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) [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) [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 [2]“. 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) [3]:
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].
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] (5) [6]. 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) [7].
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) [8]. In the past I’ve written an article on TPO antibodies [9], 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 [10]. 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) [11]. 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) [12], systemic lupus erythematosus (10) [13], and multiple sclerosis (11) [14]. 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) [15]. 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) [16].
What is Immunoporosis?
I came across another interesting journal article entitled “Immunoporosis: Immunology of Osteoporosis” (14) [4]. 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) [17], 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) [18]. 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) [19] (18) [20] (19) [21]. 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) [4]. 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 [22] (Tregs) can help to prevent autoimmunity by helping to maintain immunological self-tolerance [23] (21) [24]. They also can help to prevent osteoporosis by directly inhibiting osteoclastogenesis (22) [25].
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 [26], 2) radioactive iodine [27], 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 [28]. 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 [29], as well as environmental chemicals such as glyphosate [30]and triclosan [31].
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 [32] 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 [33], turmeric, ginger [34], 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.