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The thyroid-gut connection

July 29, 2010 in Thyroid Disorders | 2 comments

Hippocrates said: “All disease begins in the gut.” 2,500 years later we’re just beginning to understand how right he was. And, as I’ll explain in this article, hypothyroidism is no exception. Poor gut health can suppress thyroid function and trigger Hashimoto’s disease, and low thyroid function can lead to an inflamed and leaky gut – as illustrated in the following diagram:

thyroidgut

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.

  1. Stockigt, JR and Baverman LE. Update on the Sick Euthyroid Syndrome. Diseases of the Thyroid. Humana Press, Totowa, NJ, 1997, pp.49-68 ↩

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Thyroid, blood sugar & metabolic syndrome

July 23, 2010 in Obesity, Thyroid Disorders | 25 comments

ultimaAccording to the American Association of Clinical Endocrinologists, 27 million Americans suffer from thyroid dysfunction – half of whom go undiagnosed. Subclinical hypothyroidism, a condition in which TSH is elevated but free T4 is normal, may affect an additional 24 million Americans. Taken together, more than 50 million Americans are affected by some form of thyroid disorder.

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.

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The gluten-thyroid connection

July 18, 2010 in Food & Nutrition, Thyroid Disorders | 35 comments

wheatIn the first article in this series, I showed that hypothyroidism is an autoimmune disease in 90% of cases. In this article we’re going to discuss the connection between autoimmune thyroid disease (AITD) and gluten intolerance.

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.

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Welcome Mark’s Daily Apple readers!

July 15, 2010 in Uncategorized | 4 comments

welcome_matI just wanted to take a moment to welcome readers from Mark’s Daily Apple.

Let’s get logistics out of the way first: if you like what you see here, you can sign up for email updates, subscribe to my RSS feed, or follow me on Facebook and Twitter. I regularly post stuff on Facebook and Twitter that doesn’t make it to the blog, so that’s a good option if you’re a health information junkie.

If you came over for a look at my series on hypothyroidism, here’s a list of the articles I’ve written so far:

It’s a work in progress and I’ll be writing several more articles in the future on how to properly diagnose and treat thyroid disorders. Topics will include:

  • Why there’s no “one size fits all” when it comes to thyroid medications
  • How to address the autoimmune component of thyroid disease
  • The connection between gluten intolerance and Hashimoto’s
  • The gut-thyroid connection
  • The best diet for thyroid health (hint: it’s primal!)

You might have seen Mark’s recent article on acupuncture. Although it’s commonly believed in the West that acupuncture is based on mysterious energy called qi flowing through invisible lines called meridians, it turns out that idea is based on blatant mistranslations of ancient Chinese medical texts. When these texts are correctly translated, it becomes clear that acupuncture is not a “woo-woo” energy healing technique, but a complete “flesh and bones” system of medicine based on the same anatomy and physiology as western medicine. You can read all about it here.

And here are a few other special reports to check out:

  • Heart disease & cholesterol: debunks the myth that cholesterol and saturated fat cause heart disease, and explains how to treat heart disease without drugs
  • Statins: exposes the ineffectiveness and dangers of statin drugs
  • GERD/heartburn: presents evidence that heartburn & GERD are caused by too little – not too much – stomach acid, and that GERD can be effectively treated with a low carb diet and a few affordable supplements
  • EFAs, fish & fish oil: cuts through the confusion and hype about essential fatty acids, fish and fish oil and offers clear guidelines to achieving a healthy fatty acid balance
  • Depression: challenges the theory that depression is exclusively caused by a biochemical imbalance, reveals evidence that antidepressants have serious risks and are no more effective than placebo in most cases, and outlines a clear plan for treating depression without drugs

If you’re the video watching type instead of the reading type, check out my videos on cholesterol and statins:

I hope the information here helps you and those you love live healthier and happier lives. Once again, welcome to The Healthy Skeptic!

Rest in peace, China Study

July 8, 2010 in Food & Nutrition, Myths & Truths | 36 comments

coffinI know this was all over the blogosphere yesterday but I think it’s important enough for a repost.

One thing I can count on every time I write an article extolling the health benefits of animal products is someone sending me an email or posting a comment like this:

I think you’re absolutely wrong. You should read: The China Study, by Dr. T. Collin Campbell.

Sorry to be contrary, but T. Colin Campbell’s “The China Study” should put this issue to rest. Please consider the information presented there. The methodology is impressive.

Campbell recommends a vegan diet–no animal based food at all. He claims that population studies demonstrate that vegan populations do not suffer from the high incidence of cardiovascular disease and cancer that we in the West do with our diets heavy on animal protein.

In fact, those are direct quotes from comments that have been left on my blog over the past year. I can’t even show you some of the emails people have sent because the language might offend you.

Usually I direct those folks to Chris Masterjohn’s excellent critique of the China Study. Now, however, I’ll be sending them over to read Denise Minger’s freshly published China Study smackdown.

Here’s the introduction:

When I first started analyzing the original China Study data, I had no intention of writing up an actual critique of Campbell’s much-lauded book. I’m a data junkie. Numbers, along with strawberries and Audrey Hepburn films, make me a very happy girl. I mainly wanted to see for myself how closely Campbell’s claims aligned with the data he drew from—if only to satisfy my own curiosity.

But after spending a solid month and a half reading, graphing, sticky-noting, and passing out at 3 AM from studious exhaustion upon my copy of the raw China Study data, I’ve decided it’s time to voice all my criticisms. And there are many.

Denise got hold of the raw study data and took it apart with a fine-toothed comb. And what she found is that the claims Campbell made in his China Study book are not supported by the data. She also found important data points Campbell never bothered to mention in the book because they didn’t support his vegan agenda.

For example, Campbell conveniently fails to mention the county of Tuoli in China. The folks in Tuoli ate 45% of their diet as fat, 134 grams of animal protein each day (twice as much as the average American), and rarely ate vegetables or other plant foods. Yet, according to the China Study data, they were extremely healthy with low rates of cancer and heart disease; healthier, in fact, than many of the counties that were nearly vegan.

This is just one of many cases of the selective citation and data cherry picking Campbell employs in the China Study. Denise’s critique masterfully reveals the danger of drawing conclusions from epidemiological studies, which can only show correlations between variables – not causal relationships. Campbell should be well aware of this. After all, in his book he rails against the nutritional bias rampant in the scientific community. Yet nowhere is such bias more evident than in Campbell’s own interpretation of the China Study data.

Denise concludes:

Ultimately, I believe Campbell was influenced by his own expectations about animal protein and disease, leading him to seek out specific correlations in the China Study data (and elsewhere) to confirm his predictions.

Campbell’s response to previous critics of the China Study has been something to the effect of: “I’m a trained scientist. Therefore you should believe me and not my critics.” That is a weak argument – to put it mildly. You don’t need six years of graduate school to learn to think critically. Nor does having a lot of letters after your name make you immune to biased thinking or intellectual blindness. A lot of smart, educated people believed the cholesterol hypothesis for decades. But that never made it true.

You can read more – and I mean a lot more – over at Denise’s blog. I recommend starting with her article China Study: Fact or Fallacy? For many of you, it will be more than enough. But if you’re interested in this stuff, she has written several other articles worth reading.

There are also reviews of Denise’s article at Free the Animal, Whole Health Source, Robb Wolf and PaNu. If you don’t have time to read Denise’s article, read Dr. Harris’s review at PaNu. It’s the next best thing.

Rest in peace, China Study.

P.S. You might also want to check out this debate between T. Colin Campbell and Loren Cordain on human protein requirements. Notice that Cordain’s articles contain 164 citations of research studies. How many references do Campbell’s articles contain? Zero. And Campbell’s typical “I’m more educated than the other guy” won’t fly here. Dr. Cordain has some serious chops.

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5 thyroid patterns that won’t show up on standard lab tests

July 8, 2010 in Thyroid Disorders | 12 comments

diagnosis puzzleIn medicine, the key to choosing the best treatment is an accurate diagnosis. If the diagnosis isn’t correct, the treatment will be ineffective – or even cause harm.

Unfortunately misdiagnosis is common in the management of hypothyroidism. If you go to a doctor with hypothyroid symptoms, you’ll simply be given replacement hormones without any further inquiry into the cause of your condition.

Even worse, if you have hypothyroid symptoms but your lab tests are normal, you’ll be told you’re “fine”. If you insist you’re not, you might be sent home with an antidepressant, but no further clue about the cause of your symptoms.

The problem with this approach is that thyroid physiology is complex. The production, conversion and uptake of thyroid hormone in the body involves several steps. A malfunction in any of these steps can cause hypothyroid symptoms, but may not show up on standard lab tests. It’s incorrect and even negligent to assume that all cases of hypothyroidism share the same cause and require the same treatment. Yet that’s exactly what the standard of care for hypothyroidism delivers.

In this article I’ll present five patterns of thyroid dysfunction that won’t show up on standard lab tests. If you have one of these patterns, your thyroid isn’t functioning properly and you will have symptoms. But if you go to your conventional doctor, you’ll be told there’s nothing wrong with your thyroid.

A standard thyroid panel usually includes TSH and T4 only. The ranges for these markers vary from lab to lab, which is one of two main problems with standard lab ranges. The other problem is that lab ranges are not based on research that tells us what a healthy range might be, but on a bell curve of values obtained from people who come to the labs for testing.

Now, follow me on this. Who goes to labs to get tested? Sick people. If a lab creates its “normal” range based on test results from sick people, is that really a normal range? Does that tell us anything about what the range should be for health? (For more on the problems with standard lab ranges, watch this great presentation by Dr. Bryan Walsh)

The five thyroid patterns

  1. Hypothyroidism caused by pituitary dysfunction

This pattern is caused by elevated cortisol, which is in turn caused by active infection, blood sugar imbalances, chronic stress, pregnancy, hypoglycemia or insulin resistance. These stressors fatigue the pituitary gland at the base of the brain so that it can no longer signal the thyroid to release enough thyroid hormone. There may be nothing wrong with the thyroid gland itself. The pituitary isn’t sending it the right messages.

With this pattern, you’ll have hypothyroid symptoms and a TSH below the functional range (1.8 – 3.0) but within the standard range (0.5 – 5.0).

  1. Under-conversion of T4 to T3

T4 is the inactive form of thyroid hormone. It must be converted to T3 before the body can use it. More than 90% of thyroid hormone produced is T4.

This common pattern is caused by inflammation and elevated cortisol levels. T4 to T3 conversion happens in cell membranes. Inflammatory cytokines damage cell membranes and impair the body’s ability to convert T4 to T3. High cortisol also suppresses the conversion of T4 to T3.

With this pattern you’ll have hypothyroid symptoms, but your TSH and T4 will be normal. If you have your T3 tested, which it rarely is in conventional settings, it will be low.

  1. Hypothyroidism caused by elevated TBG

Thyroid binding globulin (TBG) is the protein that transports thyroid hormone through the blood. When thyroid hormone is bound to TBG, it is inactive and unavailable to the tissues. When TBG levels are high, levels of unbound (free) thyroid hormone will be low, leading to hypothyroid symptoms.

With this pattern, TSH and T4 will be normal. If tested, T3 will be low, and T3 uptake and TBG will be high.

Elevated TBG is caused by high estrogen levels, which are often often associated with birth control pills or estrogen replacement (i.e. Premarin or estrogen creams). To treat this pattern, excess estrogen must be cleared from the body.

  1. Hypothyroidism caused by decreased TBG

This is the mirror image of the pattern above. When TBG levels are low, levels of free thyroid hormone will be high. You might think this would cause hyperthyroid symptoms. But too much free thyroid hormone in the bloodstream causes the cells to develop resistance to it. So, even though there’s more than enough thyroid hormone, the cells can’t use it and you’ll have hypothyroid – not hyperthyroid – symptoms.

With this pattern, TSH and T4 will be normal. If tested, T3 will be high, and T3 uptake and TBG will be low.

Decreased TBG is caused by high testosterone levels. In women, it is commonly associated with PCOS and insulin resistance. Reversing insulin resistance and restoring blood sugar balance is the key to treating this pattern.

  1. Thyroid resistance

In this pattern, both the thyroid and pituitary glands are functioning normally, but the hormones aren’t getting into the cells where they’re needed. This causes hypothyroid symptoms.

Note that all lab test markers will be normal in this pattern, because we don’t have a way to test the function of cellular receptors directly.

Thyroid resistance is usually caused by chronic stress and high cortisol levels. It can also be caused by high homocysteine and genetic factors.

Conclusion

The five patterns above are only a partial list. Several others also cause hypothyroid symptoms and don’t show up on standard lab tests. If you have hypothyroid symptoms, but your lab tests are normal, it’s likely you have one of them.

Not only do these patterns fail to show up on standard lab work, they don’t respond well to conventional thyroid hormone replacement. If your body can’t convert T4 to T3, or you have too much thyroid binding protein, or your cells are resistant, it doesn’t matter how much T4 you take; you won’t be able to use it.

Unfortunately, if you have one of these patterns and tell your doctor your medication isn’t working, all too often the doctor’s response is to simply increase the dose. When that doesn’t work, the doctor increases it yet again.

As I said at the beginning of this article, the key to a successful treatment is an accurate diagnosis. The reason the conventional approach fails is that it skips this step and gives the same treatment to everyone, regardless of the cause of their problem.

The good news is that, once the correct diagnosis is made, patients respond very well to treatment.

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Iodine for hypothyroidism: like gasoline on a fire?

July 5, 2010 in Thyroid Disorders | 65 comments

iodizedsaltThe fantasy of both conventional and alternative healthcare practitioners is finding a single nutrient to treat hypothyroidism. For doctors, this is thyroid hormone. For alternative practitioners, it is iodine.

In the previous article I showed why, when used alone, thyroid hormone replacement often fails. In this post I’ll explain why iodine may not only be ineffective, but also cause harm.

Iodine deficiency is the most common cause of hypothyroidism worldwide. Once researchers realized this, health authorities around the world began adding iodine to table salt.

This strategy was effective in correcting iodine deficiency. But it had an unanticipated – and undesired – effect. In countries where iodine has been added to table salt, the rates of autoimmune thyroid disease have risen. The following is just a sample of studies around the world demonstrating this effect:

Why does this happen? Because increased iodine intake, especially in supplement form, increases the autoimmune attack on the thyroid.

Iodine increases the activity of an enzyme called thyroid peroxidase (TPO). In Hashimoto’s disease, TPO is the target of the immune system’s attack. Therefore, excess iodine will worsen the autoimmune response.

The extreme of this expression is called the Jod-Basedow Phenomenon. It occurs in people who are iodine deficient with elevated thyroid antibodies. When they are given supplemental iodine they develop hyperthyroid symptoms.

Only a minority of Hashimoto’s patients will develop overt hyperthyroid symptoms as a result of taking iodine. Most will have no symptoms, but tests will indicate elevated levels of TPO antibodies, suggesting an autoimmune flare-up.

On the other hand, restricting intake of iodine can reverse hypothyroidism. In one study, 78% of patients with Hashimoto’s regained normal thyroid function with iodine restriction alone.

All of this might seem confusing to people with hypothyroidism who’ve been told their condition is caused by iodine deficiency. In the U.S., however, the most common cause of hypothyroidism is not iodine deficiency, but Hashimoto’s.

The conclusion I draw from this evidence is patients with autoimmune thyroid disease (Hashimoto’s and Graves’) should not be taking iodine supplements. Since 9 in 10 people with hypothyroidism have Hashimoto’s, it’s safe to say this advice applies to the vast majority of hypothyroid patients.

I am less certain about whether iodine in food must be restricted. Foods rich in iodine, like seafood, are also rich in other essential nutrients – such as selenium and vitamin D. One dietary recommendation I can make with certainty is to use non-iodized sea salt instead of iodized salt.

The use of iodine in the treatment of thyroid disease is a controversial subject. I’m sure some readers will post comments directing me to the work of Dr. Abraham and Dr. Brownstein, both of whom have successfully treated hypothyroid patients with iodine.

I’ve read Dr. Brownstein’s book and some of Dr. Abraham’s writings, and I respect their clinical experience. But when weighed against what we know about thyroid biochemistry and physiology, and the evidence presented above linking excess iodine to autoimmune thyroid disease, I believe the argument for not using iodine with Hashimoto’s is stronger than the argument for using it.

Dr. Datis Kharrazian, author of Why Do I Still Have Thyroid Symptoms When My Lab Test Are Normal?, has written extensively about the dangers of giving iodine to patients with Hashimoto’s disease. See this recent post on his blog for a summary of research supporting his view. (If you have a thyroid condition, do yourself a favor and buy his book. It’s the best on this topic by far.)

Finally, it’s worth pointing out that for the 10% of people who have hypothyroidism caused by iodine deficiency, supplemental iodine is both necessary and effective. How do you know you’re in this group? You get your thyroid antibodies (TPO & TG) tested. If the results are positive, you have Hashimoto’s. If the results are negative, however, you need to be tested at least once more to rule out Hashimoto’s. Antibody levels fluctuate and it’s possible to get a “false negative” result if you only have a single test.

Also keep in mind that a minority of patients with Hashimoto’s confirmed by biopsy (the gold standard) never test positive for thyroid antibodies. This is probably because their immune systems are so depressed they can no longer produce antibodies. If you have a combination of hyper- and hypothyroid symptoms, I would still suspect Hashimoto’s even if your thyroid antibody tests are normal.

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Three reasons why your thyroid medication isn’t working

July 1, 2010 in Thyroid Disorders | 24 comments

medicationIn the last post I explained that, for the vast majority of patients, hypothyroidism is an autoimmune disease. This isn’t just an academic distinction. It’s the reason both conventional and alternative treatments are so often ineffective.

In this post I’m going to show you why taking replacement thyroid hormones without addressing the underlying immune imbalance is doomed to fail.

The ultimate effect of hypothyroidism, whether it’s caused by iodine deficiency or autoimmunity, is to decrease the amount of thyroid hormone available to the body. The conventional approach is to simply replace these hormones with either synthetic or bio-identical forms.

On the surface it seems like a reasonable approach. Patient doesn’t have enough hormones? Give more hormones. Simple, right?

Not so much.

Once again the conventional approach falls short because it ignores the underlying cause of the problem. It’s like taking Advil when you’ve got a pebble stuck in your shoe. It might work for a little while, and might even be necessary to dull the pain. But you’d be a lot better off if you took the pebble out of your shoe. Right?

Let’s take a closer look at why thyroid hormones often don’t work, or stop working over time. The following diagram illustrates how autoimmunity affects thyroid metabolism:

hashimotos

Immune dysregulation is another term for autoimmune disease. We still don’t know exactly what causes it, but most researchers agree it’s a mixture of genetic susceptibility and environmental factors such as iodine (excess), infection, pregnancy, diet and intestinal permeability.

In autoimmune disease the body attacks itself. It does this the same way it attacks foreign invaders like bacteria and viruses: with T-cells, B-cells, natural killer cells, and cytotoxic T cells. The immune response also involves proteins called cytokines, chemical messengers that pass messages between cells.

This self-attack by the immune system increases inflammation. And inflammation has a profound effect on all aspects of thyroid metabolism and physiology.

First, inflammation suppresses the hypothalamus-pituitary-thyroid (HPT) axis. One study showed a single injection of the inflammatory cytokine TNF-alpha reduced blood levels of TSH, T3, free T4, free T3 and TRH for 5 days. This shows inflammation disrupts the production and regulatory mechanisms of thyroid hormones. Thyroid medication will increase the levels of T4 (and possibly T3), but it doesn’t address the other effects of HPT axis suppression.

Second, inflammation decreases both the number and sensitivity of thyroid hormone receptors. If there aren’t enough receptors, or they aren’t sensitive enough, it doesn’t matter how much thyroid medication we take. The cells won’t be able to use it. It’s like when my grandpa used to turn down his hearing aids while he was watching the football game. It didn’t matter how much my grandma yelled at him – he couldn’t hear a word she said.

Third, inflammation decreases the conversion of T4 to T3. T4 is the inactive form of thyroid hormone. The body has to convert it to the active T3 form before it can be used. Most synthetic hormone medications on the market are T4. If you give a T4 medication (like Synthroid, Levoxyl, Unithroid, etc.) to someone with inflammation, it’s not going to work because they can’t convert the T4 to T3.

Patients who don’t convert T4 to T3 well do better on bio-identical hormones like Armour, because it contains both T4 and T3 (in a 4.22:1 ratio).

Inflammation disrupts thyroid metabolism in several other ways, but I think these three examples make the point.

Now let’s review.

Inflammation causes HPT axis disruption, decreased receptor function, and decreased conversion of T4 to T3. Thyroid medication only increases the levels of thyroid hormone (usually T4) in the blood. No matter how much we take, it’s not going to restore HPT axis coordination, improve receptor function, or increase conversion of T4 to T3.

The only way to do that is to address the problem at its root by regulating the immune system and decreasing inflammation. Unfortunately, this is rarely done in either conventional or alternative treatment of thyroid disorders.

Before I sign off, I just want to make one thing clear. I’m not saying thyroid medication isn’t necessary or useful. In fact, I think it’s an important part of treating Hashimoto’s – especially when TSH is consistently elevated and T4 and T3 are consistently low. My point is thyroid medication is only one piece of the puzzle, and it won’t be effective on its own unless the autoimmunity and inflammation are addressed.

If thyroid medication is the fantasy magic bullet of conventional medicine, iodine is the equivalent in alternative medicine. In the next post I’m going to explain why supplemental iodine may cause more harm than good in Hashimoto’s patients.

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The most important thing you may not know about hypothyroidism

June 28, 2010 in Myths & Truths, Thyroid Disorders, Uncategorized | 55 comments

hypothyroid patientAn estimated 20 million Americans have some form of thyroid disease. Up to 60 percent of these people are unaware of their condition. One in eight women will develop a thyroid disorder during her lifetime. Levothyroxine, a synthetic form of thyroid hormone, is the 4th highest selling drug in the U.S. 13 of the top 50 selling drugs are either directly or indirectly related to hypothyroidism. The number of people suffering from thyroid disorders continues to rise each year.

Hypothyroidism is one of the most common thyroid disorders. One recent analysis suggested up to 10% of women over 60 have clinical or subclinical hypothyroidism. It is characterized by mental slowing, depression, dementia, weight gain, constipation, dry skin, hair loss, cold intolerance, hoarse voice, irregular menstruation, infertility, muscle stiffness and pain, and a wide range of other not-so-fun symptoms.

Every cell in the body has receptors for thyroid hormone. These hormones are responsible for the most basic aspects of body function, impacting all major systems of the body.

Thyroid hormone directly acts on the brain, the G.I. tract, the cardiovascular system, bone metabolism, red blood cell metabolism, gall bladder and liver function, steroid hormone production, glucose metabolism, lipid and cholesterol metabolism, protein metabolism and body temperature regulation. For starters.

You can think of the thyroid as the central gear in a sophisticated engine. If that gear breaks, the entire engine goes down with it.

That’s why people with hypothyroidism experience everything from weight gain and depression to infertility, bone fractures and hair loss.

One of the biggest challenges facing those with hypothyroidism is that the standard of care for thyroid disorders in both conventional and alternative medicine is hopelessly inadequate.

The dream of patients with thyroid disorders and the practitioners who treat them is to find that single substance that will magically reverse the course of the disease. For doctors, this is either synthetic or bio-identical thyroid hormone. For the alternative types, this is iodine.

Unfortunately, in the vast majority of cases neither approach is effective. Patients may get relief for a short period of time, but inevitably symptoms return or the disease progresses.

So what’s the problem? Why have replacement hormones and supplemental iodine been such dismal failures?

Because hypothyroidism is an autoimmune disease.

Studies show that 90% of people with hypothyroidism are producing antibodies to thyroid tissue. This causes the immune system to attack and destroy the thyroid, which over time causes a decline in thyroid hormone levels.

This autoimmune form of hypothyroidism is called Hashimoto’s disease. Hashimoto’s is the most common autoimmune disorder in the U.S., affecting between 7-8% of the population. While not all people with Hashimoto’s have hypothyroid symptoms, thyroid antibodies have been found to be a marker for future thyroid disease.

Most doctors know hypothyroidism is an autoimmune disease. But most patients don’t. The reason doctors don’t tell their patients is simple: it doesn’t affect their treatment plan.

Conventional medicine doesn’t have effective treatments for autoimmune disease. They use steroids and other medications to suppress the immune system in certain conditions with more potentially damaging effects, such as multiple sclerosis, rheumatoid arthritis and Crohn’s disease.

But in the case of Hashimoto’s, the consequences – i.e. side effects and complications – of using immunosuppressive drugs are believed to outweigh the potential benefits. (Thanks to conventional medicine for a relative moment of sanity here.)

So the standard of care for a Hashimoto’s patient is to simply wait until the immune system has destroyed enough thyroid tissue to classify them as hypothyroid, and then give them thyroid hormone replacement. If they start to exhibit other symptoms commonly associated with their condition, like depression or insulin resistance, they’ll get additional drugs for those problems.

The obvious shortcoming of this approach is that it doesn’t address the underlying cause of the problem, which is the immune system attacking the thyroid gland. And if the underlying cause isn’t addressed, the treatment isn’t going to work very well – or for very long.

If you’re in a leaky rowboat, bailing water will only get you so far. If you want to stop the boat from sinking, you’ve got to plug the leaks.

Extending this metaphor to Hashimoto’s disease, thyroid hormones are like bailing water. They may be a necessary part of the treatment. But unless the immune dysregulation is addressed (plugging the leaks), whoever is in that boat will be fighting a losing battle to keep it from sinking.

What the vast majority of hypothyroidism patients need to understand is that they don’t have a problem with their thyroid, they have a problem with their immune system attacking the thyroid. This is crucial to understand, because when the immune system is out of control, it’s not only the thyroid that will be affected.

Hashimoto’s often manifests as a “polyendocrine autoimmune pattern”. This means that in addition to having antibodies to thyroid tissue, it’s not uncommon for Hashimoto’s patients to have antibodies to other tissues or enzymes as well. The most common are transglutaminase (Celiac disease), the cerebellum (neurological disorders), intrinsic factor (pernicious anemia), glutamic acid decarboxylase (anxiety/panic attacks and late onset type 1 diabetes).

In the next post we’ll look more closely at why Hashimoto’s can’t be treated successfully without addressing the autoimmune component, and why both the conventional and alternative approaches to treating hypothyroidism are destined to fail from the start.

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Healthcare vs. disease management

June 24, 2010 in Medical Industrial Complex | 26 comments

disease management In a recent post, The Myth of Evidence Based Medicine, I explained that conventional medicine is based not on evidence, but on profit.

So how’s this working out for us?

The U.S. spends far more than any other country in the world on healthcare – a whopping $2 trillion per year. 1

Considering this enormous expenditure, we should have the best medicine in the world. We should be reversing disease, preventing disease, and doing minimal harm.

But that’s not what’s happening at all. The U.S. ranks just 34th in the world in life expectancy and 29th for infant mortality. Of 13 countries in a recent comparison, the United States ranks an average of 12th (second from bottom) for 16 available health indicators. 2

Even worse, a study published a few years back in JAMA suggested that medical care may be the leading cause of death in the US. (For more on this, read my article The Failure of U.S. Healthcare).

Yes, you read that right. Medical care kills more people than heart disease, strokes or cancer.

How can it be that we spend nearly 16% of our GDP on healthcare, but have one of the worst health care systems in the industrial world?

The answer, in short, is that we don’t have healthcare in the U.S.. We have disease management. And there’s a world of difference between the two:

wellnesscare

Wellness care is what we need. Disease management is what we have.

Wellness care would save insurance companies billions of dollars each year. But it would devastate the bottom lines of the pharmaceutical industry.

Wellness care is what I will offer my patients. And it’s the vision I have for what medicine could be here in the U.S. and elsewhere.

I’m just not holding my breath. Until we can lessen the influence of Big Pharma, disease management will rule.

  1. Park, A. America’s Health Check Up. 11/20/2008. Time Magazine Online. ↩
  2. Starfield B. Primary Care: Balancing Health Needs, Services, and Technology. New York, NY: Oxford University Press; 1998. ↩

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