The Dr. Hedberg Show

Hashimoto’s disease can have many triggers including iodine, low birth weight, pregnancy, smoking, mercury, drugs, stress, leaky gut, environmental toxins, and of course infections.  This article will focus on the connection between infections and Hashimoto’s disease.

The infection connection and Hashimoto’s disease is something I have been investigating since 2005 when I first learned about the connection between Yersinia enterocolitica and Hashimoto’s disease.  Since then, I’ve been researching the infection connection to Hashimoto’s disease and science continues to shed more light on this area.

The vast majority of my patients with Hashimoto’s disease do have some kind of active infection that has been shown to be connected to Hashimoto’s disease.  Let’s go ahead and jump right into what the latest scientific literature has to say about this fascinating area of research.

Why do infections trigger Hashimoto’s disease?

Molecular mimicry is one explanation for bacterial trigger of the disease.  This basically means that the infection looks similar to your own thyroid tissue so your immune system launches an immune attack on the microbe and your thyroid.  Yersinia enterocolitica is a classic example of this connection.

Other explanations are complex immunologic mechanisms that I won’t go into detail here because of the technical nature of the material.  To put one mechanism simply, viruses can reside inside the thyroid gland which triggers immune activation against the virus and the thyroid.  Epstein-Barr Virus and Human Herpes Virus 6 are examples of this mechanism.

For those of you with a scientific background who would like to read more about the technical immunologic mechanisms, you can search for the phrases used in this quote, “Possible mechanisms by which infections may trigger thyroiditis include release of sequestered antigens by cell destruction or apoptosis, exposure of cryptic epitopes, molecular mimicry, or via a bystander mechanism resulting in activation of resident T- cells.” This quote is taken from this paper freely available for you to research.

Lyme disease and Hashimoto’s disease

Borrelia burgdorferi is the spirochete that causes Lyme disease and there is some evidence that this bacteria is connected to Hashimoto’s disease.  The data is limited at this point but with Lyme disease, there can be many other indirect factors and co-infections that could potentially be involved in triggering Hashimoto’s disease.

Patients with Lyme disease also tend to have some of the predisposing factors to autoimmune diseases such as a compromised digestive tract, inflammation, and tremendous oxidative stress.

Yersinia enterocolitica and Hashimoto’s disease

I have written about and recorded a podcast previously about the connection between Yersinia enterocolitica and Hashimoto’s disease.  There is good evidence of this connection so it is important to get tested if you have Hashimoto’s disease.  This can be done with a stool test and/or blood test.

Helicobacter pylori and Hashimoto’s disease

I cover this connection in detail in this article and podcast.

Viruses and Hashimoto’s disease

The following viruses have been shown to potentially trigger Hashimoto’s disease:

Coxsackievirus B

Rubella

Enteroviruses

Epstein-Barr Virus

Human Herpes Simplex Virus 6 (HHV-6)

Mumps

Parvovirus B-19

Hepatitis B

Hepatitis C

The Hepatitis C virus actually has the strongest infection connection to Hashimoto’s disease.  In fact, studies have shown that this virus can actually reside outside of the liver inside the thyroid gland thus triggering autoimmunity.

Can we be certain that the virus triggered the autoimmunity?

This can be difficult to make a definitive conclusion about the direct connection due to the interaction between the virus and the patient’s immune system.  Some viruses like the Epstein-Barr Virus and Herpes 6 can be activated inside the thyroid gland but there is no immune response to them that we can pick up on through blood testing.  This would require a biopsy of the gland and testing for specific viruses to see if they are present and active.  This is not a feasible option nor is it really necessary.  Genetic factors also play a role in how your body responds to viruses and the development of autoimmunity.

What can you do if you have an infection connection to your Hashimoto’s disease?

This depends on the infection.  Any of the bacterial triggers in the GI tract such as Yersinia and H. pylori are very straightforward and I use various supplements and herbs to get rid of them successfully.

Lyme disease is of course extremely complex so you would need to work with a “Lyme Literate” doctor who truly understands this condition.

Viruses are difficult because they require the greatest number of interventions and changes for the patient to make.  The immune system must be functioning at it’s best possible state to fully control viruses like the Epstein-Barr Virus.  Too often patients are looking for supplements and herbs to take to address Epstein-Barr Virus but that never works.  It requires a comprehensive approach addressing psychoneuroimmunology, gut health, hormones, stress, inflammation, insulin resistance etc. to be successful.

The infection connection to Hashimoto’s disease is alive and well and usually one of the most overlooked aspects of this condition along with childhood trauma.  Be sure you’re having some of these infections checked if you’re trying to heal Hashimoto’s disease.  You don’t need to have every single one tested.  Your doctor should know based on your unique health history which ones you need.

In a previous article, I covered a study that showed black cumin seed (Nigella sativa) was extremely beneficial for Hashimoto’s thyroiditis. Another exciting paper was just published which looked specifically at black cumin seeds and their effect on lipids, glucose metabolism, and anthropometric variables including body weight and body mass index (BMI).

The authors start by discussing the connection between hypothyroidism and lipids such as cholesterol, triglycerides, and LDL. High cholesterol levels are a hallmark sign of hypothyroidism which is interesting because some patients are prescribed cholesterol-lowering medication without a proper thyroid evaluation. One of the signs of successfully managing hypothyroidism is observing the drop in cholesterol levels as thyroid function improves. Hypothyroidism also increases the risk of heart attack and stroke.

The authors also state that Hashimoto’s thyroiditis is a risk factor for developing type 2 diabetes and diabetes is a common condition associated with heart disease. In fact, up to 38% of patient with type 2 diabetes also have Hashimoto’s thyroiditis.

Interestingly, the authors also discuss some of the potential negative consequences of taking the thyroid medication levothyroxine sodium which includes bone loss, cardiac dysfunction, and left ventricular hypertrophy.

They then discuss all of the known benefits of black cumin seed oil which I covered in my previous article on this supplement and Hashimoto’s disease.

How was the study done?

40 patients aged 20-50 with Hashimoto’s thyroiditis confirmed with elevated anti-thyroid peroxidase (TPOAb) antibodies and TSH, T4, and T3 were also measured. None of them had taken any supplements or followed any diets 3 months prior to the trial.

Patients in the intervention group took 2 grams of Nigella sativa powder per day and those in the placebo group took 2 grams of starches per day for 8 weeks. The black cumin seeds were milled in a grinder to make the powder. Both groups were instructed to take 1 gram with lunch and 1 gram with dinner each day.

What did they measure?

Bodyweight, BMI, waist circumference, and 3-days of food logged.

Physical activity was measured based on intensity to an average weekday.

Fasting blood tests were obtained at the beginning and end of the 8 weeks which included:

Total cholesterol

Fasting glucose

Triglycerides

HDL cholesterol

LDL cholesterol

Insulin

Nesfatin-1

Insulin resistance was measured using the homeostasis model assessment of insulin resistance (HOMA-IR) which is a calculation of glucose x insulin / 405.

What were the study results?

The weight and the BMI of those taking black cumin seed significantly reduced after 8 weeks compared to the placebo group which had no changes.

LDL and triglycerides significantly reduced in the study group.

HDL levels increased in the study group.

The atherogenic index improved in the study group which is a marker of heart disease risk.

TSH and anti-TPO concentrations decreased.

T3 levels increased slightly.

In the discussion, the authors provide information about the potential reasons for these positive outcomes. The effects on weight could be explained by the mechanism that black cumin seeds increase the feeling of fullness and satiety. Black cumin seeds also decrease the absorption of lipids which can lower cholesterol and triglyceride levels. Black cumin seeds have also been shown to decrease fat storage and the spread of fat cells as well as increasing the breakdown of fat.

We know from my previous article on black cumin seeds and Hashimoto’s thyroiditis that it is a powerful ant...

Aloe vera is one of the oldest medicinal plants we know of that was used by the ancient Egyptians who called it “the plant of immortality.” And 200 years ago Greek scientists considered Aloe vera a “universal panacea.” Aloe vera is technically named Aloe barbadensis and you most likely have heard of using Aloe topically for burns or internally for soothing an inflamed gut.

I’ve used Aloe vera over the years as one of the compounds in a gut-healing supplement I use for leaky gut, inflammatory bowel, SIBO, constipation, and irritable bowel syndrome. It works extremely well at reducing inflammation and repairing inflamed and damaged mucus membranes in the gut and the urinary tract. I have also used it quite successfully with the bladder pain caused by interstitial cystitis.

Aloe vera is rich in 200 nutritional substances most notably the following:

Minerals:

Iron

Chromium

Zinc

Selenium

Copper

Manganese

Magnesium

Sodium

Potassium

Calcium

Vitamins:

A

B1,B2,B3,B5,B6,B12

C

E

Folic acid

Enzymes:

Alkaline phosphatase

Amylase

Bradykinase

Carboxypeptidase

Catalase

Lipase

Peroxidase

Additional compounds:

Choline

Anthraquinones

Sterols

Lignins

Saponins

Salicylic acid

The above compounds explain its anti-oxidant, analgesic, antiseptic, anti-viral, and anti-inflammatory properties.

Aloe vera has been scientifically shown to be beneficial for the following:

Genital herpes

Psoriasis

Seborrheic dermatitis

Burns

Wound healing

Mucositis

Radiation dermatitis

Frostbite

Acne

Lichen planus

Apthous stomatitis

Type 2 diabetes

HIV

Cancer prevention

Constipation

Ulcerative colitis

Pressure ulcers

Traditional uses not scientifically supported yet include:

Parasites

Chronic leg wounds

Lupus

Arthritis

Alopecia

Bacterial and fungal skin infections

Tic douloureux

Promising study results on Aloe vera and Hashimoto's Disease

New research indicates that Aloe vera may be extremely beneficial for Hashimoto’s thyroiditis in patients with subclinical hypothyroidism. The study was inspired by an individual with Hashimoto’s thyroiditis who drank 50ml of Aloe Barbadensis Miller juice as a laxative and to soothe her skin. She noticed that after drinking this juice for 3 and 6 months, her TSH, Free T4, Free T3, and thyroid peroxidase antibodies (TPOAb) all improved.

Her TSH went from 5.14 to 1.83. Free T4 improved from 8.3 to 11.44. Free T3 went from 5.22 to 4.78 which indicates improved efficiency. And TPOAb decreased from 1,875 to 246.

These were quite profound changes with no other interventions and no thyroid medication.

Based on these results the authors recruited 30 women aged 20-55 with Hashimoto’s thyroiditis and subclinical hypothyroidism which was defined as having a TSH >4.0 and high TPOAb levels. These women had never been treated with thyroid medication before or taken any supplements for their thyroid issues.

All 30 subjects drank 50ml of Aloe Vera Miller Juice (ABMJ) manufactured by ZUCCARI (Trento, Italy) every morning on an empty stomach for 9 months.

TSH, Free T4, Free T3, and TPOAb levels were measured at baseline, 3 months, and 9 months.

The control group consisted of data on 15 women from a university hospital who had Hashimoto’s thyroiditis and subclinical hypothyroidism.

What did the results reveal?

The control group did not show any statistically significant changes in any of their thyroid test numbers.

At three months the study group showed statistically significant improvements in all four thyroid tests. TSH, Free T4, and TPOAb levels all improved again at the nine month mark. Free T3 levels declined at three months but then did not significantly change from three months to nine months.

Here are the basic averages during the study:

TSH Baseline: 5.19

TSH 3 Months: 3.12

TSH 9 Months: 2.01

Free T4 Baseline: 9.63

Free T4 3 Months: 10.67

Free T4 9 Months: 11.83

Free T3 Baseline: 5.29

Free T3 3 Months: 4.38

Free T3 9 Months: 4.32

Free T4:Free T3 Ratio Baseline: 1.83

Free T4:Free T3 Ratio 3 Months: 2.47

Free T4:Free T3 Ratio 9 Months: 2.78

TPOAb Baseline: 1,020

TPOAb 3 Months: 825

TPOAb 9 Months: 347

Why was it good to see T3 levels decrease slightly?

Free T3 levels will increase as a compensatory mechanism when Free T4 levels decrease. This is your body trying to balance Free T4 and Free T3 levels. As Free T4 levels increased, the peripheral deiodinase enzyme activity decreased thus slightly reducing the conversion of T4 to T3. Remember that high T3 or high/normal T3 levels have been shown to decrease lifespan due to an artificial stimulation of metabolism. This is why the short-term gain in energy and feeling of more “pep” from T3 may have long-term consequences.

Final Author Conclusions

The authors state that 100% of patients with Hashimoto’s thyroiditis and subclinical hypothyroidism at 9-months treatment with 50ml/day of Aloe vera juice restored thyroid function and markedly decreased TPOAb levels. They state that these results are possibly better than what has been shown in previous studies which looked at selenium alone and selenium plus inositol for Hashimoto’s thyroiditis. And finally, they conclude that Aloe vera juice rescues thyroid hormone production by reducing inflammation in the thyroid gland and reducing the need for conversion of T4 into T3.

Dr. Hedberg’s Comments

This study is quite impressive but the first major weakness is the lack of a control group that consumed a sham product and were told that they were taking it for their thyroid health. The placebo affect can be quite powerful which is why double-blind placebo-controlled trials have some type of sham product such as a sugar pill. However, the improvements on the blood tests for these thyroid markers would be next to impossible to achieve simply through placebo.

You’ll notice as written above that Aloe vera is rich in many substances that support thyroid health and immune health such as selenium, zinc, vitamin A, magnesium, b-vitamins, vitamin C, vitamin E, iron etc. These would have reparative properties on gut lining and also protect the thyroid gland from damage. Some of these women may have had low ferritin levels which would have slightly improved from the iron content of the Aloe vera.

Since Aloe vera is effective for repair of the intestinal barrier, it would directly address leaky gut (gastrointestinal hyperpermeability) which is a major factor in autoimmune disease. Gut repair is always one of the most important factors in healing Hashimoto’s disease. Taking Aloe vera every day for 9 months would significantly help repair any damage to the GI tract.

If some of these women were constipated, Aloe vera’s laxative effective could have potentially decreased excess estrogen levels by improving transit time. Constipation causes recirculation of estrogen and excess estrogen inhibits thyroid function and exacerbates autoimmunity in general.

We have no idea what the diet was like of each subject. Were they gluten-free or were they eating gluten? The study is out of Italy where substantial amounts of gluten are part of the diet. If they were eating gluten, these results are almost too good to be true because the aloe alone would have been able to almost completely negate the negative effects of gluten. There are many unknowns here about diet so it is hard to make any concrete conclusions.

Lastly, the authors fail to mention the infection connection to Hashimoto’s disease and the fact that Aloe vera is anti-viral against herpes viruses. Epstein-Barr virus and Herpes 6 are both significantly connected to Hashimoto’s disease and these viruses may have been suppressed by the Aloe vera. Some of the improvements we may have seen could be related to decreased viral activity.

Do you have to drink Aloe vera juice?

Aloe vera juice isn’t the most palatable option and it isn’t completely necessary. Capsules are another way to get the full benefits of Aloe vera which can be taken in a highly-concentrated form. I like the Aloe 200x by Designs for Health.

*Important Note*

I’m concerned about the use of Aloe vera in patients who are taking thyroid medication. These results indicate that the TSH decreased which may be pushed too low on a follow-up blood test creating confusion with your prescribing doctor. Additionally, if Free T4 increases then some patients may experience symptoms of hyperthyroidism because of the improvements in thyroid function in combination with the medication. This would require a delicate dance and monitoring of thyroid hormone levels on a regular basis if someone were to take Aloe vera.

This study shows some impressive and promising results for Aloe vera and Hashimoto’s disease but be sure you are working with your doctor and monitoring your thyroid hormone levels if you are on medication and decide to try Aloe vera for 9 months.

The ketogenic diet is currently sweeping the internet and the diet book world as the best thing since sliced bread for everything under the sun. Unfortunately, you can’t eat bread on the ketogenic diet and it really can be difficult to follow for some people.

Since I work with many patients who have Hashimoto’s disease and hypothyroidism, I wanted to investigate whether the ketogenic diet can cause hypothyroidism or decrease thyroid function. Let’s jump into the research and see what it has to say.

First let’s look at a study done on epileptic kids who followed a ketogenic diet since epilepsy was the first condition to be thoroughly studied and treated with a ketogenic diet. The first thing the authors point out is that we already know calorie restriction lowers T4 and T3 levels. The ketogenic diet mimics fasting so it makes sense that it could lower these thyroid hormone levels. They point out that the ketogenic diet is anti-inflammatory, anti-oxidative, and it balances neurotransmitters.

The authors state that the ketogenic has been documented to be helpful for the following conditions:

Polycystic ovarian syndrome (PCOS)

Migraine headaches

Autism

Depression

Diabetes mellitus type 2

Amyotrophic lateral sclerosis (ALS)

Alzheimer’s disease

Parkinson’s disease

Obesity

Glucose transporter protein-1 (GLUT-1) deficiency

Pyruvate dehydrogenase deficiency

In this study, 120 patients (63 male and 57 female) aged 4-10 were treated with a ketogenic diet for one year and their TSH, Free T4, and Free T3 levels were checked at 1, 3, 6, and 12 months. 20 patients (16.7%) in total developed hypothyroidism within the first 6 months which required thyroid medication. 70% of the 20 patients who developed hypothyroidism were girls as expected. Hypothyroidism was defined as a TSH level greater than 5.0 uIU/L with normal Free T4 levels.

TSH levels actually increased in everyone during the first month but dropped overall at 12 months follow-up. Free T3 levels however dropped significantly overall at 1, 3, 6, and 12 months.

The interesting thing is that the authors state that none of the kids who were diagnosed with hypothyroidism based on the TSH test developed any hypothyroid signs or symptoms. It’s also interesting to note that any kid who had been taking fish oil 6 months prior was excluded from the study since we know that fish oil improves thyroid function.

The authors point out the limitations of this study including lack of total T4 and total T3 levels as well as no testing for Hashimoto’s thyroiditis antibodies such as anti-thyroid peroxidase (TPO) and anti-thyroglobulin (TG) levels. Additionally, some of the kids were on anti-epiletic drugs which are known to disrupt thyroid function.

I don’t see how this study found anything conclusive if none of the kids developed any symptoms and hypothyroidism was based on a TSH >5.0 in growing children.

We already know that low-carbohydrate diets can work very well for fat loss such is the Volek study which had patients eat 8% carbs, 61% fat (calories from fat were 25% saturated fat, 25% monounsaturated fat, and 11% polyunsaturated fat), and 30% protein. Volek measured T4 levels which remained normal but didn’t look at T3 levels however but the subjects did extremely well with their weight loss. If thyroid function had decreased then it would have been difficult to lose weight.

We know that cutting calories and losing weight will decrease T3 levels. Not only that, we know that fasting increases reverse T3 which knocks out T3 receptors. The ketogenic diet suppresses appetite quite effectively so many people just aren’t eating enough calories on the diet which will affect thyroid hormone levels.

Why would T3 levels drop on a ketogenic diet?

Eating carbohydrates increases T3 levels because that extra T3 is required to burn glucose produced from the carbohydrates. This is why you feel warmer after eating a meal with a lot of carbohydrates. On a ketogenic diet, you don’t need as much T3 because you’re not spiking glucose levels from carbohydrates. This means that your body is more efficient at metabolizing glucose on a ketogenic diet so you don’t need higher T3 levels. It’s simply an adaptation that isn’t a bad thing as long as you’re eating enough calories.

Are low T3 levels actually a good thing?

The Leiden Longevity Study did show that lower T3 levels may be a good thing for living a long time compared to those with higher T3 levels. This is something that worries me when I work with patients who are taking T3 who haven’t investigated the potential underlying causes of lower T3 levels. About 15-20% of the population has a genetic difficulty converting T4 to T3 but the other 80-85% should be able to do fine with just T4. T3 is a powerful stimulator of metabolism so it can give the false sense of improved thyroid function when it’s really just artificially stimulating energy production. People who are taking T3 at high levels for a long period of time could potentially be shaving off some of the golden years.

The Leiden Longevity Study was then looked at again regarding thyroid hormone and longevity and this study confirmed what was found previously.

What’s the takeaway on the Ketogenic Diet and Hypothyroidism?

Decreasing calories and losing weight on a ketogenic diet are the causes of what may appear to be hypothyroidism. Since hypothyroidism and Hashimoto’s disease are complex and complicated conditions, we can’t make simple extrapolations about a single type of diet for everyone.

If you’re feeling colder, more fatigued, or having other hypothyroid issues on a ketogenic diet, first take a look at your caloric intake and make sure you’re eating enough calories. The ketogenic diet can really kill your appetitie so be careful.

Also, take a look at your fat sources. Studies have shown that polyunsatured fats from corn, soy, canola oil (rapeseed) and safflower oil inhibit thyroid function. In fact, these polyunsaturated oils were once proposed to treat hyperthyroidism.

Make sure your fats are coming from healthy polyunsaturated fat sources like fish oil, flax seeds, chia seeds etc. and balancing them with healthy monounsatured fats from avocado and olive oil as well as some saturated fat from butter or coconut.

Additionally, make sure you’re getting about 25-30% of your calories from protein. Protein has a thermic effect on metabolism so don’t go too high on fat and too low on protein.

One other thing to note is that the ketogenic diet is inherently low FODMAP. This is great for those who have SIBO (small intestinal bacterial overgrowth) but a low FODMAP diet can reduce the diversity of your gut microbiome which may not be a good thing for certain individuals who already have severe dysbiosis. You may want to eat some fermented foods like kim chi and sauerkraut as well has fiber-rich vegetables on the ketogenic diet to maintain healthy gut microlfora diversity.

I hope this allays any of your concerns about the ketogenic diet and thyroid function. Be sure you work with an experienced healthcare practitioner if you are going to try the ketogenic diet if you have a thyroid problem.

Did you know that the thyroid gland has the highest concentration of selenium compared to any organ in your body? Selenium is a powerful and essential trace mineral actually first discovered by the Swedish chemist Berzelius in 1817. Selenium mainly acts as an antioxidant, anti-inflammatory, and it is involved in the production and activation of thyroid hormone.

Selenium protects the thyroid from oxidative damage but a deficiency can lead to an increase in the weight of your thyroid which can be compounded by an iodine deficiency. When you’re deficient in selenium, you actually lose iodine more quickly so these two substances must work in perfect balance.

This is an interesting adaptation your body has developed because your thyroid has the potential to be damaged when you are deficient in selenium but you have normal iodine levels. Iodine ensures normal thyroid hormone production but the protective effects of selenium may not be there to clean up free radicals produced during hormone synthesis.

It has been found that supplementing with selenium if you are deficient in iodine can actually suppress thyroid function. This is why it may be important to have your iodine status checked before supplementing with selenium so we can figure out the best plan forward.

The catch is that supplementing with iodine can increase damage to the thyroid gland in patients with Hashimoto’s disease. This is why you should work with an experienced healthcare practitioner to help figure out the right balance for you.

Selenium acts as a “thyroid antioxidant” and is vital for the production of thyroid hormone and it is involved in the conversion of T4 (least active thyroid hormone) to T3 (most active form). One clear pattern on you thyroid labs that can indicate selenium deficiency is a high or high/normal Free T4 but low or low/normal Free T3 with a normal TSH. This indicates that your T4 isn’t converting well to T3 possibly due to a selenium deficiency.

Selenium protects the thyroid gland from the damaging effects of thyroid peroxidase (TPO-Ab) and anti-thyroglobulin (Tg-Ab) antibodies. Selenium also can protect the thyroid by binding to mercury and making it completely inert. Mercury is a major thyroid disrupting chemical but not as significant when selenium is present.

Selenium and iodine are intricately intertwined in the thyroid gland. They are both necessary for thyroid hormone production, but when iodine-deficient subjects were given selenium alone, it made their hypothyroidism much worse. Since iodine deficiency is very rare in industrialized nations, this is usually not something to be concerned about.

Can selenium help Hashimoto’s disease?

Three separate studies have shown that selenium supplementation suppress TPO-Ab and Tg-Ab levels.

A recent study by Wichman et al. Showed that selenium supplementation reduces TPO-Ab levels at 3, 6, and 12 months and Tg-Ab levels at 12 months. This was only in those treated with levothyroxine (T4), not in those who did not take thyroid hormone. This study also found that antibody levels only decreased in those taking selenomethionine but not in those taking sodium selenite. This is because selenomethionine is absorbed much better than sodium selenite.

Selenium has been found to be highly effective in patients with Hashimoto's thyroid disease. Multiple studies have shown that selenium supplementation significantly reduced thyroid antibodies which are an indicator of thyroid autoimmunity. In fact, the higher the antibody levels were at the beginning of the studies, the greater the positive effects from selenium. It was also found that selenium improved the overall sense of well-being in these individuals.

One study out of Greece found that supplementing with selenium for 12 months lowered TPO-Ab levels but once the patients stoppped taking the selenium, their antibody levels rose 4.8% after 6 months.

Another study out of Italy found the same positive TPO-Ab lowering effects after patients supplemented with selenium for 12 months.

Another recent study out of China found that areas of low selenium intake has much higher rates of thyroid autoimmunity compared to areas of China with higher intake of selenium suggesting a protective effect from autoimmune thyroiditis.

Many women develop Hashimoto's thyroiditis after they give birth. The effects of selenium supplementation were studied in pregnant women and after they gave birth. The results showed that the women who supplemented with selenium had much lower antibody levels and their thyroid glands were also protected as they did not change in size compared to the women who didn't supplement.

Selenium and the Epstein-Barr Virus

Selenium has also been shown to inhibit expression of the Esptein-Barr Virus which is a virus linked to Hashimoto's and other autoimmune diseases.  Selenium is also effective against other herpes viruses such as Herpes 6 which is also connected to Hashimoto's disease.

What is considered optimal selenium intake from food?

The current recommended dietary intake of selenium from food is 55-75 mcg/day.

What foods contain selenium?

Selenium is found mainly in high-protein foods such as:

-Meat (pork, beef, lamb, turkey, chicken)

-Tuna

-Shellfish (oysters)

-Eggs

-Brazil nuts (not recommended)

-Whole-wheat bread

-Sunflower seeds

-Mushrooms

-Rye

Be careful with whole-wheat bread and rye if you have Hashimoto’s disease because the gluten found in these grains can potentially make your Hashimoto’s much worse.

The content of selenium in foods is dependent on the soil concentration of selenium which is very low in some areas.

Which form of selenium is best and how much is a safe dose?

Sodium selenate and selenite are the most popular forms of selenium but only about 50% is absorbed. In addition, these forms of selenium increase the risk of selenium toxicity. Selenomethionine is the preferred form of selenium supplementation as it is the form found naturally in food and about 90% of it is absorbed. 200 micrograms each day is a safe dose as long as it is in the form of selenomethionine.

Can selenium be toxic?

Consumption of approximately 330 mcg/day of selenium could potentially be toxic but a safe range is 50-400 mcg/day. 850-900 mcg of selenium a day has been documented to be considered a minimum of developing selenium toxicity but I definitely would never recommend doses this high. 200mcg a day as noted above is a reasonably safe dose and it is also the dose used in the above studies on Hashmoto’s disease.

Side effects of toxicity can include:

Hair loss

Hypothyroidism

Lowered growth hormone

Depression

Diarrhea

Anorexia

Blindness

Ataxia

Respiratory disturbances

Liver and kidney damage

Hemorrhage

Nail loss

Dermatitis

Central nervous system disorders

Insulin resistance leading to diabetes

You can see that some of the symptoms from toxicity are actually the symptoms of hypothyroidism.

Why don’t you recommend Brazil nuts?

Brazil nuts can contain anywhere from .2 mcg to 253 mcg of selenium, depending on where they come from. Just imagine if you were eating 3 Brazil nuts a day from a source that was on the higher end of this range. You could easily begin to develop selenium toxicity and we would also have to factor in all the selenium you are getting from the rest of the food you are eating and any supplements such as a multivitamin. If you’re going to consume Brazil nuts, don’t take any selenium supplements and it would be wise to eat them in extreme moderation such as once a week or even once a month.

How do I put all this information together for practical use?

If you have Hashimoto’s disease then it is reasonable to supplement with selenomethionine under doctor supervision if your whole blood selenium test indicates you are deficient. But you must take into account any selenium content in other supplements you are taking as well as selenium from food to be sure you don’t go above the safe range.

Additionally, you must be certain that your iodine intake is adequate from food and a small amount from supplements so as not to further suppress your thyroid function. Since you shouldn’t supplement with large doses of iodine if you have Hashimoto’s thyroiditis, then the reasonable approach is to take a multivitamin which has about 150mcg of iodine to begin restoring any iodine deficiencies while not exacerbating your Hashimoto’s disease. Sometimes, I’ll just have patients take the multivitamin that contains some iodine and some selenomethionine so we have both bases covered.

This is definitely not something you would want to do on your own without doctor supervision so be sure to work with an experienced healthcare practitioner who can perform the proper testing needed to figure out your unique health balance.

Does a low-carbohydrate diet work best for Hashimoto’s disease? There are a number of diets out there claiming to be the best for Hashimoto’s thyroiditis but as with any condition, there is no single best diet for everyone. A recent paper entitled, “Effects of low-carbohydrate diet therapy in overweight subjects with autoimmune thyroiditis: possible synergism with ChREBP” looked at how effective a low-carbohydrate diet can be for Hashimoto’s disease. Let’s dig into what the researchers found.

180 patients with Hashimoto’s thyroiditis were enrolled in the study with a composition of 84 males and 96 females aged 30-45. All patients had blood tests done for TSH, Free T4, Free T3, anti-thyroid peroxidase (TPO) antibodies, anti-microsomal antibodies, and anti-thyroglobulin antibodies.

Body composition was also determined by body impedance analysis (BIA) which measures bodyfat percentage, total body water, and fat-free mass. Those of you who are patients of mine know we check this in the office with a scale that works through bioempedance and I also recommend a home scale to all virtual patients to do these measurements at home.

108 patients (control group) were put on a diet consisting of:

12%-15% carbohydrates

50%-60% protein

25%-30% fat

Foods consistend of leafy greens and “other types of vegetables” that were not considered to be goitrogenic. Goitrogenic foods can inhibit iodine utilization by the thyroid gland which can lead to goiter and thyroid imbalances. The authors do correctly note that cooking goitrogenic foods completely eliminates any goitrogenic effects they may have.

This control group was also instructed to avoid legumes, dairy products, bread, pasta, eggs, fruits, and rice. They were instructed to eat only lean white and red meats.

They followed this diet for only 3 weeks and then had bioimpedance testing done as well as all the original thyroid antibody and thyroid hormone tests.

The other group of 72 patients followed a simple low-calorie diet without any food restrictions. These patients were also retested after just 3 weeks with the exact same tests.

What did the study results show?

There were no statistically significant changes in TSH, Free T4, and Free T3 in either group after 3 weeks.

The group that ate the low-calorie diet but with no food restrictions only showed statistically significant changes in body weight, lean mass, and body mass index (BMI). We would expect this in virtually anyone eating fewer calories for 3 weeks. You’ll notice that they lost muscle mass which isn’t good and this is the main problem with dieting because losing muscle is not healthy.

This group also showed a statistically significant increase in thyroid antibody levels including anti-thyroglobulin and anti-microsomal antibodies but not TPO antibodies.

In contrast, the group that followed the restricted diet showed a significant decrease in all three thyroid antibody levels. This group also lost bodyfat, total body weight, and there was a reduction in BMI.

Goitrogenic intake of food in each group was taken into account but the authors did not state how these foods were prepared or the quantity consumed.

The authors conclude that this type of diet is anti-inflammatory in nature so it can help autoimmune thyroiditis which includes inflammation of the thyroid gland. They also note the effect on thyroid hormone receptors, more specifically the alpha receptor which is found in the liver and white adipose tissue involved in fat-burning in these regions of the body. This type of diet can affect gene expression in these areas in a positive way leading to more fat-burning.

The authors also briefly note the affect of thyroid disrupting chemicals on thyroid function which I...

One of the most common questions I get is, “What are optimal Hashimoto’s thyroiditis antibody levels?” For years, many patients and clinicians have been chasing thyroid peroxidase (TPO) and anti-thyroglobulin (TG) antibody levels in an attempt to get them as low as possible or even undectable as a measure of success.  This can leave many people frustrated and stressed about their condition.  Some individuals feel that these levels should become undetectable in order to consider the condition in complete remission.  But is this entirely true or necessary?

A recent study out of Germany has helped us get a clearer picture of how we should be looking at thyroid antibody levels.  The study is entitled, “Anti-thyroperoxidase antibody levels >500 IU/ml indicate a moderately increased risk of developing hypothyroidism in autoimmune thyroiditis” published in the journal Hormone Metabolism Research.

The authors were specifically looking at thyroid peroxidase and anti-thyroglobulin antibody levels and if they are associated with developing hypothyroidism.  Here is a breakdown of what the authors found:

Patients with TPO antibody levels >500 did show an increased risk of developing hypothyroidism.

Patients with TPO antibody levels <500 did not show an increased risk of developing hypothyroidism.

Patients with anti-thyroglobulin and thyroid peroxidase antibody levels <500 did not show an increased risk of developing hypothyroidism.

Anti-thyroglobulin antibody levels at any level did not show an increased risk of developing hypothyroidism.

Even those who did have elevated TSH after years of follow-up were still considered euthyroid which means they had normal functioning thyroid glands.

They did follow the patients for an average of 6 years which is a fair amount of time to make a good conclusion about how antibody levels potentially cause hypothyroidism.  Hypothyroidism was defined as a TSH >4.6. Free T4 levels weren’t statistically important in any group because they didn’t vary enough to be of concern.

Over the last 15 years, I have found that these study results hold true and that patients are usually feeling great once their antibody levels are below 500.  Some will remain in the 50-400 range no matter how well the patient eats, manages stress, improves gut function, and no matter how targeted their supplement plan is put together.

I have always followed the advice of “Treat the patient, not the labs” so when a patient is feeling great I have always discontinued focusing on these numbers.  Everyone is so unique after all that we can’t completely go by numbers and ranges on laboratory tests.  I do love testing because it almost always reveals deficiencies and imbalances that can be difficult to identify simply by talking to someone.  However, once we get deep into treatment and a patient gets well, these numbers become less and less important.

What is the takeaway?

One potential flaw in the study is the fact that hypothyroidism was defined as a TSH >4.6.  There are some clinicians who believe that the range for TSH is far to broad and that TSH should be within a tighter window such as 1.5, 2.0, or 2.5 as the upper cut-off point.  There is little evidence to support this claim for every single human being who has Hashimoto’s or hypothyroidism.

Sure, some people just feel better with a TSH that is in these lower ranges but some people also feel great with higher TSH levels.  As with everything in functional medicine, this is an individualized question which shouldn’t be set in stone.

Additionally, as pointed out above, the patients who did have TSH levels above 4.6 after the 6 year follow-up had normal thyroid function despite the higher TSH levels.

Once we’ve dealt with the most significant causes of Hashimoto’s thyroiditis including gut health, infections such as Epstein-Barr Virus, food sensitivities like vitamin D deficiency, gluten, selenium deficiency, stress, and childhood adversity, you can be confident that your immune system will continue to heal and stay in balance.

We already have enough stress in our modern day lives so this is one less thing to be worried about.  If your thyroid antibody numbers are below 500 then you’ve probably done a great job with your healing plan and you can let go of focusing on your Hashimoto’s thyroiditis antibody levels.  This includes discontinuing supplements that target autoimmunity and bringing back some variety into your diet.

In this episode of The Dr. Hedberg Show, I interview Gary Stapleton of Aerodiagnostics Laboratory answering the question, "What is the best SIBO test?"  We covered a lot of ground about the ins and outs of SIBO breath testing including the best methodology, glucose vs. lactulose, how to properly perform the test, proper test interpretation, hydrogen sulfide, when to retest and much more.

Gary is the founder of Aerodiagnostics Laboratory which I personally use in my practice and highly recommend to everyone who wants the most accurate SIBO test on the market today.  Combine that with the best customer service and support and it's a no-brainer to use them for your SIBO testing.

Below is a transcript of the entire interview with important links at the end:

Dr. Hedberg: Okay. Well, welcome, everyone. This is Dr. Hedberg and welcome to "The Dr. Hedberg Show." I'm excited today to be talking to Gary Stapleton. And Gary is the founder of Aerodiagnostics Laboratory. And this is the laboratory that I use for small intestinal bacterial overgrowth testing. Their lab offers non-invasive hydrogen and methane breath testing. It's the lab I've been using to test for SIBO because the quality is really unparalleled in the SIBO world and I've been very, very pleased with the quality of the results I've been getting and the customer service. So we're going to be talking about some really interesting items today about SIBO and SIBO testing. So, Gary, welcome to the program.

Gary: Oh, thank you, Dr. Hedberg. I really appreciate joining today and I look forward to discussing SIBO and breath testing, hydrogen and methane breath testing with the audience.

Dr. Hedberg: Excellent. Yeah, it's good to have an expert like you here because this is really a hot topic. I mean, the prevalence of SIBO is continuing to grow and we're seeing it more and more. And then, of course, our IBS population really struggles with SIBO, for the most part. So why don't you start by just talking to us about hydrogen and methane breath testing and how it works in the diagnosis of SIBO?

Gary: Yes, so thank you. And please feel free to interject if there's something that I've said or am in the process of saying that might be beneficial as well. So hydrogen and methane gas, for those listening that aren't aware, are not produced by the body. Hydrogen and methane gases are produced by bacteria that is fermenting. So the way that the test works and why it's so incredibly important to prepare correctly, to use the right devices correctly and to administer and ensure that your devices are operating correctly, to ensure that we're measuring hydrogen and methane gas appropriately, it all begins with the preparation. And then, if you prepare correctly, which means you're moving food from the GI tract, there...even if there's bacteria, there's no gas being produced because the bacteria, if it's there, needs to be fed to ferment and to produce this gas.

So if you have bacteria in your small intestine and you're not supposed to have bacteria in your small intestine, I believe it should be less than 103 colony-forming units in the small intestine. If there's bacteria there and you've prepped, which means you've removed all food, your baseline breath sample should be relatively low to no gas because, again, the bacteria's there, it's not being fed.

Now, after that baseline sample, you ingest either glucose or lactulose as a substrate that has been validated to ensure appropriate measurement of gas levels inhalation of small intestinal bacterial overgrowth. When you ingest either that glucose or lactulose, that is a food source. And that food source will now feed bacteria, if it is there. That bacteria will ferment or rot and the gas that's produced, either hydrogen or methane, will diffuse through the blood and exit via the lung air.

I'll deflect for just a moment and say everyone is aware that there's a third gas. It's called hydrogen sulfite gas. And in our experience, and I know that some of the SIBO thought leaders and some of the very good clinicians that are treating SIBO today may suggest that there's a higher prevalence of hydrogen sulfide, there's not a lot of data on that and we'll talk about that. But I will tell you we've run nearly 20,000 breath tests and by the definition of utilizing a lactulose breath test and having a flat line, we're only seeing hydrogen sulfide suspicion 1 to 2%. So it doesn't really occur that often, from our perspective.

So back to how does the test work. So if you've now prepped correctly and then you've taken a breath sample and then you ingest either the lactulose or glucose, now that lactulose and/or glucose is traveling through the small intestine. And when it meets up with bacteria, it will ferment and leak gas into the blood that exits via the lung air. We capture that and then it's tested in the lab. If it happens between zero minutes...and again, this is another of points that we will probably get into later, but the way that the test...the gold standard interpretation has been if you have a rise of gases between 0 minutes and 120 minutes, that would be a positive indication that there is bacterial overgrowth.

There are some newer data and some newer perspectives that look only at 90 minutes. And, from a laboratory perspective, it's accurate data. We want to provide you, the clinician, with accurate data. If you'd like to interpret these looking only at 0 minutes to 90, you can do that. You can look at 0 to 120 and challenge the more distance, which is what we recommend, considering then we can do that. And, again, we'll talk about that a little later.

If your choice is lactulose, then that lactulose will pass into the large intestine. And because there is bacteria, and should be, typically, you have elevated levels of hydrogen and/or methane gas when it gets into the colon. With glucose, it is absorbed and you still get some gas levels. But not necessarily elevated through the last three test tubes. Okay? So this is how the hydrogen and methane breath test actually works.

What I like about this test, with the total accuracy by the studies that were involved with it, over 90%, but what I like about it is that it's binary. If you have hydrogen and/or methane gas within that first 120 minutes or 90 minutes, that is evidence that there are bacteria producing gas. It's the only way if the patient prepared correctly. The only way you would get that gas. As I mentioned earlier, the body doesn't produce the gas. So that's the way we do that. So I'll pause there, Dr. Hedberg, and see if that answers the question.

Dr. Hedberg: Yes, yes. That's a great overview. And one of the ways I explain it to patients is just like you're putting gasoline into a car and the engine burns the gasoline and then the gas comes out. And the bacteria are basically the engine burning that fuel that you put in. And it could be either glucose or lactulose, like you said. So can you talk just a little bit about your specific methodology? Because not all labs are equal in this. And I learned that early on. So how do you ensure the data you're seeing is accurate?

Gary: Well, thank you for that question. I will tell you this is why I founded the laboratory a few years back. I think it's three and a half years ago. My wife, who is a physician, has owned and operated her own diagnostic laboratory in the pathology world. I've either owned or operated or have run large diagnostic laboratories during my career. My wife was suffering from SIBO and, of course, like many of your patients, was asked to take a breath test.

So we live in Boston and the first test was asked to go to a very well known hospital in Boston. We'll refrain from saying the exact one, but I assure you, it's a very good one. And the first process was that she had to call to organize when they would go there and have the breath collected. So there was a lot of back and forth. It was very inconvenient. And, finally, it was settled that it was going to be on a Wednesday, in Boston at 1:00 in the afternoon.

Well, as everyone knows, you have to prep for this, which includes 24 hours of a limited diet. Well, 12 hours of a limited diet and 12 hours of a fast. Clearly, you don't want to be fasting all morning. Typically, you fast overnight. So it's inconvenient for the patient there. Then, when we got there, it was to go down in the basement. And now you're in the basement for three hours with upwards of 20 other people having breath collected. No internet, no phone. For people, this is very inconvenient for obvious reasons.

And then, when the test was over, the collections were actually done, you would have . . . first of all, the prep information was not consistent with how the test was actually validated. So that led to some inaccuracies. But then, the clinician or the technicians that were collecting the breath, you could tell that they were trained by someone else, not by the equipment manufacturers or anyone directly. Almost like whispered down the lane. So things have changed and they didn't really know how to work with the devices and different things. So we were suspect from the very beginning. Needless to say, it was an inconvenient process and it wasn't that good.

So the next one was we received a kit at home because we weren't going to try again. And it was obvious that the kit was a homemade kit. The most important thing, and this goes to the question, how do you ensure accurate results, the most important thing is that you have very direct and personal involvement with that patient to help them with the prep questions. The prep is very specific.

Now, any clinician can change this, but the test has been validated on the preparation, meaning that the first 12 hours, you eat from a limited list of foods. They are very straight, very direct: chicken, fish, eggs, white rice, white bread, white potatoes. Now,...

Sometimes very simple tests provide a significant amount of valuable information when it comes to Hashimoto’s thyroiditis. One simple blood test is the red blood cell distribution width or RDW test which is included in the complete blood count (CBC). A recent study found that patients with Hashimoto’s thyroiditis have higher levels of RDW.

What is RDW?

RDW is basically a measure of the variability in size of your red blood cells. The greater the variability in size, the higher the RDW test results. Anemia is usually the cause of elevations in RDW but chronic inflammation can also cause it to elevate. Disorders such as rheumatoid arthritis, inflammatory bowel disease, high blood pressure, and Hashimoto’s thyroiditis can increase RDW. So we can confidently use RDW as a sign of inflammation along with other helpful inflammatory blood markers such as c-reactive protein, fibrinogen, erythrocyte sedimentation rate, D-dimer, and homocysteine.

What did the study show?

165 patients were included in the study with 102 of them having confirmed Hashimoto’s thyroiditis and 63 were in the healthy control group. The mean age of the participants was not statistically significant. 85 of the 102 patients with Hashimoto’s thyroiditis were women and 55 of the 63 participants in the healthy control group were women. This is no surprise since women have much higher rates of Hashimoto’s thyroiditis than men.

The complete blood count (CBC) markers were not significantly different between the groups.

Free T4 levels were significantly lower in the Hashimoto’s thyroiditis group compared to the control group. TSH levels were higher in the study group compared to the control group. We expect this since TSH levels increase in Hashimoto’s disease and Free T4 levels usually decrease.

Previous studies have shown a direct connection between lower T4 levels and increased RDW such as in this paper by Brenner et al.

Interestingly, Free T3 levels were not significantly different between the groups.

RDW levels were significantly increased in the study group compared to the healthy control group.

The main conclusion of the study was that RDW levels are increased in those with Hashimoto’s thyroiditis compared to healthy controls.

The authors point out some interesting additional findings that connect RDW to thyroid disorders. A previous paper found that elevated TSH levels are connected to elevated RDW levels entitled, “The red blood cell distribution width is associated with serum levels of thyroid stimulating hormone in the general population.”

And an additional paper found that RDW levels are higher in those with hypothyroidism.

Why does RDW increase in Hashimoto’s thyroiditis?

Since Hashimoto’s thyroiditis is a chronic inflammatory process, based on this paper and previous research, RDW increases in conditions that result in inflammation. RDW should also be assessed along with other inflammatory markers when dealing with Hashimoto’s thyroiditis.

We also know that thyroid hormone has direct effects on RDW such as in this paper it was found that RDW levels increase in hypothyroidism and hyperthyroidism.

What about Selenium?

We can actually use the RDW test to decide if we want to use selenium supplementation or not in Hashimoto’s thyroiditis. This study showed the RDW can be intimately tied to selenium status so it could be a good indicator to supplement with selenium. We already know that selenium can be very beneficial in those with Hashimoto’s thyroiditis.

I always test every patient’s blood and we look at the complete blood count which includes the RDW so we can make the best decision about what direction to go. I recommend combining it with other inflammatory markers as noted above for the best clinical picture.

Don’t forget to have a CBC done periodically if you have Hashimoto’s thyroiditis to see how your RDW is doing because it may be a key indicator of your thyroid health.

In this episode of The Dr. Hedberg Show, I interviewed Dr. David Brady about the new GI-MAP stool test by Diagnostic Solutions Laboratory.  We discussed many topics including autoimmune disease, stool testing, stealth infections, gut infections, the gut microbiome and much more.  This is the stool test I use in my practice to identify bacterial dysbiosis, viruses, parasites, yeast, and overall digestive health.

Nikolas: Well, welcome everyone. This is Dr. Hedberg. And welcome to The Dr. Hedberg Show. I'm excited today to have a long-time friend and colleague on the show, Dr. David Brady. We're gonna be talking about the GI-MAP stool test and autoimmunity. And for those of you who don't know Dr. Brady, he has 26 years of experience as an Integrative Medicine Practitioner and over 22 years in Health Sciences academia. He's a Licensed Naturopath in the State of Connecticut and also Vermont. He's board-certified in Functional Medicine and Clinical Nutrition. And he completed his initial clinical training as a Doctor of Chiropractic in 1991. He's currently the Vice President for Health Sciences, Director of the Human Nutrition Institute, and Associate Professor of Clinical Sciences at the University of Bridgeport in Connecticut.

He has a private practice called Whole Body Medicine in Fairfield, Connecticut. Dr. Brady is also an expert consultant to the professional nutraceutical and nutritional supplement and clinical medical laboratory industries. He serves as the Chief Medical Officer for Designs for Health and Diagnostic Solutions Labs. He's also an internationally sought-after presenter on nutritional, functional, and integrative medicine. He's appeared on the speaking panel of some of the largest and most prestigious conferences, this includes IFM, ACAM, A4M, IHS, AANP, and many more. And we're gonna talk about some of his papers today. So welcome to the show, Dr. Brady.

David Brady: Hey, thanks, Dr. Hedberg, great to be on your show. We go back a long way in this journey together in functional medicine and we have amazingly similar paths, although you're fortunate enough to have gone through it a little later than me which means, you're younger.

Nikolas: Right, right. Younger but...

David: Younger but we're pretty similar, so.

Nikolas: Younger but not smarter. So that's why I have you on the show.

David: Oh, I don't know about that.

Nikolas: So let's jump into autoimmunity and you've emphasized this topic a lot in some of your papers, and in a lot of your lectures, and you also work with a lot of autoimmune patients in your practice. So what do you think it was that developed your interest in autoimmunity?

David: Oh, I don't know sheer desperation, probably like yourself, you know? Just seeing so much of this stuff come in on practices over the years, and it's just grown, and grown. And, you know, even in my couple of decades in practice, I certainly see it as being so much more prevalent as a presenting concern with patients than I did back in the beginning. And what we've seen emerging in the literature in parallel to that has really made autoimmunity one of these...well not a disorder but sort of a constellation of disorders that have a similar underlying etiology.

It's really a group of disorders that is really just innately attached to the functional medicine approach, right? Because of the emphasis in functional medicine on the importance of the health of the gastrointestinal system, gut ecology. And now, we would talk about it in more detail is the microbiota and the microbiome, and certainly an appreciation of the role of toxins and things like that, just make it a natural that patients would turn to providers like us if they had an option.

And they become aware of other types of approaches and certainly with the internet coming, you know, blowing up during that same amount of time, people have access to information now including so much good information, like what you produce that makes patients realize that they have more options than Methotrexate, and Humira, and that kind of stuff. So I think we see so much of it, it's hard as a functional medicine integrative medicine practitioner, no matter what your core training, to not have to get up to speed on autoimmunity pretty darn quickly because you see it all day long.

Nikolas: Exactly. Like you said, there aren't a lot of answers from the conventional medical side other than a series of drugs, which, of course, some people need sometimes but we can do a lot as functional medicine practitioners. So this paper you published that was in the Open Journal of Rheumatology and Autoimmunity in 2013 and the title is, "Molecular Mimicry, the Hygiene Hypothesis, Stealth Infections and Other Examples of Disconnect between Medical Research and the Practice of Clinical Medicine in Autoimmune Disease."

David: Yeah. That's quite a title, huh?

Nikolas: Right, right. So why did this paper, why was it so well-received by so many in the functional medicine field?

David: Oh, it's interesting. I'm glad it was. I still get a lot of people coming up to me at speaking events, and conferences, and so forth bringing up that paper. And I've had quite a few actually faculty at different institutions be it, you know, naturopathic medical programs, nutrition programs, and so forth, saying that they used the paper in their teaching and which is a great honor to hear that. But I think the reason it probably struck a chord, for the people who have been exposed to it or have seen it is because what my intention was when I wrote it was really to pick out some of these really interesting connections and things that are in the medical research and literature [inaudible 00:06:18], such as molecular mimicry and actually, you know, looking at novel concepts of etiologies for specific autoimmune diseases based on the phenomena of molecular mimicry.

And then, in parallel to that research on the hygiene hypothesis, right, the whole idea that we're too clean now and our immune systems don't really get to adequately sample a diverse environment of potentially antigenic material while our immune system is maturing, and learning to deal with its world. And then just some other disparate types of really interesting research as it pertains to autoimmunity and how all of that information seems to be lost on the conventional practitioners who are dealing with autoimmune disease such as rheumatologists, for the most part. They really don't seem to in their very orthodox standard of practice paradigm and standards of care pay much attention to all this great research that's going on out there.

You know? How many times does a rheumatologist do a stool analysis to assess the microbiota and see if there's overgrowth of any of these organisms that the research has clearly said are often tied to a much higher incidence of the disorder. And now, beyond just association, we have actual causal data on some of these things, but they never even look there. There's been no real effort to educate people in from public health types of folks on getting young people more adequately sampling their environments so that they have a healthy immune system when they grow up.

And we have more and more atopic disease. We have kids, you can't walk through an elementary school without young kids, without every classroom has some sort of sign on it, "Food allergy this," or some sort of significant immune dysfunction that's even posted on the darn doorways. So there's clearly something major going on. It doesn't seem to be being addressed by the clinicians but yet the researchers are all over it. And I found that that was an interesting disconnect like a chasm between the researchers in Western medicine, which I think are really doing a great job when it comes to immune dysfunction and then the practice of clinical medicine, which I think is doing not a great job.

Like you said there's regimens of drugs from various anti-inflammatories to Methotrexate to response modifiers and strong immunosuppressants and certainly, those drugs have their role in the properly selected patient but it's usually when the patient is far down the line and they're actually having arrays of joint destruction or they have some other serious tissue damage going on and degenerative neurological conditions or what have you. And then, it's just basically putting the band-aid over it, and helping them out certainly symptomatically.

But what was going on in the research, I found, had the opportunity to open up a whole new approach, right, to these kind of disorders and actually climb very upstream and try to find patients, even before they have these disorders, and risk assess them for potentially getting the disorder downstream and making some significant changes in their lifestyle, and their dietary intake, and their GI health that might actually truly prevent them from getting the disorder.

So it's almost a golden opportunity for preventive medicine in its actual true form rather than the lip service that many providers both conventional and complementary painted to the whole idea of preventive medicine. And then, when you look at what they're doing, they're doing very little in the way of actual prevention.

Nikolas: Exactly. Yeah, it's interesting, you know, you bring up stealth infections in your paper, that's probably one of the most common questions I get from practitioners. And it's just interesting because, like you said, there is so much literature out there on stealth infections and autoimmunity but there aren't really any conventional interventions being developed for those, at least not that I'm aware of. But it's interesting because a lot of those drugs are immunosuppressive and...

David: Right, and counterintuitive, right?

Nikolas: Yeah. And if they have, you know, like an Epstein-Barr or a tick-borne infection or anything like that then they're just kind of goi