Before I was officially diagnosed with Graves’ Disease I knew I was going to take a natural treatment approach.  Initially I found out I had hyperthyroidism from my primary care physician, and a couple of months later I saw an endocrinologist, who officially gave me the diagnosis of Graves’ Disease.  But even though I had planned on doing things naturally for my condition, at the time I was still skeptical as to whether or not following a natural treatment protocol would help.  After all, back then I didn’t know anyone with Graves’ Disease who had successfully restored their health through natural treatment methods.

Fortunately things worked out very well for me, as I was able to get into remission without taking any medication, and years later I have still managed to maintain a state of wellness.  And many of my patients have had success in restoring their health back to normal as well.  Not everyone is able to avoid taking medication such as Methimazole or Propranolol, but even when someone needs to take medication it is of course still possible to restore one’s health back to normal.  The problem is that most people who take the medication don’t do anything to address the underlying cause of the condition, as they simply hope and pray that they will get into remission while taking antithyroid medication.  And while some people do get into remission when taking the medication alone, this state of remission is usually temporary.

Unfortunately many people with Graves’ Disease choose radioactive iodine as a first option.  And in most cases it’s because the endocrinologist they were working with convinced them that this was the very best option.  When I saw an endocrinologist for my Graves’ Disease condition I was fortunate that she didn’t try to pressure me to receive radioactive iodine treatment.  Of course even if she did recommend RAI I would have refused it, and I didn’t take the Methimazole she prescribed to me.  But many other endocrinologists recommend radioactive iodine to every single one of their patients with Graves’ Disease, which makes me very sad knowing that most of these people could have preserved the health of their thyroid gland if they had just given natural treatment methods a try.

The Problem With Receiving Radioactive Iodine As A “First Resort”

But why shouldn’t radioactive iodine be the first treatment option?  After all, hyperthyroidism can be a very scary condition to deal with.  After I found out I had hyperthyroidism I not only was in a state of disbelief, but I also was terrified.  And this was without an endocrinologist telling me that if I don’t get my thyroid gland “nuked” there is a chance I would experience a thyroid storm, or perhaps even a heart attack.  The obvious “benefit” of radioactive iodine is that it usually will eliminate hyperthyroidism, and thus will remove the risk of having a thyroid storm, along with other conditions associated with an increased heart rate.

Of course the downside is that radioactive iodine doesn’t do anything to address the autoimmune component of Graves’ Disease.  After all, it’s easy to forget that Graves’ Disease isn’t a thyroid condition, but instead is an immune system condition that affects the thyroid gland.  And while it’s important to manage the hyperthyroid symptoms, receiving radioactive iodine won’t do anything to improve the health of the immune system.  The research clearly shows that someone with one autoimmune condition is more likely to develop another autoimmune condition in the future.  And so it is very important to try to reverse the autoimmune component of Graves’ Disease, and not just focus on managing the symptoms.

How Do You Find The Underlying Cause?

It admittedly can be a challenge to determine the underlying cause of your Graves’ Disease condition.  The primary key is to try to detect the trigger or triggers which are responsible for the development of the autoimmune response.  Some common examples of triggers include stress, infections, food allergens, and environmental toxins.

There are many things you can do on your own to improve your health, such as clean up your diet, do a better job of managing your stress, and minimizing your exposure to environmental toxins.  However, it can be difficult to restore your health on your own.  This is why I think it’s wise to consult with a competent natural healthcare professional who has experience working with Graves’ Disease patients, as this will give you the guidance that you need.

On that note, in the near future I will be releasing an online group coaching program for those who have Graves’ Disease.  This new program for Graves’ Disease will be an affordable self-management/group coaching program.  Although I do think it’s a good idea for those with Graves’ Disease to work one-on-one with a competent natural healthcare professional, I realize that not everyone will choose to do this.  And even if you are currently working with a natural healthcare professional I’m sure the information provided in this program will only further help to optimize your health.

If this is something that sounds good to you I would recommend getting on my Reversing Graves’ Disease VIP priority notification list.

Click Here To Join The Reversing Graves’ Disease program VIP Priority Notification List

Lately I have been getting a lot of questions regarding essential oils.  I’ll be the first to admit that I’m not an expert in this area, although recently I have done a good amount of research on essential oils, and I figured it was time to write an article on this topic.   As I discuss these essential oils, you’ll notice that many of them have similar benefits.  For example, many of the essential oils I discuss have anti-inflammatory properties, which can greatly benefit people with Graves’ Disease and Hashimoto’s Thyroiditis.  However, this doesn’t mean that if you have an autoimmune thyroid condition that you need to take all of the essential oils with anti-inflammatory properties.

It’s important to understand that while numerous essential oils have anti-inflammatory properties, most of them have other benefits as well.  And so while there might be some overlap between different essential oils, no two oils are exactly alike.  And not everyone will respond the same to each essential oil.  For example, one person might have a favorable response to myrrh oil, but when someone else tries it they notice that it doesn’t seem to help too much.  Of course not having a positive experience with one essential oil doesn’t mean that other essential oils won’t be beneficial.  And it’s also important to understand that the quality of the essential oil is important.

What I’d like to do now is discuss five essential oils that can benefit many people with thyroid and autoimmune thyroid conditions.  Keep in mind that this list isn’t all-inclusive, as there are many other essential oils that can be beneficial, although the ones listed below have a good amount of research supporting their benefits.

1. Lemongrass.  Although there are numerous ways in which lemongrass can benefit one’s health, with regards to those with thyroid and autoimmune thyroid conditions, lemongrass is especially useful for its anti-inflammatory and antifungal effects.  One study showed that lemongrass oil inhibited the pro-inflammatory cytokines IL1 beta and IL-6 (1).  Another study concluded that lemongrass essential oil and its constituents (citral and geranial) may be a therapeutic candidate for allergic and inflammatory diseases (2).  It also appears that lemongrass essential oil may have anticancer activity (3).  Another study showed that lemongrass essential oils has antifungal effects against Candida albicans,  C. tropicalis, and Aspergillus niger (4).

2. Myrrh.  Some sources claim that rubbing two or three drops of myrrh oil on the thyroid gland on a daily basis can help support thyroid health, especially in those with hypothyroidism.  I couldn’t find any research showing that myrrh can directly benefit thyroid health.  However, in most cases it won’t hurt to give this a try, and if anyone reading this has noticed an improvement in their thyroid health by using myrrh oil please feel free to share your experience in the comments section below.  Perhaps the improvement is due to the anti-inflammatory effects of myrrh, as the research does show that myrrh can reduce pro-inflammatory cytokines (5) (6), which can help reduce the autoimmune response, and this in turn might benefit people with autoimmune conditions such as Hashimoto’s Thyroiditis.

3. Frankincense.   Frankincense is one of the main essential oils used for immune system health.  This is mainly due to the boswellic acids, which are the active compounds of frankincense (7).  The chemical structure of boswellic acids is similar to steroids, although their actions are different from most painkillers and NSAIDs (7).  Although I couldn’t find anything in the literature which shows that frankincense has a direct effect on thyroid health, just as is the case with myrrh oil, some people claim that rubbing frankincense oil directly on their thyroid gland has helped to improve their thyroid hormone levels, and in some cases even shrink thyroid nodules.  I can’t say that I have patients who have experienced this, but if anyone reading this has had a positive experience with frankincense that relates to thyroid health then please share your experience in the comments section below

But even if frankincense doesn’t have a direct effect on thyroid health, because most thyroid conditions are autoimmune, then using this essential oil can arguably help people with both Graves’ Disease and Hashimoto’s Thyroiditis.  One specific study showed how the boswellic acids in frankincense can help to reduce Th17 cytokines, which are a factor in autoimmunity (8).  The same study showed that it can also increase regulatory T cells, which help to suppress autoimmunity (8).  Another study showed how one of the boswellic acids in frankincense is a potent inhibitor of 5-lipoxygenase, which is an enzyme responsible for inflammation (9).  In addition to helping with inflammation, frankincense might also benefit people with brain and memory conditions, along with asthma, skin conditions, inflammatory bowel disease, diabetes, and cancer (10).

4. Geranium.  This essential oil has numerous benefits, but with regards to those people with thyroid and autoimmune thyroid conditions, its anti-inflammatory and antifungal effects are two of the more important properties.  A few studies reveal the anti-inflammatory effects of geranium essential oil (11) (12).  However, I would rely more on the other essential oils I have discussed thus far for inflammation, and would recommend this essential oil more for helping with candida infections, which is a common problem with my patients.  One study showed that two of three geranium oil constituents (geraniol and geranyl acetate) exhibited anti-candida activity (13).  Another study showed that the vaginal application of geranium oil or its main component, geraniol, suppressed candida cell growth in the vagina and its local inflammation (14).  Another study showed that the essential oil not only resulted in the complete inhibition of Candida albicans, but it also showed anti-microbial activity against both gram-negative and gram-positive bacteria (15).

5. Lavender.  This probably is the most well known of the essential oils I have discussed.  And lavender has many different benefits.  One study showed that lavender can protect against diabetes and oxidative stress (16).  Many know that lavender has a calming effect, and one study showed that lavender aromatherapy had a beneficial effect on insomnia and depression in women college students (17).  Many people with thyroid and autoimmune thyroid conditions have sleep issues, and so lavender oil might help in some of these cases.  Lavender also has anti-inflammatory effects, as a study showed that lavender essential oil inhibited inflammation induced by lipopolysaccharides (18).  Another study showed that lavender has antioxidant, analgesic, and anti-inflammatory effects (19).  There is also evidence that lavender has antimicrobial effects (20), and also has antifungal activity (21).

Other Essential Oils:

Although I focused on five specific essential oils in this blog post, this of course doesn’t mean that other essential oils can’t be beneficial to your health.  Other commonly used essential oils include melaleuca (tea tree oil), peppermint oil, clove oil, thyme oil, lemon oil, and marjoram.

How Do You Apply These Essential Oils?

When I first started learning about essential oils, one of the first questions I had was “how do I apply the essential oils”, and “what dosage do I use?”  In most cases you need only a very small amount of essential oil for a therapeutic effect to take place.  For example, one or two drops of these oils is frequently all someone needs.  Essential oils are usually diluted with a carrier oil, such as coconut oil or olive oil.  Other examples of carrier oils include avocado oil, sesame oil, and evening primrose oil.  Using the carrier oils reduces the chances of skin irritation occurring when the essential oils are applied topically.  And in case if you were wondering, diluting the essential oil with a carrier oil shouldn’t alter its therapeutic properties.

In summary, essential oils have some wonderful benefits, and you might want to consider incorporating them.  Myrrh oil and frankincense are two of the more well known essential oils with regards to thyroid and autoimmune thyroid conditions.  And while some claim that they have a direct effect on thyroid health, the research shows that they have a greater effect on immune system health.  I also discussed the benefits of lemongrass, geranium, and lavender, although there are many other essential oils which can benefit your health.  I’m admittedly still learning about essential oils, and if you are interested in learning more about it then you might be interested in attending the free online essential oils summit.

For those people with Graves’ Disease and Hashimoto’s Thyroiditis who are following an autoimmune paleo diet, one of the biggest challenges is to find snacks that are autoimmune paleo friendly.  And so I figured I’d put together a brief post listing some of snacks that are fine to eat for those who are following an autoimmune paleo diet.  This is an incomplete list, but for many people, the snacks I include in this post will make it much easier to follow an autoimmune paleo diet, and of course if you have other AIP-friendly snack suggestions please feel free to share these in the comments section below.

One thing to keep in mind is that while the snacks I have listed below are safe to eat for most people with Graves’ Disease and Hashimoto’s Thyroiditis, this doesn’t mean that it’s okay to overindulge in these snacks.  It’s easy to eat too many servings of fruits, sweet potato chips, and other snacks.  With regards to fruit, I would make sure to eat at least twice as many vegetables as fruits, and in many cases it’s a good idea to limit your consumption to two or three servings of fruit per day.

But how about other snacks such as plaintain chips, sweet potato chips, tiger nuts, etc?  This does depend on the person, but in most cases you will want to eat no more than one or two servings per day of these other snacks.  I realize this might be challenging to do, but one tip is to divide the snacks into smaller portions every night or morning.  So for example, if you purchase a bag of sweet potato chips or coconut flakes and if you eat them directly out of the bag then of course it’s more challenging to keep track of how much you’re eating, and before you know it you might end up eating half the bag.  On the other hand, if every night after you eat dinner you take a few minutes to portion your snacks into smaller servings then you are less likely to overindulge.

With that being said, here are nine AIP-friendly snacks:

1. Plaintain chips or crackers

2. Sweet potato chips

3. Kale chips

4. Coconut chips or flakes

5. Unsweetened coconut yogurt

6. Tiger nuts

7. AIP friendly beef jerky

8. Baby carrots and other vegetables

9. Certain fruits (i.e. apple, pear)

Preparing Your Own Snacks vs. Purchasing “Pre-Packaged” Snacks

When it comes to certain snacks such as fruit or baby carrots there shouldn’t be too many questions regarding where to purchase these foods, although I realize that not everyone will have access to organic fruits and vegetables.  But other than fruits and veggies, you will have the option of preparing your own snacks, or purchasing pre-packaged snacks.  Of course it is always best to prepare your own snacks whenever possible, as this will give you full control over the ingredients.  For example, there aren’t too many brands which carry unsweetened coconut yogurt, and most brands that are available have ingredients which might be problematic for some people.  On the other hand, I realize that many people would prefer not to prepare their own coconut yogurt.

The same concept applies with other snacks.  For example, you of course can prepare your own sweet potato chips, and if you are willing to do this then that’s great.  However, there is a brand I recently came across called “Jackson’s Honest” that has sweet potato chips with coconut oil, and there probably are a few other healthier brands that I’m not familiar with.   Although I personally don’t like beef jerky, the company “EPIC” has both beef jerky and protein bars which consist of 100% grass fed bison and beef.  Just keep in mind that not all of their products are AIP-friendly, as some of them include seeds.

It was only recently that I had the opportunity to try tiger nuts, as I was in a Whole Foods Market in New York that carried the brand Organic Gemini.  And so I decided to purchase a bag, and I must admit that I wasn’t crazy about them at first, but after awhile I got used to them, and now I really do enjoy them.  Unfortunately, they don’t offer tiger nuts at our local Whole Foods Market in Charlotte NC, but I order them online directly from the company.  Not only do I find that they make a good snack, but they are an excellent source of fiber, which is important for anyone following an autoimmune paleo diet, as some of the best sources of fiber (i.e. nuts, seeds, beans) are excluded from an autoimmune paleo diet.

What Is Your Favorite AIP-Friendly Snack?

Please feel free to share your favorite autoimmune paleo-friendly snack in the comments section below.  This can be from the list I included in this post, but of course if there are any other snacks you recommend which are AIP-friendly please feel free to share this with everyone as well.

When I consult with someone who has Graves’ Disease or Hashimoto’s Thyroiditis, it’s common for the person to have a family history of thyroid disease.  However, I also work with a lot of patients with an autoimmune thyroid condition who don’t have a family history of thyroid autoimmunity, or any other autoimmune conditions for that matter.  The National Institutes of Health estimates that up to 23.5 million Americans suffer from autoimmune disease, and that the prevalence is rising, while the American Autoimmune Related Diseases Association (AARDA) claim that the number is closer to 50 million (1).  And of course there are tens of millions of people in other countries who suffer from Graves’ Disease, Hashimoto’s Thyroiditis, and other autoimmune conditions.  But why is there an increased prevalence of autoimmunity?

Before discussing some of the different reasons for the increased prevalence of autoimmune thyroid conditions, as well as other autoimmune conditions, it’s important to point out that there is a genetic component behind most, if not all of these conditions.  And the reason why this is important to mention is because in all likelihood the genetic predisposition hasn’t changed over the last 50+ years, but there is no question that over the last few decades our environment has changed for the worse.  And if we don’t modify these environmental factors, not only will you not improve your health and therefore will remain more susceptible to developing other autoimmune conditions, but if you have children then there is an increased likelihood that they will develop an autoimmune condition.

So let’s go ahead and discuss some of the main reasons why thyroid autoimmunity is on the rise:

1. Increased C-sections and bottle feeding.  Having a Cesarean section changes the gut microbiota, as does bottle feeding.  And so being born via a C-section and/or being bottle-fed can make you more susceptible to developing an autoimmune condition in the future.  Children born via a C-section lack the benefit of protective vaginal bacteria, which may make them more susceptible to viruses, allergies, and asthma later in life, as well as type one diabetes (2) (3).  Another study showed that being born via a C-section increases the risk of developing Celiac disease (4). As for the importance of breast milk, human milk differs from formula not only with regards to nutrients, but it also has growth factors, cytokines, immunoglobulins, and digestive enzymes that are lacking in infant formula (5).  Yet another study showed that formula-feeding is associated with a shift towards Th1 cytokines, which may have an influence on the development of autoimmune disease (6).  It’s worth noting that Hashimoto’s Thyroiditis is usually a Th1-dominant condition.

Of course I realize that sometimes C-sections are necessary, and the same is true with bottle feeding.  But many C-sections are unnecessary, and some mothers don’t breastfeed their babies because they find it more convenient to bottle feed.  Another factor is that many women aren’t aware of the health benefits of breastfeeding, although I realize that most women reading this are probably aware that breastfeeding is a healthier option.  Of course I understand that some women do want to breastfeed their babies but are unable to, but the point I’m trying to make is that thousands of women are able to breastfeed their babies but choose not to do so, and most of these women don’t realize the negative impact this can have on the future health of their baby.

2. Western diet.  A “Western diet” typically includes foods that are high in sugar, unhealthy fats and oils, are frequently processed, etc.  And the reason why eating poorly can increase the risk of developing an autoimmune condition is because such diets promote inflammation.  Obesity is one factor, as this leads to the excessive accumulation of white adipose tissue and systemic inflammation (7).  In addition, processed foods and fast foods usually contain high amounts of salt, which in turn can increase Th17 cells (8) (9), which is a factor in autoimmune conditions.  In addition, Western diets will result in significantly different microbiota compositions, and one reason is because these diets are typically low in the fiber necessary to feed the good bacteria (10).  One study mentioned that a Western diet creates a specific inflammatory environment in the gut (11), and as many people reading this know, in order to have a healthy immune system you need to have a healthy gut.  A Western diet usually involves the excess consumption of omega 6 fatty acids, which also will promote inflammation.  And let’s not forget the negative impact that gluten can have on the gut.

3. Environmental toxins.  Over the past few decades there have been tens of thousands of chemicals manufactured.  One of the most well known ones is bisphenol a (BPA), which not only is an endocrine disruptor, but may play a role in the development of autoimmune conditions (12) (13) (14).  Phthalates are added to plastics to make them more flexible and harder to break, and they are found in adhesives, cosmetics, fragrances, vinyl flooring, polyvinyl chloride pipes, and certain toys and medical supplies (15).  And there is evidence that phthalates can trigger autoimmunity (15) (16).  Vaccines are also a possible factor (17) (18), and while this remains controversial, one thing that’s not debatable is that infants and children today receive many more vaccines than they did a few decades ago.  And of course there are many other environmental toxins we are exposed to, and to be honest, it would be shocking if there wasn’t an increase in autoimmunity with the stress put on our immune system by all of these chemicals.

4. Chronic Stress.  Both physical and psychological stress has been implicated in the development of autoimmune disease (19).  Of course humans have always dealt with stress, but the stressors of today are different than the stressors of the past.  In the past humans dealt more with acute stress situations, but these days we commonly deal with chronic stress.  As for how this can lead to autoimmunity, stress activates the hypothalamic-pituitary-adrenal (HPA) axis, which in turn releases cortisol, and this in turn suppresses the immune system (20) (21).  However, it is thought that the stress-triggered neuroendocrine hormones cause dysregulation of the immune system, which alters cytokine production, and this in turn leads to autoimmunity (22).  Keep in mind that this is just a theory, as the mechanism isn’t completely understood, but there does seem to be a connection.  And of course having an autoimmune condition such as Graves’ Disease or Hashimoto’s Thyroiditis can be very stressful, and so even if someone has an autoimmune thyroid condition that wasn’t triggered by stress, having the condition itself can be stressful, and this chronic stress can perpetuate the autoimmune response.

5. Antibiotics, hand sanitizer, and the hygiene hypothesis.  The hygiene hypothesis suggests that exposure to bacteria, viruses, and other “germs” can help improve your immunity.  For example, when I was a child my friends and I frequently would play outside in the dirt.  In fact, it was unusual for me to come back into the house clean.  These days I rarely see this, as it’s more common to see children and teenagers on their electronic devices.  In addition to not interacting with the environment, hand sanitizer is frequently used, and this also minimizes our exposure to these “germs”.  As a result of being too hygienic this can actually weaken our immune system, and can make us more susceptible to developing chronic inflammatory conditions, including autoimmune conditions.

What can you do about this?  Well, I would definitely minimize the use of hand sanitizer and antibacterial soaps.  I spoke about this in greater detail in an article I wrote entitled “Triclosan and Thyroid Health“.  Of course trying to avoid taking antibiotics is also important, and while there is a time and place for taking these, in many cases these are unnecessary.  And if you have children please let them play in the dirt…and feel free to go ahead and get dirty with them!

So hopefully you have a better understanding as to why the incidence of thyroid autoimmunity is increasing, along with other autoimmune conditions.  While genetics is no question a factor in the development of autoimmune thyroid conditions, lifestyle and environmental factors are primarily responsible for the increased prevalence.  Some of the main reasons for the rise in thyroid autoimmunity include increased number of C-sections, formula feeding, eating a poor diet, greater exposure to environmental toxins, chronic stress, and the hygiene hypothesis.

In the previous blog post I briefly spoke about the mechanism of action of vitamin D, and I explained the difference between vitamin D2 and vitamin D3.  I also discussed some of the more common health conditions that are affected by a vitamin D deficiency.  In this post I’m going to talk about why many people are deficient in vitamin D, and I’ll also discuss how to test for a vitamin D deficiency.  I’ll conclude the post by mentioning three ways to increase vitamin D levels.

So why are many people deficient in vitamin D?  Well, here are some of the different reasons:

1. Most people don’t get enough sunlight.  Many people work indoors and don’t get enough sunlight.  This definitely describes me, as while I’d like to say that I take a 30-minute walk in the sun during my lunch break every day, this usually isn’t the case.  And keep in mind that the amount of skin that is exposed to the sun plays a big factor.  For example, if someone takes a walk in the sun fully clothed then they will produce much less vitamin D when compared to someone who is sunbathing.  So I’ll consult with people who take a daily walk outside, or perhaps they work in their garden every day, but because they have a lot of clothing on they aren’t getting enough skin exposure.

2. Latitude.  Those who live in northern latitudes have a decreased exposure to sunlight during the winter, and thus are more likely to be deficient in vitamin D.

3. VDR polymorphism.  Vitamin D binds to the vitamin D receptor (VDR), which in turn is encoded by the VDR gene.  Many people have genetic polymorphisms of the VDR gene, which can increase one’s risk of developing a vitamin D deficiency.  And the research shows an association between VDR polymorphisms and thyroid autoimmunity (1) (2).

4. Skin pigmentation.  Those with dark colored skin absorb more UVB in the melanin of their skin, and as a result, they require more sun exposure to produce the same amount of vitamin D (3) (4).

5. Air pollution.  Air pollution can block the absorption of ultra-violet B (UBV) light.  This of course is a factor wherever you live, but if you live in a larger city then chances are you are dealing with a greater amount of air pollution.

6. Age.  Aging affects vitamin D metabolism, as the older you get, the less vitamin D is produced by the skin.

7. Frequent use of sunscreen.  Many people apply sunscreen whenever they go out in the sun, and since sunscreen blocks the absorption of vitamin D, using it frequently can lead to a vitamin D deficiency.  This isn’t meant to suggest that you should never use sunscreen, as I can understand using it if you are planning to be in the sun for many hours, but I would try to get at least 20 to 30 minutes of sun exposure daily without the use of sunscreen.

8. Deficiency in one of the cofactors.  Vitamin D works together with numerous cofactors, including magnesium, vitamin K2, zinc, boron, and vitamin A.  The vitamin D Council website has an excellent article which discusses the role that each of these cofactors has with regards to vitamin D.

What Are The Symptoms of a Vitamin D Deficiency?

Many people who are deficient in vitamin D don’t experience any noticeable symptoms.  If the vitamin D deficiency is severe then they might experience symptoms such as muscle pain or weakness.  But other factors can cause such symptoms, and not everyone with depressed vitamin D levels will experience muscle pain or weakness.  As a result, the best way to determine if you have a vitamin D deficiency is through testing.

Testing The Vitamin D Levels

25-OH vitamin D is the marker that should be tested through the blood.  Some healthcare professionals will test 1,25-dihydroxyvitamin D, and when you consider that this is the active form of vitamin D this might make sense.  However, it’s important to understand that 1,25-dihydroxyvitamin D is regulated by parathyroid hormone, and when someone has a vitamin D deficiency this results in a compensatory increase in the parathyroid hormone levels, and this in turn will increase 1,25-dihydroxyvitamin D.  And so 1,25-dihydroxyvitamin D is usually normal or elevated, even in the presence of a vitamin D deficiency.

3 Ways To Increase Vitamin D Levels

1) Sunlight.  Ideally this is the best way to increase vitamin D levels, as one hundred years ago people didn’t take vitamin D3 supplements as they do today.  However, we of course live in a different world, as many people don’t have the opportunity to go outside when it’s sunny, and most who do get regular sun exposure are fully clothed.  In addition, air pollution is a big issue, as I mentioned earlier how this affects the absorption of vitamin D.

2) Supplementation.  I personally take 5,000 IU/day of vitamin D3 on a wellness basis, and this keeps my levels at a healthy level, which I confirm through annual testing.  Does this mean that everyone should take a vitamin D3 supplement on a wellness basis?  Not necessarily, as some people do need to supplement with vitamin D3 to correct a deficiency, but are then able to maintain healthy levels through regular sun exposure.  Others need to supplement with vitamin D3 but don’t need to take as high of a dosage.

3) Indoor tanning.  Using indoor tanning beds can also be an option.  This is controversial, as indoor tanning can potentially increase the risk of skin cancer (5) (6).  However, the vitamin D Council considers tanning to be a good option if you take the following two precautions (7).  First, get half the amount of exposure that it takes for your skin to turn pink.  And second, use low-pressure tanning beds that have a good amount of UVB light, instead of the high intensity UVA light.

Can Vitamin D Be Obtained Through Diet?

Vitamin D is very low in the food supply, as it is not found in plant materials (i.e. vegetables, fruits, or grains) and it is present in small amounts in meats and other animal food sources, except in rare cases such as fish liver oils (8).  Dairy products are of course commonly fortified with vitamin D, and canned salmon, sardines, and tuna can be good sources of vitamin D (9).  But overall it is very difficult to get enough vitamin D from the diet, and it is almost impossible to correct a vitamin D deficiency through diet alone.

In summary, many people with thyroid and autoimmune thyroid conditions are deficient in vitamin D, and while a big reason for this is due to insufficient exposure to sunlight, other reasons include living in a northern latitude, having a VDR polymorphism, having dark colored skin, air pollution, frequently using sunscreen, and being deficient in one or more of the cofactors of vitamin D.  When testing for vitamin D in the blood you want to test for 25-hydroxy vitamin D, as this is more accurate than 1,25-dihyroxyvitamin D.  Sunlight and supplementing with vitamin D3 are the two main ways to increase vitamin D levels, although indoor tanning is also an option.

 

Many people are aware of the importance of healthy vitamin D levels with regards to bone health.  But vitamin D has many other important functions.  In fact, just about every tissue and cell in your body has vitamin D receptors.  Unfortunately, many people are deficient in vitamin D.  Others fall within the recommended lab reference range, but while most of the research still suggests that optimal levels should be above 30 ng/mL, some sources, including the vitamin D Council, suggest for these levels to be greater than 50 ng/mL.

I’d like to start out by discussing the mechanism of action of vitamin D.  This can get pretty complex, and so I’m just going to cover the basics.  Although vitamin D is referred to as a vitamin, the active form is actually a prohormone, and this is produced in the skin through the ultraviolet irradiation of 7-dehydrocholesterol, which is a cholesterol precursor.  So 7-dehydrocholesterol is converted into vitamin D3 (also known as cholecalciferol) in the skin.  However, vitamin D3 is biologically inert, and it needs to be metabolized to 25-hydroxy vitamin D3 in the liver, and then it gets metabolized to 1, 25 hydroxy vitamin D3 (also known as calcitriol) in the kidneys by the enzyme CYP27B1, although other tissues have this enzyme as well.

More Facts About Vitamin D

Vitamin D and its metabolites are carried in the blood mostly bound to vitamin D binding protein (DBP) (1).  So what happens is that after cholecalciferol (vitamin D3) is manufactured or taken as a supplement, it binds to DBP, and after it gets converted into calcitriol, this also is carried through the blood by DBP before binding to the vitamin D receptor.

Vitamin D increases the intestinal absorption of calcium and phosphorus, which in turn promotes bone mineralization and remodeling, and it is also involved in regulating serum calcium and phosphorus levels.  This is the main reason why most medical doctors test for Vitamin D, as they are concerned about low levels affecting bone mineral density.  However, vitamin D has numerous other functions, as it also plays a role in neuromuscular function and influences cellular growth and differentiation.  It also plays a big role in immunity, which of course is important for those with autoimmune thyroid conditions such as Graves’ Disease and Hashimoto’s Thyroiditis.  I’ll talk more about this later.

What’s The Difference Between Vitamin D2 and D3?

Supplemental vitamin D comes in two primary forms.  When someone purchases vitamin D in a health food store they are usually getting cholecalciferol, which is also known as vitamin D3.  On the other hand, when a medical doctor writes a prescription it is for ergocalciferol, which is known as vitamin D2.  Even though some sources claim that these two are equivalent, vitamin D3 has been proven to be the more potent form of vitamin D in all primate species, including humans (2).  In addition to vitamin D3 being more effective than vitamin D3, there is diminished binding of vitamin D2 metabolites to vitamin D binding protein in the plasma, a nonphysiologic metabolism, and a shorter shelf life of vitamin D2 (2).

Vitamin D and The Research                           

What I’d like to do now is discuss some of the research involving vitamin D, including numerous conditions which are affected by a vitamin D deficiency.

Vitamin D in dementia and cognition.  A few studies show that a vitamin D deficiency can increase one’s risk of dementia, and even Alzheimer’s disease (3) (4) (5).  Vitamin D receptors are abundant in the tissues of the brain, and the active form of vitamin D has neuroprotective effects which include the clearance of amyloid plaques, which is a hallmark of Alzheimer’s disease (6).

Inflammation/autoimmunity.  There are also numerous studies which show that vitamin D plays an important role in modulating the immune system and inflammation (7) (8) (9).  It appears to do this by decreasing pro-inflammatory cytokines, and is also associated with higher regulatory T cells (10) (11), which help to suppress autoimmunity.  However, some sources question whether a vitamin D deficiency is a cause of inflammation, or if it is a consequence of the inflammatory process (12) (13).

High Blood Pressure/Cardiovascular disease.  Numerous studies show that vitamin D might have antihypertensive effects in those people with essential hypertension, which in turn can help to prevent the development of a stroke (14) (15).  There is also evidence that a vitamin D deficiency can be a risk for the development of peripheral arterial disease (16) (17).  Although there is some evidence linking a vitamin D deficiency to atherosclerosis (18), other studies suggest that more research is needed in this area (19).

Osteoporosis.  One of the main functions of the active form of vitamin D is to enhance the intestinal absorption of calcium.  And this is why healthy vitamin D levels are important for healthy bone mineral density (20) (21).

Gut microbiota/Intestinal mucosal barrier.  There is evidence that vitamin D may play an important role in gut homeostasis and in the signaling between the microbiota and the host (22).  In addition, the vitamin D receptor appears to play a critical role in homeostasis of the intestinal mucosal barrier by preserving the integrity of the junction complexes (23).

Cancer.  Since vitamin D is important for optimal immune system health then it shouldn’t be surprising that some studies show that intake or synthesis of vitamin D leads to the reduced incidence and death rates of colon, breast, prostate, and ovarian cancers (24) (25) (26) (27).

Thyroid Health.  Numerous studies show a correlation between vitamin D deficiency and autoimmune thyroid disease.  A few studies have shown that low levels of vitamin D is associated with the presence of antithyroid antibodies and abnormal thyroid function (28) (29).  Both people with Hashimoto’s Thyroiditis and Graves’ Disease commonly have low levels of vitamin D (30) (31) (32).  This doesn’t mean that a vitamin D deficiency is the cause of these conditions, although having such a deficiency might make someone more susceptible to developing thyroid autoimmunity.

Autism.  There is evidence that healthy levels of vitamin D might reduce the risk of autism (33).  In addition, supplementation of vitamin D (in those who are deficient) may significantly improve the outcome of some children with Autism Spectrum Disorder through its anti-inflammatory actions, antiautoimmune effects, increasing regulatory T cells, protecting the mitochondria, and upregulating glutathione (33) (34) (35).

Infections.  Since healthy vitamin D levels are necessary for a healthy immune system, it makes sense that a vitamin D deficiency can increase one’s risk of developing infections.  There is some evidence that it can reduce the incidence of influenza (the flu), and one study suggests keeping the levels around 50 ng/mL to prevent infection (36) (37) (38).

In the next blog post I will start out by talking about why many people are deficient in vitamin D.  I will also talk about how to test the vitamin D levels, as while most healthcare professionals test for 25-OH vitamin D, since 1,25-OH vitamin D is the active form, I’m sure that some people reading this are wondering if this should be tested.  I will also discuss three ways to increase vitamin D levels.

Hashimoto’s Thyroiditis is an autoimmune thyroid condition that is characterized by elevated thyroid autoantibodies.  An encephalopathy is general term for a disease of the brain.  Hashimoto’s encephalopathy is an autoimmune condition that not only involves elevated thyroid antibodies, but it also is characterized by brain dysfunction.  In fact, the encephalopathy symptoms are usually more prominent than the thyroid symptoms.  While Hashimoto’s Thyroiditis is common, Hashimoto’s encephalopathy is a rare condition.

Because there are thyroid autoantibodies present in Hashimoto’s encephalopathy, not surprisingly one can have thyroid hormone imbalances.  This can lead to the classic hypothyroid symptoms such as fatigue, weight gain, cold hands and feet, etc.  However, many times the person with Hashimoto’s encephalopathy is in a subclinical hypothyroid state, and so while they might have elevated thyroid antibodies, they frequently will present with a normal thyroid panel and minimal hypothyroid symptoms.  As I’ll discuss below, other autoantibodies are present as well, which can lead to psychiatric manifestations, seizures and focal neurologic deficits (1).

The Autoantibodies Associated With Hashimoto’s Encephalopathy

Hashimoto’s encephalopathy involves numerous autoantibodies.  These can include elevated thyroglobulin antibodies, thyroid peroxidase antibodies, or both.  These thyroid antibodies are of course commonly seen in Hashimoto’s Thyroiditis.  But with Hashimoto’s encephalopathy, in addition to one or both thyroid autoantibodies being present, there are also autoantibodies against alpha-enolase (2) (3) (4).

Alpha-enolase, also known as Enolase 1, is a glycolytic enzyme.  These autoantibodies are found in other autoimmune conditions as well, such as Behçet’s disease (5).  Enolase exists in three different forms: α, β and γ (4). Isozyme α is found in most tissues, isozyme β in muscle, and isozyme γ is present mainly in nervous tissue (5) (6). It appears that the antibodies in Hashimoto’s Encephalopathy only involve α-enolase (4).

What’s important to understand here is that autoimmunity involves the body attacking its own cells and tissues.  What differentiates one autoimmune condition from another is that different parts of the body are attacked.  So with Hashimoto’s the immune system will attack either thyroglobulin, or the thyroid peroxidase enzymes, which is why you will see one or both of these antibodies elevated.  With Hashimoto’s encephalopathy you will not only see an increase in one or both of these thyroid antibodies, but since the immune system is attacking alpha-enolase, you will see elevated levels of these autoantibodies as well.  As for why one person will develop Hashimoto’s Thyroiditis, while another person will develop Hashimoto’s encephalopathy, it comes down to a combination of genetics, lifestyle factors, and environmental triggers.

What Is The Conventional Treatment Approach?

Corticosteroids are commonly recommended as the first line of treatment in those people with Hashimoto’s encephalopathy (7) (8).  And while many people respond very well to corticosteroids, several adverse outcomes, relapses and temporary or permanent spontaneous remissions have also been reported (8).  This doesn’t mean that I’m opposed to people using corticosteroids, as while I’m not a big fan of them, I realize that in some cases they might be necessary to take.  There have also been a few case studies where intravenous immunoglobulins were beneficial (9) (10), as they help by modulating the immune system.

Can A Natural Treatment Approach Help?            

Although conventional medical treatments might be necessary at times to help manage the symptoms, and possibly to help put the person into a state of remission, what we of course need to keep in mind is that treatments such as corticosteroids and intravenous immunoglobulins are not addressing the cause of the problem.  As a result, even if the person is put into a state of remission through modulation of the immune system, relapses are common.  This was highlighted in a case report I came across that involved a 43-year old woman with Hashimoto’s encephalopathy who experienced three relapses around the time of her menstrual cycle (11).

After the third relapse she was given thyroid hormone medication for her hypothyroidism, and she was also given estrogen and progesterone to help regulate her menstrual cycle.  After this she didn’t experience any further relapses.  If she were my patient I might have tried to address her problem without giving estrogen and progesterone, but the point I want to get across is that the apparent trigger was addressed in this situation.  Unfortunately, addressing the cause of the problem isn’t always this straightforward, but either way, one does want to ideally detect and address the cause of the problem.  So if someone has a hormone imbalance, infection, food sensitivity, toxic exposure, or another factor that is triggering the autoimmune response then of course this needs to be addressed.

You might wonder if natural agents can be used instead of corticosteroids and intravenous immunoglobulins.  In some people nutritional supplements and herbs can be used to help suppress the autoimmune response, although the cause of the problem still needs to be addressed.  But taking things that can reduce proinflammatory cytokines and increase regulatory T cells can help, including fish oils, vitamin D, curcumin, and resveratrol.  I’ve discussed this in greater detail in other articles and blog posts, and keep in mind that high doses might be necessary to help suppress the autoimmune component.

In summary, Hashimoto’s encephalopathy is an autoimmune condition that not only involves elevated thyroid antibodies, but it also is characterized by having autoantibodies against alpha-enolase.  This in turn can lead to symptoms of brain dysfunction, including psychiatric manifestations, seizures, and focal neurologic deficits.  Corticosteroids and intravenous immunoglobulins are two types of conventional treatments, with corticosteroids usually the first option.  Natural treatments might also help to put the person into remission, but whether you use natural or conventional methods to control the symptoms, the ultimate goal should be to address and remove the autoimmune trigger.

When I was dealing with Graves’ Disease I chose not to take any medication.  I decided not to take the beta blocker that was prescribed by the primary care physician who told me I had hyperthyroidism, and then I refused to take the Methimazole that was recommended by the endocrinologist who diagnosed me with Graves’ Disease.  It was approximately two months between these two doctor visits, and I didn’t begin taking bugleweed (and eventually motherwort) until after my appointment with the endocrinologist.  While everything turned out okay, I was taking a big risk by not managing my hyperthyroid symptoms for so long, and I decided to put this blog post together because unmanaged hyperthyroidism has numerous risks, and I’m going to discuss three of the main ones here.

Getting back to my situation, if the bugleweed and motherwort didn’t do a good job of managing my symptoms then I’m pretty sure I would have taken the antithyroid medication while trying to restore my health.  While it might sound hypocritical telling people with hyperthyroidism the risks of not managing their symptoms when this is exactly what I did for a couple of months, keep in mind that at the time I wasn’t working with other people who had hyperthyroidism and Graves’ Disease.  If I knew then what I know now about hyperthyroidism and Graves’ Disease I wouldn’t have gone so long without managing my symptoms.

With that being said, let’s go ahead and take a look at three of the main risks of unmanaged hyperthyroidism:

Risk #1: Decrease in bone density.  Thyroid hormones are required for skeletal development and establishment of peak bone mass (1).  In adults, T3 regulates bone turnover and bone mineral density, and normal levels of thyroid hormone are essential to maintain optimal bone strength (1).  Overt hyperthyroidism can cause accelerated bone remodeling, reduced bone density, osteoporosis, and an increase in fracture rate (2) (3).  Although this decrease in bone density is reversible (3) (4), it can take years to reverse osteopenia and osteoporosis.

In order to avoid a decrease in bone density it is important to address elevated thyroid hormone levels.  This can be accomplished through antithyroid medication such as Methimazole or PTU, or in many cases by taking an antithyroid herb such as bugleweed.  Just keep in mind that not everyone is able to lower their thyroid hormone levels by taking bugleweed, and when this is the case then it might be necessary to take antithyroid medication.  In addition to lowering the thyroid hormone levels, eating a healthy diet and engaging in some weight-bearing exercises at least a few days per week can also help to increase the bone density.

Risk #2: Thyroid storm.  A thyroid storm is a rare complication of hyperthyroidism, and is frequently caused by a secondary event such as an infection or myocardial infarction (5).  In addition to the person presenting with elevated thyroid hormone levels, they usually will have an extremely high heart rate (i.e. greater than 140 beats per minute), and a fever greater than 102 degrees Fahrenheit (>39 degrees Celsius) is almost universal (5).  Other symptoms can include persistent sweating, shaking, diarrhea, nausea, vomiting, and disorientation. The overall mortality of a thyroid storm is between 10-20% (5) (6), and this assumes that there is no delay in treatment.  This is considered to be a medical emergency, and so if you are experiencing some of the symptoms I just described then you need to take this seriously, and it probably would be wise to visit the nearest urgent care or hospital emergency center.

3) Atrial fibrillation.  An atrial fibrillation is the most common type of heart arrhythmia, and this involves an abnormal heart rate and/or heart rhythm.  Atrial fibrillation is the most common cardiac complication of hyperthyroidism, and it can increase the risk of blood clot formation inside the heart (7).  The best way for someone with hyperthyroidism to prevent atrial fibrillation from occurring is to make sure their resting heart rate isn’t too high.  I discussed this condition in greater detail in an article I wrote entitled “Hyperthyroidism and Atrial Fibrillation“.

Should You Take Medication or Herbs To Manage The Hyperthyroid Symptoms?

Some people have a difficult time deciding whether they should take antithyroid medication to manage their symptoms, or if they should choose to do this naturally through herbs such as bugleweed and motherwort.  Although I personally chose not to take the medication, some people aren’t able to effectively manage their symptoms through herbs alone.  And if this is the case, then taking medication on a temporary basis is probably a good idea.  After all, while it’s great if you can manage your symptoms naturally, even if you do need to take antithyroid medication you can still follow a natural treatment protocol.  In fact, it’s quite common for patients with hyperthyroidism to already be on antithyroid medication prior to working with me.  If you’re still not sure what to do, I would check out the following blog post I wrote entitled ” Choosing Between Prescription Drugs and Natural Supplements In Managing The Hyperthyroid Symptoms“.

In summary, while many people with hyperthyroidism and Graves’ Disease can benefit from following a natural treatment protocol, it is important to manage the symptoms while taking this approach.  There are risks of unmanaged hyperthyroidism, and three of the main risks include a decrease in bone density, thyroid storm, and atrial fibrillation.  The incidence of these three conditions can be greatly reduced by decreasing the thyroid hormone levels through the use of antithyroid medication such as Methimazole, or herbs like bugleweed.  And if you have an elevated resting heart rate then of course you also want to take action to help lower this.  Frequently the antithyroid medication or herbs will help to accomplish this, although sometimes taking an agent that specifically focuses on the cardiac symptoms is necessary, and is why some people will take a beta blocker or an herb such as motherwort.

Many people have low levels of the hormones DHEA, testosterone, estrogen, and progesterone.  And while there are numerous factors which can cause low levels of these hormones, one of the biggest factors that can cause this is something known as the pregnenolone steal, also referred to as the cortisol steal.  Many doctors will recommend bioidentical hormones to correct hormone deficiencies, and while there is a time and place for hormone replacement, it of course is preferable to correct the cause of the problem whenever this is possible.  And so in this post I’m going to discuss what the pregnenolone steal is, how it can lead to deficiencies in other hormones, and what you can do to correct this problem.

I’ve spoken about the hormone pathway in some past articles and posts, but I’m going to give a little refresher here.  First of all, it’s important to understand that all of the steroid and sex hormones are derived from cholesterol.   In other words, if you have very low cholesterol levels then this alone can result in low hormone levels.  And the reason I need to emphasize this is because many medical doctors prescribe statins to a lot of their patients, and these statins can result in low cholesterol levels.  So while you don’t want cholesterol levels that are extremely high, you also don’t want to have very low cholesterol levels.

So the hormone pathway starts with cholesterol, and the hormone pregnenolone is synthesized from cholesterol.  This takes place in the mitochondria, and so if someone has mitochondrial dysfunction then this can affect the production of pregnenolone.  But assuming this isn’t the case, pregnenolone can convert into either progesterone or DHEA, and these in turn convert into other hormones.  Let’s take a look at each of these pathways:

Conversion of Pregnenolone Into DHEA.  Pregnenolone gets converted into 17-hydroxy pregnenolone by the enzyme 17α-hydroxylase.  17-hydroxy pregnenolone will in turn get converted into dehydroepiandrosterone (DHEA) by the enzyme 17,20 lyase.  DHEA is the precursor of androstenedione, which in turn is a precursor of testosterone.  Testosterone in turn can convert into estradiol via the enzyme aromatase, and dihydrotestosterone (DHT) via the enzyme 5α-reductase.

Conversion of Pregnenolone into Progesterone.   Pregnenolone converts into progesterone, which in turn gets converted into 17-hydroxy progesterone by the 17α-hydroxylase enzyme.  17-hydroxy progesterone will in turn be converted into 11-deoxycortisol, which in turn is converted into cortisol by the enzyme 11beta-hydroxylase.  17-hydroxy progesterone can also convert into androstenedione, with the help of the enzyme 17,20 lyase.  So progesterone ultimately leads to the formation of cortisol, although it can also lead to the formation of androstenedione.  Progesterone can also be converted into aldosterone, which takes place in multiple steps.

What Is The Pregnenolone Steal?

The pregnenolone steal is what happens when someone deals with prolonged chronic stress.  Out of all of the hormones I listed above, the production of cortisol is a priority.  And if someone is in a stressed out state, cortisol will be produced at the expense of DHEA.  So with the hormone pathway I discussed, you’ll recall that pregnenolone can be converted into both progesterone and DHEA, which in turn will convert into the other hormones I mentioned.  If someone is stressed out then this will inhibit the enzyme 17,20 lyase, which  helps to convert 17-OH pregnenolone into DHEA, and 17-OH progesterone into androstenedione.

So what is the consequence of this?  Well, if these enzymes are inhibited then this will result in a decrease of DHEA and androstenedione.  And remember that these hormones are precursors to testosterone, and this hormone converts into estradiol and DHT.  As a result, the pregnenolone steal can result in decreased levels of DHEA, androstenedione, testosterone, estradiol, and DHT.  Keep in mind that not all of these hormones will instantaneously become depleted, and so initially you might see some of these hormones depressed, while other hormones will look fine.

So the pathway that converts pregnenolone into progesterone will predominate.  However, cortisol is a priority over progesterone, and so progesterone will also decrease in order to produce more cortisol.  This is why this process is also referred to as the “cortisol steal” by some sources.

How Can The Pregnenolone Steal Be Diagnosed?

Sometimes it can be challenging to tell if someone is going through the pregnenolone steal, but in most cases you will see elevated cortisol levels, followed by low levels of one or more of the sex hormones.  If cortisol is high and all of the sex hormones are low or depressed, then you can be confident that the pregnenolone steal is a factor.  But wait, if someone is in postmenopause, isn’t it normal for the sex hormones to be depressed?  In other words, is it possible that if all of the sex hormones are low it’s simply due to the aging process?

Well, without question the hormones do decrease as we age.  However, this doesn’t mean that they should be depressed.  And if cortisol is elevated, then this is a pretty good sign that the pregnenolone steal is at least part of the problem.  Sure, there can always be other factors, such as one’s age, but if chronic stress is a factor then this needs to be addressed.

What are some of the symptoms someone will experience during the pregnenolone steal?  Since this involves high cortisol and low sex hormones, then the symptoms will usually correlate with this.  So for example, if someone is experiencing hot flashes or a low libido, then this probably is due to a deficiency of one or more of the sex hormones.  Other symptoms can include menstrual irregularities, anxiety or depression, vaginal dryness, insomnia, irritability, fatigue, and numerous other symptoms.  So when someone has one or more of these symptoms then it’s possible that the pregnenolone steal is the root cause of the problem.

How Can You Reverse The Pregnenolone Steal?

As for how you can halt and reverse this process, the two most important things you can do is to 1) reduce the stress in your life, and 2) improve your stress handling skills.  I realize that sometimes people can’t reduce their stress levels, but either way it is important to work on stress management.  Remember that chronic stress will inhibit the enzymes which lead to the production of DHEA, along with the androgens and estrogens.  And so if you don’t do anything to improve your stress handling skills,  then your body will continue to produce cortisol at the expense of your sex hormones.

So you need to block out time to manage the stress in your life.  I personally use a biofeedback program by the company Heart Math, as I block out 12 to 15 minutes each night before I go to bed.  Sure, I probably should be doing more than this, but it’s definitely better than nothing.  And in my opinion it’s better to spend 10 to 15 minutes EVERY DAY on stress management than 30 minutes three times per week.  Of course you don’t need to use Heart Math, as many people improve their stress handling skills through techniques such as yoga and meditation.  And there are other mind body medicine techniques as well.  I talk more about this in my article entitled “Mind Body Medicine and Thyroid Health“.

In summary, the pregnenolone steal occurs when someone is in a stressed out state.  When this is the case the body will do everything it can to produce cortisol, which in turn will inhibit the enzymes that lead to the formation of the androgens and estrogens.  So if someone has elevated cortisol levels and low sex hormones, then this is an indication that the pregnenolone steal is occurring.  And in order to halt this process you need to reduce your stress levels and improve your stress handling skills.  Some ways to accomplish this is through yoga, meditation, and biofeedback.

Just about everyone with thyroid and autoimmune thyroid conditions have some type of inflammatory process.  This is especially true with those patients with Graves’ Disease and Hashimoto’s Thyroiditis.  And while the inflammatory markers on a blood test or stool panel won’t always be positive in the presence of inflammation, I still thought it would be beneficial to discuss some of the more important markers which relate to inflammation.

Before talking about the different inflammatory markers, I’d like to briefly discuss the inflammatory process, as this will help you to better understand the purpose behind testing for these markers.  First of all, why does someone experience inflammation?  The inflammatory process occurs when someone is exposed to a trauma, infection, food allergen, toxin, or something else that puts stress on the body.  Without going into too much detail, let’s look at an example of what happens when someone is exposed to a bacterial infection. In this situation there will be an activation of white blood cells, along with the release of something called arachidonic acid.  The arachidonic acid will lead to inflammatory substances known as leukotrienes and prostaglandins, and this in turn will stimulate neutrophils, which are a type of white blood cell in your body.  In fact, when you get a complete blood count with differential one of the things it will test for is neutrophils, and if the neutrophils are elevated, then this usually indicates an acute inflammatory process.

In any case, inflammation not only results in an increase in neutrophils, but it can also cause an increase in free radicals, which causes oxidative stress and tissue damage.  And your body will also release proinflammatory cytokines, which I’ve discussed in other articles as being a factor in autoimmunity.  This process also involves something called nuclear factor kappa B (NFkB), which results in more inflammation, and one of the problems with autoimmune conditions is that NFkB gets chronically upregulated.  I spoke about NFkB in greater detail in a past blog post entitled “The Role of Cytokines In Autoimmune Thyroid Conditions”.

Hopefully you have a better understanding of the inflammatory process.  Now I’d like to go ahead and talk about the different inflammatory markers:

C-reactive protein.  C-reactive protein (CRP) is one of the main inflammatory markers commonly tested for by healthcare professionals.  It increases as interleukin 6 (IL6) is secreted by immune system cells, with an example being macrophages.  IL6 is a proinflammatory cytokine, which I’ll discuss a little later.  CRP is not a specific test.  In other words, if it is positive it means you have inflammation, but it won’t tell you where the inflammation is located.  Ideally you want the levels to be less than 1.0 mg/L, but any value greater than 3.0 mg/L doesn’t only mean that the person has a good amount of inflammation, but it also might mean that you have an increased risk of developing cardiovascular disease (1).  When getting this test it’s best to order “high sensitivity” C-Reactive protein, also known as hs-CRP.

Reference range: Most labs use a reference range of 1.0 to 3.0 mg/L, and while greater than 3.0 mg/L seems to be a cardiovascular risk, ideally you want to see this less than 1.0 mg/L.

Erythrocyte sedimentation rate (ESR).  This is another inflammatory marker commonly recommended by healthcare professionals, and this marker represents the rate at which red blood cells sediment in a one hour period.  Like CRP, an elevated ESR confirms the presence of inflammation, but it doesn’t pinpoint specifically where the inflammation is in the body.  CRP is usually preferred because these levels increase in the blood quicker after the inflammatory process begins.

Reference range: The range will vary depending on the age and gender, as most labs use a reference range less than 15 mm/hr for men under 50 years old, less than 20 mm/hr for women under 50 years old, less than 20 mm/hr for men over 50 years old, and less than 30 mm/hr for women over 50 years old (2).

Fibrinogen.  This is a protein produced by the liver, and it helps to stop bleeding through the formation of blood clots.  This marker isn’t commonly used to measure inflammation, although it frequently elevates in the presence of inflammation.

Reference range: Most labs use a reference range of 200 to 400 mg/dL

Calprotectin.  Calprotectin is a marker tested in the stool that is used to detect intestinal inflammation.  It is a calcium-binding protein that is found in large amounts in neutrophils, and during inflammation, calprotectin is released from the activated neutrophils (3).  Although you can’t use calprotectin by itself to diagnose a certain condition, it can help to differentiate between inflammatory bowel disease (i.e. Crohn’s disease and ulcerative colitis) and non-inflammatory conditions (4) (5).  It can also be used to monitor the progress of someone with inflammatory bowel disease (IBD).  Just keep in mind that calprotectin can increase with certain gut infections (which can of course cause intestinal inflammation but doesn’t necessarily mean that someone has IBD), as well as with colorectal cancer (6).  However, calprotectin is usually normal or very low in those with irritable bowel syndrome (7).  So if someone has high calprotectin then they have some type of intestinal inflammation, perhaps IBD, and most likely not IBS.  On the other hand, if someone has normal calprotectin then they probably don’t have intestinal inflammation.

It’s important to know that the intake of non-steroidal anti-inflammatory drugs (NSAIDS) increases calprotectin levels (8) (9).  Also, since intestinal inflammation is more common in those with an increased body mass index (BMI), it shouldn’t be surprising that elevated calprotectin is associated with obesity (10) (11) (12).  Although the focus here is on fecal calprotectin levels, there is evidence that serum calprotectin is increased in those with papillary thyroid carcinoma, and significantly decreases after total thyroidectomy (13).

Reference Range: The labs I’m familiar with use a reference range of less than 50 mcg/g

Lactoferrin.  Fecal lactoferrin can also be a useful marker for determining if someone has intestinal inflammation.  It is an iron-binding protein, which comes mainly from neutrophils (14).  Lactoferrin is usually significantly increased in IBD, but it can also increase with infective diarrhea, colon cancer, and after taking NSAIDS (14).  Like calprotectin, lactoferrin may also be useful in monitoring the treatment one is receiving for IBD.  And since lactoferrin is usually negative in IBS, this marker can also help to differentiate IBD from IBS (15).

Reference range: Doctor’s Data uses a reference range of less than 7.3 mcg/mL

Secretory IgA.  Secretory IgA (SIgA) is found on the mucosal surfaces of the body, and it plays an important role in providing protection by separating the outside environment from the inside of the body (16).  This is a process called immune exclusion, as it limits the entry of pathogens and antigens (16).  As a result, it is common for there to be elevated levels of secretory IgA in the presence of an infection, and sometimes a food allergen.  There is also evidence of elevated secretory IgA levels in inflammatory bowel disease (17), although it seems as if calprotectin and lactoferrin are better markers.  On the other hand, chronic stress can result in a decrease in SIgA, which in turn can increase one’s susceptibility of having an infection or an increase in intestinal permeability (18).

Reference range: The reference range seems to depend on the lab, as Doctor’s Data uses a reference range of 51-204 mg/dL, while Genova Diagnostics uses a range less than 885, with the units not specified.

Lysozyme.  Lysozyme is an enzyme that is secreted at the site of inflammation in the gastrointestinal tract.  Lysozyme levels also seem to be elevated in people with IBD (19).  One study showed that neutrophils cause elevated fecal lysozyme levels in ulcerative colitis and macrophages cause elevated serum lysozyme levels in Crohn’s disease (20).

Reference range: The labs I’m familiar with use a reference range of less than 600 ng/mL

Eosinophilic Protein X.  There is evidence that eosinophils are involved in the pathophysiology of numerous inflammatory conditions of the gut.  Eosinophils contain different proteins which are cytotoxic, and are released from the eosinophils after being activated.  One of these proteins includes eosinophil protein X (EPX).  Some suggest that EPX might be a better marker of low grade inflammation, whereas other markers such as calprotectin and lactoferrin usually don’t test positive until someone has a significant amount of intestinal inflammation.  A few studies show that EPX is positive in inflammatory bowel disease (21) (22) (23).

Reference range: Genova Diagnostics is the only lab I know of which tests for this, and they use a reference range of less than 4.6 mcg/g

Autoantibodies.  Although autoantibodies aren’t considered to be inflammatory markers, the presence of elevated autoantibodies usually correlate with an inflammatory process.  In other words, when someone has elevated autoantibodies, inflammation will also be present.  There are many different autoantibodies one can test for, but with regards to thyroid autoimmunity, the most common ones include thyroid peroxidase antibodies, thyroglobulin antibodies, and thyroid stimulating immunoglobulins.   The first two autoantibodies I mentioned are associated with Hashimoto’s Thyroiditis, while thyroid stimulating immunoglobulins are commonly found in patients with Graves’ Disease.

Reference range: These are common reference ranges for the following thyroid antibodies:

Thyroglobulin antibodies: 0-0.9 IU/mL

Thyroid peroxidase (TPO) antibodies: 0-34 IU/mL

Thyroid stimulating immunoglobulins (TSI): <140%

Proinflammatory Cytokines.  Autoimmunity involves the presence of proinflammatory cytokines, and although I don’t test the cytokines in my patients, some doctors do.  Some examples of proinflammatory cytokines that can be tested include Interleukin-1 beta (IL-1β, Interleukin-6 (IL-6), Interleukin-8 (IL-8), and tumor necrosis factor alpha (TNF-α).

Which Inflammatory Markers Should You Test For?

I have most of my patients test for hs-CRP through the blood.  I don’t always test for ESR, although some healthcare professionals will test hs-CRP and ESR on all of their patients.  I do test for the thyroid antibodies in my patients.  As I mentioned earlier, I don’t do testing for cytokines.  As for calprotectin, lactoferrin, lysozyme, and some of the other stool markers, there are times when I will do stool testing on my patients, although it’s not something I do with every patient.  If someone is having a lot of gut issues and/or symptoms of inflammatory bowel disease then obtaining a stool panel might be a good idea.  However, there are functional medicine doctors who will recommend a comprehensive stool panel with every single one of their patients, and especially those with autoimmune thyroid conditions.

In summary, inflammation is a factor with just about every autoimmune condition, including Graves’ Disease and Hashimoto’s Thyroiditis.  Some of the different inflammatory markers include C-reactive protein (CRP), erythrocyte sedimentation rate (ESR), calprotectin, lactoferrin, lysozyme, secretory IgA, Eosinophilic Protein X, and proinflammatory cytokines.  Although autoantibodies aren’t considered to be an inflammatory marker, if an autoimmune thyroid condition is suspected then it makes sense to test the thyroid antibodies.  In addition to testing the thyroid antibodies, I commonly test for hs-CRP, and while I don’t do testing for cytokines, there are times when I will recommend testing for one or more of the other inflammatory markers.