Mythbusters: Thyroid Edition

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By David A. Cohen, MD, FACE, ECNU and Sahil Parikh, MD
mythbusters thyroid edition

There are countless myths and misconceptions associated with this silver dollar-sized tissue that have spread throughout the mainstream health and fitness culture... The purpose of this article is to shed evidence-based light on some of the more debated topics in thyroidology and separate fact from fiction.

The thyroid gland is the small butterfly-shaped organ at the base of your neck that regulates your body’s metabolism. Every cell in the body counts on an appropriate amount of thyroid hormone. Too much thyroid hormone (called hyperthyroidism) can be a problem, leading to damage to the heart, bones, muscles and so much more, while causing many symptoms, including weakness, anxiety, and insomnia. On the other hand, too little thyroid hormone (called hypothyroidism) can damage the same organs, and contribute to weight gain, “brain fog,” and infertility, just to name a few. However, there are countless myths and misconceptions associated with this silver dollar-sized tissue that have spread throughout the mainstream health and fitness culture. From mild cognitive impairment to intractable chronic pain to morbid obesity (and just about everything in between), almost any symptom can be attributed to being a “thyroid issue”. While abnormal thyroid function absolutely will lead to significant symptoms, we need to be careful not to wrongly attribute every symptom to the thyroid. There now exists a small but vocal community that advocates for unproven solutions regarding thyroid testing and treatments. The purpose of this article is to shed evidence-based light on some of the more debated topics in thyroidology and separate fact from fiction.

"While eating healthy is beneficial for maintenance of overall health, there are no clinical studies or scientific data to show that any particular diet can prevent or treat thyroid disease."

To rT3 or not to rT3?

The thyroid gland makes thyroxine hormone, called T4, which is then converted into either triiodothyronine (T3) or reverse T3 (rT3). If there is not enough T4 or T3, the pituitary gland responds by releasing more Thyroid Stimulating Hormone (or TSH) in order to drive increased production of T4 and T3, maintaining hormone levels within the normal ranges. Therefore, the first lab finding that is seen in hypothyroidism is an elevated TSH. On the other hand, TSH decreases in hyperthyroidism. TSH goes in “the opposite direction” of the function.

While T3 is the active form of thyroid hormone, reverse T3 is simply a breakdown product and has no effect on the body. Though evidence-based guidelines advise measuring only TSH, T4, and/or T3 to understand thyroid function, many continue to push for routine checking of rT3. We know from our understanding of physiology, extensive well-validated studies, and tremendous experience working together with our patients that a good clinical history of symptoms, a detailed physical exam, and measurement of the appropriate hormones are more than enough to diagnose a patient with thyroid disease. Evidence supporting routine rT3 checks is scant to say the least. Reverse T3 levels exist in the body for a very short time (compared to T3 and T4) and can be affected by many factors including illness and medications. Additionally, all medications used to treat hypothyroidism and hyperthyroidism will affect rT3 levels. For example, if a patient is taking T4 or T3 replacement, rT3 will rise for a very short time after taking the medicine; therefore, checking rT3 may make one think that the medicine is too much or too little. All of this makes rT3 level interpretations highly unreliable for thyroid evaluation and treatment, rendering routine testing unnecessary and costly. Therefore, most healthcare providers rightfully refrain from routine checking of rT3 levels.

The Thyroid Diet, Supplements, Vitamins, and Minerals

Iodine is the building substrate for thyroxine hormone. Iodine deficiency and its subsequent effects on thyroid gland are well known. Fortunately, in the United States, most people can obtain sufficient iodine (approximately 150 micrograms/day) through their daily dietary intake. In many individuals, excess iodine intake can actually cause hypothyroidism (called the Wolff-Chaikoff Effect) or hyperthyroidism (called the Jod-Basedow Phenomenon).

Selenium is another micronutrient that is needed for normal production and use of thyroid hormone. Selenium also appears to act as an antioxidant (protecting the thyroid from free radical damage) with anti-inflammatory properties. Evidence shows that selenium supplementation improves eye disease in patients with autoimmune hyperthyroidism (called Graves’ Disease), but this benefit is likely limited to individuals with selenium deficiency. If there is a concern for a lack of selenium (which is very rare in the United States), replacement with 50-100 micrograms per day may be beneficial.

Zinc helps convert T4 to T3. Its deficiency can lead to increased production of rT3, which, as stated above, is biologically inactive. Therefore, zinc replacement is unlikely to have any benefit.

Vitamin A and D deficiencies have been associated with hypothyroidism and autoimmunity. However, there is no evidence that their deficiencies actually cause thyroid disease. It is worthwhile to check vitamin D levels in patients with thyroid disease and to provide supplementation if there is a deficit, but this isn’t expected to improve thyroid function.

Iron is necessary for normal thyroid hormone production. Healthcare practitioners will often check for iron deficiency in patients who have thyroid disease, particularly given the increased risk of autoimmune gastrointestinal conditions (such as celiac disease and gastritis) in patients with thyroid disease.

Many advocate for various special diets, including gluten free, anti-inflammatory, paleo, and keto as cures for hypothyroidism. Unfortunately, while eating healthy is beneficial for maintenance of overall health, there are no clinical studies or scientific data to show that any particular diet can prevent or treat thyroid disease.

Euthyroid Hashimoto’s & Subclinical Hypothyroidism: Where Do We Draw the Line in the Sand?

Hypothyroidism can be caused by many different things. The cause can be as straightforward as surgical removal. Severe and prolonged iodine deficiency can also be a cause. In the Western world, autoimmune inflammation called Hashimoto’s thyroiditis, thought to be a combination of genetic susceptibility and environmental factors, is the most common cause of hypothyroidism. Hashimoto’s thyroiditis is highly suggested in the setting of certain blood tests (thyroglobulin antibodies or TPO antibodies) or evidence from a thyroid ultrasound (which isn’t typically recommended or necessary).

There are no symptoms related to Hashimoto’s thyroiditis, other than if the chronic autoimmune inflammation causes gland failure (hypothyroidism). This destructive process varies widely from patient to patient - it can be very rapid or can evolve slowly over many, many years.

“Euthyroid Hashimoto’s” is the term used when people have one or both of the antibodies to the thyroid gland, but their TSH and T4 levels are normal. There is no treatment of the Hashimoto’s thyroiditis, only thyroid hormone replacement if hypothyroidism occurs. Where genuine controversy does exist within the medical community is the precise point at which thyroid replacement is warranted, considering that a mildly elevated TSH has been suggested to perhaps be a normal manifestation of aging. There are some conditions in which there are (or may be) adverse effects associated with mild hypothyroidism (termed subclinical hypothyroidism):

  • Obesity and diabetes
  • Cholesterol
  • Increased risk of heart attack, heart disease, and death from heart disease
  • Stroke
  • Depression and bipolar disease
  • Muscle weakness and exercise intolerance
  • Hip fractures
  • Pregnancy-related complications, including pre-eclampsia, infertility, postpartum hemorrhage, miscarriage, and preterm delivery

It is essential that we remember that “association does not mean causation,” so we shouldn’t jump to treating everyone who has subclinical hypothyroidism and falls into one of the above categories. Rather, this is best approached individually with each patient, deciding to treat based on what together the health care practitioner and the patient think is best for the patient.