Americans are infatuated with pills, thanks to decades of conditioning from the pharmaceutical industry. It doesn’t matter whether they come from the pharmacy or the health food store, we have a cultural fixation with finding that magic bullet. It’s no wonder—making genuine, lasting changes to your health takes hard work and discipline, the two last things you’ll see advertised on commercials during your favorite television show.

If you want to continue feeling sick, then continue eating the Standard American Diet (SAD). If you want to feel better and you have autoimmune Hashimoto’s, you’ll need to say a permanent goodbye to gluten. Someone emailed recently saying she had Hashimoto’s and wasn’t feeling better even though she was 90 percent gluten-free. When you have Hashimoto’s that’s like being 90 percent pregnant, you need to commit to a 100 percent gluten-free diet, which, thanks to an exploding gluten-free market, is getting easier every day.

You’ll need to repair a leaky gut by removing the foods to which you are intolerant. The worse your leaky gut the longer this list of foods could be. Also, I and many other practitioners are increasingly finding many patients require a diet free of grains, starchy vegetables, and sweets, and need to follow something akin to the GAPS or Specific Carbohydrate Diet (SCD). Newer research shows that healing of the small intestine, the seat of digestion and absorption as well as food intolerances, requires a lengthy abstinence from these foods.

To support all these efforts you also have to balance your blood sugar imbalances with a diet that is significantly lower in carbohydrates than most Americans are accustomed to, and ditch the unfounded fear of healthy fats.

Going gluten-free is vital first step

Removing gluten is a vital first step if you have Hashimoto’s. Even if you don’t have Hashimoto’s, chances are removing this ubiquitous toxin from your diet will help you greatly. Numerous studies from several countries show a strong link between gluten intolerance and Hashimoto’s. When immune antibodies tag gluten for removal from the bloodstream, where it landed thanks to a leaky gut, this stimulates production of antibodies against the thyroid gland as well. In other words, every time you eat gluten, your immune system launches an attack not only against gluten but also against the thyroid gland. This immune response to gluten can last up to six months each time it’s ingested. It’s just not worth it. Also, as I continue my research and practice in neurology, I never cease to be amazed at how profoundly one’s brain health, a concern for all those struggling with hypothyroidism, can be impacted by removing gluten from the diet.

When gluten-free isn’t enough

Some people with Hashimoto’s give up gluten and feel only marginally better. Many practitioners have found in these cases a diet free of grains, starchy vegetables, legumes, and most sweeteners may be necessary. This type of diet, called a monosaccharide (single sugar) diet, is more commonly known today as the Gut and Psychology Syndrome (GAPS) diet, or the Specific Carbohydrate Diet (SCD). It is based on consuming a diet free of foods that contain disaccharides or polysaccharides, more complex sugars and carbohydrates, such as those in all grains, most beans, and most sweeteners. These complex sugars feed harmful bacteria in the small intestine that prevent its repair or proper function.

Elimination/Provocation diet

People become so accustomed to eating certain foods that they don’t realize those foods are harming them. Instead they think a foggy brain, skin rashes or rosacea, chronic respiratory issues, joint pain, water retention, a distended belly, chronic digestive issues, and more are a normal part of life. Foods that most commonly trigger these reactions are gluten, dairy, eggs, corn, soy, and yeast. Sometimes nuts are a problem. Technically a person can develop an intolerance to any food, especially one that is eaten repeatedly when a leaky gut is an issue.

In the book I outline how to undergo the Elimination/Provocation diet. Basically you eliminate the foods I just mentioned for two to three weeks, then reintroduce each food, one at a time, every 72 hours. Monitor yourself closely for reactions, which can be physical, psychological, or emotional. If you react, then you know that is a food you need to remove from your daily diet. After undergoing the monosaccharide diet or a protocol for leaky gut, you later may be able to add back in one of the formerly offending foods (except for gluten of course). I go over a protocol for repairing leaky gut in the book.

Balancing blood sugar

Gut health is dependent on balanced blood sugar—blood sugar imbalances create stress, which in turn inflames the digestive tract.  The nice thing about the monosaccharide diet (GAPS, SCD) is that its low-carb nature automatically makes it conducive to both balancing blood sugar and repairing the digestive tract. Outside of that diet, plenty of books and websites are devoted to low-carb diets and how they can balance blood sugar. The average American diet and even the USDA food pyramid are simply too high in carbohydrates, which is not conducive to good hormonal health. I do not advise people to eat a specific amount of carbohydrates as everyone’s needs are different. Instead I ask you to monitor whether you feel sleepy or crave sugar after a meal. If so, you just ate too many carbs for your system. Other tell tale signs can include insomnia or waking up at 3 or 4 a.m., an energy crash in the late afternoon, feeling spacey, irritable or light-headed if you go too long without eating, constant hunger, constant craving for sweets, and difficulty losing weight. If you have any of these symptoms you may have hypoglycemia, insulin resistance, or a combination of the two.

Putting diet to work

One practitioner, Yolanda Loafer, DC, emailed our website to report back on her success with a patient in Romania with whom she had been working long distance. (We get emails from around the world, but only have trained practitioners in the United States.) Because this woman is not able to get any U.S. supplements through Romanian customs, Dr. Loafer worked with her on diet alone and the patient quickly noticed significant improvements. For my upcoming book on brain chemistry I have also received a number of stories on how changing the diet radically improves brain health.

I realize making drastic dietary changes takes a re-education, negotiating meal times with your family, and a sorrowful goodbye to some old favorites. Many people balk at the idea of giving up gluten because they cannot imagine life without toast or delivered pizza. However once they take the plunge, they also realize it’s not nearly as hard as they thought it would be. More limited diets, such as the monosaccharide diet, can mean even more severe changes to your lifestyle and your pantry. So what keeps people going? The huge benefits they reap. I know people whose suicidal tendencies disappeared on a gluten-free diet, or whose chronically distended, upset bellies flattened and quieted on a monosaccharide diet. If compliance is an issue, you may benefit from an online or in-person support group (such as at http://drkforum.com), hypnotherapy, counseling, or some other method to motivate you to stick to your diet and better your health. You’re worth it.

It can be difficult to stick to a thyroid-healthy diet when practically every television commercial, every billboard, and every person around you is tempting you with starchy, processed junk foods. But when people complain they want to eat like a normal person, I say fine, then you will be sick like a normal person.

When it comes to thyroid antibodies, those definitive markers for Hashismoto’s, confusion sometimes arises. For instance, do your high antibody counts mean your Hashimoto’s is worse than your friend’s, whose counts are low? Or how come you first presented with negative antibodies, and now that you’re on your practitioner’s protocol and feeling significantly better your antibody counts are suddenly positive? And why is iodine producing negative antibody results? Does that mean it’s “curing” Hashimoto’s?

As you’ll learn, if your practitioner sees negative antibodies and proclaims you are “cured” of Hashimoto’s, he or she clearly does not understand some basic immune principles.

In this article I review thyroid antibody panels, what they really mean, how to accurately test the status of your autoimmune condition, and whether your protocol is working for you.

First of all, we all make antibodies against cell tissue. The presence of some antibodies is healthy and normal. As old tissue cells die to be replaced by new ones, the immune system tags these dead cells with antibodies, just as it would tag an invading virus or infection to destroy and remove. In the autoimmune process however, this highly organized and complex system runs awry, and antibodies tag healthy tissue. This is the case in Hashimoto’s, an autoimmune disease in which the body’s immune system tags healthy thyroid tissue for destruction and removal.

We identify Hashimoto’s by measuring thyroid peroxidase antibodies (TPO Ab) and thyroglobulin antibodies (TgAb). TPO is the most commonly elevated antibody in Hashimoto’s, however TgAb should always be checked too, even though it is not as common. To assess whether these antibodies are positive we use the lab ranges, which vary from lab to lab.

Why you can have negative antibody results and still have Hashimoto’s

Say all your symptoms point to Hashimoto’s but your antibody tests are negative. Does this mean you don’t have Hashimoto’s? Not necessarily. As you’ll learn, if your practitioner sees negative antibodies and proclaims you are “cured” of Hashimoto’s, he or she clearly does not understand some basic immune principles.

The waxing and waning immune system

When I have a patient who is struggling with symptoms of both hyperthyroidism and hypothyroidism, a strong indication of Hashimoto’s, and the antibody test comes back negative, I run a second panel. Because the autoimmune response waxes and wanes, the patient may test negative one week and positive the next.  Sometimes I may even ask the patient to enjoy extra sugar and gluten in their diet before the second test, as sugar will drive up inflammation and gluten will provoke the autoimmune response, both of which better the chances of producing a positive result on an antibody lab panel.

Many times these people will not test positive for Hashimoto’s or start to feel better until their compromised immune system improves in health.

Overall immune weakness

Some people with Hashimoto’s test negative because their overall immune health is weak and they do not produce enough antibodies. Their immune systems have been so stressed for so long that their total white blood cells and B-cells are too low to be able to make antibodies. You have to have some degree of immune fitness to produce antibodies. Many times these people will not test positive for Hashimoto’s or start to feel better until their compromised immune system improves in health.

These are the people who, after several weeks on a gluten-free diet or on a protocol from their practitioner start feeling great, yet are dismayed when a follow-up antibody panel shows antibodies are significantly higher, or are positive when they were initially negative. In some cases this is a sign that immune health has been restored to the point where antibody production kicks back into action.

TH-1 is higher than TH-2

A TH-1 dominance may be another reason for negative antibodies. As I explain in the book, we can roughly divide the immune system into two sides. TH-1 is the side that reacts immediately to an invader whereas TH-2 is the delayed response that produces antibodies. In a healthy immune system TH-1 and TH-2 are balanced, however in Hashimoto’s one of these becomes overly dominant. When TH-1 soars too high this suppresses TH-2 and hence antibody production. As a result antibody counts on a lab panel may show as low or negative. When you bring these two systems into balance, however, antibody counts on a panel may temporarily increase before balancing out.

This also explains why the use of iodine can produce a negative antibody panel in Hashimoto’s. Iodine has been shown to stimulate the autoimmune attack against the thyroid, which increases inflammation, a TH-1 response. In a TH-1 dominant person—statistically most people with Hashimoto’s—this further stimulates TH-1 while suppressing TH-2, again producing negative antibody results and giving many the impression the Hashimoto’s has been “cured.” Also, high doses of iodine can stimulate the production of TPO, the enzyme that is the target of autoimmune attack, to the point that it becomes inactive and the autoimmune attack ceases. However TPO is necessary for thyroid function and this is not a desirable approach when we have other methods that work better.

If either of these factors is a possibility, I tell people to check for inflammatory cytokine levels (the compounds that make up the TH-1 system), such as IL-2, IL-12, TNFa, and interferon. They should also check the CD4/CD8 ratio, which is the ratio between T-suppressor and T-helper immune cells. If inflammatory cytokines are high and the CD4/CD8 ratio is out of balance, this indicates an inflammatory condition that is suppressing TH-2 and perhaps artificially producing a negative result for Hashimoto’s. This is especially important to check in those using iodine to address Hashimoto’s.

(If all this immune terminology is confusing, please refer to the book, where it is explained in detail.)

Beyond thyroid antibodies to gluten

These reasons explain why Jane can have really low or even negative antibody counts and feel worse than her friend Mary, who also has Hashimoto’s but whose antibody counts are higher. Jane’s overall immune function is weaker or more out of balance. This is also why I caution people about the results from labs that test for intolerances to gluten, dairy, and other foods. A negative result does not necessarily mean you’re free to resume eating breads, pastas, and other gluten foods. In fact I heard of a woman with all the classic symptoms of Hashimoto’s, celiac disease, and rheumatoid arthritis (an autoimmune joint condition) who barely tested positive for a gluten intolerance. Unfortunately her doctor, who does not understand these immune basics, interpreted this as meaning she is only a little bit intolerant to gluten and can still eat it, just in smaller amounts, and she continues to suffer.

As I explain in the book, the Elimination/Provocation Diet is the best test for food intolerances.

Some people always test negative

Interestingly, studies also show some people always test negative for Hashimoto’s on antibody panels, while follow-up biopsies confirm that Hashimoto’s is present. That’s why it’s imperative to test other immune markers, remove gluten from the diet, and avoid iodine if Hashimoto’s is suspected.

Reacting to both TH-1 and TH-2 stimulators

In the book I explain how a challenge using designated herbal and nutritional compounds can determine a TH-1 or TH-2 dominance. One practitioner emailed with a question about a patient who reacted negatively to both TH-1 and TH-2 compounds. I have seen this before in those whose gut barrier is extremely compromised and who react to many things. In this case the focus would first be to first restore health to the gut and then try the challenge again some time later.

Trepanation, drilling a hole in the head, used to be a medical technique. In the future, people will view the way we treat heart disease today as just as absurd.

Heart disease is a gut-immune-hormone disease

An ancient surgical procedure, called trepanation, consisted of drilling a hole in the head and removing a piece of the

skull. It is thought this practice was used to release evil spirits that caused mental illness, migraine headaches and other ills. Nowadays, however, if you went to your naturopath with complaints of headaches and she pulled out her drill, you would bolt from her office in horror.

Sadly, when it comes to heart disease, it seems we haven’t advanced all that much. When future humans look back to 2010 and the way we treat heart disease, they will shake their heads in disbelief. Much of heart care today, in both conventional and alternative medicine, ranges from harmful to hopelessly misguided.

Although cancer recently took the top spot, heart disease has long been the leading cause of death since the advent of processed foods almost 100 years ago, and it’s no wonder. The root of disease almost always begins in the gastrointestinal (GI) tract, with problems compounding in the immune and endocrine (hormone) systems, which in turn stress the heart. That gut health and immunity status affects the heart is lost on most conventional doctors, including many holistic ones.

These days we see two extreme viewpoints of cholesterol, both of which are incomplete. In conventional medicine, cholesterol is the defining marker for heart disease. While your local MD’s approach to treating high cholesterol has been seriously questioned and successfully challenged by reputable science, the standard of treatment — low-fat diets and Lipitor, for example — hasn’t budged. And when this model fails to prevent heart disease, as it often does, doctors simply blame the patient for not toiling long enough in the prison of low-fat diets.

In holistic medicine, on the other hand, cardiovascular health is often dismissed when symptoms are lacking, and high cholesterol is brushed away. Although the nutritional model is safer (for statin drugs can have devastating side effects), it too falls short when it doesn’t address the risk of high cholesterol levels.

Consider inflammation

As always, the answer lies in the middle of these two extremes. Conventional doctors miss the mark when they look at cholesterol levels in isolation, as do holistic doctors when they hardly consider it at all. The truth is, high cholesterol is a risk when inflammation is present.

When looking at what causes heart disease and how to treat it, atherosclerosis, the formation of plaque within the arteries, is the bottom line. But it’s shortsighted to simply blame atherosclerosis on high cholesterol. Rather, atherosclerosis comes from an immune response. The immune response creates inflammation, with this inflammation gradually worsening into lesions in the arterial walls. Since the body’s priority is to stay alive now, even if means self-sabotage in the long run, it speedily delivers cholesterol to the lesions to patch them up, hence causing atherosclerosis.

The key for the practitioner then is not simply to lower cholesterol, leaving the arterial walls more vulnerable to failure, but rather to ferret out what’s driving the inflammation. This is where the skill and ongoing education of the practitioner come in. For instance, newer research shows that some people develop atherosclerosis due to an autoimmune disease in which the body attacks it’s own arterial wall tissue. Is a prescription for either Lipitor or CoQ10 going to do much for these folks? Obviously not.

The sleuthing for inflammation starts by understanding that atherosclerosis starts where the gastrointestinal, hormonal, and immune systems meet (and yes, they do meet!). But for the sake of simplicity, lets look at each individually.

The gut connection to heart disease

Although many practitioners understand that poor digestion creates inflammation, a couple of problems specific to the GI tract can trigger atherosclerosis. For instance, bile secreted by the gallbladder escorts cholesterol out of the body. However, with dysbiosis — when there is more bad bacteria than good bacteria in the gut — this process falters or fails. The result is a rise in cholesterol (not to mention estrogen and various toxins). In this case, a simple gut detox and inoculation with beneficial bacteria lowers cholesterol.

Also critical is the link between helicobacter pylori infection and atherosclerosis. H.pylori, a bacterium unique in its ability to survive the highly acidic environment of the stomach, is best known for causing peptic ulcers, gastritis, and duodenitis. What’s less known, however, is that h.pylori also destroys vascular tissue; autopsies are turning up h.pylori in the lesions of stroke and heart attack victims.

Our gut is exposed to many pathogens, including h.pylori, daily. A healthy stomach sufficient in hydrochloric acid (HCl) destroys pathogens as soon as they enter. It’s estimated that 90 percent of Americans are deficient in HCl, and that h.pylori can be found in 50 percent of the world’s population, so it’s easy to see why this may be the most common infectious disease worldwide. Not to mention that most, if not all, chronic users of antacids harbor excess h.pylori.

So why hasn’t medicine launched a full-scale attack? Because an h.pylori infection is asymptomatic, quietly wreaking havoc before more telltale signs such as gastric ulcers enter the picture. And since most practitioners, both conventional and natural, practice based on symptoms, it can easily go unnoticed until it’s too late.

I do not like using the serum antibody test for h.pylori. A retest will not show whether we have successfully treated the infection, for the antibody levels stay elevated for up to a year after treatment. The breath test is more useful diagnostically. Because this bacteria is so contagious (by saliva), I have found treating an individual for h.pylori does not have lasting success unless the entire family is treated. I once had a patient whose h.pylori infection kept rebounding, despite treating his family. It was when he sheepishly brought in his mistress for treatment that we were finally able to kick the infection for good.

The immune system and the heart

We typically don’t think of a weak immune system as having much to do with heart health, but as with h.pylori, undetected viruses and other antigens can prey on the cardiovascular system. Although I am wary of making diagnoses based on symptoms, my patients who complain of chronic pain and fatigue are often suspects for chronic viruses. Most often they are the ones I screen for antibodies to antigens associated specifically with atherosclerosis: Cytomegalovirus, coxsackievirus, chlamydia pneumonia and porphyromonas gingivitis (for this last one, proper oral hygiene is key). I then track the treatment with follow-up tests that look at antibodies and the viral load, even if patients report they are feeling wonderful. Sometimes nutritional support helps relieve symptoms tremendously, but the virus persists and we either need to dig deeper or find a more effective treatment. Asking, “How do you feel?” to treat your patients is a standard for failure.

Natural medicine offers the most effective treatment against viruses, compared to the prescription drug Interferon, which has caused more suicides than all other drugs combined throughout history. The goal, along with correcting the patient’s diet and digestion, is to boost the natural killer cells to combat the virus. This can be done quite nicely with a synergistic combination of botanicals.

When considering heart disease and immunity, one also needs to consider liver function, especially when running tests for C-Reactive Protein (CRP) and homocysteine. CRP is made in the liver as a response to inflammation. If your patient’s CRP comes back normal while other markers for atherosclerosis are present, it could be due to fatty liver, the use of multiple drugs, or other issues that impair liver function. When the liver is impaired, it simply won’t crank out the CRP like it should, and lab levels for CRP will come back normal. Likewise, statin drugs lower CRP and produce a kosher lab panel, but this is rather like removing the engine light instead of fixing the engine.

Another heart culprit is the amino acid homocysteine, which destroys arterial walls and promotes atherosclerosis. Most people understand high homocysteine levels to be related to B vitamin deficiencies, but hypochlorhydria (too little stomach acid), and the use of estrogen creams and birth control pills can also raise homocysteine. A lesser-known culprit is poor liver function, when the liver’s methylation pathway is not functioning. Therefore this pathway should always be supported in conjunction with the usual homocysteine-lowering therapies. Methly-B12 and Metacrin DX both support clearing the liver’s methylation pathway.

Hormones and the heart

When we think of hormones, we typically think of the sex hormones and how clumsily they function for many people. What most provokes atherosclerosis, however, is a less glamorous but exceptionally touchy hormone that we tend to abuse: Insulin. After years of a high-carb, sugar-laden diet that calls on the pancreas repeatedly to flood the system with insulin, the body’s cells become insulin resistant. This leaves excess amounts of insulin circulating through the bloodstream, leading to high blood pressure, thicker blood (which can gum up the cardiovascular system), and an increase of the enzyme activity that elevates cholesterol. In men, testosterone protects the cardiovascular system, just as estrogen does for women. In cases of insulin resistance, however, we see men becoming estrogen dominant (developing “breasts”) and women becoming testosterone dominant (growing “beards”), and we know cardiovascular destruction is well under way. These are the folks who fatigue after meals, whose fasting blood sugar is over 100 and who typically show high LDL and triglyceride levels. For these folks, regulating dysglycemia is imperative to heart health.

Thyroid health also plays an important role in cholesterol levels and heart health. When a person’s thyroid is under functioning, he or she makes fat more quickly than it is burned, which drives up triglycerides, cholesterol and LDL cholesterol. Hypothyroidism also makes the liver and gallbladder sluggish, which contributes to high cholesterol.

The autoimmune or neurological connection to the heart

There are times when I have exhausted all the possibilities, and still arterial inflammation and high cholesterol persist. It is then that I suspect autoimmune disease, when the body is attacking it’s own arterial walls, hormones or environmental compounds such as heavy metals, that in turn lead to high cholesterol and atherosclerosis. At that point we run an immune panel for direction in taming the autoimmune response. This information is vital in knowing specifically how to treat each autoimmune case, as the wrong approach can exacerbate the condition. Additionally, an understanding of functional neurology is important. When brain degeneration is accelerated due to autoimmune disease, insulin surges, nutrient deficiencies and other factors, autonomic function can begin to fail. Knowing how to assess and address neurological function can aid in heart health.

For ideas on how to modulate an autoimmune condition, see my book Why Do I Still Have Thyroid Symptoms? Although it addresses the thyroid, the autoimmune mechanics are the same for any tissue being affected.

To lower or not to lower cholesterol?

As long as we are addressing the source of inflammation, I still feel it is prudent to lower overly high cholesterol in order to put the brakes on artery-clogging atherosclerosis. I do this with compounds that contains red yeast rice extract, which studies show to be more effective than statin drugs, while absent of the dangerous side effects. (This compound proved so beneficial that the FDA banned it, citing it was “too effective to be a natural agent.” When the ban was lifted and it came back on the market, the pharmaceutical industry successfully bankrupted about half the manufacturers through expensive litigation.) If cholesterol levels refuse to lower with these compounds, I then look for gallbladder congestion. As mentioned earlier, bile escorts cholesterol from the body, so a sluggish and congested gallbladder will hamper this mechanism.

Doing the work

Like other practitioners, I also prescribe sufficient essential fatty acids, antioxidants and vitamin D on top of specific therapies. Healing cardiovascular damage naturally requires patience, dedication and thoroughness, not only from the practitioner, but especially from the patient. As all practitioners know, noncompliance can sabotage the best of care. When my patients present with inflammation markers and poor cardiovascular health, I always ask them, “How deep do you want to go? Here are 10 steps I’d like to take with you,” and I outline what I have presented in this article. In the end it’s up to them whether they want to do the work, but it’s only when I give them all their options that I can sleep at night. I need to know I have done more than the modern equivalent of drilling a hole in their head.

Most hypothyroidism patients are treated with thyroid hormones while the underlying cause, immune dsyregulation or a breakdown in the thyroid hormone pathway, is ignored. As a result they may suffer from the consequences of poor thyroid function, one of the most serious being compromised bone health.

When looking at bone health, it’s important to consider not just bone density but also bone quality. One may have good bone density but poor bone quality — in other words the bone’s architecture is weakly engineered.

Because of the interactions between thyroid function and calcium regulation, people with hypothyroidism tend to have higher than normal bone density, while those with hyperthyroidism lose bone density.

However studies have shown higher bone density does not correlate with more bone strength. In fact, they show that hypothyroidism is accompanied by an increased risk for fractures. That’s because what’s more important is how well the bone is constructed. The following features are included when assessing bone quality:

• Microarchitecture
• Accumulated microscopic damage
• Collagen quality
• Mineral crystal size
• Bone turnover

All of these qualities combined that allow bone to successfully resist fractures. Unfortunately no definite tests exist at this time to monitor bone quality, however managing a hypothyroid condition should be paramount when addressing bone health.

Studies have also shown that people with hyperthyroidism lose bone density and are at a higher risk for bone fractures, even if proper thyroid function has been restored. Similarly, people whose thyroid condition is improperly managed with the excessive or unnecessary use of thyroid hormones are also at risk for loss of bone density.

References

Kosinska A, Syrenics A, Syrenicz, et al. The influence of treatment of substituvie or suppressive doses of thyroxine on biochemical bone turnover markers. Ann Acad Med Stetin. 2005;51:94-97.

Lakatos P. Thyroid hormones: beneficial or deleterious for bone? Calcif Tisue Int. 2003 Sep;73(3):205-9.

Licata A. Bone density vs bone quality: what’s a clinician to do? Cleve Clin J Med. 2009 Jun76(6):331-6.

Do you even need thyroid hormone replacement? Hashimoto’s accounts for 90 percent of hypothyroidism cases in the United States. When the autoimmune disease is successfully managed, thyroid hormones may not be necessary…However not taking them when you truly need them can have disastrous consequences for your health and well-being.

Choosing the right thyroid hormone

When choosing the appropriate thyroid hormone, three factors must be considered:

Sensitivity to fillers

Some people, especially those with autoimmune diseases such as Hashimoto’s, are sensitive to the dyes and fillers in thyroid hormone medications. Cornstarch, found in many brands, is a common trigger. Synthroid®, Westhroid, and Thyrolar contain cornstarch. A good example of how fillers can affect people occurred recently when Armour was reformulated with increased cellulose, decreased dextrose, and added cornstarch, which caused problems for many users.  Nature-Thyroid appears to be the most hypoallergenic brand.

Bio-identical versus synthetic hormones

I personally prefer my patients use a bio-identical thyroid hormone such as Armour. Lab tests can measure bio-identical hormones in your system, whereas they cannot measure synthetic hormones (only TSH is an effective marker when synthetic hormones are used). However, some people clearly do better with synthetic hormones, such as Synthroid®.

Why is that? This is common in people with an autoimmune thyroid disease, especially Graves’, who have developed an autoimmune attack against T3 and T4. In other words, their immune system is attacking their thyroid hormones. Because bio-identical hormones contain both T3 and T4, this stimulates the autoimmune attack and makes the person feel worse. In these cases, a synthetic T4 may be a better option. Currently there are no lab tests to test for antibodies against T3 and T4, however one is in development.

The function of T3 hormones

T3 is the active form of thyroid hormone, having the greatest impact on metabolism, but also carries the greatest risk of overdosing. People who have difficulty converting T4 to T3, or whose cells have become resistant to thyroid hormones, do better with thyroid hormones that include T3.

However some people develop hyperthyroid symptoms with T3 support — feeling wired, nervousness, insomnia, heart palpitations, etc. This scenario is most common in Hashimoto’s patients who have constant immune attacks against their thyroid gland, which releases excess thyroid hormone into the bloodstream. These people typically do better with a T4-only medication.

Assessing responses to thyroid hormones

Many thyroid hormone users have a history of trying various meds. Some thyroid hormones make people feel wired, jittery or nervous. Others bring TSH into a normal range but do not alleviate symptoms. Some worked really well. All of these reactions provide insight into the mechanisms involved in the hypothyroidism.

No significant response, but normal TSH

This is very common with those who have Hashimoto’s. Chronic inflammation, whether it is from unmanaged Hashimoto’s or other sources (injury, surgery, infection, cancer, overtraining), can cause three scenarios:

• Prevents the conversion of T4 to T3
• Hampers communication between the pituitary gland in the brain and the thyroid gland.
• Inhibits thyroid receptors on cells from responding to thyroid hormones

In these cases, the response to T4-only medications will be poor. Another factor to consider is that the person may have many other conditions affecting thyroid health, such as insulin resistance, hormonal imbalances, gut infections, food intolerances, and more.

Only felt better with bio-identical hormones

This scenario can occur for several reasons:

• Unable to convert T4 to T3 when using T4-only medication
• Sensitivities to dyes or fillers in synthetic compounds that are not in bio-identical compounds
• May need T3 due to problems with the thyroid hormone receptors on cells
• Receptor sites on cells simply respond better to bio-identical than synthetic hormones

Only felt better with T3 combination hormones

If a person consistently does better with isolated T3 hormones, whether synthetic or bio-identical, a couple of factors are possible. One is difficulty converting T4 to T3. The other is that receptor sites on cells are resistant to thyroid hormones due to high cortisol, low progesterone, inflammation, high homocysteine, vitamin A deficiencies, and more.

Only felt better with synthetic hormones

This may occur in individuals who have an overactive metabolism and can’t tolerate additional T3. As mentioned earlier, this is common in those with Hashimoto’s who experience repeat immune attacks against the thyroid, or when the immune system is attacking T4 and T3, such as with Graves’ disease or multiple autoimmune diseases.

Felt over-stimulated with T3 or bio-identical hormones

Again, this may occur in the person with Hashimoto’s whose immune system is constantly attacking the thyroid gland, releasing excess thyroid hormone into the bloodstream. It also occurs in those with high epinephrine, an adrenal hormone, due to excess caffeine or nicotine, severe psychological stress, constant overtraining, or genetic mechanisms.

Felt fatigued and run down with thyroid hormones

This is almost always related to sensitivities to dyes or fillers in the thyroid hormone medication. It may also occur if the person is having an autoimmune response against their thyroid hormones, such as in Graves’ or in those with multiple autoimmune diseases.

Do you even need thyroid hormones?

Another factor to consider is whether you even need thyroid hormone replacement. Hashimoto’s, an autoimmune attack against the thyroid, accounts for 90 percent of hypothyroidism cases in the United States. When the autoimmune disease is successfully managed, thyroid hormones may not be needed at all, and taking them unnecessarily can do more harm than good. Another consideration is poor thyroid function caused by breakdowns in thyroid  pathways that need addressing, instead of true hypothyroidism (this is discussed in Chapter Four of the book).

However if damage to the gland is substantial enough, then thyroid hormones are necessary. Not taking thyroid hormone replacement when you truly need it can have disastrous consequences on your total health and well-being. If a person shows repeated and continuous elevations of TSH, thyroid hormones should be considered.

Even when thyroid hormone replacement is used, it is still vitally important to manage the autoimmune condition. This will enhance the effectiveness of the medication, preserve the integrity of the thyroid gland, and prevent the progression of the autoimmune condition into attacks on other areas of the body.

Thyroid replacement hormones

Brand Name Thyroid Hormones

• Synthroid – synthetic T4 only
• Levothroid – synthetic T4 only
• Levoxyl – synthetic T4 only
• Unithroid – synthetic T4 only
• Cytomel – synthetic T3 only
• Thyrolar – synthetic fixed ratio of T3 and T4
• Armour – bio-identical fixed ratio of T3 and T4 combination
• Westhroid – bio-identical fixed ratio of T3 and T4 combination
• Nature-Throid – bio-identical fixed ratio of T3 and T4 combination

Generic Thyroid Hormones

• Levothyroxine – synthetic T4 only
• L-Thyroxine – synthetic T4 only
• Liothyronine – synthetic T3 only
• Liotrix – synthetic fixed ratio of T3 and T4 combination
• Dessicated Thyroid – bio-identical T3 and T4 combination

Synthetic Thyroxine (T4) Hormones

• Synthroid – Brand Name
• Levothroid – Brand Name
• Levoxyl – Brand Name
• Unithroid – Brand Name
• Levothyroxine – Generic
• L-Thyroxine – Generic

Synthetic Triiodothyronine (T3) Hormone

• Cytomel – Brand Name
• Liothyronine – Generic

Synthetic T3 and T4 Combination

• Thyrolar – Brand Name
• Liotrix – Generic

Bio-Identical T3 and T4 Combination

• Armour –Brand Name
• Westhroid – Brand Name
• Nature-Throid – Brand Name
• Dessicated Thyroid – Generic

Although adequate iodine consumption is important for thyroid hormone production and iodine deficiency is the most common cause of hypothyroidism worldwide, its supplemental use in autoimmune thyroids is contraindicated. Iodine is the major cofactor and stimulator for thyroid peroxidase (TPO). TPO is the enzyme that is under attack with Hashimoto’s thyroiditis. It appears that increased iodine intake, especially as a supplement, increases the immune attack on the thyroid.(1) The extreme of this clinical expression is called the Jod-Basedow Phenomenon.(2) This phenomenon is portrayed as individuals who are iodine-deficient in conjunction with elevated thyroid antibodies. When these individuals are given exogenous iodine supplements they develop a hyperfunction autoimmune response. Although this phenomenon does take place in clinical practice at times, iodine supplementation with autoimmune thyroids does not always lead into thyroid hyperfunction. Rather one observes increased levels of TPO autoantibody levels that multiply dramatically with iodine supplements, and in many instances increased production of thyroid overactive symptoms.

In areas of the world where iodine has been added to sodium chloride (table salt), the rates of autoimmune thyroid have risen. In China, participants enrolled in a baseline study in 1999, and during the five-year follow-up through 2004, the effect of regional differences in iodine intake on the incidence of thyroid disease was examined. Of the 3761 unselected subjects who were enrolled at baseline, 3018 (80.2 percent) participated in this follow-up study. Levels of thyroid hormones and thyroid autoantibodies in serum, and iodine in urine, were measured, and B-mode ultrasonography of the thyroid was performed at baseline and follow-up. The study concluded that more than adequate or excessive iodine intake may lead to hypothyroidism and autoimmune thyroiditis.(3)

A study was conducted to evaluate the evolution of thyroid autoimmunity in relation to the change in goiter prevalence during 3 years of iodine prophylaxis in Sri Lanka. These results indicate an evolution of thyroid autoimmune markers during the course of iodine prophylaxis, which has not been described before.(4) A study evaluated the effects of iodine intake on the prevalence of thyroid dysfunction, autoimmunity, and goiter in two regions with different iodine status after two years of iodization in Turkey. In total, 1733 adolescent subjects were enrolled into the study. They measured free thyroxine (fT4), thyrotropin (TSH), antithyroid peroxidase antibodies (Anti-TPO), antithyroglobulin antibodies (Anti-Tg), and urinary iodine (UI), and examined the thyroid gland by ultrasound. The research study concluded that iodine supplementation in Turkey has resulted in the elimination of iodine deficiency in the Eastern Black Sea Region, and this has been accompanied by an increase in the prevalence of autoimmune thyroiditis and thyroid dysfunction.(5)

A study observed the effects of iodine on the level of CD4/CD8 cells and the production of thyroglobulin autoantibody (TGAb) and thyroid peroxidase autoantibody (TPO Ab), and investigated the role of iodine in thyroid autoimmunity. The study concluded that iodine might exert influence on the level of CD4/CD8, and thus the production of thyroid antibodies might directly or indirectly take part in the process of thyroid autoimmunity. Both low iodine and 100 times normal iodine intakes might activate the immune state on some degrees. The effects of iodine on immune responses of TG and TPO antigens in thyroid autoimmunity might not be completely the same.(6)[i] A research study concluded that thyroglobulin polymorphisms, combined with the explosive mix of iodine, TPO Ab, and H2O2 necessary for thyroid hormone synthesis, inadvertently provide the trigger for the autoimmune thyroid response.(7)

A study evaluated the prevalence of chronic autoimmune thyroiditis (CAT) and iodine-induced hypothyroidism, hyperthyroidism (overt and subclinical), and goiter in a population exposed to excessive iodine intake for 5 years (table salt iodine concentrations: 40-100 mg/kg salt). This was a population-based, cross-sectional study with 1085 participants randomly selected from a metropolitan area in São Paulo, Brazil, and conducted during the first semester of 2004. Thyroid ultrasound examination was performed in all participants and samples of urine and blood were collected from each subject. Serum levels of thyroid-stimulating hormone, free thyroxine, and anti-thyroid peroxidase (TPO) antibodies, urinary iodine concentration, thyroid volume, and thyroid echogenicity were evaluated. The study also analyzed table salt iodine concentrations. At the time the study was conducted, table salt iodine concentrations were within the new official limits (20-60 mg/kg salt). Nevertheless, in 45.6% of the participants, urinary iodine excretion was excessive (above 300 microg/l) and, in 14.1%, it was higher than 400 microg/l. The prevalence of CAT (including atrophic thyroiditis) was 16.9% (183/1085), women were more affected than men (21.5 vs 9.1% respectively, P=0.02). Hypothyroidism was detected in 8.0% (87/1085) of the population with CAT. Hyperthyroidism was diagnosed in 3.3% of the individuals (36/1085) and goiter was identified in 3.1% (34/1085). The study concluded that after five years, iodine intake by the Brazilian population may have increased the prevalence of chronic autoimmune thyroid and hypothyroidism in subjects genetically predisposed to thyroid autoimmune diseases. Appropriate screening for early detection of thyroid dysfunction may be considered during excessive nutritional iodine intake.(8)

It has been reported that hyperthyroidism is associated with an altered endothelial function and increased risk of arterial thromboembolism. A study was conducted to estimate chosen markers of endothelial dysfunction in iodine-induced thyrotoxicosis (IIT). The groups studied consisted of 41 hyperthyroid subjects, who had been treated with amiodarone (n = 6) or vitamin preparations supplemented with iodine (n = 35) and 40 persons with normal thyroid function. The following parameters were measured: thyroglobulin antibodies (TG Ab), thyroid peroxidase antibodies (TPO Ab), THS receptor antibodies (TR Ab), soluble adhesion molecules: sVCAM-1 and sICAM-1, von Willebrand factor (vWF), plasminogen activator inhibitor-1 (PAI-1), C-reactive protein (CRP), fibrinogen and urine iodine concentration. RESULTS: Patients with IIT had significantly higher levels of sVCAM-1 (p < 0.01), IL-6 (p < 0.005), fibrinogen (p < 0.005) and CRP (p < 0.05) in comparison to healthy subjects, whereas sICAM-1, PAI-1 and vWF concentrations did not differ between the groups studied. The highest sVCAM-1 levels were observed in patients with amiodarone induced thyrotoxicosis, and fibrinogen and CRP–in subjects receiving vitamin preparations. There were significant correlations between sVCAM-1 concentration and the levels of sICAM-1 (r = 0.341; p = 0.029) and PAI-1 (r = 0.347; p = 0.026), as well as with urine iodine concentration (r = 0.448; p = 0.004). IL-6 concentration correlated with vWF (r = 0.456; p = 0.003), TPO Ab (r = 0.328; p = 0.036) and PAI-1 level (r = 0.319; p = 0.042). The study concluded that iodine induced thyrotoxicosis is associated with an increase of sVCAM-1 and IL-6 levels, possibly reflecting inflammatory and destructive processes in the thyroid gland. However, increased procoagulant activity was not found in patients with IIT.(9)

A study was conducted to assess the relationship between the biological exposure to iodine and hypothyroidism. METHODS: Logistic regression model was used to analyze the risk factors of hypothyroidism, according to the epidemiologic data of 3761 adults in 3 kinds of rural communities: mild iodine deficiency area (4 natural villages in Panshan County, Liaoning Province), more than adequate iodine (7 natural villages of Zhangwu County, Liaoning Province), and excessive iodine area (2 natural villages of Huanghua City, Hebei Province). The study concluded that more than adequate iodine and excessive iodine were independent risk factors of subclinical hypothyroidism (OR = 3.172 and 6.391, P < 0.05) and overt hypothyroidism (OR = 3.696 and 9.213, P < 0.05). When interactions of iodine exposure and thyroid peroxidase antibody (TPOAb) or thyroglobulin antibody (TgAb) were included, more than adequate iodine was still a risk factor of subclinical hypothyroidism (OR = 2.788, P < 0.01), but had no such effect on overt hypothyroidism. Interaction of more than adequate iodine and positive TgAb significantly affected subclinical hypothyroidism and overt hypothyroidism (OR = 2.656 and 3.347, P < 0.05). In conclusion, more than adequate and excessive iodine exposure are independent risk factors of hypothyroidism. The risk of hypothyroidism goes up and thyroid dysfunction becomes more serious with the increasing biological exposure
to iodine.(10)

The current iodine status and the impact of silent iodine prophylaxis on the prevalence of autoimmune thyroiditis among schoolchildren in a formerly iodine-deficient community in northwestern Greece were investigated. The findings were compared to those obtained from a similar survey conducted 7 years previously in the same area. A total of 302 schoolchildren (12-18 years of age) from a mountainous area of northwestern Greece were examined for the presence of goiter, and blood and urine samples were collected for assessment of thyroid function, antithyroid antibodies and urinary iodine excretion. In those children (n = 42) with palpable goiter or positive antibodies and/or a thyrotropin (TSH) level greater than 5 mU/L, thyroid ultrasonography was performed to estimate thyroid gland size and morphology. Median urinary iodine concentration in the children was 20.21 microg/dL, indicating sufficient iodine intake. Thyroid function was normal in all but 7 children, who had subclinical hypothyroidism (2.5%). Antithyroid antibodies (antithyroid peroxidase [TPO] and/or antithyroglobulin [Tg]) were positive in 32 children, including those with subclinical hypothyroidism (10.6%). Twenty-nine of these children (9.6%) also had the characteristic echo pattern of thyroiditis on ultrasound and were diagnosed to have autoimmune thyroiditis. In comparison to data from our previous survey 7 years ago, there has been a threefold increase in the prevalence of autoimmune thyroiditis among schoolchildren. In conclusion, silent iodine prophylaxis resulted in the elimination of iodine deficiency in Greece, and this has been accompanied by an increase in the prevalence of autoimmune thyroiditis.(11)

In the mountainous areas of Azerbaijan, the schoolchildren suffer from severe Iodine Deficiency (ID) with median Urinary Iodine Excretion (UIE) 36 mcg/l and prevalence of goiter 99% (estimated by US). In a population of 293,000 schoolchildren aged 8-14 y.o., a study administered capsules containing 190 mg of iodized oil (Lipiodol-Guerbet, Cedex, France) twice yearly in 6 months apart (total 380 mg). The aim of the present study was to evaluate the efficacy, the benefits, as well as the possible side-effects in a follow-up period of 6 and 12 months after the initial administration of iodized oil. Six and 12 months after the initial administration of iodide, two representative samples of 391 and 326 children respectively were examined. The evaluation included: estimation of goiter by US, determination of UIE and serum measurements of T3, T4, TSH, Tg, autoantibodies against thyroid peroxidase (anti-TPO) and thyroglobulin (anti-Tg). The results found that there was an improvement in median UIE, which increased from 36 mcg/l to 68 and 81 mcg/l after 6 and 12 months of treatment respectively. The prevalence of goiter decreased from 99% to 54% and 26% respectively. Tg was decreased at 6 and 12 months from the first administration, whereas TSH remained unchanged at 6 months and decreased at 12 months when compared to the latter value. Hypothyroidism was detected in 7% of children after iodide administration both at 6 and 12 months, but overt hypothyroidism was observed only in 0.5% at 12 months. Subclinical hyperthyroidism was detected in 2% and 6% after iodide administration both at 6 and 12 months. There was a significant increase in the title of thyroid auto antibodies in 6 months, which was retained and increased in 12 months. There was no relation between the appearance of thyroid dysfunction and the positive thyroid auto antibodies. It was concluded that the dose of 190 mg iodide administered twice yearly, improved iodine deficiency and endemic goiter in schoolchildren. The increase of UIE resulted from iodide administration, was accompanied by an increased title of thyroid auto-antibodies and an increased prevalence of hyper and hypo-thyrotropinemia apparently of no autoimmune etiology.(12)

Lifelong thyroid hormone replacement is indicated in patients with hypothyroidism as a result of Hashimoto’s thyroiditis. However previous reports have shown that excess iodine induces hypothyroidism in Hashimoto’s thyroiditis. A study investigated the effects of iodine restriction on the thyroid function and the predictable factors for recovery in patients with hypothyroidism due to Hashimoto’s thyroiditis. The subject group consisted of 45 patients who had initially been diagnosed with hypothyroidism due to Hashimoto’s thyroiditis. The subjects were divided randomly into two groups. One group was an iodine intake restriction group (group 1) (iodine intake: less than 100 micro g/day) and the other group was an iodine intake non-restriction group (group 2). The thyroid-related hormones and the urinary excretion of iodine were measured at the baseline state and after 3 months. After 3 months, a recovery to the euthyroid state was found in 78.3 % of group 1 (18 out of 23 patients), which is higher than the 45.5% from group 2 (10 out of 22 patients). In group 1, mean serum fT4 level (0.80 +/- 0.27 ng/dL at the baseline, 0.98 +/- 0.21 ng/dL after 3 months) and the TSH level (37.95 +/- 81.76 micro IU/mL at the baseline, 25.66 +/- 70.79 micro IU/mL after 3 months) changed significantly during this period (p < 0.05). In group 2, the mean serum fT4 level decreased (0.98 +/- 0.17 ng/dL at baseline, 0.92 +/- 0.28 ng/dL after 3 months, p < 0.05). In the iodine restriction group, the urinary iodine excretion values were higher in the recovered patients than in non-recovered patients (3.51 +/- 1.62 mg/L vs. 1.21 +/- 0.39 mg/ L, p=0.006) and the initial serum TSH values were lower in the recovered patients than in the non-recovered patients (14.28 +/- 12.63 micro IU/mL vs. 123.14 +/- 156.51 micro IU/mL, p=0.005). In conclusion, 78.3% of patients with hypothyroidism due to Hashimoto’s thyroiditis regained an euthyroid state iodine restriction alone. Both a low initial serum TSH and a high initial urinary iodine concentration can be predictable factors for a recovery from hypothyroidism due to Hashimoto’s thyroiditis after restricting their iodine intake.(13)

A study looked at the effect of iodine on autoimmune thyroiditis. Autoimmune thyroiditis is an organ-specific autoimmune disorder characterized by infiltration of the thyroid gland by lymphocytic inflammatory cells, often followed by hypothyroidism due to destruction and replacement of the follicular tissue. Dr. Noel Rose and members of his laboratory at Johns Hopkins University have continued to study autoimmunity using autoimmune thyroiditis as a model. Autoimmune thyroiditis is multifactorial, with both genetic and environmental factors involved. We have studied familial association of thyroid antibodies in juveniles with either autoimmune thyroiditis or Graves’ disease. Epitope analysis of thyroglobulin autoantibodies showed that autoantibodies from unrelated patients with disease had greater similarity of epitope binding than members of their own family. Subclass analysis of thyroglobulin autoantibodies indicated that IgG2 was dominant in autoimmune thyroiditis. Much of our work focused around iodine as an environmental trigger of autoimmune thyroiditis. We showed that iodination of the human thyroglobulin molecule alters its immunoreactivity. We explored the role of excess iodine ingestion in exacerbating thyroiditis using the NOD.H2h4 mouse as a model. We found multiple effects of excess iodine, including changing the immunogenicity of the thyroglobulin molecule and the upregulation of ICAM-1 and ROS in the thyrocyte itself. These observations may help to delineate the mechanisms by which iodine exacerbates thyroiditis and to explain differences in the host response of genetically susceptible individuals compared to those who are resistant to disease.(14)

Citations

1 SurksM, Sievert R. Drugs and thyroid function. NEJM, 1995;333(25):1688.

2 Weetman A. Graves’ Disease. NEJM 2000;343(17):1236.

3 Effect of iodine intake on thyroid disease in China. N Engl J Med. 2006 Jun 29;354(26):2783-93.

4 Evolution of thyroid autoimmunity during iodine prophylaxis0the Sri Lankan experience. Eur J Endocrinol. 2003 Aug;149(2)103-10.

5 High prevalence of thyroid dysfunction and autoimmune thyroiditis in adolescents after elimintion of iodine deficiency in the Eastern Black Sea Region of Turkey. Thyroid 2006 Dec;16(12):1265-71.

6 Experimental study on effects of iodine deficiency and excess on thyroid autoimmunity. Zongua Yu Fang Xue Za Zhi. 2006 Jan;40 (1):18-20.

7 Why measure thyroglobulin autoantibodies rather than thyroid peroxidase autoantibodies? Thyroid 2004 Jul;14(7):510-20.

8 Camargo RY, Tomimoria Ek, Neves Sc, et al. Thyroid and the environment: exposure to excessive nutritional iodine increases the prevalence of thyroid disorders in Sao Paulo, Brazil. Eur J Endocrinol. 2008 Sep;159(3):293-9.

9 Zonenberg A, Tolejko B, Scelachowska M, et al. Markers of endothelial dysfunction in patients with iodine induced hyperthyroidism. Endokryonol Pol. 2006 May-Jun;57(3):210-7.

10 Chong W, Shit Xg, Teng WP, et al. Multifactor analysis of relationship between the biological exposure to iodine and hypothyroidism. Zhongua Yi Za Zhi. 2004 Jul 17:84(14):1171-4.

11 Zois C, Stavrou I, Kalogera C, et al. High prevalence of autoimmune thyroiditis in school children after elimination of iodine deficiency in northwestern Greece. Thyroid. 2003 May;13(5):485-9.

12 Markou KB, Georgopoulous NEA, Makri M, et al. Improvement of iodine deficiency after iodine supplementation in school children of Azerbaijan was accompanied by hypo and hyperthyrotropinemia and increased title of thyroid autoantibodies. J Endocrinol Invest. 2003;26(2 Suppl):43-8.

13 Yoon SJ, Choit SR, Kim DM, et al. The effect of iodine restriction on thyroid function in patients with hypothyroidism due to Hashimoto’s thyroiditis. Yonsi Med J. 2003 Apr 30;44(2):227-35.

14 Lynne Burek C. Autoimmune thyroiditis research at Johns Hopkins University. Immunol Res. 2010 Jan 20. [Epub ahead of print]

Do you need to take the Leaky Brain Challenge? Read on to find out.

The most disturbing thing I see in regards to Hashimoto’s is that although people’s TSH may be managed with thyroid hormones, their immune dysregulation goes unchecked. This leaves other areas of the body vulnerable to attack, the most profound being the brain.

There are three ways Hashimoto’s can affect the brain. First, many people with Hashimoto’s also have an autoimmune attack against their nervous system. On a blood test this can be identified by positive antibodies to neurological tissue.  Second, unrelated to an autoimmune attack against the nervous system, the inflammatory response generated by Hashimoto’s can activate the brain’s immune system, hence promoting inflammation in the brain. Third, Hashimoto’s can lead to low thyroid hormones, which are necessary to dampen the brain inflammation caused by the previous two factors.

Depression, fatigue, and brain fog

It’s important to know that we all experience brain degeneration on an ongoing basis. A more common term for accelerated brain degeneration is simply known as aging. The trick is to prevent the brain from degenerating any faster than it has to.

Unfortunately, it is very common to see advanced brain degeneration in long-term, unresolved Hashimoto’s cases, with the most common symptoms being depression (from decreased firing of the frontal cortex), fatigue (from brain fatigue due to neurodegeneration), and brain fog (from brain inflammation).

True, these are also symptoms of hypothyroidism, but in some cases, particularly when the condition is long standing or still persistent despite successful management of thyroid levels, the impact of an unresolved thyroid condition on the brain should be investigated.

How Hashimoto’s affects the brain’s immune system

The brain is made up of two types of cells: neurons and microglia cells. Neurons are responsible for communication within the brain and everything we associate with brain activity, such as our intelligence, emotions, and the ability to automatically breathe, digest or maintain a heartbeat.

The microglia cells are the brain’s immune cells. It’s their job to react to foreign invaders, clean up debris and plaque, and dissolve dead neurons. The microgia are necessary for optimal neuronal communication and healthy brain function.

Although microglial cells function as the brain’s immune system, they are unlike the immune system in the rest of the body. When a virus or bacteria invades your body, the body’s immune system orchestrates a comlex and multi-faceted response, as described briefly in Chapter Three of my book. For instance, once an antigen (a foreign invader) is successfully dispatched, the immune system’s T-suppressor cells call off the attack and send the troops home.

Not so with the brain’s immune system. If an antigen makes its way into the brain, there is no complex orchestration, but rather an all-out assault by the brain’s microglial cells on the invader and, as a consequence, inflammation and degeneration of surrounding brain tissue. What’s worse is that there are no T-suppressor cells to call off the attack, and the glial cells, in their unrestrained assault, create brain inflammation and chew up brain tissue in a degenerative cascade.

Hashimoto’s is a double whammy for the brain

Unfortunately, Hashimoto’s activates microglia cells in two ways.  First, thyroid hormones are integral to brain health, and Hashimoto’s can lead to low thyroid hormone status. Thyroid hormones dampen overactivity of the microglial cells, thus preventing or slowing down this cascade that causes inflammation and degeneration in the brain.(1-8)

Second, the inflammatory response caused by Hashimoto’s increases the activity of the brain’s microglia cells, hence promoting brain inflammation.(9)

So failing to address the autoimmune attacks of Hashimoto’s is a double whammy on the brain — the inflammation caused by Hashimoto’s increases microglial activity, while low thyroid hormone status fails to adequately dampen the microglial cells.

The effect of Hashimoto’s on the blood-brain barrier

The microglia cells not only make up more than half of the total mass of the brain, but they also make up the blood-brain barrier, a thin barrier that lines the brain and allows necessary, nano-sized substances to pass through. The blood-brain barrier is important for keeping antigens (foreign invaders, such as viruses or bacteria) and environmental toxins out of the brain.

Unfortunately, the blood-brain barrier can develop “leaks” for a variety of reasons, including poor blood-sugar stability (particularly insulin resistance),(10) chronic stress,(11) chronic inflammation,(12) poor gut health, poor diet with unhealthy fats,(13) and unchecked autoimmune activity, such as Hashimoto’s disease (alcohol and high homocysteine are other recognized factors(14-16)). If you are familiar with leaky gut, as discussed in the book, then you’ll understand leaky brain, as both the gut and the brain are immune barriers vulnerable to the same problems.

When the blood-brain barrier develops leaks, bad guys get in, the microglial cells go nuts, and a whole lot of brain tissue gets chewed up. This creates inflammation, which in felt in some as “brain fog,” and leads to accelerated brain degeneration.

The Leaky Brain Challenge

How do you know if your blood-brain barrier is leaky? A simple and easy way to find out is to do Blood-Brain Barrier Challenge. To do this, simply take 1000 mg of straight GABA (not GABA precursors such as theanine).

GABA is a neurotransmitter synthesized in the brain and is responsible for calming or inhibiting over activity. Although some companies sell GABA supplements, the reality is the GABA molecule is too large to pass through an intact blood-brain barrier. The fact that this supplement sells so well is a testament to the integrity of the average American’s blood-brain barrier.

So, if several hours after taking 1000 mg of GABA, you feel calm, relaxed or sleepy, you know that GABA, a molecule too large to pass through the blood-brain barrier, has nevertheless made it into your brain and is performing its calming duties. This means your blood-brain barrier has become compromised and your brain is highly susceptible to the immune rampages I discussed above.

Some people, instead of feeling relaxed, will find GABA makes them feel more anxious or jittery. There are other reasons for this that will be discussed in my next book, however any reaction at all indicates a leaky brain barrier.

If you felt no change after taking GABA, that is a good sign that your blood-brain barrier is intact and functioning well. (For accurate results, be sure to take this test during the day and not at bedtime.)

What to do about a leaky brain barrier

Addressing the areas that helped cause a permeable blood-brain barrier is the best place to start if you want to restore integrity. First make sure your diet is strictly void of gluten. Then do an Elimination/Provocation diet, as explained in my book, to determine whether other foods, such as dairy or eggs, are also provoking the immune system.

Continue on with the other strategies explained in the book: Balancing blood sugar, addressing gut health and gut infections, and supporting adrenal health so your adrenal hormones are neither too high or too low. All of these will help quench inflammation, a notorious saboteur of brain health. Also, ask your practitioner about the supplements I have created specifically for blood-brain barrier integrity, brain inflammation and increased blood flow to the brain (which will be discussed in my next book). Other strategies include enhancing the liver’s methylation pathway (Chapter Eight of the thyroid book) and supplementing with alpha-lipoic acid.

Modulating your autoimmune disease is a vital step to protecting the integrity of your blood-brain barrier and the health of your brain. The longer Hashimoto’s or any autoimmune disease goes on unchecked, the more vulnerable your brain is to autoimmune disease, degeneration, and inflammation.

References

1 Pumirat J. Prog Neurobiol. 1992;39:281-294.

2 Limr FRS, et al. J Endocrinol. 1997;154:161-175.

3 Gomes FCA, et al. Adv Exp Med Biol. 1997;429:99-108.

4 Mallet M, et al. Adv Exp Med Biol. 1997;429:99-108.

5 Dobbertin A, et al. J Neuroscie. 1997;17:5305-5315.

6 Bernal J, et al. Thyroid hormones and brain development. Eur J Endocrinol;133:390-398.

7 Calza L, et al. Thyroid hormone-induced plasticity in the adult rat brain.  Brain Res Bull. 1997;44(4):549-57.

8 Flavin RSL, et al. Regulation of microglial development: A novel role for thyroid hormones. The Journal of Neuroscience. 2001;21(6):2028-2038.

9 Flavin RSL, et al. Regulation of microglial development: A novel role for thyroid hormones. The Journal of Neuroscience. 2001;21(6):2028-2038

10 Kamada H et al. Influence of hyperglycemia on oxidative stress and matrix metalloproteinase-9 activation after focal cerebral ischemia/reperfusion in rats. Stroke. 2007;38:1022-1049.

11 Espositie, P, et al. Acute stress increases permeability of the blood-brain barrier through activation of brain mast cells. Brain Research. 2001;888(1):117-127.

12 Haroh J, et al. Oxidative stress activates protein tyrosine kinase and matrix metalloproteinases leading to blood-brain barrier dysfunction. J neurochem. 2007;22(1).

13 Jali C, et al. Cyclooxygenase inhibition limits blood-brain barrier diruption following intracerebral injection of tumor necrosis factor-alpha in the rat. JPET. 2007;323(2):488-498.

14 Haorah J, et al. Alcohol0induced oxidative stress in brain endothelial cells causes blood-brain barrier dysfunction. Journal of Leukocyte Biology. 2005;78:1223-1232.

15 Atul F, et al. Elevated levels of homocysteine compromise blood-brain barrier integrity in mice. Blood. 2005.

16 Homocysteine attenuates blood-brain barrier function by inducing oxidative stress and the junctional proteins. FASEB. 2008;22:734-7.

I never thought when I started practicing that I would one day write a thyroid book and teach thyroid classes, as I am not inherently passionate about the thyroid.

But I have invested so much time into the thyroid because the majority of my patients have some degree of thyroid dysfunction. I quickly learned you can’t help a chronically sick person if you ignore the thyroid, as every cell in the body has receptors for thyroid hormones. Poor thyroid function affects bone health, neurological function, hormone balancing, immune function, and so on. As a practitioner, you have to be an expert in the thyroid if you want to get anywhere with your patients.

Thyroid Hormones Don’t Complete the Care

This was once a problem for me because, like a lot of doctors, I did not know how to truly influence thyroid function beyond thyroid hormones. No other disorder has frustrated me more — I used to dread it when a thyroid case walked in because it pushed me to the edge and made me feel like a poor practitioner. Add to this that I was up against the Thyroid Dream: The idea that patients will take the right thyroid hormone, get skinny, and have no more symptoms. They also frequently come in with bagfuls of supplements, a testament to their endless search for that magic bullet.

The truth is, although thyroid hormones are necessary in many cases, there is rarely one magic medication or supplement to cure thyroid disease. Instead it’s a whole web of dysfunction that needs to be unraveled, and the trick is knowing which thread to pull first.

The Immune Connection

So I started running antibody tests, looking for Hashimoto’s, because I noticed my failure rate was the highest when an immune component was active. To add to the frustration, some tests came back negative when Hashimoto’s seemed so evident. Turns out some Hashimoto’s patients will always test negative for the disease. Biopsies, however, show Hashimoto’s is nevertheless active and present in these individuals.

I learned that not only do the immune surges of Hashimoto’s directly affect the thyroid gland, but they also affect the various thyroid pathways: conversion of T4 to T3, the brain’s communication with the thyroid, the number of thyroid-binding proteins that transport thyroid hormones, and how well cellular receptor sites accept thyroid hormones. This was not exactly an overnight discovery.

To compound the confusion, thyroid hormones themselves modulate immune activity. In other words, having sufficient thyroid hormones in your body helps keep your immune system under control so that it doesn’t go haywire and attack your own body tissue. You can see how Hashimoto’s, which often leads to a thyroid hormone deficiency, fires up the immune system in a vicious, compounding cycle. This is one reason it is so important to quench the immune attacks.

The Brain Connection

And if that all wasn’t enough, the brain plays a significant role in matters. As a practitioner trained in neurology, I constantly deal with the neurological fall-out of hypothyroidism: depression, brain fog, balance issues, and autoimmune attacks in the brain. The immune surges of Hashimoto’s and the resultant hypothyroidism depress neurotransmitter levels and activity, which are needed for healthy thyroid function (and vice versa). If Hashimoto’s goes unchecked, it can eventually lead to autoimmune attacks in the brain with devastating consequences.

I have also come to learn that hypothyroidism suppresses autonomic function, with symptoms such as chronic gastric distress and leaky gut, poor gallbladder function, dry eyes, incontinence and more. What’s more, taking thyroid hormone medications, even though they may be necessary for optimal function, also have a suppressive effect on autonomic function, and these patients will need to incorporate lifelong modifications to their diet and lifestyle as a result.

Goiters, Nodules and Masses

Goiters, nodules and masses are other facets of poor thyroid function that don’t always have clear-cut answers. For instance, goiter is not always related to iodine deficiency, and there are a variety of questions that have to be asked and tests run to determine the relevant mechanism when a patient presents with any of these.

Unraveling the Web

These are just some of the ways hypothyroidism and Hashimoto’s can weave a tangled web. I haven’t even addressed diet, iodine or the fact that some people develop sensitivities to the fillers in their thyroid hormones!

Too many practitioners have been lulled into looking for hypothyroidism in their 40-something, overweight female patients with cold hands and feet, when the reality is that hypothyroidism and Hashimoto’s affects both men and women of all body types and ages, presenting with a variety of symptoms. And Hashimoto’s is all too often dismissed, because for most doctors, diagnosing it doesn’t change how they will treat their patients.

These topics are a sampling of what I will discuss more deeply in bi-weekly newsletters. I hope you will subscribe to receive articles on thyroid function and other facets of functional medicine, and that they will benefit you on your journey toward better thyroid health. Please also stay tuned for an upcoming forum where readers can share experiences, successes and challenges, hopefully creating a space for further education.