Testing TSH only or even TSH and T4 does not work!
If you suffer from thyroid symptoms (fatigue, hair loss, brittle nails, feeling cold, difficulty losing weight, brain fog, infertility menstrual irregularity) and they did thyroid testing by running just a TSH or maybe a TSH and a free T4, it wasn’t enough. If you are currently on medication and they are only testing TSH or maybe a TSH and a free T4 it is not enough! Let’s look at some thyroid physiology to understand why TSH and T4 are not enough, by themselves, to accurately assess how your thyroid is functioning.
Thyroid Testing Basics
TSH is produced by the anterior pituitary gland and it tells the thyroid gland to produce more thyroid hormone. The thyroid produces mainly T4 which then gets converted to T3 in peripheral tissues (liver, intestines, and lungs mainly). T3 is the “active” thyroid hormone. By saying T3 is the active thyroid hormone, it means that if you have thyroid symptoms, you ultimately have some kind of a problem with normal, healthy T3 activity in the cells. This is a big deal! Normal TSH, and normal T4 follow by low or functionally low T3 is one of the most common patterns I see in patients.
The production of your thyroid hormones looks like this:
TSH>T4>T3>Hormone Activity
The current standard in thyroid testing is to run only T4 and TSH and then assume that if they are ok you are converting from T4 to T3 correctly. This is wrong! Let’s explore a little more about this thyroid conversion process. I think a picture can help here.
The above picture illustrates how someone has low T3 in the body due to decreased activity of the D1 enzyme, but sufficient T3 in the pituitary due to normal activity of the enzyme D2. This leads to low T3 in the body creating thyroid symptoms, but normal T3 in the pituitary creating a normal TSH.
You’ll notice from the picture that two separate enzymes can convert T4 to T3. Deiodinase type 1(D1) is the dominant form found in the liver where roughly 80% of T4 to T3 conversion takes place while deiodinase type 2(D2) is abundant in the pituitary gland. This is an important distinction because there appears to be many physiological shifts that alter D1 activity but not D2[i],[ii],[iii]! The net effect of having poor D1 activity is the thyroid will be low in the active thyroid hormone T3 for the body. The deadly combination is that as long as D2 works the pituitary will not be low in the active thyroid hormone T3! What happens when the body is deficient in T3, but the pituitary gland is not? You will have symptoms of low T3 (fatigue, hair loss, brittle nails, feeling cold, difficulty losing weight, brain fog, infertility menstrual irregularity), but your pituitary marker of thyroid metabolism (TSH)will look normal.
Yes, I would like to work with Dr. Warren or Dr. Deglmann
The next question is what causes these decreases in D1 activity and thus a low peripheral T3 level?
This discussion is actually a huge can of worms and why helping someone with a thyroid problem can get a little complicated. Here is a brief list of things we know can alter the activity of the deiodinase enzyme and reveal a “Normal TSH and T4” but a low T3 with proper thyroid testing.
- Deficiency of selenium
- Imbalanced serotonin (depression)
- Imbalanced dopamine (depression and anxiety)
- Imbalance cortisol, stress hormone(sleep, energy, and food cravings)
- Imbalance of testosterone
- Decreased growth hormone
- Blood sugar imbalances (reactive hypoglycemia, insulin resistance, and diabetes)
- Chronic pain
- Environmental toxin exposures
- Iron deficiency
- Inflammation
Your Body Is Intelligent
I would like to take a brief pause here and admire the amazing intelligence of your body. This system of thyroid hormone conversion is a built in protection mechanism! This system is designed to slow you down during times of stress to protect your body from harm. The most dramatic studies on this conversion process come from people who are critically ill, starving, or suffering from inflammation[iv],[v]. Let’s use starvation as an example because it is fairly simple.
When you do not eat food for a long period of time, you decrease the T3 in your body. Why? It slows down your metabolism to help you survive longer under this stress. What would happen if you decreased T3 in the pituitary at the same time you decreased it in the body? The pituitary would sense the low T3 and want to send instructions to make more thyroid hormone. This is not what we want! The body is trying to protect itself from a stress by lowering the active thyroid hormone availability. Therefore, we have a system in place that lets us lower the active T3 in the body while keeping the pituitary levels of T3 adequate (and thus the TSH looks normal).
This system is basically triggered by massive stress which can have various sources. You can find studies on starvation, critically ill people, and but it happens to people who are inflamed and those who struggle with chronic illness. You do not have to be on death’s doorstep for this phenomena to happen to you. A study in 2011 found that people with elevated IL-6 (an inflammatory cytokine) showed this decrease in T3 production in the body, but the pituitary was unaffected. They also found that when you got rid of the inflammation and the IL-6 went down that the thyroid conversion went back to normal![vi]If more doctors ran T3 with their thyroid testing panels they would see this, but insurance companies tell the doctors T3 is not important! How is the active thyroid hormone not the MOST important piece to actually test?
Solving the Problem
Before I end this I just want to talk briefly about what to do when thyroid testing reveals a low T3 problem. Many patients come to me after going to websites or reading books and believe that a T3 medication (like Armour or Cytomel) will solve their symptoms. Let me make this very clear. I think T3 medication can help a ton of people and should be used in the majority of hypothyroid cases. However, can you see that if the imbalance in T3 is caused by…inflammation, or a problem with testosterone, or an adrenal problem, or iron deficiency…it is a bad idea to take T3 medication and ignore what caused this imbalance in the first place? Check out some other great websites, and you’ll find they agree with me on thyroid testing:
www.thyroidbook.com
www.nahypothyroidism.org
http://chriskresser.com/thyroid
One of the great secrets of helping someone with a thyroid problem is understanding how other processes affect the thyroid. (The details at each website may vary, but the basic message of TSH/T4 testing not being enough, T3 being important, and other health problems affecting the thyroid are the central piece here). Proper thyroid testing always includes TSH, T4, and T3.
Contact Restorative Health Solutions for a free 15 minute consult. Click HERE to go to our CONTACT US page and get a personal answer to your questions.
[i] Dentice M, Salvatore D. Deiodinases: the balance of thyroid hormone: local impact of thyroid hormone activation. J Endocrinology2001. Jun; 209(3):273-82.
[ii] Bates JM, St Germain DL, Galton VA. Expression profiles of the three iodothyronine deiodinases, D1, D2, and D3, in the developing rat. Endocrinology. 1999 February; 140(2):844-51
[iii] Arrojo E, Drigo R, Fonseca TL, Werneck-deCastro JP, Biano AC. Role of the type 2 iodothyronine deiodinase (D2) in the control of thyroid hormone signaling.
[iv] Peeters RP, Wouters PJ, Kaptein E, Van Toor H, Visser TJ, Van den Berghe G. Reduced activation and increased inactivation of thyroid hormone in tissues of critically ill patients. Journal of Clinical Endocrinology and Metabolism. 2003 Jul;88(7):3202-11.
[v] Debaveye Y, Ellger B, Mebis L, Van Herck E, Coopmans W, Darras V, Van den Berghe G. Tissue deiodinase activity during prolonged critical illness: effects of exogenous thyrotropin releasing hormone and its combination with growth hormone-releasingpeptide-2. Endocrinology. 2005 Dec;146(12)5604-11.
[vi] Wajner SM, Goemann IM, Bueno AL, Larsen PR, Maia AL. IL-6 promotes nonthyroidal illness syndrome by blocking thyroxine activation while promoting thyroid hormone inactivation in human cells. J Clin Invest. 2011 May; 121(5):1834-45.
