If you have read some of the posted comments from thyroid and autoimmune thyroid forums and Facebook groups, chances are you’ll come across people with Graves’ disease and Hashimoto’s who experienced dramatic improvements in their health just by changing their diet.  Some people do nothing but eliminate gluten from their diet, and yet feel significantly better.  Others need to be more strict with their diet in order to receive great results.  However, one question you might have is whether or not eating well simply helped to improve the health of these people, or did making these dietary changes reverse the autoimmune component of their condition?  I’m going to discuss this in this blog post.

Although the focus of this blog post is on whether changing one’s diet alone can reverse Graves’ disease and Hashimoto’s, I’d like to briefly review the triad of autoimmunity and discuss the four main categories of autoimmune triggers.  According to the triad of autoimmunity, in order for autoimmunity to develop you need 1) a genetic predisposition, 2) an environmental trigger, and 3) an increase in intestinal permeability (a leaky gut).  As you know, we can’t change your genes, but we can reverse autoimmunity by removing the trigger and healing the gut.

Focusing on the environmental triggers, there are four main categories of these triggers:

1. Food

2. Stress

3. Chemicals

4. Infections

As you can see, one of the main categories is food.  So it is possible that food can be a trigger, and if a specific food is the sole trigger, then eliminating this food from one’s diet can reverse the autoimmune component.  If this is the case, then why do some people who eliminate gluten, or perhaps even follow a strict autoimmune Paleo diet for a few months, not get into remission?  There are a few obvious answers, with one being that food isn’t a trigger in everyone.  In many people the main trigger is stress, chemicals, and/or infections.  If this is the case, then eating well alone won’t reverse one’s condition.

Another reason why a person who follows a strict AIP diet might not get into remission is because they have multiple triggers.  In other words, certain foods might be a trigger, but they might have one or more triggers from the other categories I listed above.  I see this quite frequently, as a person might feel significantly better when eliminating certain foods, but they are still symptomatic, their thyroid antibodies are still high, etc.  This usually means that not all of the triggers have been removed.

It’s also worth mentioning that a person might clean up their diet and not feel better, and then prematurely decide that food wasn’t the main trigger, when the real problem is that they weren’t strict enough with their overall diet.  For example, someone might completely go gluten and dairy free, but they might react to another food (i.e. corn).  Or perhaps cross contamination is an issue, as a person might think they’re completely avoiding a certain food, but somehow they’re getting exposed to it.  This is especially a concern when eating out.  These are just a few things to consider when evaluating your diet.

Which Foods Can Be Triggers?

The truth is that you can have an immune system reaction to any food.  However, this doesn’t mean that all foods are potential autoimmune triggers.  For example, while I don’t do a lot of IgG food sensitivity testing, I have done such testing on some of my patients, and I’ve seen people test positive for healthy foods such as broccoli and asparagus.  While one can argue that eating these foods might cause inflammation (if one is sensitive to them), and perhaps even prevent the gut from healing in this situation, they aren’t autoimmune triggers.

On the other hand, gluten, dairy, and corn are potential triggers of autoimmunity.  This is why most natural healthcare practitioners will advise their autoimmune patients to avoid these foods.  This is especially true when trying to restore one’s health, but a strong argument can be made to continue avoiding these common allergens even after achieving a state of remission.

How Can Food Trigger Autoimmunity?

Something called molecular mimicry may explain why certain foods can trigger autoimmunity.  I’ve discussed molecular mimicry in past articles and blog posts, as it seems that certain foods contain antigenic substances that have amino acid sequences similar to those of human proteins (1).  When someone eats these foods, this can result in the production of antibodies that not only react against the food antigens, but the body’s own tissues.  An example of this is gluten, as there is some evidence that gluten has a similar amino acid sequence to the thyroid gland, which can cause the body to develop antibodies not only against gluten, but the thyroid gland as well.

Removing Your “Leaky Gut Triggers”

In addition to environmental triggers playing an important role in thyroid autoimmunity, it’s also important to mention that different factors can cause a leaky gut.  In the past I’ve mentioned how gluten causes a leaky gut in everyone, and so if gluten is the only autoimmune trigger and is also the only “leaky gut” trigger, then avoiding gluten alone might be the solution to reversing the autoimmune component of Graves’ disease or Hashimoto’s.  I say “might” be the solution because even after removing the trigger and healing the gut, you might need to do things to reduce proinflammatory cytokines and increase regulatory T cells, which is also necessary to suppress the autoimmune component.

Cure vs. Remission vs. Improvement

In some of my webinars and articles I’ve discussed the difference between “cure” and “remission”, and how Graves’ disease and Hashimoto’s can’t be permanently cured since they involve a genetic component.  While “getting into remission” doesn’t sound as good as “being cured”, this still involves the elimination of one’s symptoms, normalization of thyroid markers (include thyroid antibodies), and correcting other imbalances related to the autoimmune thyroid condition.  And it is possible to stay in remission for a prolonged period of time, as I’ve been in remission from Graves’ disease since 2009, although I’ve dealt with some other health issues over the years, most notably Lyme disease, which I discussed in a previous blog post.

On the other hand, many people experience an improvement in their symptoms and/or labs upon changing their diet, but they don’t go into remission.  For example, they might have a reduction of their symptoms, but they don’t completely go away.  Or their blood tests might improve, but they’re still not in balance.  Keep in mind that in some cases of Hashimoto’s the thyroid panel can’t be normalized, which is why you also want to monitor the thyroid antibodies, along with other tests that were out of range.  If you experience some positive changes after modifying your diet but don’t get into remission, please don’t become discouraged, as this is very common.  When this is the case, in most cases there are other triggers/imbalances that need to be addressed.

How Do You Know If Food Is Your Only Trigger?

As for how to know if food is your only trigger, in my opinion, the best way to find out is through an elimination and reintroduction diet.  If you avoid all of the allergenic foods (gluten, dairy, corn, etc.) and your symptoms resolve and your thyroid panel and antibodies normalize, then you know that food was the main culprit.  On the other hand, if your symptoms don’t improve and/or your blood tests don’t normalize, then there are most likely other triggers present.  As I briefly mentioned earlier, sometimes removing the trigger alone isn’t sufficient, as you might need to do other things to reduce the inflammation.

I mentioned IgG food sensitivity testing earlier, and you might wonder if this is something you should consider doing.  In some cases this can detect food triggers, although false results are common, which is why I don’t recommend such testing to all of my patients.  Earlier I also mentioned that not every food that tests positive on an IgG food sensitivity panel is an autoimmune trigger. I realize that many people don’t want to stop eating foods that have gluten and dairy, but this is the best way to find out of these are triggers.  Plus, even if gluten isn’t a trigger it’s best to be avoided, especially while healing your gut.

Is It Necessary To Eat A Strict Diet If Food Isn’t The Main Trigger?

If you’re pretty sure that certain allergens aren’t a trigger in your case, you might wonder if it necessary to continue avoiding these.  For example, if you followed an elimination diet for at least 30 days and didn’t experience any improvement in your symptoms or thyroid markers, is it okay to reintroduce gluten, dairy, and other common allergens?  I get this question asked a lot, and I usually recommend to continue avoiding the “allergenic foods” at least until one’s health has been restored…even if they aren’t responsible for triggering autoimmunity.

This is especially true with gluten, as I reminded you earlier how the research shows that gluten causes a leaky gut in everyone.  And since dairy and corn cross react with gluten (eating these foods can produce gluten antibodies), one can argue that it’s best to avoid these foods as well.  In fact, some natural healthcare practitioners recommend for people with autoimmune conditions of all types to permanently avoid gluten, dairy, and corn.  I’d be lying if I told you that I’ve avoided all of these 100% since I’ve been in remission.  But I’ll also admit that anytime myself or anyone else with an autoimmune condition is exposed to these food allergens they’re taking a risk.

What’s Your Experience With Avoiding “Food Triggers”?

Please feel free to share your experience with eliminating some of the allergenic foods discussed in this blog post.  If you received good results when avoiding gluten, dairy, corn, etc., and perhaps even achieved a normalization of your thyroid antibodies after doing this, please feel free to share your experience in the comments section below.  On the other hand, if you strictly avoided these common allergens and didn’t see any positive changes, I’d like to hear from you as well.  Perhaps you didn’t notice a difference in your health when avoiding gluten, dairy, or corn, but noticed a significant improvement when avoiding another food or allergen (i.e. soy, eggs, nightshades, etc.)

The kidneys are vital organs that play an important role in filtering our blood.  Since thyroid hormone affects every cell and tissue in the body, it shouldn’t be a surprise that having hypothyroidism or hyperthyroidism can have an impact on kidney health.  In this blog post I’m not only going to discuss the relationship between the thyroid gland and the kidneys, but I’m also going to give you some information that will help you to determine if your kidneys are working properly.  As a result, this blog post won’t only be beneficial for those with thyroid and autoimmune thyroid conditions, but will be valuable to anyone with kidneys (which hopefully describes YOU!).

I’d like to start out by discussing some of the basics of kidney function.  First of all, each kidney consists of filtering units called nephrons, and each nephron includes a filter called the glomerulus, along with a tubule.  These structures are part of the renal cortex, which is the outer part of the kidney.  The glomerulus filters your blood, and the tubule helps to remove toxins, reabsorbs ions, water, and nutrients, which in turn helps to maintain blood pH and electrolyte balance.  There is also something called a collecting duct, which reabsorbs solutes and water, which in turn forms urine.

Let’s go ahead and list some of the functions of the kidney in bullet-point format:

• Acid-base balance
• Maintaining fluid balance
• Regulation of electrolytes
• Removal of waste materials from food, medications, and toxic substances
• Regulation of blood pressure
• Production of certain hormones (i.e. erythropoietin) that help to produce red blood cells
• Activation of vitamin D

Health Conditions Involving The Kidneys

There are many health conditions associated with the kidneys, and I’m going to list a few of them below:

• Chronic kidney disease
• Kidney stones
• Glomerulonephritis
• Acute nephritis
• Polycystic kidney disease
• Urinary tract infections
• Acidosis
• Uremia
• Nephrotic syndrome

What Is Chronic Kidney Disease?

I’m not going to discuss all of these conditions I listed above, but I do want to discuss chronic kidney disease (CKD).  CKD is a common condition that refers to a long-term loss of kidney function.  It is identified by the presence of an abnormality of kidney structure or function (or both) for at least 3 months (1).  Some of the common risk factors for developing CKD include a family history, smoking, high blood pressure, diabetes, and obesity.  I’ll talk about the relationship between thyroid hormone imbalances and CKD shortly.

How is Chronic Kidney Disease Diagnosed?

As I mentioned earlier, CKD is identified by the presence of an abnormality of kidney structure and/or function for at least 3 months.  Specifically, one of the following needs to be present for at least 3 months (2):

• Decreased estimated glomerular filtration rate (eGFR) (<60 mL/min/1.73 m2)
• Albuminuria (urinary albumin-to-creatinine ratio ≥30 mg/g)
• Structural abnormalities (from imaging)
• Urine sediment abnormalities (hematuria, red or white blood cell casts, oval fat bodies or fatty casts, granular casts, and renal tubular epithelial cells)
• Electrolyte and other abnormalities due to tubular disorders
• Histological abnormalities
• Previous history of kidney transplantation

While diagnosing CKD might seem to be complex, in many cases a simple comprehensive metabolic panel (CMP) can provide the necessary information.  A urinalysis can also come in handy.  Some of the markers related to kidney function on a CMP include:

• Estimated glomerular filtration rate (eGFR)
• Blood urea nitrogen (BUN)
• Creatinine
• Electrolytes (sodium, potassium)

Of these, the eGFR is the most helpful, with creatinine next.  If someone has an elevated creatinine and depressed eGFR, this is an indication that there is kidney dysfunction occurring.  However, there are a few important things you need to understand.  Since CKD is diagnosed if the abnormality is present over a period of 3 months, you can’t diagnose CKD by one abnormal CMP.  In other words, if a SINGLE test shows that you have elevated creatinine levels and a low eGFR, this isn’t diagnostic of CKD.  I’ve had patients who showed these findings on a CMP, only to have these values normalize upon retesting them.

I also mentioned that a urinalysis can be helpful in diagnosing kidney dysfunction.  Protein in the urine (proteinuria) can be an important indicator of renal disease and the types of proteins found in the urine help to distinguish glomerular and tubular disorders (3).  In addition, if casts and/or blood cells are present in the urine then this can also provide some important clues about the causes of kidney dysfunction (3).

The Different Stages of Chronic Kidney Disease

Another thing to keep in mind is that there are different stages of chronic kidney disease.  The stage of CKD is based on the eGFR and the level of proteinuria.  Patients are classified as G1-G5 based on the eGFR, and A1-A3 based on the albumin:creatinine ratio (4).  What’s important to understand is that the lower the eGFR, the worst the kidney function.  For example, if someone has a GFR between 45 and 59, this is considered to be a mild to moderate reduction in kidney function, whereas if they have a GRF between 15 to 29 this is considered to be a severe reduction, with a GFR <15 indicating kidney failure.

The Kidney Stone-Oxalate Connection

Although I’m not going to discuss kidney stones in this blog post, in the past I’ve written an article about oxalates, which are a common cause of kidney stones.  If this is something that interests you please check out my article “Oxalates, Kidney Stones, and Thyroid Health”.

The Relationship Between Thyroid Health and Kidney Health

Thyroid hormones affect the development and physiology of the kidneys.  As a result, thyroid dysfunction can affect renal blood flow, glomerular filtration rate, tubular function, electrolyte homeostasis, and kidney structure (5).  Similarly, kidney disease can have a negative effect on thyroid health.  What I’d like to do next is specifically look at the relationship between hypothyroidism and kidney health, as well as hyperthyroidism and kidney health.

Hypothyroidism and Kidney Health

Multiple case studies have shown that overt hypothyroidism can cause elevations in creatinine, reduced renal blood flow, and decreased GFR (6).  However, this usually won’t cause chronic kidney disease, and correcting the thyroid hormone imbalance will usually result in normalization of these markers.  That being said, I did come across a case report involving a 75-year old woman who had CKD caused by hypothyroidism (7).  As for the impact of kidney dysfunction on thyroid health, mild to moderate kidney dysfunction usually won’t cause thyroid hormone imbalances, although as I’ll discuss shortly, chronic kidney disease can cause overt hypothyroidism.

Hyperthyroidism and Kidney Health

Hyperthyroidism causes an increase in renal blood flow and GFR, with the GFR increasing about 18–25% among hyperthyroid patients (8).  Thyroid hormones increase the plasma renin, angiotensin II, and serum angiotensin converting enzyme levels (8).  If you have elevated thyroid hormone levels and you get a comprehensive metabolic panel you probably will see a decreased creatinine.  This is not only due to an increase in the filtration rate, but also is caused by a decrease in muscle mass (9).  Usually the serum sodium and potassium will be normal on a CMP, although there are exceptions, with hypokalemia (low potassium) being more common than hyponatremia (low sodium).  The good news is that most of these imbalances are reversed upon balancing the thyroid hormone levels, although sometimes the person will need to rebuild muscle mass (i.e. do weight-bearing exercises) to increase the creatinine.

Chronic Kidney Disease and Thyroid Health

Now I’d like to look more specifically at the relationship between chronic kidney disease and thyroid hormone imbalances:

Hypothyroidism and Chronic Kidney Disease

Recent studies show that hypothyroidism is associated with a higher risk of cardiovascular disease and death in CKD (10).  There is also increasing evidence that hypothyroidism is a risk factor for the development of CKD, as well as its progression (10).  The reverse seems to be true as well, as the research shows a higher prevalence of subclinical and clinical hypothyroidism in those with chronic kidney disease (11).

Since thyroid hormones affect every cell and tissue in the body, it probably isn’t surprising to learn that hypothyroidism can have a negative effect on kidney health.  But how can severe kidney dysfunction cause hypothyroidism?  There are a few possible mechanisms.  One involves the retention of iodine due to impaired kidney excretion (11).  This actually may be a mechanism that can also cause hyperthyroidism in some people with CKD.  In addition, CKD may cause dysregulation of the hypothalamic-pituitary-thyroid (HPT) axis (11).  Finally, the peripheral conversion of T4 to T3 may be impaired in CKD, resulting in low T3 levels (12).

When someone has CKD and low T3 levels, along with an elevated TSH, many practitioners would look to address this by giving the patient thyroid hormone replacement.  However, when doing research for this blog post I came across a few different sources which mentioned how clinicians need to exercise caution in treating patients with low T3 levels/elevated TSH, as this can lead to a negative nitrogen balance (12).

This poses a bit of a dilemma for someone with CKD who has low T3 levels, as having healthy thyroid hormone levels is very important.  While giving thyroid hormone replacement might not be wise in some cases of CKD, addressing the cause of the conversion problem is an option to consider.  In the case of CKD, some of the factors that commonly affect the conversion of T4 to T3 include chronic metabolic acidosis, chronic protein malnutrition, and decreased clearance of proinflammatory cytokines (12).

Hyperthyroidism and Chronic Kidney Disease

Although hyperthyroidism doesn’t cause CKD, it can accelerate it (12).  The problem is that many people in the earlier stages of CKD aren’t aware that they have any kidney issues.  If you had one of the risk factors (i.e. smoking, high blood pressure, obesity, diabetes) prior to developing hyperthyroidism then of course there is a greater chance that you have CKD, which means that in someone with hyperthyroidism there is an even greater urgency to decrease the thyroid hormone levels.

Conventional Treatment Methods for CKD

The treatment for CKD depends on the severity of the condition.  Of course with any type of kidney disease you want to make sure you address some of the risk factors I mentioned earlier.  Unfortunately this frequently is accomplished through medication, which further stresses out the kidneys.  For example, if someone has high blood pressure, medication very well might be necessary, but this shouldn’t be the only treatment recommended.  Similarly, if someone has type 2 diabetes, medication such as Metformin might be a good idea to take on a temporary basis, but doing other things to address the cause of the condition is important.  Of course if someone is smoking then quitting is the only good solution, although I realize that it’s not easy to do.

If someone reaches what’s referred to as “end-stage” kidney disease, then the two options usually given are dialysis or having a kidney transplant.  Dialysis is a treatment that removes waste products and extra fluid from your blood (since your kidney is no longer able to do this).  And a kidney transplant is when someone donates a healthy kidney which replaces one of your non-functioning kidneys.  Of course neither of these options are desirable, which is why you want to do everything you can to maintain the health of your kidneys.  Perhaps in the future stem cell therapy will be an option (13), but even if this is the case in the future keep in mind that 1) stem cell therapy is expensive, and 2) my guess is that not everyone with CKD will be a candidate to receive it.

Can Homeopathy Help With Chronic Kidney Disease?

In November of 2015 my cat “Cookie” was diagnosed with chronic kidney disease.  Cookie lived a great life, and she was 17 years old at the time, but I was still sad when she was diagnosed with CKD.  The veterinarian gave Cookie 2 to 3 months to live.  I gave her fluids daily, but after a few weeks she was going downhill fast, vomiting frequently, and her appetite was decreasing.  I should add that I brought Cookie to the vet for some acupuncture treatments, which didn’t seem to help much.

One day I was in a pet store, and I asked the owner if she could suggest any natural remedies for my cat.  She suggested a homeopathic formula called RenoAid by the company HAMPL.  And so I started giving Cookie the homeopathic formula.

To make a long story short, I was very skeptical about the homeopathy helping, but I figured I had nothing to lose but the $35 I spent on the bottle.  It was the least I could do to try to help Cookie.  Cookie gained her appetite back and seemed to be back to her old self.  I know for certain it was the homeopathic formula that helped, as a few weeks later we went away on a one-week cruise, and we left Cookie with a friend.  The friend did give Cookie the homeopathic formula while we were away, but only once or twice per day (I had been giving it to her six times per day), and when we came back from the cruise Cookie started losing her appetite again.  I gave her the RenoAid more frequently and fortunately her health improved.

Cookie passed away in July 2017, approximately 18 months after the vet told me she had only 2 or 3 months to live.  The homeopathy didn’t cure her CKD, but it allowed her to live a happy life for 1 1/2 years.  I’m telling this story not to encourage people with CKD to receive homeopathy, but just as a reminder that natural treatment options can be powerful.  Unfortunately I’m unaware of a similar homeopathic product for humans, but I’d like to discuss some things you can do naturally to support the health of your kidneys.

Natural Treatment Options For Kidney Health

1. Eat a healthy diet.  This of course is the case with any chronic health condition, as you want to eat mostly whole foods, including plenty of vegetables.  I need to mention that if someone has already been diagnosed with CKD then they will want to make sure not to eat too much protein.  This frequently is the case for those with Graves’ disease or Hashimoto’s who follow an autoimmune Paleo (AIP) diet, as many people will eat a lot of meat.  Just keep in mind that you don’t need to eat a lot of meat when following an AIP diet.  I realize that many people eat a lot of meat because they don’t feel full unless if they eat meat with every meal…this is especially true with those who have hyperthyroidism.  But ideally you want to eat mostly vegetables, which is true with just about any healthy diet.

2. Stay hydrated.  Drinking plenty of water is important for optimal kidney health.  I recommend to drink purified water or a good quality spring water out of a glass bottle, and to try your best not to drink tap water or water in plastic bottles.  I realize this might not be possible 100% of the time, as if you go to a restaurant or travel then there might be times when you drink tap water or water out of a plastic bottle.  But don’t underestimate the impact that chemicals in the water will have not only on your kidney health, but your overall health as well.  One thing to keep in mind is that while there are no studies which show that bisphenol A (BPA) can cause or contribute to CKD, BPA (and other chemicals) will build up when the glomerular filtrate rate decreases (14).

3. Minimize your consumption of sugar.  I mentioned how having diabetes is a risk factor for CKD.  But being prediabetic is associated with a modest increase in CKD (15).  And let’s face it, many people with prediabetes will eventually develop “full blown” diabetes.  After all, it’s not as if someone has healthy blood sugar levels one day and the next day they develop type 2 diabetes.  Obviously it takes time for this condition to develop.  If you have high blood glucose and/or insulin levels but haven’t progressed to type 2 diabetes yet I’d check out my blog post entitled “Insulin Resistance, Hypoglycemia, and Thyroid Health”.  If you already have diabetes then you can read my article on the 4 types of diabetes.

4. Normalize your blood pressure.  As I discussed in a past article I wrote on blood pressure, hypertension is common with both hyperthyroidism and overt hypothyroidism.  But many times high blood pressure is unrelated to thyroid hormone imbalances.  Other causes of hypertension include smoking, obesity, stress, adrenal problems, and sleep apnea.  Sometimes it can be challenging to find the cause of hypertension.  While medication is an option to consider in some cases, if you have high blood pressure it makes sense to also try to improve your diet and lifestyle, and certain nutritional supplements may also be beneficial, including fish oils, CoQ10, and aged garlic.

5. Balance your thyroid hormone levels.  After reading this blog post you should have a basic understanding as to how both hyperthyroidism and hypothyroidism can affect the health of the kidneys.  Even if the thyroid hormone imbalance isn’t the primary cause of the kidney dysfunction, having either hyperthyroidism or hypothyroidism can worsen the kidney condition.  This is especially true if someone has hyperthyroidism in the presence of CKD.

6. Reduce your toxic load.  Exposure to certain environmental chemicals can cause renal injury due to excessive oxidative stress (16).  Two of these chemicals include perfluoroalkyl acids and dioxins.  Heavy metals can also have a negative effect on the kidneys, although the extent and the expression of renal damage depend on the species of metals, the dose, and the time of exposure (17).  I came across another study which showed that arsenic exposure can be related to CKD (18).  While it’s impossible to completely eliminate your exposure to environmental toxins, you can 1) minimize your exposure to environmental chemicals and 2) do things to eliminate chemicals from your body.

7. Lower high oxalate levels.  Oxalates not only can cause kidney stones, but in some cases oxalate crystals are associated with renal inflammation, fibrosis and progressive renal failure (19).  In the past I have tested high for oxalates, which I’m certain was due to my diet, as I was eating plenty of high oxalate foods at the time (i.e. spinach, berries, and nuts).  Having high oxalates doesn’t mean that you need to eliminate all foods high in oxalates, but it probably would be a good idea to minimize your exposure to them.  The test I recommend is the Organic Acids Test from Great Plains Laboratory.

8. Take natural agents to support kidney health.  I don’t think this is necessary for everyone to do, and I can’t say that I commonly recommend supplementation for kidney health, but if you have a current kidney issue then this is something to consider.  When doing research in this area I found some of the following natural agents to be beneficial for the kidneys:

Cordyceps sinensis.  There is evidence that cordyceps can improve renal function and specifically decrease serum creatinine, increase creatine clearance, reduce proteinuria, and alleviate CKD-associated complications (20) (21).

Astragalus.  There is evidence that astragalus can improve the renal function of CKD patients (22) (23).

Poria cocos.  This is a medicinal fungus that showed to benefit rats who had CKD (24).

Green tea polyphenols.  One study I came across showed that green tea polyphenols can help with early renal damage (25).

Curcumin.  Curcumin can help with many different health conditions, and a few studies show that it can help those with CKD by reducing inflammation and oxidative stress (26) (27).  Another study showed that it can be useful in the prevention and treatment of renal fibrosis (28).

Resveratrol.  A few different studies show that resveratrol can prevent renal injury due to its antioxidative properties (29) (30).

Glutathione.  The kidneys are highly dependent on an adequate supply of glutathione to maintain normal function (31), and so doing things to increase glutathione levels is important.  This can be accomplished through diet (i.e. consumption of cruciferous vegetables), taking glutathione precursors (i.e. N-acetylcysteine), or an acetylated or liposomal glutathione supplement.

You may have noticed that most of the natural agents listed can help to reduce inflammation and oxidative stress, which is why they can help with CKD.  If someone has CKD then perhaps they’ll want to take a kidney support product consisting of a few of the agents I listed here, but otherwise I would just focus on eating well, making sure you’re well hydrated, perhaps drink green tea on a regular basis, and do what’s necessary to have healthy glutathione levels.

Have you seen any relationship between your thyroid condition and kidney function?  If so, please share your experience in the comments section below.  Remember that you can find out some good information by doing a simple comprehensive metabolic panel and looking at the eGFR. You can also get some valuable information from a urinalysis.

 

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.