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.

Over the last year I’ve had a few patients with Hashimoto’s thyroiditis ask me about the benefits of black cumin.  This is based off of a study which demonstrated that black cumin had a positive effect on the TSH and TPO antibodies in Hashimoto’s patients.  And so based on these requests I decided to do some research on black cumin and put together my own blog post on this topic.  However, unlike a few other articles written by healthcare practitioners, I’m not just going to focus on the study related to Hashimoto’s, as I’ll dive deeper and discuss some of the other health benefits of black cumin.

Black cumin is also known as Nigella sativa (N. sativa), which is a medicinal plant and belongs to the Ranunculaceae family (1).  The seeds of black cumin are the main source of its active ingredients (2) (3).  It’s most prominent constituent that has well-known antioxidant, anti-inflammatory, and anti-cancer properties is thymoquinone (4).  Although I’ll discuss how black cumin might help those people with Hashimoto’s, as I mentioned in the opening paragraph, I’ll also discuss some of the other health benefits of this herb.

Black Cumin and the Hashimoto’s Study

So let’s go ahead and talk about the study.  This involved forty patients with Hashimoto’s thyroiditis, aged between 22 and 50 years old (5).  They were split into two groups, where one group consumed 2 grams of black cumin per day in powder form for 8 weeks, while the other group consumed a placebo (2 grams of starches).

These are the markers that were evaluated:

• Thyroid stimulating hormone (TSH)
• Thyroid peroxidase (TPO) antibodies
• Serum T3
• Serum Vascular Endothelial Growth Factor (VEGF)
• Nesfatin-1

Many people reading this are familiar with the first three markers I listed above, but some aren’t familiar with the fourth and fifth ones.  VEGF is a glycoprotein, and it has been proposed that VEGF is present in epithelial cells of the thyroid gland and contribute to the development and function of thyroid epithelial cells (6).  One of the typical characteristics of Hashimoto’s thyroiditis is high TSH levels, and this promotes VEGF secretion.  In other words, VEGF levels are usually high in Hashimoto’s patients.  As for Nesfatin-1, this is a peptide, and some studies have demonstrated a role of Nesfatin-1 in thyroid conditions (7) (8).

It’s also worth mentioning that anthropometric markers were measured, including weight, BMI, and waist circumference.

So what happened to those people with Hashimoto’s who supplemented with black cumin?  Well, their TSH and TPO antibodies decreased, the serum T3 increased, and there was also a reduction in serum VEGF.  Changes in Nesfatin-1 were not significant.  In addition, those who took black cumin experienced a significant reduction of weight, BMI, and waist circumference.  As a result, the authors concluded that it can be regarded as a useful therapeutic approach in the management of patient’s with Hashimoto’s.

Should Everyone With Hashimoto’s Take Black Cumin?

It’s difficult to recommend black cumin to everyone with Hashimoto’s based on a single human study, especially since it involved only 40 participants.  I should mention that there was a separate animal study which showed that black cumin can benefit those with hypothyroidism.  It’s also important to let you know that there are studies showing that black cumin can benefit those with other autoimmune conditions, including multiple sclerosis (9) and rheumatoid arthritis (10).

While there needs to be more studies done on autoimmune patients before we can conclude that black cumin is something that everyone should take, the research shows that there are many other health benefits of this herb:

Antibacterial activity.  H. pylori is a potential trigger of thyroid autoimmunity, and there is evidence that black cumin seeds have antimicrobial properties against H. pylori that’s comparable to triple therapy (11).  There is also evidence that it can inhibit the growth of Staphylococcus aureus (12).  This study also demonstrated that there can be a difference in the antimicrobial effectiveness of black cumin depending on the source of the black cumin seeds.

Antifungal activity.  Black cumin has demonstrated antifungal activity against most pathogenic fungi (13) (14).  A few studies have shown that black cumin can specifically help with Candida overgrowth (15) (16).

Anti-parasitic activity.  Schistosoma mansoni is one of the parasites causing schistosomiasis, and a few studies demonstrate that black cumin can help with the eradication of these parasites (17) (18).  A couple of in vitro studies showed that it can also be effective against blastocystis hominis (19) (20).  Blastocystis hominis is a parasite that is a potential trigger of thyroid autoimmunity.

Antidiabetic activity.  One study looked at the effect of black cumin seeds on the glycemic control of patients with type 2 diabetes (21).  The results of the study showed that black cumin at a dose of 2 grams per day caused significant reductions in fasting blood glucose and hemoglobin A1C, while insulin resistance reduced significantly, and beta cell function increased (21).  It’s also worth mentioning that 1 gram per day showed improvement but wasn’t statistically significant, while 3 grams per day provided no further benefit.  A few rat studies have also showed that black cumin has anti-diabetic properties (22) (23).

Anticancer activity.  As if eradicating infections and helping with type 2 diabetes wasn’t impressive enough, there is also evidence that black cumin has anti-cancer properties.  Experimental findings strongly suggest that black cumin could serve, alone or in combination with known chemotherapeutic drugs, as effective agents to control tumor initiation, growth, and metastasis (24).  Another journal article discussed how the main bioactive component of black cumin (thymoquinone) can be considered as a promising therapy for cancer treatment (25), although the main focus of the review was to demonstrate how thymoquinone can improve the efficacy of conventional cancer treatments, including surgery, radiotherapy, and chemotherapy.  Yet another journal article summarized the actions of thymoquinone and crude oil of black cumin against different cancers, and showed that it has positive effects on breast cancer, liver cancer, skin cancer, and renal cancer (26).

Immunomodulatory, anti-inflammatory, and antioxidant effects.  In the study on Hashimoto’s I mentioned how consuming black cumin led to a decrease in TPO antibodies.  This shouldn’t be surprising when you look at the research, as besides the study on Hashimoto’s, there is additional evidence showing that black cumin has immunomodulatory, anti-inflammatory, and antioxidant effects.  One review showed that thymoquinone has anti-inflammatory properties that prevent the biosynthesis of proinflammatory cytokines such as interleukins and TNF-alpha (27), which are both associated with autoimmunity.  Another comprehensive review mentioned that black cumin extracts and thymoquinone can potentially be used in the regulation of immune reactions implicated in various infections and non-infectious conditions including different types of allergies, autoimmune conditions, and cancer (28).  A few studies have demonstrated the antioxidant properties of black cumin (29) (30).

Lipid lowering effects.  One study showed that 8-week supplementation of 2 grams of black cumin per day combined with an aerobic exercise program provides significant improvements in LDL-cholesterol and HDL-cholesterol (31).  Although regular aerobic exercise is important, it would be interesting to see what the results would have looked like with people taking black cumin alone.  And while it was nice to see LDL decrease and HDL increase, I’d like to see if it positively affects markers such as LDL particle size.

Hepatoprotective effects.  A few studies show that black cumin can protect the liver and cause a decrease in lipid peroxidation and liver enzymes (32) (33).  Although this blog post focuses on how black cumin can help with Hashimoto’s, many of my patients with hyperthyroidism and Graves’ disease have elevated liver enzymes, and so black cumin might be of benefit in this situation.

Other health conditions.  There are studies showing that black cumin can protect the gastrointestinal tract (34), cardiovascular system (35), and kidneys (36).  It’s important to mention that the antioxidant and anti-inflammatory properties of black cumin seem to be the main features of preventing and protecting these and other areas of the body from injury.  So the truth is that black cumin not only can help those with Hashimoto’s thyroiditis, but other autoimmune conditions as well.

Can Black Cumin Be Toxic In High Doses?

There have been a number of animal studies on black cumin seeds evaluating its toxicity, and overall it seems to be very safe.  One study looked to evaluate the toxicity effect of black cumin on the liver function of rats (37).  The results showed that consuming high doses of black cumin resulted in no significant change in the liver enzymes (alanine aminotransferase and aspartate aminotransferase).  This shouldn’t be surprising, as I mentioned earlier how black cumin can actually protect the liver.

What is the Ideal Dosage of Black Cumin, and Where Can You Purchase It?

According to the research, it seems that 2 grams per day (in divided doses with meals) is ideal.  But of course everyone is different, and for some people it might be wise to start with lower doses.  As for where to purchase it, you can visit your local health food store, do an online search, or click here for a product I recommend, which includes one gram of black cumin seed per serving, along with mixed tocotrienols.

Should YOU Take Black Cumin?

While I can’t say with certainty that everyone with Hashimoto’s should take black cumin based on the single study I discussed earlier, it’s easy to see how many people in general can benefit from taking this, let alone those with autoimmune conditions such as Hashimoto’s.  After reading through all of the research I’m excited to start recommending black cumin to some of my patients.

What’s Your Experience With Black Cumin?

I’d be interested in hearing from anyone who has supplemented with black cumin.  And so if you have already have taken black cumin please feel free to share your experience in the comments section below.  If you took black cumin and noticed positive benefits please let me know!  If you took black cumin and didn’t notice any benefits please let me know!  And if you took black cumin and felt worse please feel free to share your experience as well!

I’d like to wish everyone a very happy Thanksgiving!  I’m sure everyone has had some ups and downs in 2018, especially those currently dealing with a thyroid or autoimmune thyroid condition.  But most of us really do have a lot to be grateful for, including myself!  I am grateful for having a wonderful wife and two amazing daughters!  Even though I’ve dealt with some health challenges this year unrelated to Graves’ disease (to be revealed in a future blog post) I’m grateful that right now I’m currently feeling great!  Of course I’m also grateful for the opportunity to share my knowledge and experience in helping you to optimize your health!

Please feel free to share what you’re grateful for in the comment sections below!