This article is part of a special report on Thyroid Disorders. To see the other articles in this series, click here.
In the last article in this series I discussed several lines of evidence suggesting that inflammation is one of the primary causes of Low T3 Syndrome.
In this article we’re going to discuss another common, but lesser known, cause: autoimmune hypopituitarism.
Say what? I know that’s a mouthful. Let’s break it down.
The pituitary gland is located just below the hypothalamus, but outside the blood-brain barrier. It’s primary job is to monitor the levels of hormones produced by various endocrine organs (like the thyroid), and release stimulating hormones (like TSH) that direct those organs to produce their respective hormones (like T4 and T3).
The pituitary gland can be the target of inflammatory response to local infections, cancer or autoimmune reactions. When an autoimmune mechanism is involved, lymphocytic adenohypophysitis (LAH) or autoimmune hypopituitarism are the terms used to describe the condition. (I’ll refer to this condition as LAH throughout the article.)
What is autoimmune hypopituitarism?
LAH is characterized by progressive destruction of pituitary tissue, which over time produces a decline in the function of the pituitary gland. (1) When the pituitary is damaged more than one hormone is affected, especially as the disease becomes more advanced.
It was originally believed that LAH occurred exclusively in pregnant women. (2) But although prevalence is still much higher in that population, we now know it also occurs in non-pregnant women, men and children. (3)
Adrenocorticotropin (ACTH) deficiency is most common (60%), followed by thyrotropin (TSH) deficiency (47%), gonadotropin (FSH/LSH) deficiency (42%), growth hormone deficiency (42%) and prolactin deficiency (34%).
What is remarkable about this condition is how unknown it is in spite of its prevalence. It’s true prevalence is unknown, but most investigators believe it is under-reported because it is often misdiagnosed. I’ve seen some estimates that it may affect up to 0.5% of the population and up to 40% of Hashimoto’s patients.
How is autoimmune hypopituitarism diagnosed?
The reason it’s so often misdiagnosed is that it’s difficult to pin down. It is strongly associated with other autoimmune diseases, which further complicates the clinical picture. In fact, concurrent autoimmune conditions are reported in 20-50% of LAH cases. (4)
Interestingly, Yoon et al. injected hamsters with Rubella virus glycoproteins and consistently induced LAH, as evidenced by autoantibodies to pituitary cells and infiltration of the pituitary gland by lymphocytes. (5) This finding suggests there may be some connection between viral infections and LAH.
Other investigators have identified antibodies to growth hormone (GH), thyrotropin (TSH), and luteinizing hormone (LH) in cases of LAH. (6) Unfortunately, the only conclusive test for LAH is a tissue biopsy, which is obviously problematic due to the location of the pituitary gland.
Low levels of the pituitary hormones can indicate LAH, but they can also be a sign of other functional problems with feedback in the hypothalamus or a primary problem with the hypothalamus itself.
What are the signs and symptoms of LAH?
The hallmark sign of LAH is atrophy of the gonads, adrenals and thyroid gland. Endocrine tissue is similar to muscle tissue in the sense that it will atrophy if it’s not stimulated regularly (similar to how men who take testosterone have shrunken testes).
- Impaired vision
- Loss of appetite
- Hormone imbalances
However, LAH is difficult to characterize because it can mimic so many other conditions. A problem with the pituitary gland can affect the entire endocrine system, because the pituitary sends out the stimulating hormones that direct the organs (thyroid, adrenals, ovaries, testes, etc.) to produce their respective hormones. This is, of course, how LAH can lead to low T3 levels.
It’s also interesting to note that there appears to be a connection between LAH and celiac disease. (What isn’t connected with celiac disease?) Delvecchio et al found that about 40% of newly diagnosed celiac patients had anti-pituitary antobidies in their blood and it resulted in – at a minimum – growth hormone deficiency. (7) This is an important finding that I have rarely seen discussed.
How is autoimmune hypopituitarism treated?
Not very well, in the conventional model. Some doctors use immunosuppressants like prednisone, azothioprine and methotrexate, but the risks and side effects of these drugs can often be worse than the disease itself.
The first step to take is to make sure you’re eating a diet that is free of foods that tend to provoke an autoimmune response. A Paleo-type diet is the best starting place, but you may also want to remove dairy, nightshades and eggs for at least 30 days because those foods can be problematic for people with autoimmune disease.
It’s also important to focus on nutrients that support proper T-regulatory cell function, like vitamin D and glutathione, and nutrients that support overall immune health like vitamin C, iodine and selenium.
I would also consider low-dose naltrexone (LDN), a medication that is being used to successfully treat a wide range of autoimmune diseases – including Hashimoto’s and Graves’. In most cases I don’t recommend pharmaceuticals because they tend to suppress symptoms without improving function. LDN, however, actually improves the function of the body by upregulating endogenous endorphin production and balancing the immune system.
Articles in this series:
- Low T3 Syndrome I: It’s Not About The Thyroid!
- Low T3 Syndrome II: Myths and Misconceptions
- Low T3 syndrome III: Inflammation Strikes Again
- Low T3 Syndrome IV: An Autoimmune Disease You’ve Never Heard Of?
- Low T3 syndrome V: Should It Be Treated With Thyroid Hormone?