It is now clear that not only do these conditions share the same underlying causes – and thus require the same treatment – they are 100% preventable and, in many cases, entirely reversible.

Because of these similarities, Dr. Francine Kaufman coined the term diabesity (diabesity + obesity) to describe them. Diabesity can be defined as a metabolic dysfunction that ranges from mild blood sugar imbalances to full-fledged type 2 diabetes. Diabesity is a constellation of signs that includes:

• abdominal obesity (i.e. “spare tire” syndrome);
• dyslipidemia (low HDL, high LDL and high triglycerides);
• high blood pressure;
• high blood sugar (fasting above 100 mg/dL, Hb1Ac above 5.5);
• systemic inflammation; and,
• a tendency to form blood clots.

The subjective symptoms of diabesity include (but aren’t limited to):

• sugar cravings, especially after meals;
• eating sweets does not relieve cravings for sugar;
• fatigue after meals;
• frequent urination;
• increased thirst and appetite;
• difficulty losing weight;
• slowed stomach emptying;
• sexual dysfunction;
• visual problems; and,
• numbness and tingling in the extremities.

The term diabesity is misleading in one respect: it suggests one must be obese to experience the metabolic problems I just described above. That’s not true. Thin people can suffer from the entire spectrum of blood sugar imbalances, all the way up to full-fledged type 2 diabetes. The term sometimes used for someone who is thin, yet has insulin resistance, dysglycemia and dyslipidemia is “metabolically obese”. Their metabolism behaves as if they’re obese, even when they’re not.

It’s almost impossible to overstate how serious and far-reaching a problem diabesity is. It affects more than one billion people worldwide (1), including 100 million Americans and 50% of Americans over 65.

More than half of Americans are overweight, and a full one-third are clinically obese. 24 million Americans have type 2 diabetes, with one in three unaware that they have it. (2)

Diabesity is the leading cause of modern, chronic disease. The “diabese” have increased risk of heart disease, stroke, dementia, cancer, kidney failure and blindness – to name only a few.

In the U.S. today, every ten seconds someone dies from diabetes-related causes. (3) Diabetes and cardiovascular disease have now outpaced infectious disease as the primary cause of morbidity and mortality worldwide. In Dr. Bernstein’s Diabetes Solution, Dr. B claims that diabetes is now the 3rd leading cause of death. But death certificates don’t list diabetes or hyperglycemia as the underlying cause of heart attacks, strokes or fatal infections. Nor do they consider the role of obesity, insulin resistance and inflammation in these conditions. If they did, it’s quite possible that diabesity is not only the leading cause of disease, but also the leading cause of death.

Diabesity is literally bankrupting our health care system. The direct and indirect costs of type 2 diabetes were $174 billion in 2007. The cost of obesity in that same year was $113 billion. So the total cost of diabesity to society can be conservatively estimated at nearly $300 billion per year. (4) To put that in perspective, diabesity has cost the U.S. $3 trillion over the past decade. That’s three times the estimated cost of fixing our entire health care system. And it’s only going to get worse. the projected cost of diabetes alone is expected to rise to more than $330 billion by 2034. (5)

With numbers like this, you’d expect a state of emergency to be declared. You’d think we’d be doing everything in our power to figure out the cause of these conditions and how to treat them successfully.

But the reality is that the conventional treatment of diabesity has been a dismal failure. This is reflected in the shocking growth of the conditions that fall under the diabesity umbrella over the past two decades, and the equally alarming projections for the future.

Recent reports suggest that one-third of people born in 2010 will develop diabetes at some point in their lives. (6) What is particularly horrifying about this statistic is that many of those who develop diabetes will be kids. Type 2 diabetes used to be a disease of the middle-aged and elderly. No longer. A recent Yale study indicated that nearly one in four kids between the ages of 4 and 18 have pre-diabetes (glucose intolerance). Some regional studies show type 2 diabetes in kids has jumped from less than 5% before 1994 to 50% in 2004. (7)

Each year, kids are getting fatter. Among American children 2-5 years of age, more than 10% are now obese. (8) Even more alarming is the rise of obesity in infants under 2 years of age. Research from Harvard shows infant obesity has risen more than 70% since 1980. (8) And this isn’t because babies are eating more donuts and cheese doodles while cutting back on their Stairmaster workouts, either. Clearly there’s more to the diabesity story than eating junk food and not exercising enough. But I digress. We’ll be covering causes in future articles.

From 1993 to 2008, the number of people in the world with diabetes increased seven-fold from 35 million to 240 million, and is expected to rise to 380 million by 2030. This is ten times the number of people affected by HIV/AIDS worldwide. In the U.S., the incidence of diabetes is projected to increase to 44 million in the year 2034. (9)

What accounts for such an explosion of new cases? One reason is that the standard treatment for diabesity is not only ineffective, it’s contributing to the problem. Once they have developed, diabetes and obesity are characterized by insulin resistance, which in turn results in carbohydrate intolerance. Yet prominent organizations such as the American Diabetes Association have been recommending a low-fat, high-carbohydrate diet as a treatment for diabetes for decades. It didn’t work in 1985, and it still doesn’t work. Einstein once said that insanity is doing the same thing over and over, and expecting a different result. Clearly the conventional approach to treating diabesity is insane.

In this series, we’re going to get the bottom of the diabesity epidemic. We’ll leave the conventional model of understanding diabesity – which is now about 40 years old – in the dust and replace it with an updated 2010 model that reflects the current scientific literature. We’re going to uncover the real causes of of diabesity, and we’re going to find out exactly how it can be prevented and even reversed in the majority of cases.

As we go along we’ll be busting a number of conventional and alternative myths about diabesity. We’ll learn that:

• Obesity isn’t as simple as eating too much and not exercising enough.
• Diabetes isn’t always progressive, and can be reversed in many people.
• Diabetes isn’t caused by eating too many carbohydrates.
• A fasting blood sugar of 95 mg/dL and Hb1Ac of 5.5% isn’t “normal”.
• Thin people can get type 2 diabetes.
• And more…

As we begin, I’d love to hear from you. Do you have any specific questions about diabesity? Anything you’ve always wondered about but haven’t found the answer to? Leave a comment, and I’ll do my best to address it at some point in the series.

Related posts:

1. Thyroid, blood sugar & metabolic syndrome
2. Medical care is 3rd leading cause of death in U.S.

What we haven’t discussed yet, however, are specific strategies for bringing the immune system back into balance. That will be the focus of this article.

Originally, I planned to go into considerable detail on the specific mechanisms of immune dysfunction that occur with Hashimoto’s, including a review of immunology, immune system classification (i.e. Th1 or “cell-mediated” immunity vs. Th2 or “humoral immunity”) and immune cell organization. It quickly became clear that such an approach would require an entire series of its own.

So, as fascinating as all of that stuff is, I decided to cut to the chase and focus on the practical, clinical applications. But there’s a caveat. Although I’ll be offering some general guidelines here for how to balance the immune system, if you have Hashimoto’s (or any other autoimmune condition) it’s in your best interest to find someone who understands immunology and is current with the latest nutritional and botanical protocols for treating autoimmune disease.

Why? Because autoimmune disease is not only extremely complex, but also highly individualized. Hashimoto’s in one person is not the same as Hashimoto’s in the next person. In one person, Hashimoto’s could present as a Th1-dominant condition. In another, it may present as Th2 dominant. In still another, both the Th1 and Th2 systems might be overactive, or underactive. And each of these cases requires a different approach. For example, botanicals like echinacea and astragalus stimulate the Th1 system. If someone with Th1 dominant Hashimoto’s takes these herbs, they’ll quite possibly get worse. On the other hand, antioxidants like green tea and Gotu Kola stimulate the Th2 system, and would be inappropriate for those with Th2 dominant Hashimoto’s. (For more information on the specifics of Hashimoto’s autoimmune physiology, see this article on Dr. Kharrazian’s blog and pick up a copy of his book.)

The good news, though, is that there are general approaches to balancing the immune system that are suitable for all types of Hashimoto’s regardless of the specific pattern of immune dysregulation. These approaches can be broken into three categories: removing autoimmune triggers, enhancing regulatory T cell function and reducing inflammation.

Removing autoimmune triggers

We’ve already discussed the role of gluten, iodine, stress and a leaky gut in triggering an autoimmune response. Other potential triggers include estrogens, infectious agents, and environmental toxins.

Estrogen fluctuations can trigger the gene expression of Hashimoto’s in the presence of inflammation and genetic susceptibility. In addition to turning on the genes associated with Hashimoto’s, estrogen surges have been shown to exacerbate the autoimmune attack on the thyroid. This may explain why the expression of Hashimoto’s is so common during pregnancy and perimenopause – both times when estrogen may be fluctuating wildly.

Environmental toxins are associated with autoimmune disease, and Hashimoto’s is no exception. Certain antigens like mercury that bypass our barrier system cause a potent immune response that can become chronic and overactive. If you suspect environmental toxicity may be contributing to your condition, it’s probably a good idea to get a test for chemical haptens and heavy metal antibodies.

Autoimmune thyroid disease has also been associated with a variety of infectious agents, including Rubella, Rubeolla, Epstein-Barr Virus, Retrovirus, Influenza B virus, Coxsakie virus and Yersinia. The mechanism in all cases is theorized to be cross-reaction between thyroid stimulating hormone (TSH) receptors and infectious agents. Once again, if you suspect an infectious agent is involved in your condition, a screening for these pathogens is a good idea.

Enhancing regulatory T cell function

These strategies are all designed to enhance the function of regulatory T cells (also referred to as the Th3 system). Regulatory T cells are used to balance the activity between T-helper cells (Th1 & Th2) and T-suppressor cells (which “turn off” the immune attack).

Vitamin D has been shown to influence regulatory T cells, which in turn modulate T helper cell expression and balance the Th1 and Th2 response. For more on this see The Role of Vitamin D Deficiency in Thyroid Disorders.

The gut flora play a significant role in both cell-mediated (Th1) and humoral (Th2) immunity. Studies show that this protective role can be maintained and modulated by taking probiotics. Specific probiotic strains can influence the secretion of cytokines to help direct naïve helper T cells towards either a Th1 dominant, cell-mediated immune response or towards a Th2 dominant, humoral immune response.

Acupuncture has recently been shown to regulate the Th1 and Th2 immune response. In this study of patients with depression, both Prozac and acupuncture were shown to reduce inflammation. But only acupuncture restored the balance between the Th1 and Th2 systems. In another study, acupuncture reduced inflammation and lessened the symptoms of asthma by regulating the balance between Th1 and Th2 cytokines.

Reducing inflammation

Essential fatty acids (EFAs) play an important role in preventing and reducing inflammation. I’ve written an entire series of articles on this topic, which I’d recommend reading if you haven’t already.

The ideal ratio between omega-6 and omega-3 fatty acids is between 1:1 and 3:1. The average American ratio is closer to 25:1, and as high as 30:1, thanks to diets high in processed and refined foods. The result of this imbalance is – among other things – inflammation.

Two steps are required to bring this ratio back into balance. First, dramatically reducing consumption of omega-6 fats, and second, moderately increasing consumption of omega-3 fats. I explain how to do this in considerable detail in this article.

Another benefit of increasing intake of omega-3 fatty acids is that they have also been shown to help balance the Th1 and Th2 systems.

Aside from ensuring a proper balance of omega-3 and omega-6 fatty acids, following an anti-inflammatory diet/lifestyle and avoiding dietary triggers like gluten and iodine is essential.

Putting these general approaches to balancing the immune system into action should give you a good start towards getting the autoimmunity under control. But if you don’t see the results you’d like, I’d recommend working with someone who knows how to address your particular immune imbalance more specifically.

Related posts:

1. The gluten-thyroid connection
2. Three reasons why your thyroid medication isn’t working
3. The role of vitamin D deficiency in thyroid disorders

Statements like “Synthroid is best” or “I prefer to use synthetic T4 with my patients” or “I only use bio-identical hormones” demonstrate a lack of understanding of thyroid pathology. Why? Because, as I’ve explained in this series, the underlying causes of thyroid dysfunction are diverse.

Giving all patients the same thyroid medication without understanding the mechanisms involved is analogous to not checking a patient’s blood type before doing a transfusion. Granted, the consequences may not be as severe, but the underlying principle is the same.

Before we continue, let me remind you that I’m not a doctor and I’m not offering you medical advice. My intent is to educate you about the various considerations that should be made when choosing a thyroid medication, so you can discuss them with your doctor. Understood? Great. Let’s move on.

Choosing the right thyroid medication requires answering the following three questions:

1. What’s the mechanism that led to the need for medication in the first place?
2. Are there any mechanisms that may interfere with the actions of the medication?
3. Does the patient have sensitivities to the fillers used in the medications?

Let’s look at each of these in turn.

What’s the mechanism that led to the need for medication in the first place?

If you’ve been following this series, you know that there’s no single cause for low thyroid function. Do you have an autoimmune disease (Hashimoto’s) causing destruction of your thyroid gland? Do you have high levels of estrogen causing an increase in thyroid binding proteins and a decrease in free thyroid hormone? Do you have a systemic inflammatory condition affecting your ability to convert T4 to T3, or decreasing the sensitivity of the cells in your body to thyroid hormone?

In order to choose the right hormone, you have to know what the underlying mechanism causing the dysfunction is. Let’s look at an example.

Say you have a problem converting T4 to T3. In this situation, your TSH may or may not be slightly elevated, but let’s say it is, and your doctor prescribes Synthroid. Synthroid is a synthetic T4 hormone. Will this help you?

No. It won’t help because your problem in this example isn’t a lack of T4, it’s an inability to convert T4 to the active T3 form. You could take T4 all day long, and it won’t do a thing unless your body can convert it.

The first step in this case would be to address the causes of the conversion problem (i.e. inflammation), in the hopes that you may not need replacement hormone. If that doesn’t work, though, what you’d need in this situation is either a so-called bio-identical hormone that has a combination of T4 and T3, or a synthetic T3 hormone (like Cytomel). These will deliver the T3 you need directly, bypassing the conversion problem.

Are there any mechanisms that may interfere with the actions of the medication?

The vast majority of long-term hypothyroid patients that haven’t been properly managed find that they constantly need to increase the dose of their medication, or switch to new medications, to get the same effect.

There are several reasons for this. First, inflammation (which is characteristic of all autoimmune diseases, and Hashimoto’s is no exception) causes a decrease in thyroid receptor site sensitivity. This means that even though you may be taking a substantial dose of replacement hormone, your cells aren’t able to utilize it properly.

Second, elevations in either testosterone or estrogen (extremely common in hypothyroid patients) affect the levels of circulating free thyroid hormone. For example, high levels of estrogen will increase levels of thyroid binding protein. Thyroid hormone is inactive as long as it’s bound to this protein. If you take thyroid replacement, but you have too much binding protein, there won’t be enough of the active form to produce the desired effect.

Third, there are several medications that alter the absorption or activity of T4. These include commonly prescribed drugs like antibiotics & antifungals (i.e. sulfonamides, rifampin, keoconazole), anti-diabetics (Orinase, Diabinese), diuretics (Lasix), stimulants (amphetamines), cholesterol lowering medications (Colestid, Atromid, LoCholest, Questran, etc.), anti-arrhythmia medications (Cordarone, Inderal, Propanolol, Regitine, etc.), hormone replacement (Premarin, anabolic steroids, growth hormone, etc.), pain medication (morphine, Kadian, MS Contin, etc.), antacids (aluminum hydroxides like Mylanta, etc.) and psychoactive medications (Lithium, Thorazine, etc.).

All of these factors must be considered if a particular medication isn’t having the desired effect.

Does the patient have sensitivities to the fillers used in the medications?

Another important consideration in choosing the right hormone is the fillers contained in each medication. Many popular thyroid medications contain common allergens such as cornstarch, lactose and even gluten. As I explained in a previous post, most hypothyroid patients have sensitivities to gluten, and many of them also react to corn and dairy (which contains lactose).

Synthroid, which is one of the most popular medications prescribed for hypothyroidism, has both cornstarch and lactose as a filler. Cytomel, which is a popular synthetic T3 hormone, has modified food starch – which contains gluten – as a filler.

Even the natural porcine products like Armour suffer from issues with fillers. In 2008, the manufacturers of Armour reformulated the product, reducing the amount of dextrose & increasing the amount of methylcellulose in the filler. This may explain the explosion of reports by patients on internet forums and in doctor’s offices that the new form of Armour was either “miraculous” or “horrible”. Those that had sensitivities to dextrose were reacting less to the new form, and experiencing better results, while those that had sensitivities to methylcellulose were reacting more, and experiencing worse results.

The best choice in these situations is to ask your doctor to have a compounding pharmacy fill the prescription using fillers you aren’t sensitive to. Unfortunately, insurance companies sometimes refuse to cover this.

Other considerations

Another common question that is hotly debated is whether bio-identical or synthetic hormones are best. Once again, the answer is: “It depends.” In general I think bio-identical hormones are the best choice. A frequently perpetuated myth (in Synthroid marketing, for example) is that the dosages and ratio of T4:T3 in Armour aren’t consistent. Studies have shown this to be false. Armour contains a consistent dose of 38 mcg T4 and 9 mcg T3 in a ratio of 4.22:1.

However, in some cases patients do feel better with synthetic hormones. One reason for this is that a small subset of people with Hashimoto’s produce antibodies not only to their thyroid tissue (TPO and TG), but also to their own thyroid hormones (T4 and T3). These patients do worse with bio-identical sources because they increased the source of the autoimmune attack.

Another issue is the use of T3 hormones. As we’ve discussed, T3 is the active form and has the greatest metabolic effects. The flip side of this, however, is that it’s far easier to “overdose” on T3 than on T4. Patients with trouble converting T4 to T3 do well on synthetic T3 or bio-identical combination T4:T3 products. But for many patients with Hashimoto’s, which is can present with alternating hypo- and hyperthyroid symptoms, T3 can push them over the edge. They are generally better off with T4 based drugs.

As you can see, the best thyroid hormone for each patient can only be determined by a full thyroid work-up and exam, followed by trial and error of different types of replacement medications. Such a work-up would include not just an isolated TSH test, but also a more complete thyroid panel (including antibodies), other important blood markers (glucose, lipids, CBC with diff, urinary DPD, etc.) and possibly a hormone panel. A history must be taken with particular attention paid to the patient’s subjective response to replacement hormones they may have tried in the past.

Unfortunately, this rarely happens in the conventional model, where the standard of care is to test only for TSH. If it’s elevated, the patient will get whatever hormone that particular practitioner is fond of using without any further investigation. And all too often, as many of you can attest, this simplified and incomplete approach is doomed to failure.

Related posts:

1. Three reasons why your thyroid medication isn’t working
2. Why thyroid medication is often necessary
3. The most important thing you may not know about hypothyroidism

However, I have no problem with pharmaceuticals if:

1. they work,
2. they do more good than harm, and;
3. there are no non-drug alternatives with the same effect.

It turns out that thyroid medication meets these criteria in cases of hypothyroidism with chronically elevated TSH. Elevated TSH indicates that the body is not producing enough thyroid hormone to meet metabolic needs. And thyroid hormone is so important to the proper function of the body that the benefits of replacing it far outweigh any potential side effects of the medication.

Remember that every cell in the body has receptor sites for thyroid hormone. Thyroid hormones are responsible for the most basic and fundamental aspect of physiology: the basal metabolic rate. Since the basal metabolic rate affects every system of the body, low thyroid hormone causes a global decline in cellular function.

Here’s a list of things that can go wrong when thyroid hormones are low. It’s not complete, but it should give you some idea of how important the thyroid is to proper function.

• Decreased energy production and metabolism in all cells of the body
• Decreased bone quality and increase in fractures
• Elevated cholesterol
• Impaired phase II detoxification
• Anemia
• Decreased stomach acid production
• Constipation, intestinal dysbiosis, malabsorption
• Intestinal inflammation
• Blood sugar imbalances
• Gallstone formation
• Vascular and arterial plaquing
• Neurodegeneration, cognitive problems, depression
• Weight gain
• Hair loss
• Dry skin
• Cold hands and feet
• Infertility and reproductive dysfunction
• Weakened immune system

I could go on, but I think you get the point. If your thyroid hormones are low, you can’t be healthy. Period.

90% of people with hypothyroidism in the U.S. have Hashimoto’s disease. Hashimoto’s is an autoimmune condition that causes destruction of the thyroid gland over time. As this destruction progresses, the thyroid gland becomes less and less able to produce enough hormones to meet metabolic needs. This is reflected in an increase in thyroid-stimulating hormone (TSH).

Persistently elevated TSH is a sign that the body needs more thyroid hormone than it can produce on its own. This is one clear sign that it’s time for replacement medication. But it isn’t the only one. Some people with TSH in the normal lab range still find that they benefit from replacement.

Note that I’m not saying everyone with hypothyroid symptoms should be on medication. In a previous post, I discussed 5 different patterns of low thyroid function that present with normal TSH levels. These include underconversion of T4 to T3, problems with thyroid binding proteins, pituitary dysfunction and thyroid receptor-site resistance. In these cases, the problem isn’t with the thyroid gland itself or its ability to produce enough hormones, but is either “upstream” (in the case of pituitary dysfunction) or “downstream” (in the case of conversion problems, binding protein issues or resistance.) For these patterns, replacement hormones are often unnecessary.

There are many in my profession (natural healthcare) that vehemently oppose the use of medication under any circumstances. I think that’s foolish. I’m more concerned about the dangers of Big Pharma than most. But that doesn’t mean we should ignore the important role drugs play in treating certain conditions.

In fact, my philosophy on healthcare can be simply stated as: whatever works best and causes the least harm. It’ not often that a drug fits the bill. But in the case of hypothyroidism with elevated TSH, I believe replacement medication is a necessary part of a larger strategy that includes balancing blood sugar, adrenals and the immune system and fixing the gut.

In the next post I’ll discuss the many different considerations when choosing a thyroid medication.

Related posts:

1. Three reasons why your thyroid medication isn’t working
2. 3 steps to choosing the right thyroid hormone
3. 5 thyroid patterns that won’t show up on standard lab tests

The main obstacle most Americans face in implementing dietary changes, as Dr. K points out, is their addiction to the idea of a “quick fix”:

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.

As long as this mentality prevails, we’ll continue to suffer from increasing rates of disease and morbidity, and our “disease-care” system will continue to buckle and, eventually, collapse.

Dietary and lifestyle changes aren’t easy, but they’re the key to promoting health and preventing disease. And that’s just as true with Hashimoto’s as it is with type 2 diabetes and heart disease.

Related posts:

1. Basics of immune balancing for Hashimoto’s
2. Low-carb diet best for weight loss
3. The gluten-thyroid connection

I won’t have time to respond to comments while I’m away, but please do leave them and I’ll answer when I come back. I’ve got a few more articles in the thyroid series, and next up after that will be type 2 diabetes & metabolic syndrome. Have a great August!

Vitamin D is all the rage. It seems like every day another article is published in medical journals or the mainstream press about the dangers of vitamin D deficiency, and the benefits of supplementation. In this article we’re going to discuss the impacts of vitamin D on thyroid physiology and wade into the increasingly murky topic of vitamin D supplementation – specifically as it relates to thyroid disorders.

Vitamin D deficiency has been associated with numerous autoimmune diseases in the scientific literature. Vitamin D plays an important role in balancing the Th1 (cell-mediated) and Th2 (humoral) arms of the immune system. It does this by influencing T-regulatory (Th3) cells, which govern the expression and differentiation of Th1 and Th2 cells.

Vitamin D deficiency is also specifically associated with autoimmune thyroid disease (AITD), and has been shown to benefit autoimmune-mediated thyroid dysfunction.

Vitamin D has another little-known role. It regulates insulin secretion and sensitivity and balances blood sugar. This recent paper showed that vitamin D deficiency is associated with insulin resistance. And as we saw in a previous article, insulin resistance and dysglyemcia adversely affect thyroid physiology in several ways.

“Okay, big deal,” you say. “I’ll just take vitamin D supplements or get more sun.”

Not so fast. Research over the past two decades has identified a variety of mechanisms that reduce the absorption, production and biologic activity of vitamin D in the body.

• Since vitamin D is absorbed in the small intestine, a leaky and inflamed GI tract – which is extremely common in people with low thyroid function – reduces the absorption of vitamin D.
• High cortisol levels (caused by stress or medications like steroids) are associated with lower vitamin D levels. They synthesis of active vitamin D from sunlight depends on cholesterol. Stress hormones are also made from cholesterol. When the body is in an active stress response, most of the cholesterol is used to make cortisol and not enough is left over for vitamin D production.
• Obesity reduces the biologic activity of vitamin D. Obese people have lower serum levels of vitamin D because it gets taken up by fat cells.
• Not eating enough fat or not digesting fat properly reduces absorption of vitamin D. Vitamin D is a fat-soluble vitamin, which means it requires fat to be absorbed. People on low-fat diets, and people with conditions that impair fat absorption (like IBS, IBD, gall bladder or liver disease) are more likely to have low levels of vitamin D.
• A variety of drugs reduce absorption or biologic activity of vitamin D. Unfortunately, these include drugs that are among the most popular and frequently prescribed – including antacids, replacement hormones, corticosteroids, anticoagulants and blood thinners.
• Aging reduces the conversion of sunlight to vitamin D becomes.
• Inflammation of any type reduces the utilization of vitamin D.

“Okay, fine,” you say. “I’ll just get my vitamin D measured, and if it’s low, I’ll take supplements.”

If only it were that simple. We now know that certain people with normal serum levels of vitamin D still suffer from deficiency symptoms. How is this possible?

In order for circulating vitamin D to perform its functions, it must first activate the vitamin D receptor (VDR). The problem is that many people with autoimmune disease have a genetic polymorphism that affects the expression and activation of the VDR and thus reduces the biologic activity of vitamin D. Studies have shown that a significant number of patients with autoimmune Hashimoto’s disease have VDR polymorphisms.

In plain English, here’s what this means: if you have low thyroid function, you might be experiencing vitamin D deficiency even if your blood levels of vitamin D are normal. It also means that, if you have a VDR polymorphism, it’s likely you’ll need to have higher than normal blood levels of vitamin D to avoid the effects of vitamin D deficiency.

“Okay, I get it,” you say. “I may need higher vitamin D levels than the average person if I have one of those genetic defects. So tell me what my levels should be!”

Well, this is where we venture into murky territory. The question of how high vitamin D levels should be is very difficult to answer in the case of someone with autoimmune thyroid disease. Studies suggest the optimal 25(OH)D level is 35 ng/mL for the average person. Some researchers (notably Dr. John Cannell and colleagues at the Vitamin D Council) have suggested that 50 ng/mL should be the minimum level.

The bulk of the evidence, however, doesn’t support that claim. For starters, the other authors of the study Dr. Cannell used as the basis for his 50 ng/mL recommendation came to a very different conclusion from the same data. In the paper they published in the American Journal of Clinical Nutrition, they wrote that their data confirmed the previously acknowledged optimal level of 35 ng/mL – not the 50 ng/mL suggested by Dr. Cannell.

What’s more, some recent studies have shown that higher isn’t better when it comes to vitamin D. A study in the American Journal of Medicine found that, in most people, maximum bone density occurs at 25(OH)D levels between 32-40 ng/mL. When levels are pushed above 45 ng/mL, as recommended by Dr. Cannell, bone density starts to decrease. Another study published in the European Journal of Epidemiology found that South Indians 25(OH)D levels above 89 ng/mL were three times more likely to have suffered from heart disease than those with lower levels.

If you’ve been following this blog for a while, you know that we don’t put too much faith in epidemiological studies. They don’t prove causation. They only show a relationship between two variables. But the relationship of vitamin D to calcium levels also provides a plausible mechanism by which high 25(OH)D levels could increase the risk of heart disease.

Complicating the matter further, recent work by researcher Chris Masterjohn suggests that the harmful effects of vitamin D toxicity are at least in part caused by a corresponding deficiency in vitamins A & K2. The fat-soluble vitamins A, D & K2 work synergistically, as Masterjohn has described in his Cod Liver Oil Debate article and a recently published scientific paper.

Masterjohn’s hypothesis, which has been confirmed by others, raises the possibility that the higher levels of 25(OH)D that were linked with lower bone density and heart disease may be safe if vitamin A & K2 levels are sufficient. Unfortunately, there is no clinical evidence (that I’m aware of) that helps us to answer this question.

“Okay, okay,” you say. “Just tell me how much to take already!”

I wish it were easier to answer this question. Really, I do. I think about it a lot for my own patients. The research is clear that 35 ng/mL is the minimum level for optimum function for healthy people. But people with autoimmune thyroid conditions aren’t healthy. They often have GI disorders, inflammation, stress, excess weight, VDR polymorphisms and other factors that impair their production, absorption and utilization of vitamin D. This suggests that the minimum 25(OH)D level for those with AITD may be significantly higher than for healthy people.

My current approach with these patients is to do a cautious trial of raising their serum levels to a range of 60-70 ng/mL. If their symptoms improve at this level, I will then switch them to a maintenance dose while watching for clinical signs of vitamin D toxicity. These include kidney stones (also a sign of vitamin K2 deficiency), low appetite, nausea, vomiting, thirst, excessive urination, weakness and nervousness. I will also monitor serum calcium levels, because elevated calcium in the blood is a sign of vitamin D toxicity and a significant risk factor for cardiovascular disease (especially in the presence of vitamin K2 deficiency). Calcium levels above 11-12 mg/dL (or 2.8-3 mmol/L) are indicative of vitamin D toxicity.

I will also make sure these patients are getting adequate amounts of vitamin K2 and vitamin A in their diets. Sources of vitamin A include organ meats, cod liver oil and full-fat milk and cream from grass-fed cows. Sources of vitamin K2 include fermented foods like natto, hard cheeses and kefir as well as egg yolks and butter from grass-fed cows. I may also use a vitamin K2 supplement (MK-4/MK-7 combo) if patients can’t tolerate fermented foods.

Finally, if you’re interested in finding out if you have a VDR polymorphism that could be affecting your metabolism of vitamin D, Genova Diagnostics has an Osteogenomics panel that tests for them. I’m not sure how much value this test has clinically, however, since it doesn’t provide any information about how the VDR polymorphism affects vitamin D metabolism in each specific case. That’s still something that would have to be figured out using the “trial and error” process I described above.

In time we can hope that the explosion of research being conducted on vitamin D will lead to more clarity on the question of appropriate serum 25(OH)D levels for people with autoimmune diseases. For now, we have to make our best guess based on clinical results and anecdotal reports.

Related posts:

1. The thyroid-gut connection
2. The gluten-thyroid connection
3. Iodine for hypothyroidism: like gasoline on a fire?

The adrenals are two walnut-shaped glands that sit atop the kidneys. They secrete hormones – such as cortisol, epinephrine and norepinephrine – that regulate the stress response. But these hormones play other crucial roles, many of which are directly related to thyroid health. In fact, as we’ll see in this article, proper thyroid function depends on healthy adrenal glands.

Most people are aware of the obvious forms of stress that affect the adrenal glands: impossibly full schedules, driving in traffic, financial problems, arguments with a spouse, losing a job and the many other emotional and psychological challenges of modern life.

But other factors not commonly considered when people think of “stress” place just as much of a burden on the adrenal glands. These include blood sugar swings, gut dysfunction, food intolerances (especially gluten), chronic infections, environmental toxins, autoimmune problems and inflammation. All of these conditions sound the alarm bells and cause the adrenals to pump out more stress hormones. In this context, stress is broadly defined as anything that disturbs the body’s natural balance (homeostasis).

Adrenal stress is probably the most common problem we encounter in functional medicine, because nearly everyone is dealing with at least one of the factors listed above. Symptoms of adrenal stress are diverse and nonspecific, because the adrenals affect every system in the body. But some of the more common symptoms are:

• Fatigue
• Headaches
• Decreased immunity
• Difficulty falling asleep, staying asleep and waking up
• Mood swings
• Sugar and caffeine cravings
• Irritability or lightheadedness between meals
• Eating to relieve fatigue
• Dizziness when moving from sitting or lying to standing
• Gastric ulcers

Weak adrenals can cause hypothyroid symptoms without any problem in the thyroid gland itself. In such cases, treating the thyroid is both unnecessary and ineffective, and addressing the adrenals themselves is the key to improving thyroid function.

The most significant indirect effect the adrenals have on thyroid function is via their influence on blood sugar. High or low cortisol – caused by any of the chronic stressors listed above – can cause hypoglycemica, hyperglycemia or both. And as we saw in a previous article, blood sugar imbalances cause hypothyroid symptoms in a variety of ways.

But adrenal stress also has more direct impacts on thyroid function. The following five mechanisms are the most important.

1) Adrenal stress disrupts the HPA axis

By now many people have heard of the hypothalamic-pituitary-adrenal (HPA) axis. It’s a complex network of interactions between the hypothalamus, the pituitary and the adrenal glands that regulates things such as temperature, digestion, immune system, mood, sexuality and energy usage – in addition to controlling the body’s reaction to stress and trauma.

Countless studies show that chronic adrenal stress depresses hypothalamic and pituitary function. And since these two organs direct thyroid hormone production, anything that disrupts the HPA axis will also suppress thyroid function.

Studies have shown that the inflammatory cytokines IL-1 beta, IL-6 and TNF-alpha, which are released during the stress response, down-regulate the HPA axis and reduce levels of thyroid stimulating hormone (TSH). Another study showed that one single injection of tumor necrosis factor alpha (TNF-alpha), an inflammatory peptide, reduced serum TSH, T3, free T4, free T3 and hypothalamic TRH for 5 days. TNF-alpha was also found to decrease the conversion of T4 to T3, reduce thyroid hormone uptake, and decrease the sensitivity of the thyroid to TSH.

2) Adrenal stress reduces conversion of T4 to T3

We discussed under-conversion of T4 to T3 in a prior article. Remember that although 93% of the hormone produced by the thyroid gland is T4, it is inactive in that form and must be converted into T3 before it can be used by the cells. The inflammatory cytokines I listed above not only disrupt the HPA axis, they also interfere with the conversion of T4 to T3.

The enzyme 5′-deiodinase catalyzes the conversion of T4 into T3 in peripheral tissues such as the liver and the gut. Both Th1 and Th2 inflammatory cytokines – IL-6, TNF-alpha, IFN-gamma and IL-1 beta – have been shown to suppress the conversion of T4 to T3. In patients without thyroid illness, as levels of IL-6 (a marker for inflammation) rise, levels of serum T3 fall. And injections of inflammatory cytokines into healthy human subjects resulted in a rapid reduction of serum T3 and TSH levels, and an increase in the inactive reverse T3 (rT3) form, while T4 and free T4 levels were only minimally changed.

3) Adrenal stress promotes autoimmunity by weakening immune barriers

The GI tract, lungs and the blood-brain barrier are the primary immune barriers in the body. They prevent foreign substances from entering the bloodstream and the brain. Adrenal stress weakens these barriers, weakens the immune system in general, and promotes poor immune system regulation.

As we discussed in my previous article on the gut-thyroid connection, when these immune barriers are breached large proteins and other antigens are able to pass into the bloodstream or brain where they don’t belong. If this happens repeatedly, the immune system gets thrown out of whack and we become more prone to autoimmune diseases – such as Hashimoto’s.

4) Adrenal stress causes thyroid hormone resistance

In order for thyroid hormone circulating in blood to have a physiological effect, it must first activate receptors on cells. Inflammatory cytokines have been shown to suppress thyroid receptor site sensitivity.

If you’re familiar with insulin resistance, where the cells gradually lose their sensitivity to insulin, this is a similar pattern. It’s as if the thyroid hormone is knocking on the cell’s door, but the cells don’t answer.

While there’s no practical way to measure receptor site sensitivity in a clinical setting, the research above suggests it is decreased in autoimmune and other inflammatory conditions. A perfect example of this in practice is the Hashimoto’s patient who is taking replacement hormones but still suffers from hypothyroid symptoms – often in spite of repeated changes in the dose and type of medication. In these patients, inflammation is depressing thyroid receptor site sensitivity and producing hypothyroid symptoms, even though lab markers like TSH, T4 and T3 may be normal.

5) Adrenal stress causes hormonal imbalances

Cortisol is one of the hormones released by the adrenals during the stress response. Prolonged cortisol elevations, caused by chronic stress, decrease the liver’s ability to clear excess estrogens from the blood. Excess estrogen increases levels of thyroid binding globulin (TBG), the proteins that thyroid hormone is attached to as it’s transported through the body.

When thyroid hormone is bound to TBG, it is inactive. It must be cleaved from TBG to become “free-fraction” before it can activate cellular receptors. (These free-fraction thyroid hormones are represented on lab tests as “free T4 [FT4]” and “free T3 [FT3]“.)

When TBG levels are high, the percentage of free thyroid hormones drops. This shows up on labs as low T3 uptake and low free T4/T3.

Aside from adrenal stress, the most common causes of elevated TBG secondary to excess estrogen are birth control pills and estrogen replacement (i.e. Premarin).

Balancing the adrenals

Here’s the tricky thing about adrenal stress: it’s almost always caused – at least in part – by something else. These causes include anemia, blood sugar swings, gut inflammation, food intolerances (especially gluten), essential fatty acid deficiencies, environmental toxins, and of course, chronic emotional and psychological stress.

When they exist, these conditions must be addressed or any attempt to support the adrenals directly will either fail or be only partially successful. With that in mind, here are some general guidelines for adrenal health:

• Avoid or at least greatly minimize stimulants
• Stabilize blood sugar (via a moderate or low-carb diet)
• Practice stress management and relaxation techniques
• Have fun, laugh and make pleasure a regular part of your life
• Avoid dietary causes of inflammation (refined flours, high-fructose corn syrup and industrial seed oils in particular)
• Ensure adequate intake of DHA & EPA

Specific nutrients such as phosphatidyl serine and adaptogenic botanicals like Panax ginseng, Siberian ginseng, Ashwagandha and Holy basil leaf extract are also helpful in modulating the stress response and supporting the adrenals. However, these are potent medicines and should be taken under the supervision of a trained practitioner.

Related posts:

1. 5 thyroid patterns that won’t show up on standard lab tests
2. Why thyroid medication is often necessary
3. The thyroid-gut connection

The gut-thyroid-immune connection

Have you ever considered the fact that the contents of the gut are outside the body? The gut is a hollow tube that passes from the mouth to the anus. Anything that goes in the mouth and isn’t digested will pass right out the other end. This is, in fact, one of the most important functions of the gut: to prevent foreign substances from entering the body.

Another important function of the gut is to host 70% of the immune tissue in the body. This portion of the immune system is collectively referred to as GALT, or gut-associated lymphoid tissue. The GALT comprises several types of lymphoid tissues that store immune cells, such as T & B lymphocytes, that carry out attacks and produce antibodies against antigens, molecules recognized by the immune system as potential threats.

Problems occur when either of these protective functions of the gut are compromised. When the intestinal barrier becomes permeable (i.e. “leaky gut syndrome”), large protein molecules escape into the bloodstream. Since these proteins don’t belong outside of the gut, the body mounts an immune response and attacks them. Studies show that these attacks play a role in the development of autoimmune diseases like Hashimoto’s.

We also know that thyroid hormones strongly influence the tight junctions in the stomach and small intestine. These tight junctions are closely associated areas of two cells whose membranes join together to form the impermeable barrier of the gut. T3 and T4 have been shown to protect gut mucosal lining from stress induced ulcer formation. In another study, endoscopic examination of gastric ulcers found low T3, low T4 and abnormal levels of reverse T3.

Likewise, thyrotropin releasing hormone (TRH) and thyroid stimulating hormone (TSH) both influence the development of the GALT. T4 prevents over-expression of intestinal intraepithelial lymphocytes (IEL), which in turn causes inflammation in the gut.

The gut-bacteria-thyroid connection

One little known role of the gut bacteria is to assist in converting inactive T4 into the active form of thyroid hormone, T3. About 20 percent of T4 is converted to T3 in the GI tract, in the forms of T3 sulfate (T3S) and triidothyroacetic acid (T3AC). The conversion of T3S and T3AC into active T3 requires an enzyme called intestinal sulfatase.

Where does intestinal sulfatase come from? You guessed it: healthy gut bacteria. Intestinal dysbiosis, an imbalance between pathogenic and beneficial bacteria in the gut, significantly reduces the conversion of T3S and T3AC to T3. This is one reason why people with poor gut function may have thyroid symptoms but normal lab results.

Inflammation in the gut also reduces T3 by raising cortisol. Cortisol decreases active T3 levels while increasing levels of inactive T3. ¹

Studies have also shown that cell walls of intestinal bacteria, called lipopolysaccharides (LPS), negatively effect thyroid metabolism in several ways. LPS:

• reduce thyroid hormone levels;
• dull thyroid hormone receptor sites;
• increase amounts of inactive T3;
• decrease TSH; and
• promote autoimmune thyroid disease (AITD).

Other gut-thyroid connections

Hypochlorhydria, or low stomach acid, increases intestinal permeability, inflammation and infection (for more on this, see my series on acid reflux & GERD). Studies have shown a strong association between atrophic body gastritis, a condition related to hypochlorhydria, and autoimmune thyroid disease.

Constipation can impair hormone clearance and cause elevations in estrogen, which in turn raises thyroid-binding globulin (TBG) levels and decreases the amount of free thyroid hormones available to the body. On the other hand, low thyroid function slows transit time, causing constipation and increasing inflammation, infections and malabsorption.

Finally, a sluggish gall bladder interferes with proper liver detoxification and prevents hormones from being cleared from the body, and hypothyroidism impairs GB function by reducing bile flow.

Healing the gut-thyroid axis

All of these connections make it clear that you can’t have a healthy gut without a healthy thyroid, and you can’t have a healthy thyroid without a healthy gut. To restore proper function of the gut-thyroid axis, both must be addressed simultaneously.

Healing the gut is a huge topic that can’t be covered adequately in a few short sentences. But I will say this: the first step is always to figure out what’s causing the gut dysfunction. As we’ve reviewed in this article, low thyroid is one possible cause, but often hypochlorhydria, infections, dysbiosis, food intolerances (especially gluten), stress and other factors play an even more significant role. The second step is to address these factors and remove any potential triggers. The third step is to restore the integrity of the gut barrier. My preferred approach for this last step is the GAPS diet.

The influence of thyroid hormones on the gut is one of many reasons why I recommend that people with persistently high TSH and low T4 and T3 take replacement hormones. Low thyroid hormones make it difficult to heal the gut, and an inflamed and leaky gut contributes to just about every disease there is, including hypothyroidism. Fixing the gut is often the first – and most important – step I take with my patients.

Related posts:

1. Three reasons why your thyroid medication isn’t working
2. The gluten-thyroid connection
3. Why thyroid medication is often necessary

Metabolic syndrome (MetS), also affects 50 million Americans, and insulin resistance, one of the components of metabolic syndrome, affects up to 105 million Americans. That’s 35% of the population. Metabolic syndrome has become so common that it’s predicted to eventually bankrupt our healthcare system. Both metabolic syndrome and insulin resistance are risk factors for heart disease and diabetes, two of the leading causes of death in the developed world.

With such a high prevalence of both thyroid dysfunction and metabolic syndrome, you might suspect there’s a connection between the two. And you’d be right.

Studies show an increased frequency of thyroid disorders in diabetics, and a higher prevalence of obesity and metabolic syndrome in people with thyroid disorders.

That’s because healthy thyroid function depends on keeping your blood sugar in a normal range, and keeping your blood sugar in a normal range depends on healthy thyroid function.

How high blood sugar affects the thyroid

Metabolic syndrome is defined as a group of metabolic risk factors appearing together, including:

• abdominal obesity;
• high cholesterol and triglycerides;
• high blood pressure;
• insulin resistance;
• tendency to form blood clots; and,
• inflammation.

Metabolic syndrome is caused by chronic hyperglycemia (high blood sugar). Chronic hyperglycemia is caused by eating too many carbohydrates. Therefore, metabolic syndrome could more simply be called “excess carbohydrate disease”. In fact, some researchers have gone as far as defining metabolic syndrome as “those physiologic markers that respond to reduction in dietary carbohydrate.”

When you eat too many carbs, the pancreas secretes insulin to move excess glucose from the blood into the cells where glucose is used to produce energy. But over time, the cells lose the ability to respond to insulin. It’s as if insulin is knocking on the door, but the cells can’t hear it. The pancreas responds by pumping out even more insulin (knocking louder) in an effort to get glucose into the cells, and this eventually causes insulin resistance.

Studies have shown that the repeated insulin surges common in insulin resistance increase the destruction of the thyroid gland in people with autoimmune thyroid disease. As the thyroid gland is destroyed, thyroid hormone production falls.

How low blood sugar affects the thyroid

But just as high blood sugar can weaken thyroid function, chronically low blood sugar can also cause problems.

Your body is genetically programmed to recognize low blood sugar as a threat to survival. Severe or prolonged hypoglycemia can cause seizures, coma, and death. When your blood sugar levels drop below normal, your adrenal glands respond by secreting a hormone called cortisol. Cortisol then tells the liver to produce more glucose, bringing blood sugar levels back to normal.

The problem is that cortisol (along with epinephrine) is also a sympathetic nervous system hormone involved in the “flight or fight” response. This response includes an increase in heart rate and lung action and an increase in blood flow to skeletal muscles to help us defend against or flee from danger. Cortisol’s role is to increase the amount of glucose available to the brain, enhance tissue repair, and curb functions – like digestion, growth and reproduction – that are nonessential or even detrimental in a fight or flight situation.

Unfortunately for hypoglycemics, repeated cortisol release caused by episodes of low blood sugar suppresses pituitary function. And as I showed in a previous article, without proper pituitary function, your thyroid can’t function properly.

Together, hyperglycemia and hypoglycemia are referred to as dysglycemia. Dysglycemia weakens and inflames the gut, lungs and brain, imbalances hormone levels, exhausts the adrenal glands, disrupts detoxification pathways, and impairs overall metabolism. Each of these effects significantly weakens thyroid function. As long as you have dysglycemia, whatever you do to fix your thyroid isn’t going to work.

How low thyroid function affects blood sugar

We’ve seen now how both high and low blood sugar cause thyroid dysfunction. On the other hand, low thyroid function can cause dysglycemia and metabolic syndrome through a variety of mechanisms:

• it slows the rate of glucose uptake by cells;
• it decreases rate of glucose absorption in the gut;
• it slows response of insulin to elevated blood sugar; and,
• it slows the clearance of insulin from the blood.

These mechanisms present clinically as hypoglycemia. When you’re hypothyroid, your cells aren’t very sensitive to glucose. So although you may have normal levels of glucose in your blood, you’ll have the symptoms of hypoglycemia (fatigue, headache, hunger, irritability, etc.). And since your cells aren’t getting the glucose they need, your adrenals will release cortisol to increase the amount of glucose available to them. This causes a chronic stress response, as I described above, that suppresses thyroid function.

How to keep your blood sugar in a healthy range

It’s important to understand that whether you have high or low blood sugar, you probably have some degree of insulin resistance. I described how high blood sugar causes insulin resistance above. But insulin resistance can also cause low blood sugar. This condition, called reactive hypoglycemia, occurs when the body secretes excess insulin in response to a high carbohydrate meal – causing blood sugar levels to drop below normal.

In either case, the solution is to make sure your blood sugar stays within a healthy range. There are two targets to consider. The first is fasting blood glucose, which is a measure of your blood sugar first thing in the morning before eating or drinking anything. I define the normal range for fasting blood glucose as 75 – 95 mg/dL. Although 100 is often considered the cutoff for normal, studies have shown that fasting blood sugar levels in the mid-90s were predictive of future diabetes a decade later. And although 80 mg/dL is often defined as the cutoff on the low end, plenty of healthy people have fasting blood sugar in the mid-to-high 70s (especially if they follow a low-carb diet).

The second, and much more important, target is post-prandial blood glucose. This is a measure of your blood sugar 1-2 hours after a meal. Several studies have shown that post-prandial blood glucose is the most accurate predictor of future diabetic complications and is the first marker (before fasting blood glucose and Hb1Ac) to indicate dysglycemia.

Normal post-prandial blood sugar one to two hours after a meal is 120 mg/dL. Most normal people are under 100 mg/dL two hours after a meal.

Now that we know the targets, let’s look at how to meet them. If you’re hypoglycemic, your challenge is to keep your blood sugar above 75 throughout the day. The best way to do this is to eat a low-to-moderate carbohydrate diet (to prevent the blood sugar fluctuations I described above), and to eat frequent, small meals every 2-3 hours (to ensure a continuous supply of energy to the body.

If you’re hyperglycemic, your challenge is to keep your blood sugar below 120 two hours after a meal. The only way you’re going to be able to do this is to restrict carbohydrates. But how low-carb do you need to go? The answer is different for everyone. You figure your own carbohydrate tolerance by buying a blood glucose meter and testing your blood sugar after various meals. If you’ve eaten too many carbs, your blood sugar will remain above 120 mg/dL two hours after your meal.

I highly recommend you pick up a blood glucose meter if you have a thyroid and/or blood sugar problem. It’s the simplest and most cost-effective way to figure out how much carbohydrate is safe for you to eat. There are tons of meters out there, but one that gets a lot of good recommendations is the ReliOn Ultima. It’s pretty cheap, and the test strips are also cheap, which is where the major expense lies.

Finally, if you have poor thyroid function it’s important that you take steps to normalize it. As I’ve described in this article, the cycle works in both direction. Dysglycemia can depress thyroid function, but thyroid disorders can cause dysglycemia and predispose you to insulin resistance and metabolic syndrome.

Related posts:

1. 5 thyroid patterns that won’t show up on standard lab tests
2. Why thyroid medication is often necessary
3. Diabesity: the #1 cause of death and disease?

Several studies show a strong link between AITD (both Hashimoto’s and Graves’) and gluten intolerance. [1, 2, 3, 4, 5] The link is so well-established that researchers suggest all people with AITD be screened for gluten intolerance, and vice versa.

What explains the connection? It’s a case of mistaken identity. The molecular structure of gliadin, the protein portion of gluten, closely resembles that of the thyroid gland. When gliadin breaches the protective barrier of the gut, and enters the bloodstream, the immune system tags it for destruction. These antibodies to gliadin also cause the body to attack thyroid tissue. This means if you have AITD and you eat foods containing gluten, your immune system will attack your thyroid.

Even worse, the immune response to gluten can last up to 6 months each time you eat it. This explains why it is critical to eliminate gluten completely from your diet if you have AITD. There’s no “80/20″ rule when it comes to gluten. Being “mostly” gluten-free isn’t going to cut it. If you’re gluten intolerant, you have to be 100% gluten-free to prevent immune destruction of your thyroid.

So how do you find out if you’re gluten intolerant? Unfortunately, standard lab tests aren’t very accurate. They test for antibodies to gluten in the bloodstream. But antibodies in the blood will only be found in cases where the gut has become so permeable that gluten can pass through. This is a relatively advanced stage of disease. Blood tests will miss the many milder cases of gluten intolerance that haven’t yet progressed to that stage.

Stool analysis is far more sensitive, because it detects antibodies produced in the digestive tract that aren’t yet escaping into the bloodstream. Using this method at Entero Lab, Dr. Kenneth Fine, a pioneer in the field, has found that up to 35% of Americans are gluten intolerant.

In addition to the stool analysis, Dr. Fine’s lab uses a cheek swab to test for the genes connected with gluten intolerance and celiac disease. People with HLA DQ genes are more likely than the general population to have autoimmune disease, celiac disease and gluten intolerance. Dr. Fine’s research shows that more than 80% of Americans have one of these gene types.

When I first read Dr. Fine’s research, I was astounded by the implications. It suggests that 1 in 3 Americans are gluten intolerant, and that 8 in 10 are genetically predisposed to gluten intolerance. This is nothing short of a public health catastrophe in a nation where the #1 source of calories is refined flour. But while most are at least aware of the dangers of sugar, trans-fat and other unhealthy foods, fewer than 1 in 8 people with celiac disease are aware of their condition. I would guess that an even lower proportion of people are aware they are gluten intolerant.

One reason gluten intolerance goes undetected in so many cases is that both doctors and patients mistakenly believe it only causes digestive problems. But gluten intolerance can also present with inflammation in the joints, skin, respiratory tract and brain – without any obvious gut symptoms.

As much improved as Dr. Fine’s methods are, they aren’t perfect. In some patients with autoimmune disease, their immune system is so worn out they can no longer produce many antibodies.

Hashmioto’s, the most common autoimmune thyroid condition, is primarily a Th1 dominant condition. I’ll explain what this means in further detail in a future article. For now, what you need to understand is that in Th1-dominant conditions, the Th2 system is suppressed. The Th2 system is the part of the immune system responsible for producing antibodies. When the Th2 system is severely depressed, the body’s ability to produce antibodies is impaired. The levels may be so low that they won’t show up on a test. So, even if you have gluten intolerance, your test for gluten antibodies may be falsely negative if you have Th1-dominant Hashimoto’s.

This is why I recommend that you avoid gluten if you have AITD, regardless of whether tests show an active antibody response. This is especially true if you have one of the genes (HLA DQ1,2, or 3) that predisposes you to developing gluten intolerance. In my opinion continuing to eat gluten when you have a confirmed autoimmune condition simply isn’t worth risking the immune destruction it could cause.

In fact, the more I learn about gluten and its effects on the body, the more I think we’d all probably be better off not eating it. Mark Sisson has written extensively about the dangers of gluten and gluten-containing grains, so head over there and have a look if this is new to you. The short version: foods that contain gluten (both whole grains and flours) contain substances that inhibit nutrient absorption, damage our intestinal lining, and – as I’ve described in this article – activate a potentially destructive autoimmune response. What’s more, there are no nutrients in gluten-containing foods that you can’t get more easily and efficiently from foods that don’t contain gluten.

The good news is that if you have AITD and are gluten intolerant removing gluten completely from your diet will dramatically improve your health. It’s not easy, but it’s worth it.

Related posts:

1. The thyroid-gut connection
2. 3 steps to choosing the right thyroid hormone
3. Iodine for hypothyroidism: like gasoline on a fire?