I was talking with a colleague a few weeks ago about functional medicine, and what that looks like in practice. “So, how would you treat someone with hypothyroidism, for example?” He asked me. My answer was far from simple, and that’s because no two cases of hypothyroidism are exactly the same.
In the world of functional medicine, we categorize “hypothyroidism” in seven different ways. In a traditional doctor’s office, that isn’t the case, which leads to the multitude of diverse and unique patient cases getting treated exactly the same. (Read: Synthroid) For those with primary hypothyroidism, AKA “underactive thyroid,” or a thyroid that just isn’t doing its job of producing adequate hormone, replacement therapy is appropriate. But what if the reason someone has low thyroid function doesn’t begin and end with the thyroid? In fact, most of the time, the diagnosis and solution isn’t so linear…
The Seven Thyroid Patterns
1. Primary Hypothyroidism (Underactive Thyroid)
Primary hypothyroidism basically boils down to a thyroid gland that isn’t doing its job of manufacturing thyroid hormone. If thyroid hormone isn’t being made, it can’t carry out its function in the body. Thyroid hormones come in two basic forms, T3 (triiodothyronine) and T4 (tetraiodothyronine). Both of these hormones basically consist of an amino acid molecule (tyrosine) attached to three (T3) or four (T4) molecules of iodine. T3 is considered the “active” form of thyroid hormone, which floats around in the blood, doing its job. T4 has some direct effects on the body, but it’s most known for acting as a reserve for T3. When T3 start to drop, rather than simply making more T3 right away (this might take too long), an enzyme removes one of the four iodine molecules from T4, thereby converting it to T3, the “active form.” The thyroid produces these hormones in proportions roughly equal to 5% T3 and 95% T4, give or take.
Underactivity of the thyroid can result from two things. One, the thyroid might not have access to the raw materials needed to manufacture thyroid hormones (namely, tyrosine and iodine) or two, the machinery just might not work. To effectively treat an underactive thyroid, we would need to substitute either thyroid hormone or tyrosine/iodine, depending on which is needed.
2. Hypothalamic Hypothyroidism (Stress-Induced)
Although thyroid hormones are made by the thyroid, the thyroid gland itself isn’t the control center. Rather, an area of the brain called the hypothalamus calls the shots. The hypothalamus secretes a hormone called TRH, thyrotropin-releasing hormone, which in turn signals to the pituitary gland to increase or decrease TSH, thyroid stimulating hormone, which is the hormone that directly tells the thyroid what to do. This whole process is referred to as the Hypothalamic Pituitary Thyroid Axis.
To make things more complicated, thyroid hormone production doesn’t quite begin and end at the hypothalamus, either. Although the hypothalamus acts as the control center for thyroid hormone regulation, other processes in the body can suppress the activity of the hypothalamus–namely, stress.
Stress comes in many forms (too much exercise, too little sleep, not eating enough, overworking ourselves, relationship problems, illness etc…) but they all affect the hypothalamus (and thyroid) the same way. If a patient’s hypothyroidism results from stress, hormone replacement therapy would help, yes. But is it the best way to help this patient heal? No. The obvious answer would be stress reduction, and supporting the body in overcoming the dangerous effects of stress.
3. Hashimoto’s Thyroiditis (Autoimmune)
Autoimmune hypothyroidism is a subset of primary hypothyroidism in that the thyroid-hormone-making-machinery is malfunctioning. But the difference between Hashimoto’s thyroiditis and the type of hypothyroidism described in #1 is that the cause of the thyroid dysfunction is known: autoimmunity. In this case, the body mistakes the thyroid gland for a pathogen, and the immune system begins attacking and destroying the thyroid tissue, affecting its ability to produce thyroid hormone. Once again, hormone replacement therapy would help the situation, but the best solution would be to treat the autoimmune process and help prevent it from getting out of control.
Hashimoto’s thyroiditis, like other autoimmune conditions, has a genetic predisposition that can be triggered by factors in the environment. Sometimes stress can trigger the autoimmunity, as can nutritional problems, environmental exposure to toxins, viral infections, and more. Either way, the best solution is to treat the autoimmunity and teach the patient how to manage their condition.
4. Peripheral Conversion Defect (Thyroid Hormone Metabolism)
As a quick refresher on what we’ve already discussed, T3 is the “active” form thyroid hormone, produced in small amounts. The thyroid produces T4, the “inactive” form at rates nearly 20x higher, which floats around in the blood stream to be converted to T3 as needed.
Mainly, the conversion of T4 to T3 takes place in the liver, but the digestive system, heart, muscle, and nerve cells all also are involved in the conversion process. However, sometimes this conversion process gets interrupted, leading to blood levels of T3 that are too low. The reason for this can be complicated, but some of the main drivers of this so-called peripheral conversion defect (or problem with thyroid hormone metabolism) include oxidative stress and nutritional deficiencies. Correcting nutritional deficiencies is pretty straightforward (change the diet, supplement, correct absorption problems) but oxidative stress is a whole other animal. Oxidative stress results from inflammation, which can be triggered by anything from chronic disease, to infections, to a high-stress lifestyle. Once again, this form of hypothyroidism is highly individual.
5. Hormone Receptor Competition (Toxins)
Once T4 has been converted into its active form of T3, it’s time for the hormone to do its job. Thyroid hormone is responsible for regulating body temperature, metabolism heart rate, digestion, cognitive function, fertility…you name it, thyroid hormone affects it. Thyroid hormone acts like an on/off switch in the body. When it binds to its receptors, it either amplifies or suppresses the ongoing response. If no T3 is around, the switch can’t get flipped.
But of course, nothing is quite as simple as flipping a switch (except, you know…flipping a switch.) Really, the relationship between the T3 hormone and our bodily systems is more like a lock and key mechanism. T3 is like the key, and the receptor is like a lock, which is only supposed to be accessed by its specially designated key. Unfortunately, there are quite a few molecules in the world that look a lot like T3, and can fit into the T3 receptor (like a keyhole). Unlike thyroid hormone, these molecules can’t actually turn on or off the switch, but they do fit nicely into the receptor, preventing T3 from accessing it.
These “look alike” molecules obviously aren’t supposed to be in our bodies. Typically, they’re toxins that result from contaminated food and water, poor quality air, exposure to mold/fungus, or hazardous chemicals. Unlike some of the other types of hypothyroidism we’ve already discussed, supplementing with thyroid hormone won’t correct the problem. The body already has plenty of T3 floating around, and adding more hormone isn’t going to have much effect. Sure, it might crowd out the toxins, out competing them for the receptor site, but typically the therapeutic dose used for patients isn’t sufficient to have an effect. The only solution is to remove the source of the exposure and support the body’s detoxification efforts.
6. Binding Globulin Availability (Sex Hormone Imbalances)
Remember all those details about TRH, TSH, T3, and T4? Well, there are three more hormones to add to the list to make things just a little more confusing: rT3 (reverse T3), free T3, and free T4.
When thyroid hormones travel through the blood stream, they aren’t just floating around willy-nilly, waiting to find their receptor. Instead, they’re bound to carrier proteins, called globulins, which help protect them from damage and shuttle them to where they need to go. While on the bus (attached to the hormone binding globulin), the thyroid hormone is inactive. Only when it detaches from the globulin, metaphorically getting off the bus, can it do its job of binding to the receptor. Sometimes, the ratio of globulin to thyroid hormone becomes distorted, with too much globulin. The result of this is that the thyroid hormone gets all bound up, making it inactive by preventing it from accessing the receptor site. In order to truly be “active,” thyroid hormone needs to be unattached from globulin. In this situation, we call the thyroid hormone “free T3” and “free T4.” As you might guess, a person might have normal and healthy levels of total T3 and T4, but the amount of free T3 and free T4 are too low because the amounts of hormone binding globulin are too high.
What causes elevated levels of hormone binding globulins? Lots of things, but most often excess amounts of estrogen (from birth control pills, pregnancy, or other reasons) and estrogen “look alike” molecules, such as plastics, soy products, and other toxins. The best way to treat a patient in this situation is to uncover the cause of the excess globulins, remove the source, and support the body’s detoxification as it returns to a functional baseline.
7. Nutrient Deficiencies
If we circle back to point #1, we remember that thyroid hormones (T4 and T3) are named as such because of the number of iodine molecules they contain. So, what happens when a person needs to synthesize more thyroid hormone but they don’t have enough iodine in order to do so?
You guessed it, thyroid hormone deficiency. However, iodine isn’t the only nutrient which, when depleted, can induce a state of hypothyroidism. Zinc, selenium, vitamin D and magnesium are all necessary for thyroid hormone production, and low levels mean bad news for thyroid health. (Additionally, hypothyroid patients also tend to be low on vitamin B12, though that isn’t necessarily something that causes hypothyroidism.)
If that sounds complicated, it’s because it is! What makes it even more complicated is the fact that you can’t possible know whether or not you have vitamin deficiencies that predispose you to hypothyroidism, or what type of hypothyroidism you actually have (if you have it at all) unless you have a thorough lab workup done by your doctor.
The causes of hypothyroidism are complicated and multi-faceted, even more so than I’ve been able to cover in this blog post! But the main takeaway is that you shouldn’t settle for a simple diagnosis if your doctor simply tells you you have hypothyroidism. There’s always more to the picture, and there are likewise a lot more options for education and management. Many people don’t need a lifelong prescription for Synthroid. In some cases, it’s possible to completely reverse the hypothyroidism, prevent it from worsening, and even heal related conditions (like sex hormone imbalances, toxin exposure, or autoimmune disease.)
If you’re suffering with thyroid disease, first of all, I’m so sorry. But more importantly, there’s hope for you! Ask your doctor to dig a little deeper, or find a new healthcare provider who will help get to the bottom of your symptoms and empower you to manage your health according to your values.