference ranges for the same autoantibodies.  As a result, you might test positive for a specific autoantibody with one lab, but test negative for the same autoantibody with a different lab.  So how do you know which lab reference range is accurate?  First of all, you do need to keep in mind that everyone is different, and we can make the argument that some people might be fine even if their thyroid antibodies are slightly elevated according to the lab reference range.

For example, the Labcorp reference range for TPO antibodies is currently 0-34 IU/mL.  The Quest Diagnostics reference range for TPO antibodies is <9 IU/mL.  I don’t know which reference range is more accurate, and we need to keep in mind that although the units are the same with these two labs, the methodologies can differ between labs, and there are other reasons why different labs have different ranges for the same marker.

In any case, if someone has TPO antibodies that are well above the reference range (i.e. 2,000 IU/mL), then we can conclude that this is abnormal.  On the other hand, if someone has TPO antibodies that are consistently around 50 IU/mL does this mean that the autoimmune response isn’t as big of a concern?  There’s some debate here, as some well known practitioners will say that a lower number doesn’t necessarily correlate with the severity of the autoimmune response, but I think it’s safe to say that most practitioners would still like to see the antibodies on the low side.

It’s also important to understand that it’s not always easy to decrease and normalize thyroid antibodies.  In some people the thyroid antibodies will gradually decrease until they normalize without any setbacks.  For others there will be more of a “rollercoaster” pattern, as the antibodies might fluctuate back and forth until they normalize.  Then there are people with Graves’ disease and Hashimoto’s who don’t experience any significant decrease in thyroid antibodies, and in some cases their antibodies gradually increase over time.  During this latter scenario this usually means that the person’s triggers haven’t been detected and/or removed, the gut hasn’t been healed, and/or there are other underlying imbalances that need to be addressed.  I’m about to discuss this further.

4 Steps To Lower Thyroid Antibodies Naturally

Earlier I discussed the triad of autoimmunity, and how this will determine whether someone will develop elevated thyroid antibodies.  So for example, if someone has a genetic predisposition for Graves’ disease or Hashimoto’s and they are exposed to a specific environmental trigger and at the same time they have an increase in intestinal permeability (a leaky gut), then autoimmunity is likely to develop.  As a result, it shouldn’t be a surprise to learn that in order to lower thyroid antibodies you need to address these factors:

Step #1: Find the triggers.  Not finding the triggers is probably the biggest reason why someone’s thyroid antibodies don’t decrease.  Finding the triggers can admittedly be challenging at times, and usually involves doing a comprehensive health history, along with the appropriate testing.  In 2018 I wrote a book that focuses on triggers, and while the title of the book is “Hashimoto’s Triggers“, a lot of the information in this book can benefit people with Graves’ disease as well.  I also discuss triggers in my book “Natural Treatment Solutions for Hyperthyroidism and Graves’ Disease“.

Here are some potential autoimmune triggers:

• Food triggers (gluten, dairy, corn)
• Stress
• Pathogenic bacteria
• Viruses (i.e. Epstein-Barr)
• Parasites
• Heavy metals
• Xenoestrogens
• Overtraining
• Estrogen dominance

Step #2: Remove the triggers.  Once the triggers have been detected, obviously the next goal should be to remove them.  Sometimes this is easier said than done.  For example, if someone discovers that a specific food is a trigger, then of course they can remove this food from their diet.  On the other hand, if an infection or chemical is the trigger, then it can be challenging to address these at times.  Certain infections can be difficult to eradicate, regardless of whether someone takes prescription antibiotics or natural antimicrobials.  And some chemicals are more challenging to eliminate from the body than others.

Step #3: Correct underlying imbalances.  Sometimes other underlying imbalances can interfere with healing, which can in turn prevent thyroid antibodies from lowering.  For example, inflammation is associated with autoimmunity, and while finding and removing the triggers will frequently resolve the inflammation, this isn’t always the case.  Sometimes further action is required to resolve the inflammation, such as taking higher doses of natural anti-inflammatory agents (i.e. curcumin, resveratrol, glutathione).  Having deficiencies in vitamin D, selenium, and omega-3 fatty acids can make it very challenging to lower thyroid antibodies.

Step #4: Restore the health of the gut microbiome.  Having a healthy gut is necessary for a healthy immune system, and in some people, healing the gut can be challenging as well.  Although there is a lot of great information on the Internet and in books on gut healing, most people need to do more than just take gut-healing supplements and eat gut-healing foods, as you need to make sure to remove those factors which are interfering with gut healing.  This may sound like common sense, but many people only focus on reinoculation (with probiotics) and gut healing, and while these are important, doing these alone many times isn’t sufficient to restore the health of the gut.  For more information on this please read my blog post entitled “What Is The 5-R Protocol?”

Can Low Dose Naltrexone (LDN) Lower Thyroid Antibodies?

I spoke about LDN in a past article entitled “Low Dose Naltrexone and Thyroid Autoimmunity“, and so I definitely would check this out for more information on LDN.  This is an option for some people with Graves’ disease and Hashimoto’s to consider, as LDN can lower thyroid antibodies in some cases by modulating the immune system.  However, while I’m not opposed to my patients taking LDN, you need to keep a couple of things in mind.  First of all, LDN doesn’t work for everyone.  Second, even when it does work, LDN isn’t doing anything to address the underlying cause of the problem.  That being said, I mentioned earlier how sometimes it can be challenging to find and/or remove autoimmune triggers, and when this is the case there’s nothing wrong with taking LDN to modulate the immune system while still trying to address the cause of Graves’ disease or Hashimoto’s.

Is There a Role for IgG Autoantibodies in a Healthy Immune System?

Over the years some of the labs have lowered their reference range for thyroid autoantibodies, which suggests that there should be no autoantibodies found in healthy people.  For example, some labs use a reference range of ≤1 IU/mL for thyroglobulin antibodies. But multiple journal articles discuss that small amounts of autoantibodies are present even in healthy individuals (3) (4).

One study found 66 autoantibodies that are common and abundant in the population, regardless of age, gender and disease status (3).  It was suggested that IgG autoantibodies might be necessary and perform some key physiological function, including the clearance of intracellular debris during inflammation.  Perhaps some autoantibodies have important physiological functions, and thus should be present in small amounts, while others don’t offer any benefits.  Either way I think it’s safe to say that we don’t know everything about autoantibodies, and I’m sure we’ll learn even more about them in the future.

What Have You Done To Lower Thyroid Antibodies?

If you have the antibodies for Graves’ disease or Hashimoto’s (or both), please let me know what you have personally done to try to lower them, and if you were successful in doing so.  If you were successful in lowering and/or normalizing them please let me know!  And if you were unsuccessful please let me know!  Thank you for sharing your experience with everyone.

Over the last few years there has been a lot of buzz about cannabidiol, also known as CBD.  CBD can be derived from hemp or cannabis, which are both members of the same plant species, Cannabis sativa.  While both hemp-derived CBD oil and cannabis-derived CBD oil offer certain health benefits, not everyone will respond the same to each of these.  Although cannabis-derived CBD oil seems to be a much richer source of phytochemicals and cannabinoids, including a compound called tetrahydrocannabinol (THC), this doesn’t mean that hemp-derived CBD oil can’t benefit people with different types of health conditions…including thyroid and autoimmune disorders.

As for how CBD oil can help with thyroid and autoimmune thyroid conditions, cannabinoids are potent anti-inflammatory agents that can decrease proinflammatory cytokines, while increasing T-regulatory cells (Tregs) (1).  As I have discussed in past articles and blog posts, proinflammatory cytokines promote inflammation, while Tregs suppress autoimmunity.  One of the main proinflammatory cytokines associated with autoimmunity is interleukin-17 (IL-17), which is produced by Th17 cells.  And there is evidence that CBD oil can reduce levels of IL-17 (2) (3).

Of course just as is the case with other natural anti-inflammatory agents, CBD oil doesn’t do anything to address the underlying cause of the condition.  So while CBD oil might be able to help to reduce symptoms by decreasing inflammation, you still want to find and detect the triggers and correct underlying imbalances.  In other words, if you have Graves’ disease or Hashimoto’s, taking CBD oil alone probably isn’t the solution, as you need to remove your autoimmune triggers, correct other underlying imbalances, heal the gut, etc.  That being said, it’s important to add that at times removing the triggers won’t break the inflammatory cycle, and CBD oil might be helpful in this case as well.

Have You Tried CBD Oil?

The purpose of this blog post isn’t to get into detail about the benefits of CBD oil, but instead is to learn about the experiences those with thyroid and autoimmune thyroid conditions have had when taking this.  If you have taken CBD oil to improve your thyroid health (or for any other purpose) please share your experience in the comments section below.  Did you take hemp-derived or cannabis-derived CBD oil?  If you took it for your Hashimoto’s or Graves’ disease condition I’d be especially interested to see if it benefited you, how long it took before you noticed positive changes, and anything else you’d be willing to share to help others who might be interested in using CBD oil.