In treating patients with hypothyroidism and Hashimoto’s Disease, most physicians rely too much on the TSH (thyroid-stimulating hormone) level on a lab blood test. Part I addressed the fact that a patient’s TSH level is only part of a larger picture that includes transporting thyroid-hormone to cells; getting that hormone inside receptor sites; converting the inactive form of thyroid hormone (T4) into the active form (T3); and much more.
At Carolinas Thyroid Institute, I look for the deeper cause of low-thyroid symptoms, by assessing whole-body systems (nervous, immune, gastrointestinal, and endocrine/hormonal). I offer a free, informative 15-minute phone consultation to anyone in the U.S. who is taking thyroid medication and is still suffering with hypothyroid symptoms. Scheduling is easy on our Contact Us page or by calling (704) 853-8000.
Blocking Thyroid Hormone: Homocysteine, Toxins, and Oxidative Stress
Inside each cell in the body is a nucleus. The nucleus is surrounded by a nuclear membrane, where there are “receptors” for thyroid hormone. Both cortisol and reverse T3 (covered in Part I) block these thyroid-hormone-receptor sties, which results in low-thyroid symptoms—even where there is enough thyroid hormone in the blood and there is a normal lab result on a TSH and T4 blood test. In this case, a patient’s cells would not benefit from the thyroid hormone she is making or the prescription she is taking.
In addition to cortisol and reverse T3, a high level of homocysteine in the body will block thyroid-hormone-receptor sites. Homocysteine is a chemical in the blood, which is produced when methionine (an amino acid) is broken down by the body, in a process called methylation. To lower the amount of homocysteine (by turning it back into methionine), both B12 and folate are needed.
If a patient doesn’t secrete enough stomach acid, she will probably be deficient in both B12 and folate, which would allow homocysteine to increase and to block thyroid hormone. People with Hashimoto’s Hypothyroidism often have insufficient stomach acid (a condition called hypochlorhydria). At Carolinas Thyroid Institute, every patient is given a blood test to measure homocysteine and is evaluated for gastrointestinal health.
Another problem with thyroid-hormone-receptor sites involves chemical exposure. Environmental toxins, such as Bisphenol A (BPA), reduce thyroid-hormone-receptor-site sensitivity. BPA is a toxin found in plastics, in the coatings of some food cans, and in dental sealants. Anyone with thyroid problems should choose BPA-free water bottles and BPA-free food cans.
Oxidative stress is a condition in which the body produces an abundance of free radicals that cause cellular damage. Antioxidants (glutathione; vitamins C and E; betacarotene in egg yolks, carrots, yams, cantaloupe, etc.) counteract the effect of free radicals. Without enough antioxidants present in the body, oxidative stress will cause thyroid-hormone-receptor-site resistance, which results in hypothyroid symptoms.
Blocking Thyroid Hormone: Chronic Inflammation
Chronic inflammation interferes with thyroid hormone in several ways. First, inflammation reduces the number of thyroid-hormone receptors. If there are fewer receptors, there are fewer places where thyroid hormone can attach and deliver its chemical message. The information in this chemical message allows cells to perform properly.
Not only does inflammation reduce thyroid-hormone receptors, it decreases the sensitivity of existing thyroid-hormone-receptor sites.
Inflammation in the body is caused by food sensitivities; pesticides and environmental chemicals; autoimmune disease; poor blood-sugar regulation; hormonal imbalances; infections; injury; and stress. Some inflammation is necessary and helpful. The immune system uses inflammatory messengers, called cytokines, to respond to infections and to trigger short-term inflammation so that the body can heal. Continual, chronic inflammation is very destructive, however.
Autoimmune patients with Hashimoto’s Disease, for instance, often have chronic inflammation, because their “autoimmune attacks” produce cytokines. The cytokines block thyroid-hormone-receptor sites. (See Hashimoto’s Disease, under Low-Thyroid Problems, in the Menu.)
Inflammatory chemicals have another effect, too: they halt the conversion of inactive T4 into T3—the active form of thyroid hormone, the form that cells can use. Lowering inflammation, therefore, is so important for anyone with a thyroid problem. Reducing or eliminating these inflammatory foods will help thyroid patients to avoid chronic inflammation: sugar, gluten, all grains, soy, dairy products, and artificial ingredients.
One way to gauge how much inflammation is in the body is to measure the following on a lab blood test: HDL Cholesterol (50-65 is optimal); C Reactive Protein; ESR; Ferritin; and Fibrinogen. All thyroid patients at Carolinas Thyroid Institute are tested for these inflammatory markers.
Conversion Trouble: Enzymes and Poor Blood-Sugar Control
As already stated, thyroxine (T4) must be converted into the active form of thyroid hormone (T3) to be used by the body. A healthy thyroid gland will release thyroid hormone that is about 93% T4 and about 7% T3, so most of the thyroid hormone released by a healthy thyroid needs to be converted. Most of this conversion takes place inside a healthy liver. Conversion also takes place within other healthy organs: the gut, lungs, kidneys, and brain.
If a patient is taking synthetic thyroid-hormone medication, such as Synthroid (levothyroxine), that patient may have sufficient T4 in the blood and, therefore, a normal TSH level; but the conversion of that T4 to T3 is essential. Anything that interferes with conversion will cause hypothyroid symptoms, regardless of medication dosage. Switching to a natural form of thyroid hormone will provide this patient with medication that is 7% T3, but this small amount does not compensate for poor conversion in the body.
To understand the conversion process, it’s helpful to know what three (5′ deiodinase) enzymes do. They are called D1, D2, and D3. Compared to D2, D1 is inefficient. D2 is a thousand times better at converting T4 into T3 than D1 is.
D1 is responsible for converting T4 into T3 everywhere in the body, but there is only a little D1 in the pituitary (in the brain). D2, on the other hand, converts T4 to T3 in the brain only. Therefore, D2 is present in the pituitary, which benefits from this much more efficient conversion enzyme. The pituitary would likely have enough T3, even when the rest of the body does not.
Poor blood-sugar control has a negative effect on this conversion process. When a patient has insulin resistance, there is more inflammation, which suppresses D1 activity. D2, however, is actually energized by problems like inflammation, stress, and autoimmune diseases—the very things that suppress D1.
When someone has poor blood-sugar control, D1 doesn’t convert enough inactive T4 into active T3 in the body, but the pituitary (thanks to an energized D2) will have more than enough T3. This patient’s body would not have enough thyroid hormone, but her TSH (released by the pituitary) wouldn’t reveal it.
The enzyme D3 is unlike D1 and D2. D3 converts T4 into reverse T3, and there is none in the brain (which means there is none in the pituitary). As covered in Part I, reverse T3 gets rid of excess T4 in the blood and blocks active free T3 from entering a cell’s thyroid-hormone-receptor sites. Too much reverse T3 is a cause of hypothyroid symptoms.
It’s clear that simply taking thyroid-hormone medication does not solve the problem of hypothyroid symptoms in most cases. Hypothyroidism and Hashimoto’s Disease involve the entire body, and only a whole-body Functional Medicine approach can uncover the real reason for continuing symptoms. For a free, 15-minute phone consultation with me, Dr. Steven Roach, schedule on our Contact Us page or call (704) 853-8000.
