The thyroid gland itself is only responsible for roughly 7% of your total body’s active thyroid hormone. If you have read my previous articles you know that around 93% of what your thyroid gland produces is inactive thyroid hormone (T4). The other 7% of the hormones coming out of the gland is the active form (T3).
So where does the majority of my active form of thyroid hormone come from?
If your thyroid was like your boss who gave you a paycheck, your liver is the bank in which you can cash this check for usable money. In this analogy, the paycheck is like the inactive form of thyroid hormone (T4) and actual usable money is the active form of thyroid hormone (T3). Your liver produces more active thyroid hormone than the thyroid gland does itself. Some thyroid experts (1) report that up to 60% of your total T3 depends on healthy liver function.
This has been known for decades now in the literature, and yet it still doesn’t get much recognition.One study (2) showed that 23 patients with extreme liver function also showed a significant portion of these people with enlargement of their thyroid gland called a goiter. A goiter is often seen in those with more severe hypothyroidism. What was even more interesting is that after their liver recovered all but one person’s goiter was clinically undetectable. The same study also showed that after liver recovery all thyroid variables were normalized. We can see that in studies that look at other liver functions (like the flow and production of bile) demonstrate a clear association with a decrease in bile flow and those with hypothyroid. (3,4) When you decrease bile flow, you also increase the prevalence of gallstones. It is no surprise that there is an increased prevalence of gallstones in those with hypothyroidism (5,6). One of the many other functions the liver has is cholesterol production and metabolism. There have been animal studies showing that cholesterol metabolism is impaired with lower thyroid hormone. This actually was reversed when the animals were given thyroid hormone (7). So there is a clear relationship in the literature in thyroid dysfunction with liver dysfunction, and this relationship is a two-way street. So liver function affects thyroid hormone and thyroid hormone affects liver function.
What the end goal is to live a lifestyle that promotes harmony of all systems in the body so you don’t have to medicate these symptoms.Using the paycheck and bank analogy above, when it comes to thyroid hormone, having a good liver is like having a friendly bank. A friendly bank that has very little fees can turn convert pretty much all of that paycheck into actual money. Now let’s say you were a part of a different bank, one that would charge you fees for everything under the sun. You want to go inside and talk to the teller? There’s a fee for that. You didn’t keep a minimum balance? I’m sorry there’s a fee for that, too. Oh, and that ATM you used back in December? Yeah, we had to charge a fee for that. Now that we are talking about fees you have Paper Statement fees, and returned mail fees that will go into effect next week. So you said you wanted to make a deposit? Just don’t make it too big because we have a big deposit fee too…The point being is that with a fee ridden bank you are going to end up with less actual money than what is said on that paycheck. A dysfunctional liver is like a dysfunctional bank, you are going to get less actual active hormone T3 conversion compared to a healthy functioning liver.
The conversion of T4 to active T3Since the majority of thyroid hormone released from the thyroid gland is inactive, we need to rely heavily on the conversion of its inactive form to the active form. Remember, the liver is responsible for 60% of this conversion to active T3. The enzyme that produces active T3 from the inactive T4 comes from a class of enzymes called the deiodinase enzymes. This enzyme will strip one of the four iodine molecules off of T4, and thus leave it with three iodine molecules left, T3. This is why it is called a DE-iodinase enzyme. To make things even a little bit more complex is that there are multiple types of deiodinase enzymes. The reason why the body is suspected to have different types of deiodinase enzymes is thought to be a regulatory mechanism. The liver primarily has two different types: both Type 1 Deiodinase (DIO1) and Type 3 Deiodinase (DIO3). DIO1 is responsible for producing active T3, while DIO3 actually produces something called reverse T3 which is inactive. When an individual is stressed, sick, inflamed or all three this upregulates DIO3 in the liver (8) which will in turn produce more inactive reverse T3. So it is important to look at stress and inflammation in those with thyroid issues for this very reason. These deiodinase enzymes are also heavily dependent on selenium, which is a very important nutrient for thyroid function.
Thyroid Binding Globulin – It can be Your Private Jet or Your Ball-and-Chain
Thyroid binding globulin is the transport molecule of thyroid hormone. It is considered to be another layer of this vast regulatory mechanisms that involve thyroid hormones. Many people call Thyroid binding globulin a taxi cab, I like to call it the private jet. When levels of thyroid binding globulin are just right, thyroid hormones are shuttled to their destination swiftly like a private jet. Too much of these binding globulins and they can act like a ball-and-chain and bind up thyroid hormone which renders them useless. Like goldilocks and the pourage, we want Thyroid Binding globulin to be at just the right level. Not too high, or not too low. Thyroid binding globulin is considered to be an acute phase reactant (9), which means it is elevated under times of inflammation and stress. Elevated estrogens have been shown to elevate Thyroid binding globulin 2-3 fold (10). Birth control has also been shown to elevate thyroid binding globulins as well (11).
Homocysteine and your thyroid gland
Homocysteine is a molecule that is overproduced when a process in the liver called methylation is impaired. Methylation is highly depended on vitamin B status, as well as many other compounds. There are also many genes as well as gene mutations that can affect methylation (this is a topic in and of itself). Elevated homocysteine can contribute to atherosclerosis, brain degeneration, and it can actually bind to thyroid receptors and block the entrance of thyroid hormone into the nucleus of the cell (12)
Your Liver, Your Gut Bacteria, and Thyroid Hormone
In a previous article, I mentioned that your liver will produce two different compounds called T3-Sulfate (T3S) and T3-aceticacid (T3AC). These two compounds are then sent to the gut in which our gut microbes can convert these compounds into T3. It is estimated that this can account for 20% of your total T3 (1).
When looking at someone with thyroid dysfunction it is also important to look at the other tissues that help play a role in thyroid hormone production. Now I want to hear from you! Have you had your liver, gut, or kidneys looked at from a thyroid hormone perspective?
(1) Kharrazian, Datis. “Chapter 1.”Why Do I Still Have Thyroid Symptoms?: When My Lab Tests Are Normal. Garden City, NY: Morgan James Pub., 2010. 3-4. Print.