Most cases of Graves’ disease and Hashimoto’s thyroiditis are relatively easy to distinguish from one another.  But every now and then it’s not clear as to which autoimmune thyroid condition someone has.  Of course there are also people with non-autoimmune thyroid conditions, but I’m not referring to these cases here.  Instead I’d like to focus on Hashitoxicosis, which sometimes can be mistaken for Graves’ disease, but is actually Hashimoto’s that involves transient hyperthyroidism.

Based on what I just said, if you are experiencing hyperthyroidism, then the next question you may have is “how do I know if my hyperthyroid condition is due to Hashitoxicosis or Graves’ disease?”  Well, let’s first go ahead and look at how Graves’ disease and Hashimoto’s thyroiditis are typically diagnosed, and then you should have a better understanding as to how Hashitoxicosis is diagnosed.

How Graves’ Disease is Diagnosed

Many reading this know that I was diagnosed with Graves’ disease in 2008.  Initially I was diagnosed with hyperthyroidism, which is characterized by a depressed (and usually undetectable) thyroid stimulating hormone (TSH), along with elevated T3 and T4 levels.  I also had many of the classic symptoms associated with hyperthyroidism, including an elevated resting pulse rate, heart palpitations, tremors, weight loss, an increased appetite, more frequent bowel movements, etc.

Upon visiting an endocrinologist I had my thyroid antibodies tested.  The thyroid stimulating immunoglobulins (TSI) are the most specific antibodies associated with Graves’ disease, and these were elevated, which confirmed my Graves’ disease diagnosis.  It’s also worth mentioning that TSI is a type of TSH receptor antibody (TRAB), and many times this is tested for instead of TSI, while sometimes both of these are tested by endocrinologists.

Endocrinologists also commonly recommend the radioactive iodine uptake test as a way to determine that someone has Graves’ disease.  I didn’t have this test done, and to be honest, most people with Graves’ disease don’t need to have this test done.  If you have hyperthyroidism in the presence of elevated TSI levels then this confirms that you have Graves’ disease.  Some doctors will argue that the radioactive iodine uptake test can also reveal whether someone has hot or cold nodules, which is true, but of course a thyroid ultrasound can also detect thyroid nodules, and the characteristics of an existing thyroid nodule on an ultrasound can give an idea as to whether a nodule is malignant or benign.  It’s not perfect, but neither is the radioactive iodine uptake test, and an ultrasound is much less invasive than the radioactive iodine uptake scan.

So let’s go ahead and summarize how Graves’ disease is diagnosed:

• Depressed (usually undetectable) thyroid stimulating hormone (TSH)
• Elevated thyroid hormone levels (T3 and T4)
• Elevated thyroid stimulating immunoglobulins (TSI)
• Elevated radioactive iodine uptake test (remember that this isn’t needed to diagnose Graves’ disease if the TSI is positive)

How Hashimoto’s Thyroiditis is Diagnosed

Hashimoto’s thyroiditis frequently takes longer to diagnose than Graves’ disease, and the main reason for this is because if someone is experiencing hyperthyroidism the person is more likely to seek immediate medical attention, whereas if someone is experiencing hypothyroid symptoms (i.e. fatigue, weight gain, cold hands and feet) they are less likely to take immediate action.  The reason why many people with these symptoms don’t consult with a doctor sooner than later is because many other factors can cause similar symptoms, and so it can be challenging to make the connection purely from a symptomatic standpoint.  On the other hand, the symptoms of hyperthyroidism are usually more alarming, as if someone has an elevated resting heart rate of 100+ BPM along with palpitations, tremors, weight loss, in some cases the symptoms of thyroid eye disease, etc., then they are much more likely to schedule an appointment with a doctor.

What also makes it challenging is that many people with Hashimoto’s don’t have overt hypothyroidism, but instead they have subclinical hypothyroidism.  This means that they have elevated thyroid stimulating hormone (TSH) levels, but their thyroid hormone levels look fine…at least from a lab reference range perspective.  Regarding Graves’ disease, some people with this condition do experience subclinical hyperthyroidism, but this is not as common as subclinical hypothyroidism.  In fact, it’s safe to say that just about everyone with Hashimoto’s will present with subclinical hypothyroidism prior to developing overt hypothyroidism.

I discussed this in a past blog post entitled “What Causes Thyroid Autoimmunity?“, where I discussed the autoimmunity timeline.  With Hashimoto’s, the development of thyroid autoantibodies occurs first, and then over time the TSH usually becomes elevated.  After this it can take months or years before the thyroid hormone levels become out of range.  It’s important to mention that in many people the thyroid hormones will never become overtly depressed, but there is a good chance that eventually they will become less than optimal.  In other words, they might look fine on a blood test report, but be outside of the “functional reference range”.  But even in this situation it usually takes time for this to occur.

In any case, there are two thyroid autoantibodies commonly associated with Hashimoto’s.  These include thyroid peroxidase (TPO) and thyroglobulin antibodies.  If someone has an elevated TSH and at least one of these antibodies are elevated, then this is when they are typically diagnosed as having Hashimoto’s thyroiditis.  Once again, this can happen in the present of normal, depressed, or less than optimal thyroid hormone levels.  This is why some doctors don’t even bother to test the thyroid hormone levels, but will only look at the TSH (keep in mind that this isn’t something I recommend, as I feel it’s important to also measure the thyroid hormone levels).  It’s also worth mentioning that some sources will refer to those who have an elevated TSH, depressed thyroid hormone levels, and elevated TPO and/or thyroglobulin antibodies as having “Hashimoto’s hypothyroidism”.  For the sake of simplicity I always refer to this condition as “Hashimoto’s thyroiditis” in my blog posts.

So let’s go ahead and summarize how Hashimoto’s thyroiditis is diagnosed:

• Elevated thyroid stimulating hormone (TSH)
• Elevated thyroid peroxidase (TPO) and/or thyroglobulin antibodies
• Normal, less than optimal, or depressed thyroid hormone levels (T3 and T4)
• Negative radioactive iodine uptake test (usually not recommended when Hashimoto’s is suspected)

How Is Hashitoxicosis Diagnosed?

After reading this you now know that Graves’ disease is diagnosed when someone has a depressed TSH, elevated thyroid hormone levels, and elevated TSI levels (or an elevated radioactive iodine uptake test).  On the other hand, Hashimoto’s thyroiditis is diagnosed with an elevated TSH, along with elevated TPO and/or thyroglobulin antibodies.  As for how Hashitoxicosis is diagnosed, the person will present with hyperthyroidism (depressed TSH and elevated thyroid hormone levels), but unlike Graves’ disease, the TSI levels and radioactive iodine uptake test will both be negative.  However, at least one of the autoantibodies associated with Hashimoto’s (TPO and thyroglobulin antibodies) will be positive.

So let’s go ahead and summarize how Hashitoxicosis is diagnosed:

• Depressed thyroid stimulating hormone (TSH)
• Elevated thyroid hormone levels (T3 and T4)
• Elevated thyroid peroxidase (TPO) and/or thyroglobulin antibodies
• Normal thyroid stimulating immunoglobulins (TSI)
• Negative radioactive iodine uptake test

Why Do Some People With Hashimoto’s Have Hashitoxicosis?

So just as a reminder, Hashitoxicosis is a state of hyperthyroidism that occurs in some people with Hashimoto’s, but it’s differentiated from Graves’ disease in that people won’t have elevated TSI levels.  So essentially the person will have hyperthyroidism in the presence of Hashimoto’s antibodies.  But why do some people with Hashimoto’s thyroiditis also have Hashitoxicosis?  In other words, why would someone experience hyperthyroidism if they have Hashimoto’s antibodies (and not Graves’ disease antibodies)? The hyperthyroidism experienced in someone with Hashitoxicosis is caused by the release of preformed thyroid hormones caused by the destruction of the thyroid follicles (1).

Having Antibodies For Both Graves’ Disease and Hashimoto’s

If for any reason you’re confused at this point, please go back and look at the summaries listed above.  And before wrapping up this blog post I’ll give a final summary below to further clarify everything.  But before doing this, I think it’s important to mention that it’s possible for someone to have thyroid antibodies for both Graves’ Disease and Hashimoto’s.  In fact, not only is it possible, but it is quite common.  This can occur in any of the following combination:

• Elevated TSI and TPO antibodies
• Elevated TSI and thyroglobulin antibodies
• Elevated TSI, TPO, and thyroglobulin antibodies

This may bring up another question…if someone has any combination of Graves’ disease antibodies (TSI) and Hashimoto’s antibodies (TPO, thyroglobulin), AND if they are presenting with hyperthyroidism, do they have Graves’ disease or Hashitoxicosis?  If someone has hyperthyroidism in the presence of elevated TSI levels, then this is diagnostic of Graves’ disease.  Now truth to be told, if someone has the antibodies for both Graves’ disease and Hashimoto’s and is presenting with hyperthyroidism, it’s very difficult to know for certain whether the hyperthyroidism is being caused by stimulation of the TSH receptor antibodies (typical of Graves’ disease), or by the release of thyroid hormone by the thyroid follicles (typical of Hashitoxicosis).  But to be honest, it doesn’t matter in this situation, as the treatment will be the same regardless.

In other words, from a symptom management perspective, a person with a depressed TSH, elevated thyroid hormone levels, and elevated TSI levels will want to do things to suppress the thyroid hormone levels, even in the presence of TPO and/or thyroglobulin antibodies.  And if someone has any type of thyroid autoantibody (TSI, TPO, and/or thyroglobulin antibodies), the goal should be to do whatever is necessary to reverse the autoimmune component and normalize the antibodies.  The challenge is that different types of autoantibodies can have different triggers.  For example, someone who has the antibodies for both Graves’ disease and Hashimoto’s might follow a natural treatment protocol and remove one or two triggers, thus causing normalization of one thyroid autoantibody, while another thyroid autoantibody remains elevated.  When this is the case, the goal should be to find the remaining triggers.

What’s The Best Treatment Approach For Hashitoxicosis?

Another challenge is that the hyperthyroidism associated with Graves’ disease usually will last longer than in someone who has Hashitoxicosis.  From a conventional medical standpoint, antithyroid medication such as Methimazole or PTU is commonly recommended for those with Graves’ disease.  Some people with Hashitoxicosis are also prescribed antithyroid medication, but the concern here is that since the hyperthyroidism is usually transient, the person with Hashitoxicosis who takes antithyroid medication might become overtly hypothyroid sooner than later.  As a result, if Hashitoxicosis is diagnosed then the person might be prescribed a beta blocker and not antithyroid medication.

The problem with only taking a beta blocker is that some people with Hashitoxicosis will experience hyperthyroidism for a few months.  And while a beta blocker can help to address the cardiac symptoms, elevated thyroid hormone levels shouldn’t be taken lightly, as they can have a negative effect on bone density.  In my practice I commonly recommend bugleweed to my Graves’ disease patients who aren’t taking antithyroid medication, and I have no problem recommending this herb on a temporary basis to people with Hashitoxicosis.  When this is the case it’s a good idea to do regular thyroid panels (i.e. every 2 to 4 weeks), and if someone starts experiencing hypothyroid symptoms then this is a good sign that the bugleweed needs to be reduced or stopped.

Low dose naltrexone (LDN) is also something to consider in those with Hashitoxicosis.  The downside is that LDN doesn’t address the cause of the problem, and it doesn’t work in everyone, but the upside is that when it does work it modulates the immune system, and thus the person with Hashitoxicosis might not have to take either a beta blocker or antithyroid medication/herbs (which also don’t address the underlying cause).  So what ideally would happen is that someone with Hashitoxicosis would take LDN, and the immune system would no longer damage the thyroid follicles as I mentioned earlier, and thus the person wouldn’t be hyperthyroid.

Consider a Natural Treatment Approach for Hashitoxicosis

While some people with autoimmune conditions benefit from taking LDN, of course the long term goal of Hashitoxicosis should be to reverse the autoimmune component.  This is true with any autoimmune condition, and it’s no exception with Hashitoxicosis.  While it’s important to manage the hyperthyroid symptoms, at the same time you want to find and remove environmental triggers, heal the gut, etc.  I talk about this in greater detail in other articles and blog posts.

FINAL SUMMARY

If you understand the difference between Hashitoxicosis and Graves’ disease then you probably don’t need to read this “final summary”.  On the other hand, if you’re still confused I’ll try to clarify one last time…

You Probably Have Hashitoxicosis if You Have ALL of the following:

• Depressed TSH
• Elevated thyroid hormones (T3 and T4)
• Elevated TPO and/or thyroglobulin antibodies
• Negative TSI levels
• Negative radioactive iodine uptake test (for those who get this done)

You Probably DON’T Have Hashitoxicosis if You Have ANY OF THE FOLLOWING:

• Elevated TSH
• Normal or low thyroid hormones (T3 and T4)
• Negative TPO and/or thyroglobulin antibodies
• Positive TSI levels
• Positive radioactive iodine uptake test (for those who get this done)

By now it should be obvious that if you don’t have hyperthyroidism (depressed TSH and elevated thyroid hormones) then you don’t have Hashitoxicosis.  Similarly, if you don’t have elevated TPO and/or thyroglobulin antibodies then you probably also don’t have Hashitoxicosis.  If you’re still confused as to whether you have Graves’ disease, Hashimoto’s, or Hashitoxicosis then please feel free to post your thyroid panel and antibody results in the comments section below and I’ll briefly give you my feedback.  Just keep in mind that I can’t officially diagnose your condition, and I’ll also ask to please refrain from posting other lab values in the comments, as I’ll only be providing feedback to those who post their TSH, thyroid hormone levels, and thyroid antibodies.  And if anyone reading this has experienced Hashitoxicosis and would like to share their experience please feel free to post your comment as well.

Many people use essential oils to improve their health.    Some of the different reasons people use essential oils include to help reduce anxiety, to improve sleep, to combat infections, relieve aches and pains, to reduce inflammation, they’re used as natural pesticides, as cleaning agents, and there are many, many other uses.  Not surprisingly, people with thyroid and autoimmune thyroid conditions can also benefit from using essential oils, which I’ll discuss in this blog post.

Over the years I’ve learned a lot about essential oils, and in 2018 a book was written by Dr. Eric Zielinski called “the Healing Power of Essential Oils”.  It’s an excellent book, and one that I highly recommend.  In this book he not only discusses many of the health benefits of essential oils, but also how to apply them, how to choose a reputable oil brand, etc.  While those who are new to essential oils will definitely find value from reading this book, even if you have been using essential oils for many years I think you’ll greatly benefit from some of the information.

Although I’m going to mention a few pearls from Dr. Zielinski’s book in this blog post, for those who have absolutely no knowledge of essential oils I’m going to dedicate a few sentences to describe what they are.  Essential oils, also known as volatile oils, are secondary metabolites of plants whose constituents are basically a complex mixture of terpenic hydrocarbons, especially monoterpenes and sesquiterpenes, and oxygenated derivatives such as aldehydes, ketones, epoxides, alcohols, and esters (1).  Essential oils greatly differ in their compositions. Even the composition of essential oils extracted from the plants of the same species differ in different geographic locations (2).  As for the mechanism of action of essential oils, this depends on their chemical composition (3).

Despite their name, essential oils aren’t truly essential.  They are termed “essential” because they represent the very essence and the most important part of the plant. Generally, essential oils are produced through steam distillation or mechanical expression while simple plant extracts often involve the use of solvent such as acetone, ethanol or hexane for extraction (4). During distillation, water condensate is separated by gravity leaving a very small amount of volatile liquid that is the essential oil (4).  As a result, they are extremely concentrated due to the nature of the extraction process.

The Application of Essential Oils

Let’s go ahead and take a look at some of the different ways that you can apply essential oils.

• Topical therapy. When applying essential oils topically they will be absorbed through the skin.  Using a carrier oil such as fractionated coconut oil, olive oil, or avocado oil is recommended to dilute the essential oil, which is important since they are so concentrated.  Doing this won’t reduce its effectiveness, but it will prevent skin irritation from occurring when applying the essential oil topically.  Where on your body should you apply essential oils?  Although many people apply essential oils to the bottom of their feet, according to Dr. Zielinski, applying essential oils to the bottom of your feet isn’t the most effective way to get the healing compounds into your bloodstream.  This is based on a study that discusses transdermal drug delivery, and mentions that the genitals is said to have the highest permeability followed by skin from the head and neck region, the skin at the trunk (chest, stomach, back), the skin at the arm, and finally the skin of the legs. The authors from the same study recommend that transdermal formulations should be applied to the trunk or arm since there is usually less potential for sensitization and the lower density of hair follicles leads to better tack and ease of removal.  That being said, I’m sure there are people reading this who have been applying essential oils to the bottom of their feet and still received wonderful results.
• Inhalation.  Putting essential oils in a diffuser or inhaler can also be beneficial.  A diffuser will break the essential oils down into very small compounds, and the air will carry these small doses into your respiratory system.  As for what diffuser you should use, Dr. Zielinski recommends the ultrasonic variety.
• Oral consumption. Some essential oils are safe for ingestion, and people unknowingly ingest essential oils every day when consuming certain foods and beverages.  That being said, you want to exercise caution, and it probably is a good idea to consult with an expert first.  Dr. Zielinski does mention how you shouldn’t add undiluted essential oils to a beverage or capsule.  As is the case when applying essential oils topically, when adding essential oils to a beverage or capsule he recommends diluting the oil with an edible carrier oil, such as coconut oil.  He also recommends to limit the use to two or three drops at a time.

Choosing Quality Essential Oils

My goal isn’t to promote or criticize any specific companies, but you need to remember that not all essential oils are created equal.  The chemical composition of essential oils varies widely depending upon the geographical location, botanical origin, genetics, bacterial endophytes, and extraction techniques (5).

Here are some tips to help you choose good quality essential oils:

• Try choosing an oil that is certified organic
• Find out about the sourcing
• Choose companies that use a third party to test their oils
• Request a batch report
• Test a couple of them out and see how you feel

Don’t overlook the last bullet point I listed.  While it’s ideal to use essential oils that are certified organic and third-party tested, this doesn’t mean that essential oils that don’t fit under this category aren’t effective.  If you’re currently using essential oils that aren’t organic and/or third party tested and are pretty certain that they are benefiting your health, then feel free to continue using them.  On the other hand, if you have used such essential oils and didn’t notice any therapeutic benefits then the quality could very well have been a factor.  This isn’t only true with regards to essential oils, but nutritional supplements and herbs as well.

According to Dr. Zielinski, if you try an essential oil and do not get the desired result, this doesn’t mean that the oil isn’t pure.  In his book he mentioned how this may be due to the chemical constituents that are within each batch, and that you may need to try a few different brands to find the one that works best for you.  This all relates to the last bullet point listed above, which is to test a few brands and see which one provides the greatest therapeutic benefits.

How To Use Essential Oils To Improve Thyroid Health

I think it’s safe to say that essential oils alone won’t provide a cure for thyroid autoimmunity.  If you have Graves’ disease or Hashimoto’s thyroiditis, then there are a few different ways to use essential oils to benefit your thyroid health:

1. Apply essential oils directly to your thyroid gland.  Although there is no research demonstrating that rubbing essential oils on the thyroid gland will offer any benefit, some people have reported positive changes by doing this.  As I mentioned earlier, always use a carrier oil when using any essential oils topically, including on the thyroid gland.  As for which essential oils can be applied topically to the thyroid gland, myrrh and frankincense are commonly recommended by many natural healthcare practitioners, but other essential oils can be beneficial as well.

2. Use essential oils to improve your immune system health.  While myrrh and frankincense can be rubbed directly into the thyroid gland (when combined with a carrier oil), they don’t need to be utilized this way to benefit people with Graves’ disease and Hashimoto’s.  Both of these essential oils can greatly help with the inflammatory component of autoimmune conditions, and I discussed this in an article entitled “Can Myrrh and Frankincense Benefit Thyroid Health?”

3. Use essential oils to address autoimmune triggers and underlying imbalances.  In addition to taking anti-inflammatory and immune-modulating essential oils such as myrrh and frankincense, other essential oils can potentially address the triggers of Graves’ disease and Hashimoto’s, along with some other underlying imbalances.  For example, H. pylori can be an autoimmune trigger, and while I can’t say that I commonly use essential oils in patients who test positive for this, there is evidence that certain essential oils, including lemongrass, can eradicate H. pylori (6).  And while essential oils won’t help to eliminate stress, certain essential oils such as lavender can help people to better cope with stress and anxiety (7) (8), which is a big factor in many health conditions.

What You Need To Know About Essential Oils Research

Although essential oils can benefit people with Graves’ disease and Hashimoto’s, the truth is that there is no research showing that essential oils can specifically help people with these conditions.  This isn’t to suggest that essential oils can’t help with thyroid autoimmunity (or else I wouldn’t have written this blog post), but only that there haven’t been studies which show that taking specific essential oils can benefit people with Graves’ disease and Hashimoto’s.  Similarly, I also mentioned earlier how numerous practitioners recommend for their thyroid and autoimmune thyroid patients to rub essential oils directly on their thyroid gland (combined with a carrier oil).  While some people do find this to be helpful, this isn’t based on any research study which has demonstrated that doing so can be beneficial for thyroid health.  Of course just because something isn’t in the research doesn’t mean it can’t be beneficial, and to be fair, there is also no research showing that using essential oils topically on the thyroid gland isn’t beneficial!

In Dr. Zielinski’s book he has a section entitled “Deciphering The Research”, and in this section he discusses how the majority of the research is based on “constituent studies”.  In other words, these studies focus on isolated chemicals that make up essential oils, and not the oils themselves.  And just because a study demonstrates a specific effect of an isolated chemical doesn’t mean the same effect will apply to the whole essential oil.  In his book Dr. Zielinski gives an example of menthol, which is a constituent found in peppermint.  He discusses how menthol has a different therapeutic effect than peppermint, as while peppermint does include menthol, it also includes other constituents as well.

Another thing to consider is that many studies involving essential oils are animal studies.  Now to be fair, a lot of studies involve animals, and many of them are useful and in some cases can apply to humans.  That being said, you can’t always apply the results of animal studies to humans.

Can Essential Oils Be Beneficial If You Had a Thyroidectomy?

While most of my patients have a thyroid gland, when doing some research for my blog post I came across another blog post written by someone who has a thyroid gland, and the author claimed that she was taking essential oils as a substitute for thyroid hormone replacement.  In the comments section of her post I noticed that a few people who had thyroidectomies asked if they can benefit from taking essential oils, and a few of these people wondered if they can use essential oils instead of thyroid hormone replacement.

If someone has Hashimoto’s and an intact thyroid gland, then conceivably essential oils might help with the autoimmune component, thus reducing the damage taking place to the thyroid gland, which in turn may allow them to take this in place of levothyroxine or desiccated thyroid.  This probably is an exception to the rule, although if anyone reading this has successfully used essential oils as a substitute for thyroid hormone replacement I’d love to hear from you in the comments section below.  On the other hand, if someone has had a complete thyroidectomy then there is no gland to produce thyroid hormone.  And while essential oils might help to support other areas of the body in someone who has had their thyroid gland removed, they won’t take the place of thyroid hormone.

Are There Risks With Taking Essential Oils?

Although the risks of using essential oils are minimal, this doesn’t mean they are risk-free.  There are risks with any natural agent, including nutritional supplements, Chinese herbs, and it’s no exception with essential oils.  First of all, just as anyone can have a negative reaction to an herb, it’s also possible to have a negative reaction to an essential oil.  And remember that they are very concentrated, which is another reason to be cautious, and why only a few drops diluted in a carrier oil is usually required to have a therapeutic effect.  In most cases people will do fine using essential oils in very small amounts topically with a carrier oil, or inhaling them through a diffuser or inhaler.  As I mentioned earlier, oral consumption comes with greater risks.

What’s Your Experience With Essential Oils?

I’d love to hear about your experience with essential oils in the comments section below.  If essential oils have benefited your thyroid health, immune health, or other aspects of your health please let me know!  If you used essential oils and didn’t notice any improvement in your health please let me know!   And if you have anything else to share that will benefit those interested in learning more about essential oils please feel to share this as well.

Osteoporosis affects almost 44 million men and women aged 50 and older in the United States, and evidence shows that the incidence is rising (1).  Fractures caused by osteoporosis can cause significant morbidity and loss of productivity, and the mortality rate in the first year after a hip fracture is 20 to 30% (1).  Having a thyroid or autoimmune thyroid condition can greatly affect the health of your bones, and in some cases can increase the risk of developing osteoporosis.

In 2014 I wrote an article entitled “Bone Density and Thyroid Health“.  While there will be some overlap between the past article and this current blog post, there will be also be some updated information.  One big difference between this and the previous information is that in this post I will focus more on how thyroid autoimmunity affects bone density.  It’s not just about thyroid hormone, as the inflammation associated with Graves’ disease, Hashimoto’s, and other autoimmune conditions can play a big role in the development of osteoporosis.

Bone Cells

Although many people think of bone as being static, bone undergoes continuous remodeling thanks to a few different types of bone cells.  The following comprise the four major cell types in the skeleton (2):

1. Chondrocytes.  These are responsible for forming cartilage.

2. Osteoblasts.  These are responsible for forming bone.

3. Osteocytes.  Osteocytes are produced as a result of matrix calcification of osteoblasts under the influence of an enzyme called alkaline phosphatase (3).

4. Osteoclasts.  These are responsible for bone resorption (breaking down bone).

Of these, chondrocytes, osteoblasts, and osteoclasts are responsive to thyroid hormone.  On the other hand, we’re currently unaware of the effects of thyroid hormone on osteocyte function.  In order to have healthy bones it’s essential to have a balance between bone forming osteoblasts and bone resorbing osteoclasts.

Effects of Thyroid Hormone on Bone Health

As I discussed in the previous article on bone density and thyroid health, thyroid hormones have important effects on skeletal development, as well as linear growth and the maintenance of adult bone mass and strength.  Just as a reminder, the thyroid gland secretes mostly T4, which converts into the biologically active T3.  Many people have problems converting T4 into T3, which in turn can have a negative effect on bone health.  On the other hand, too much T3 also isn’t a good thing when it comes to bone health.

Overt Hypothyroidism.  Hypothyroidism results in low bone turnover with a decrease in osteoblastic bone formation and reduced osteoclastic bone resorption.  In other words, low thyroid hormone levels will have a negative effect on both bone formation and bone resorption.

Overt Hyperthyroidism.  On the other hand, hyperthyroidism causes high bone turnover with an increase in bone formation and resorption rates.  The remodeling time is shortened with an imbalance between resorption and formation that results in a net loss of approximately 10% of bone per remodeling cycle (4) (5).  What this means is that hyperthyroidism causes accelerated bone loss, which can eventually lead to osteoporosis.  So while many people are understandably concerned about the cardiac risks associated with elevated thyroid hormone levels, it’s also important to be aware of the risks of prolonged hyperthyroidism on bone health.

Subclinical hypothyroidism.  This refers to an elevated TSH in the presence of normal thyroid hormone levels.  There aren’t a lot of studies which show the effect of subclinical hypothyroidism on bone health, although it’s worth mentioning that many people with Hashimoto’s have subclinical hypothyroidism, and shortly I’ll discuss the effects that thyroid autoimmunity has on bone health.

Subclinical hyperthyroidism.  This is characterized by a depressed TSH in the presence of normal thyroid hormone levels.  There has been a decent amount of research demonstrating that even subclinical hyperthyroidism can have a negative effect on bone health.  One large meta-analysis involving 70,298 subjects showed that an undetectable TSH (i.e. <0.01 mU/L) was associated with a 2- and 3.5-fold increased risk of hip and spine fractures (6).

Can Elevated TPO Antibodies Decrease Bone Density and Increase Fracture Risk?

Now that I’ve discussed the relationship between bone health and hyperthyroidism, hypothyroidism, and subclinical thyroid conditions, let’s take a look at how autoimmunity affects bone health.  When specifically talking about thyroid autoimmunity, it can be difficult to separate the effects of thyroid hormone and the immune system on bone density.  After all, many people with autoimmune thyroid conditions have elevated or depressed thyroid hormone levels, and we even mentioned how subclinical thyroid imbalances can impact bone health as well.

That being said, before discussing how the immune system mediators present in autoimmunity can directly affect bone health, I’d like to first talk about a study that looked at the impact that elevated TPO antibodies had on bone density and fracture risk (7).  In the past I’ve written an article on TPO antibodies, and while these are more commonly associated with Hashimoto’s thyroiditis, they are also frequently found in people with Graves’ disease.

As for the study, it involved 189 postmenopausal women, 110 of who had normal TSH and thyroid hormone levels, and 79 who were diagnosed with subclinical hypothyroidism.  Based on what I said earlier we would perhaps expect those with subclinical hypothyroidism to have less than optimal bone health, and sure enough, the study showed that TSH was a better predictive value for fractures in those women who had subclinical hypothyroidism.

However, the study demonstrated that the inflammation associated with thyroid autoimmunity can also have a negative effect on bone quality.  The authors specifically stated that “disturbance in osteoclastic activity in new bone formation might be a consequence of chronic inflammatory autoimmune disorders leading to decreased bone mineral density”.  They also mentioned how “immune mediators found to play a role in most autoimmune disorders could also be involved in promoting bone loss in autoimmune thyroid disease”.  In other words, the inflammation associated with autoimmunity can play a role in bone loss, thus leading to osteoporosis.

And this was proven in the study, as a prognostic tool called the “FRAX score” was used to assess the risk of fractures in the different participants of the study.  The study showed that the FRAX score for major osteoporotic fractures and hip FRAX was significantly higher in the euthyroid group (normal TSH and thyroid hormone levels) with elevated TPO antibodies when compared to those who had normal TPO antibodies.  So the authors concluded that the presence of TPO antibodies is a potential marker of higher fracture risk.

Although this study specifically focused on TPO antibodies, having elevated thyroglobulin antibodies and/or thyroid stimulating immunoglobulins would probably have a similar effect. In fact, another study I came across showed that TSH receptor antibodies (TRAb) play an important role in bone turn-over (8).  This study involved fifty-seven euthyroid women with a history of hyperthyroidism due to Graves’ disease, and while we know that elevated thyroid hormone levels affect bone density, the authors of this study suggested that the presence of elevated TRAb may affect the bone metabolism as well.

While this blog post focuses on the effect thyroid autoimmunity has on bone health, based on what I said earlier about how inflammation can affect bone density, it shouldn’t be surprising to learn that other autoimmune conditions are also associated with an increased risk of osteoporosis.  This includes rheumatoid arthritis (9), systemic lupus erythematosus (10), and multiple sclerosis (11).  To be fair, other factors can also play a role in osteoporosis in different types of autoimmune disorders, but it still is very important to address the inflammation associated with these conditions.

Role of Immune Mediators In Bone Density

So how can immune mediators associated with Graves’ disease and Hashimoto’s (and other autoimmune conditions) affect bone density?  Apparently these immune cells can cause an increase in osteoclasts, which you learned earlier, can increase bone resorption.  In addition, some of these immune cells can negatively affect bone damage in other ways (12).  Certain proinflammatory cytokines, including TNF-alpha and IL-17 can increase bone loss either by increasing osteoclast generation and activation, or by inducing RANKL expression by the osteoblasts (13).

What is Immunoporosis?

I came across another interesting journal article entitled “Immunoporosis: Immunology of Osteoporosis” (14).  Immunoporosis was proposed by the authors as the specific role of the immune system in osteoporosis, and this article discussed how T helper (Th) cells play major roles in bone homeostasis.  In other words, it discusses how these T cells can either directly or indirectly modulate bone health and thereby affect bone remodeling.  Four of these T cells (Th1, Th2, Treg, Th17) play a role in thyroid autoimmunity, and so I thought it would be a good idea to focus on these.

Th1 Cells and Bone Health

An increase in Th1 cells is associated with most autoimmune conditions, including Hashimoto’s thyroiditis.  While there is still some controversy over this, most sources consider Hashimoto’s to be a Th1-dominant condition.  In any case, Th1 cells secrete certain proinflammatory cytokines, and I mentioned earlier how these can increase osteoclasts, thus resulting in a greater amount of bone resorption.  However, the journal article on “immunoporosis” discussed how the majority of cytokines produced from Th1 cells inhibit osteoclastogenesis (15), which means that it possibly can have a protective role in the pathogenesis of osteoporosis.  These conflicting findings suggest that more research needs to be conducted in this area.

Th2 Cells and Bone Health

Whereas Hashimoto’s is considered by most sources to be predominantly a Th1-dominant condition, Graves’ disease is considered by numerous sources to be a Th2-dominant condition.  In other words, there are a greater number of Th2 cells, including IL-4, IL-5, and IL-13, and these cytokines have also been associated with the inhibition of osteoclastogenesis (16).  So it looks like Th2 cells might also have a bone protective role.

Th17 Cells and Bone Health

Th17 cells seem to be the main cells that are primarily responsible for the development of autoimmune conditions.  While many of the cytokines associated with Th1 and Th2 cells can help to protect bone health, the proinflammatory cytokines associated with Th17 cells (IL-1, IL-6, IL-17, TNF-alpha) enhance osteoclastogenesis (17) (18) (19).  In fact, according to the authors of the journal article, Th17 cells in the blood and peripheral tissues can serve as an important marker for osteoporosis (20).  As a result, the goal should be to do whatever is necessary to decrease Th17 cells.

Treg Cells and Bone Health

While Th17 cells play a role in promoting autoimmunity, regulatory T cells (Tregs) can help to prevent autoimmunity by helping to maintain immunological self-tolerance (21).  They also can help to prevent osteoporosis by directly inhibiting osteoclastogenesis (22).

What Can You Do To Increase Bone Density?

In the past article I wrote on bone density and thyroid health, I discussed doing the following to increase bone density:

• Correct the thyroid hormone imbalance
• Eat a healthy diet
• Consume nutrients important to bone health
• Engage in weight bearing exercises
• Have healthy levels of estrogen and progesterone

In this current blog post I reinforced the importance of having healthy thyroid hormone levels, although I also mentioned that subclinical hypothyroidism and subclinical hyperthyroidism can affect bone health.  But I also discussed how proinflammatory mediators can have a negative effect on bone health, thus increasing the risk of developing osteoporosis.  This is yet another reason why it’s important for those with Graves’ disease and Hashimoto’s thyroiditis to address the autoimmune response.

Most people with Hashimoto’s are told to take thyroid hormone replacement without addressing the autoimmune component.  As for Graves’ disease patients, they are usually given an option of 1) antithyroid medication, 2) radioactive iodine, or 3) thyroid surgery.  Without question conventional medical treatment is sometimes necessary, but not doing anything to improve the health of the immune system can have many negative consequences, including an increased risk of osteoporosis.

How To Decrease Immune Mediators Associated With Osteoporosis

While diet and exercise are important factors in having healthy bones, by reading this blog post you know that decreasing Th17 cells and proinflammatory cytokines (and increasing Treg cells) are also important.  I’ve spoken in greater detail about this in past articles and blog posts, but here are some of the things to consider doing:

1. Find and remove the autoimmune triggers.  This is probably the most important thing to do, as you need to detect and then remove your autoimmune triggers.  As I’ve mentioned in the past, this can be challenging to do, even when working with a natural healthcare practitioner, but is even more difficult when trying to do it on your own.

2. Heal the gut and restore the health of the microbiome.  According to the triad of autoimmunity, everyone with Graves’ disease and Hashimoto’s (and other autoimmune conditions) has a leaky gut.  In addition, there are many factors that can have a negative effect on our gut microbiome, including medications such as antibiotics and proton pump inhibitors, infections, as well as environmental chemicals such as glyphosate and triclosan.

3. Eat an anti-inflammatory diet.  While there is no diet that fits everyone perfectly, it makes sense to eat mostly whole foods while avoiding refined foods, sugars, and fast food.  And eating plenty of vegetables is also a good idea.

4. Make sure you have healthy vitamin D levels.  Vitamin D is not only important for bone health, but it also plays a major role in immune system health as well.  As a result, it’s almost impossible to have healthy bones if you have low vitamin D levels.

5. Consider other nutrients and herbs to reduce inflammation.  Some nutrients and herbs that can reduce inflammation include omega-3 fatty acids, selenium, turmeric, ginger, and resveratrol.

6. Take nutrients/herbs that increase Tregs.  Some natural agents you can take that can help increase Tregs include probiotics, vitamin A, vitamin D, omega 3 fatty acids, turmeric, and drinking green tea.

7. Manage stress and get sufficient sleep.  Compromised adrenals due to high stress levels/poor stress handling skills can lead to inflammation, and not getting enough sleep can also cause this.  So this is yet another reason to block out time for stress management and to do everything you can to get 7 to 8 hours sleep each night.

So hopefully you have a better understanding of how thyroid autoimmunity can cause osteoporosis.  In the case of someone with Graves’ disease or Hashimoto’s thyroiditis, even if the person is taking medication to balance the thyroid hormone levels, it’s also important to address the autoimmune component.  Failing to do so not only can increase the risk of developing other autoimmune conditions in the future, but it can also have negative consequences on your bone health.Please feel free to share your experience regarding bone density and osteoporosis in the comments section below.

For those with hyperthyroidism and Graves’ disease who choose to see an endocrinologist, it can be very frustrating being told that the only three treatment options someone has are 1) antithyroid medication, 2) radioactive iodine, and 3) thyroid surgery.  Without question there is a time and place for conventional medical treatment, and while antithyroid medication such as Methimazole and PTU commonly causes side effects, they usually do a wonderful job of lowering thyroid hormone levels.  There are even situations when more extreme treatment methods such as thyroid surgery are necessary.  But while conventional treatment methods are sometimes necessary, it’s ludicrous that most endocrinologists don’t do anything to address the cause of the condition.

Why do most endocrinologists only give three treatment options to their hyperthyroid patients, and not try to address the cause of the problem?  One obvious reason is the training they receive in medical school.  But this isn’t the only reason, as these days there are many medical doctors who practice functional medicine, and most of these medical doctors were also brainwashed while attending medical school.  Perhaps two of the main characteristics that result in some medical doctors practicing functional medicine are 1) having an open mind, and 2) being willing to deviate from the norm.  In other words, having a closed mind and/or being afraid of deviating from the norm are probably the main two reasons why most endocrinologists refuse to practice functional medicine, and thus fail to address the cause of the hyperthyroid condition.

One more thing I’ll say here is that I’m not suggesting that endocrinologists shouldn’t prescribe antithyroid medication, recommend surgery in some cases, etc.  What I am suggesting is that more endocrinologists should practice functional medicine, while utilizing conventional medical treatment whenever necessary.  In fact, even if an endocrinologist chooses to recommend antithyroid medication to EVERY patient with hyperthyroidism, but at the same time does things to address the cause of the condition, this would dramatically reduce the number of patients who ended up receiving radioactive iodine or thyroid surgery.

So what I’d like to do now is discuss 7 things most endocrinologists don’t know (or won’t admit) about hyperthyroidism and Graves’ disease.

1. The autoimmune component of Graves’ Disease can be reversed.  Please keep in mind that this isn’t just my opinion, and of course it’s important to elaborate on the meaning of “reversed”.  I’m not suggesting that Graves’ disease can be permanently cured.  I’ve been in remission from Graves’ disease since 2009, and while I would love to say that I permanently cured my Graves’disease condition, the truth is that for those with Graves’ disease who restore their health, there is always a possibility of experiencing a relapse if you don’t do a good job of maintaining your health and are exposed to specific triggers.

When I say the autoimmune component can be reversed, this means that by removing the autoimmune trigger and healing the gut, and doing other things to reduce proinflammatory cytokines and increase regulatory T cells, the autoimmune response can be suppressed.  This admittedly isn’t an easy process, as there are times when finding the trigger can be challenging, and many people struggle making the necessary dietary and lifestyle changes.  But if someone is willing to take responsibility for their health AND their autoimmune triggers are detected and removed, then it is very possible to achieve a state of remission and maintain your health thereafter.  In other words, the goal should be to achieve a state of PERMANENT remission.

2. Eating healthy can play an important role in your recovery.  Over the years I’ve had numerous patients bring up diet to their endocrinologists.  In most cases an endocrinologist will tell the patient that diet isn’t a factor in the development of their condition, and because of this, eating well won’t do anything to improve their thyroid and immune system health.  The truth is that certain foods can be a trigger, but this doesn’t mean that food is a trigger in everyone with hyperthyroidism and Graves’ disease.

That being said, certain foods are inflammatory, and since Graves’ disease is an inflammatory condition, it makes sense to avoid anything that will promote inflammation.  Once again, this doesn’t mean that everyone will achieve remission by eating whole healthy foods, but it will be very difficult to restore your health if your diet consists mostly of refined foods, fast food, etc.  In the past I’ve mentioned the triad of autoimmunity, and one component of this triad is a leaky gut.  I’ve also mentioned in the past how the research demonstrates that gluten causes a leaky gut in everyone.  As a result, it makes sense for anyone with Graves’ disease (or any other autoimmune condition) to avoid gluten while trying to restore their health.

3. There are natural agents that can lower thyroid hormone levels.  Every now and then a patient will tell me that their endocrinologist is familiar with bugleweed, which is an herb that has antithyroid properties.  But many endocrinologists aren’t familiar with bugleweed.  L-carnitine can also lower thyroid hormone levels when taken in higher doses, but most endocrinologists also aren’t aware of this.  Earlier I mentioned how some people do need to take antithyroid medication, as while many of my patients do fine taking natural agents such as bugleweed, this approach isn’t effective in everyone.

You may wonder whether or not you should take antithyroid medication, or give an herb such as bugleweed a try.  When I was dealing with Graves’ disease I chose not to take antithyroid medication, but this doesn’t mean that this is the best decision for everyone.  If you’re currently taking antithyroid medication, aren’t having any negative side effects, and are concerned that bugleweed won’t effectively manage your symptoms then by all means continue taking it.  On the other hand, if you’re taking antithyroid medication and are experiencing side effects then you might want to give bugleweed a try.

If you were recently diagnosed with hyperthyroidism and haven’t taken any antithyroid medication then you might choose to start with bugleweed and see if it helps, and if not you can always switch to the medication.  Those who are familiar with my “Graves disease story” know that I started with bugleweed and a few weeks later added motherwort to further help with my heart palpitations.  Some people with hyperthyroidism take lemon balm and/or L-carnitine.  Lithium is another option, although I can’t say it’s something I commonly recommend to my patients.

4. Genetics isn’t the main reason why people develop Graves’ disease.  Although some endocrinologists will flat out tell their Graves’ disease patients that they don’t know why they developed this condition, other doctors will blame their patient’s Graves’ disease condition on genetics.  While it’s true that genetics is a factor, it isn’t the most important factor.  Earlier I mentioned the triad of autoimmunity, and the three components of this triad are 1) a genetic predisposition, 2) an environmental trigger, and 3) a leaky gut.  So while you do need to have a genetic predisposition to develop Graves’ disease or any other autoimmune condition, you also need to be exposed to at least one trigger, and according to the triad of autoimmunity you also need to have a leaky gut.  Similarly, in order to achieve a state of remission you need to remove any triggers and heal the gut.

The truth is that most people who have the genetics for Graves’ disease won’t develop this autoimmune thyroid condition.  In fact, when conducting the case history during an initial consultation, it’s not uncommon for the patient to tell me that they are unaware of any family members who have been diagnosed with Graves’ disease.  If Graves’ disease was solely a genetic condition then I would imagine that when conducting my initial consultations a lot more family members would be mentioned as having Graves’ disease.  If you’re wondering if there is any family history of Graves’ disease in my case, as far as I know there isn’t anyone in my family who has been diagnosed with Graves’ disease.  Once again, I’m not denying that genetics isn’t a factor, but only that it’s not the main factor.

5. Chronic stress and adrenal imbalances can be the primary factor in the development of Graves’ disease.  While genetics isn’t the main factor in the development of Graves’ disease, chronic stress and compromised adrenals seem to be major culprits in many people.  It admittedly can be challenging to confirm this, as correlation doesn’t always mean causation.  In other words, just because someone dealt with a lot of stress prior to developing Graves’ disease doesn’t mean that stress was the trigger.

That being said, I’m pretty sure stress was the main reason why I developed Graves’ disease.  And while I can’t say that stress is the main factor in everyone I work with, it’s common for people I consult with to tell me that in their opinion, stress was their primary trigger.  Keep in mind I’m not just referring to emotional stressors.  Physical stressors can also be a culprit.  For example, while emotional stress was a factor in my situation, prior to being diagnosed with Graves’ disease I was overtraining, which also will negatively affect the adrenals over time.  So in my case I’m pretty confident that it was a combination of emotional and physical stressors that wrecked havoc on my adrenals, and set the stage for my Graves’ disease condition.

6. Some people with hyperthyroidism benefit from iodine supplementation.  This is going to be a bit controversial, as I’m sure that many people reading this blog post agreed with the first five things listed here, but can’t believe that I listed iodine as potentially being beneficial for hyperthyroidism.  First of all, I’d like to say right off of the bat that not everyone does well when supplementing with iodine, and I don’t have all of my patients take iodine.  In fact, even if you’re open to taking iodine, it is wise to first test to determine if you have an iodine deficiency, and even if you’re deficient in iodine you need to increase your antioxidant status and start with small doses.

Most endocrinologists will advise their patients with hyperthyroidism and Graves’ disease to avoid iodine, not only in supplement form, but food sources as well.  The reason is because iodine is a precursor to thyroid hormone, and so they’re concerned that taking iodine will exacerbate one’s hyperthyroid condition.  But many decades ago, before radioactive iodine treatment was commonly recommended, Lugol’s solution was used to manage the symptoms of hyperthyroidism.  And if someone is unable to take antithyroid medication and bugleweed isn’t helping to lower their thyroid hormone levels, there are times when iodine supplementation should be considered…especially if your endocrinologist is pressuring you to receive radioactive iodine.

7. Radioactive iodine doesn’t “cure” Graves’ disease.  I think it’s safe to say that many people with Graves’ disease reading this understand that radioactive iodine isn’t a cure.  But that won’t stop many endocrinologists from labeling it as a cure.  While they can make an argument that in many cases radioactive iodine will be a permanent solution for hyperthyroidism, remember that Graves’ disease is primarily an immune condition, not a thyroid condition.  So just to clarify, radioactive iodine treatment many times will permanently eliminate hyperthyroidism, but it will do absolutely nothing for the autoimmune component of Graves’ disease.  And it’s obviously the same concept with thyroid surgery.

Why is this significant?   The reason why this is important to understand is because having one autoimmune condition increases the likelihood of developing other autoimmune conditions in the future.  Thus, if someone receives radioactive iodine, but nothing has been done to remove the autoimmune trigger and heal the gut, then you can’t conclude that Graves’ disease has been cured.  In fact, earlier I mentioned how I don’t consider Graves’ disease to be completely curable due to the genetic component, and thus I mentioned how I try to help my patients achieve a state of “permanent remission”.   On the other hand, someone who receives radioactive iodine shouldn’t be considered to be in remission, because while their hyperthyroidism very well may never return, the autoimmune component hasn’t been addressed.

As for those who have toxic multinodular goiter, I still wouldn’t consider radioactive iodine to be a “cure”, mainly because it doesn’t do anything to address the underlying cause of the condition.  So while there might not be the same concern as with Graves’ disease (a risk of developing other autoimmune conditions in the future), there still is an underlying cause of toxic multinodular goiter.  And not addressing this can lead to other health issues in the future.  It’s also worth mentioning that I’ve worked with patients who had toxic multinodular goiter AND thyroid autoantibodies.

If you have a hyperthyroid condition and have seen an endocrinologist, please share your experience in the comments section below.  If you had a negative experience please let me know!  If you happened to have a positive experience with your endocrinologist please let me know!  And if there is anything else you’d like to add regarding what most endocrinologists don’t know about hyperthyroidism please feel free to share this as well.

A few months ago I wrote a blog post entitled “The Lyme-Thyroid Connection”.  It was a very detailed post, but one thing I didn’t reveal was the motivation behind it.  The reason why I decided to write about Lyme disease was because the previous month I personally was diagnosed with chronic Lyme disease.  Although I was thinking about revealing that I had Lyme disease in the previous blog post, I decided to hold off for a few reasons.  One reason is because the blog post was long enough without my personal story!  In addition, I figured I’d wait until I went through a few months of treatment (to be discussed below), as I didn’t want current and future patients to be concerned about my state of health.  Before moving on, I do want to say that I currently feel great!

As most people reading this know, I was diagnosed with Graves’ disease.  When I first found out I had hyperthyroidism I was shocked.  Once I started developing symptoms related to Lyme disease I was also quite surprised.  I was probably even more surprised with the chronic Lyme disease diagnosis, as overall I felt like I had been taking good care of my health.  In 2016 I had shingles, and without question this was related to stress, as we sold our home and purchased a new one, which was a very stressful process, and then right after moving into our new home I broke my fifth metatarsal.  While 2016 was very stressful, I can’t say that I had abnormally high stress levels in 2018.  In addition, I do block out time for stress management on a daily basis.

You might wonder what having Lyme disease has to do with stress?  After all, this is a condition that is due to getting bit by a tick, right?  While it is true that the bacteria associated with Lyme disease (Borrelia burgdorferi) is commonly transmitted through the bite of a tick, this doesn’t mean that everyone who gets infected with Borrelia burgdorferi will present with the symptoms of Lyme disease.  This is true of other types of infections as well, as the health of the host’s immune system plays a big role in the symptoms they will present with in any infection.  What makes it even more puzzling is that most years I experience some type of temporary head cold, but this wasn’t the case in 2017 and the first half of 2018.  I figured this was a sign that my immune system was in a good state of health.  Apparently I was mistaken.

My Lyme Disease Story

I’d like to go ahead and share my “Lyme disease story”.  In July of 2018 I visited Bear Mountain State Park in New York for a family reunion.  Six days later I developed a mild cold, and I didn’t think much of it.  In fact, that weekend I attended a 3 day nutritional conference, and although I wasn’t feeling 100%, I was able to stay focused and alert.  A few days later I began feeling better.  However, one week after developing the “cold-like” symptoms I began experiencing some neurological symptoms.

The very first neurological symptom I experienced was numbness on the left side of my face.  Coincidentally, when I had attended the nutritional conference, a friend I hadn’t seen for a few years also attended, and he had numbness in his face as well.  This was caused by Bell’s Palsy, which in most cases is caused by a viral infection.  And so when I developed the facial numbness I was thinking that perhaps I also coincidentally had Bell’s Palsy.  I was also concerned about the possibility of a stroke, and my wife encouraged me to call a medical doctor, which I did.  He advised me to go to the ER, and I decided against this, mainly because I didn’t have the risk factors of a stroke, no family history, etc.  I admit I was taking a risk, but I was pretty confident that the numbness I was experiencing wasn’t related to a stroke.

Anyway, in addition to the face numbness, I began experiencing some “electric shock” sensations in my hands and feet, and I realized that something was seriously wrong when one day I experienced weakness in my right leg.  I should backtrack and let you know that when the leg weakness developed I had been taking some anti-viral herbs, as up until the leg weakness I was thinking that it might be some type of virus, perhaps even Epstein-Barr.  When I started experiencing the leg weakness I did think of Lyme disease, but I also was concerned that it might be something else, such as multiple sclerosis.  After all, I had Graves’ disease, and having one autoimmune condition increases the risk of developing another autoimmune condition in the future.

The leg weakness started on a Saturday, and on that Monday I scheduled an appointment with a local functional medicine practitioner (her name is Carrie) who has a lot of experience working with Lyme disease patients, and she also had personally dealt with chronic Lyme disease herself.  Like me, she also went through the Institute for Functional Medicine certification.  The problem was that I would have to wait a few days to see her, and while this wasn’t too long of a wait, I decided that I would keep my appointment with Carrie, but I saw another doctor on that Monday.

This turned out to be a waste of time, as not only didn’t he think I had Lyme disease (since I didn’t have classic Lyme disease symptoms, a bull’s-eye rash, etc.), but he wanted to refer me to a neurologist.  To be honest, this wasn’t too surprising, and I should have known better.  I was just impatient and was hoping to find answers sooner than later.  I also wasn’t 100% certain I had Lyme disease, but if I did have it then I wanted to get this addressed as soon as possible, and so I chose not to see a neurologist.  Keep in mind that if I did have Lyme disease I was suspecting that I might have “acute” Lyme disease, and not “chronic” Lyme.

Why Did I Suspect That I Had Lyme Disease?

I think it’s important to talk about the decision not to see a neurologist, as many people with Lyme disease had made this mistake initially.  And in some cases it led to their condition becoming debilitating.  This is the reason why I decided not to go to a neurologist, as while I wasn’t sure if I had Lyme disease, I figured that if I had multiple sclerosis or something else then it can wait a few weeks, but if I had acute Lyme disease this needed to be treated as soon as possible.

Not seeing a neurologist turned out to be a good decision in my case, as if I had chosen to see a neurologist first I not only would have had to wait at least a few weeks, but I probably would have spent thousands of dollars on unnecessary testing.  In the blog post I wrote on Lyme disease in September I spoke about how Lyme disease can mimic multiple sclerosis, and so there is a chance that I might have been falsely diagnosed with multiple sclerosis, or perhaps another condition.  Another possibility is that after extensive testing by the neurologist everything would have come back negative, and I would have been back to square one.

Of course I’m not criticizing those with chronic Lyme disease who initially chose to see a neurologist first.  They were just following the recommendations of their doctor.  It admittedly can be a tough decision to make, as if someone is experiencing neurological symptoms it of course is understandable why they would choose to see a neurologist sooner than later.  But since I was familiar with Lyme disease I went with my gut instinct and decided not to see a neurologist.  So I’m not trying to discourage anyone from seeing a neurologist, but if there is even a small possibility that your symptoms might be related to Lyme disease then it’s important to look into this, and not to delay for too long.

My Appointment With The Lyme Disease Specialist

I saw the functional medicine practitioner on a Thursday morning, and my wife accompanied me.  The appointment lasted well over an hour, as it included a consultation and exam.  I also ended up getting some blood work.  At the time Carrie also thought I had ACUTE Lyme disease, and I had to decide whether or not to take antibiotics.  Just a reminder that prior to the appointment I was taking some antimicrobial herbs, and I got a little more aggressive when my leg weakness developed.  Overall I was taking the herbs for about 2 weeks, and they didn’t seem to be helping with the neurological symptoms.  And to be honest, I came to the appointment knowing that there was a good chance that antibiotics would be recommended, and I made the decision to take them…specifically Doxycycline.

So I took Doxycycline while waiting for the results of the tests.  I’m sure some people will frown upon my decision to take antibiotics, and I admit it wasn’t an easy decision.  I will say that I’ve mentioned in the past how taking antibiotics might be a good idea for ACUTE Lyme disease, and since I thought my Lyme disease was acute I figured the “benefit” of eradicating the infection and preventing the development of chronic Lyme disease outweighed the risks of the antibiotics disrupting my gut microbiome.  The truth is that I was afraid of developing chronic Lyme disease after working with some patients who had it and seeing how debilitating it could be.

Two weeks after starting the Doxycycline I had another consultation with Carrie, and this is when I found out I didn’t have acute Lyme disease, but CHRONIC Lyme disease!  Although my practice focuses on thyroid and autoimmune thyroid conditions, I’ve had patients who also had chronic Lyme disease, and some of them had been on antibiotics for years!  I knew I wasn’t going to follow this route, as I was upset enough that I took the Doxycycline for 2 weeks.

Herbs, Antibiotics, UV Light, and Ozone Therapy

After finding out I had chronic Lyme disease, Carrie told me there were a few different treatment options.  I can take an herbal/homeopathic approach, I can take antibiotics for a few months, or I can receive UV light and ozone therapy.  I asked her what treatment she recommended, knowing that there was no way I was going to take antibiotics on a long term basis.  She recommended UV light and ozone, and so this is what I decided to do.

Although I heard some great things about ozone, I also had heard stories of people with chronic Lyme disease who felt great after a few months of treatment with ozone, only to have their symptoms return.  I decided to go this route anyway, understanding that at the same time I would have to work on further improving my immune system health.  Of course I thought my immune system was in a good state of health, as while I did deal with shingles in 2016, overall I’ve been healthy, and I have been in remission from Graves’ disease since 2009.

You might argue that getting Lyme disease wasn’t under my control, as I was bit by a tick.  While this might be true, the fact is that I had chronic Lyme for a period of time, yet for some reason didn’t experience symptoms until a later date.  I discussed this earlier when I spoke about how the host’s immune system plays a big role n the development of symptoms.

How Do I Currently Feel?

As I mentioned in the opening paragraph, I currently feel great!  However, I must admit that I never felt terrible to begin with, which is why the medical doctor who wanted to refer me to a neurologist didn’t think it was Lyme disease.  Throughout this process I have never felt fatigued, which is very common with Lyme disease.  And while I had some “electric shock” sensations in my hands and feet, this was intermittent, whereas many people with chronic Lyme disease have severe pain.  Even the numbness in my face was pretty mild.  I can’t say the same about the weakness in my right leg, which is what prompted me to schedule the appointment with Carrie.  Fortunately I only experienced the weakness in my leg a few times, and as of writing this post I haven’t had this symptom since September (knock on wood!).

Overall I can’t complain, as while I wish I didn’t have Lyme disease, I’m very grateful that my symptoms haven’t been severe thus far.  Plus, similarly to when I was diagnosed with Graves’ disease, I feel that being diagnosed with Lyme disease will force me to learn more about this condition.  While I think my focus will always be to help those with Graves’ disease and Hashimoto’s, I’m confident that my experience will benefit those with thyroid and autoimmune thyroid conditions who also have Lyme disease.  What’s scary is that there is a good chance that some of my current patients have chronic Lyme disease and don’t know it, just as was the case with me.

How Did I Develop Chronic Lyme Disease?

You might wonder how I developed Lyme disease in the first place?  I have no idea, as I don’t recall ever getting bit by a tick or having a bull’s-eye rash.  It’s also important to know that there is evidence of Lyme disease being transmitted by fleas and biting flies as well.  Either way, apparently I had gotten bit by a tick, flea, or biting fly in the past, and what I think happened is that when I went to Bear Mountain State Park this summer I got another tick bite.  That evening my dog was all over me, and so it’s very possible that there was a tick on him and he passed it on to me.

Anyway, my theory is that I somehow got infected in the past, but my immune system kept the infection in check until getting bit by a tick when visiting Bear Mountain.  Of course there is no way to prove this, as I didn’t have the classic “bull’s-eye” rash, but it makes sense since my symptoms started approximately one week after visiting Bear Mountain.  Plus, as I mentioned in the previous blog post I wrote on Lyme disease, many people with Lyme disease never present with a bull’s-eye rash.

Some people reading this know my staff person Kate, and when I suspected I had Lyme disease her initial reaction was “no way!”  Her husband gets exposed to ticks frequently when he’s working, while I’m in an office setting most of the time.  But it’s just another lesson that anyone can get Lyme disease.  We do have two dogs (we have cats too but they stay indoors), and so besides potentially getting exposed this past summer in New York, it’s also possible that over the last few years I got exposed to one or more ticks.  Or perhaps the first exposure was through a flea or biting fly.

I Also Tested Positive For Bartonella

Most people with Lyme disease also have one or more coinfections.  This was the case with me, as I tested positive for Bartonella.  Bartonella is a type of gram-negative bacteria, and while it can be transmitted through the bite of a tick, it also can be transmitted through cat scratches, and thus is sometimes referred to as “cat scratch disease”.  I do have three cats, and so I suppose it’s possible that it was transmitted this way, but as I just mentioned, it also can be transmitted through the bite of a tick.  For the Bartonella I was advised to take a homeopathic formula for 2 months.

Concern With A Graves’ Disease Relapse

When I was officially diagnosed with Lyme disease, one of my main concerns was that it would potentially re-trigger my Graves’ disease condition.  And while I didn’t feel any overt hyperthyroid symptoms, I did order a thyroid panel with antibodies shortly after being diagnosed with Lyme disease, and I’m thankful that everything looked fine.  Of course this doesn’t mean that I’m in the clear yet, as it probably would be a good idea to do a thyroid panel with antibodies at least one or two more times in the near future, just to be on the safe side.

What Would I Have Done Differently?

I don’t really have any regrets so far, although if I knew that I had chronic Lyme disease I wouldn’t have taken the antibiotics and I instead would have started with UV light/ozone therapy right away.  Sometimes I do wonder if I should have taken a “Lyme-focused” herbal approach instead of the UV light/ozone therapy.  Although I did take some herbs when I first started experiencing symptoms, they were more specific for viruses, although I also added an herbal antimicrobial called Biocidin, which in some cases can help with chronic Lyme.

My Current And Future Treatment Approach

While I’m currently receiving UV light/ozone treatment every other week, I also started taking some herbs that are recommended by the herbalist Stephen Buhner in his excellent book “Healing Lyme”.  Since the Doxycycline no doubt disrupted my microbiome, further compromising my immune system, I’ve also been working on restoring my microbiome health and doing things to promote gut healing.  And of course I’m making sure to eat well, manage stress, get plenty of sleep, minimize exposure to environmental toxins, etc.  I thought I was doing a good job in these areas before, but I’m doing an even better job now.

Advice For Others With Chronic Lyme Disease

As for what advice I have for others with chronic Lyme disease, I’ll just remind you that while addressing the infection is important, it’s even more important to focus on improving your immune system health.  And while taking antibiotics sometimes is necessary, especially when someone has acute Lyme disease, if you have chronic Lyme disease you need to strongly consider the pros and cons of long-term antibiotic use.  I felt bad enough taking the Doxycycline when I thought my Lyme disease was acute, but there are some people who are on antibiotics for months or years.

Without question antibiotics can be a blessing when it comes to acute infections, and I’m not just talking about Lyme disease, but other types of infections that can be serious, and in some cases even life-threatening.  On the other hand, we can’t ignore the impact that antibiotics have on the good bacteria of the gut.  Even taking antibiotics for one or two weeks can significantly disrupt the microbiome, let alone taking them for many months or years.

So for those reading this who currently have chronic Lyme disease, if you aren’t taking antibiotics that’s wonderful!  Try everything you can to avoid taking them in the future.  If you took antibiotics like me, even for a short period of time, then hopefully you took time to restore your microbiome health, which doesn’t just mean taking high potency probiotics for a few weeks (although taking high potency probiotics is also a good idea).  Perhaps restoring the microbiome is a topic I will discuss in a future blog post in 2019.

For those who currently have chronic Lyme disease and have been taking antibiotics for a few months or years, I hope that one of your goals in the near future is to devise a plan to wean off of the antibiotics.  This very well might mean working with a natural healthcare practitioner who focuses on Lyme disease.  I’ll add that I have worked with a few patients who were seeing some alternative-minded medical doctors who focused on Lyme disease, yet still took antibiotics for months or years.  If this describes you then it might be time to switch to a different practitioner.

Should EVERYONE Get Tested For Lyme Disease?

I have no idea how long I was dealing with chronic Lyme disease, as it could have been a few months, or a few years.  Either way, based on my experience, you might wonder if everyone should be tested for Lyme disease.  First of all, I would read my blog post from September, as I talk about testing, including possible false negatives.  In other words, a negative ELISA and/or Western Blot won’t always rule out Lyme disease.  Some labs are better than others, as many practitioners use IGeneX, which is a lab I considered using, but Carrie recommended Medical Diagnostic Laboratories.

Sometimes I do wonder if it would have made a difference if I knew I had chronic Lyme disease sooner.  For example, while I was already living a pretty healthy lifestyle, if I knew I had Lyme disease even a few months sooner perhaps I would have started taking the herbs recommended by Stephen Buhner, which might have prevented the onset of symptoms.  Of course there is no way of knowing this for certain, but I’m bringing this up because while everyone reading this should already be living a healthy lifestyle, some people aren’t, and if you were to find out you had Lyme disease ahead of time you might be more strict with your diet, make sure you’re getting enough sleep, blocking out time for stress management, etc.  Once again, I realize that some people are already doing this, but many people aren’t.

At the same time I don’t want everyone reading this to become paranoid and think that they have Lyme disease.  The truth is that we all have microbes in us that can be potentially pathogenic.  For example, most adults have Epstein-Barr in their body, and while in many people it is inactive, if you don’t take care of your health it can reactivate and cause a lot of problems.  As I mentioned earlier, Lyme disease wasn’t the only pathogen I’ve dealt with recently, as in 2016 I had shingles, which no doubt was a consequence of extreme stress, and I discussed this in a blog post I wrote entitled “Can Shingles Trigger Graves’ Disease and Hashimoto’s?”.

What Can You Do To Prevent Yourself From Getting Lyme Disease?

In order to prevent yourself from getting Lyme disease, you obviously want to try everything you can to minimize your exposure to ticks.  Of course this is easier said than done, although when hiking you can try to avoid walking across grassy fields, wear long pants and socks, inspect your clothes and skin for ticks, etc.  Just a reminder that your dogs and cats can pass ticks onto you, and they can also be infected by ticks.

Oil of lemon eucalyptus can also be used as a tick repellent (1).  So can chemical repellents containing DEET, but I’d stick with the essential oils!  Stephen Buhner also has formulated this tick repellent, and he says that the primary herb for prevention is astragalus, and to take a minimum of 1,000 mg per day if you live in a Lyme endemic area.  I will say that there is some controversy over using astragalus in those with autoimmune conditions such as Graves’ disease and Hashimoto’s.

If you have already been bit by a tick and discover it while it’s still attached, use a tick removal device to release it from your skin.  According to Stephen Buhner, applying Andrographis tincture as soon as the tick is removed can be effective.  As a result, it might be a good idea to have some Andrographis tincture handy.

Even if you don’t have Lyme disease I hope you found this post to be interesting and informative.  If you have any questions or comments based on my “Lyme disease story” (or your “Lyme disease story”) please post them in the comments section below.