Optimal function of the thyroid gland is essential for vibrant health and yet thyroid dysfunction is often overlooked or inadequately treated even by so called thyroid doctors. It is estimated that at least 27 million adults in the U.S. have some form of thyroid-related illness, with up to 40% of the population living with suboptimal thyroid function. Thyroid issues are much more common in women than in men. Weighing just 20-60 grams in a healthy individual, this butterfly-shaped gland located under the larynx (voice box) is tasked with producing master metabolism hormones that control every cell of the body. These hormones include Triiodothyronine (T3), Thyroxine (T4), and Diiodothyronine (T2).
Basic Thyroid Physiology
In healthy individuals, low blood levels of T3 and T4 signal the hypothalamus to produce thyrotropin-releasing hormone (TRH), which in turn causes the pituitary to release thyrotropin (also known as Thyroid Stimulating Hormone, or TSH). TSH is what signals the thyroid to make more thyroid hormones, T3 and T4, and release them into the blood. This completes the feedback loop to raise blood levels and from there these thyroid hormones are transported into the cells of the body to perform their many metabolism-related functions such as weight control, temperature regulation, and growth. T4 is considered the inactive or storage form of thyroid hormone and a portion of it is converted by enzymes, called deiodinases, into T3, the active form. When T4 is in excess, some of it is converted into another hormone, called Reverse T3 (RT3). It’s thought that about 40% of T4 gets converted to T3 and about 20% gets converted to RT3.
However, part of what makes the effects of thyroid dysfunction so far-reaching and complicated is that thyroid hormones are dependent on other hormones to function optimally. This includes insulin, cortisol, and sex hormones. When things go awry with the thyroid itself or any of the other related organs, glands, or these related hormones, the resulting dysfunction can present itself as any one of the following types of thyroid conditions.
Hypothyroidism occurs when the thyroid does not produce enough thyroid hormones or when there is poor conversion of T4 to T3, resulting in a sluggish or underactive metabolism.
- Primary Hypothyroidism – usually caused by iodine deficiency
- Secondary Hypothyroidism – caused by a problem within the pituitary that results in decreased secretion of TSH
- Hypothalamic/Tertiary Hypothyroidism – caused by decreased secretion of TRH related to certain chronic diseases or congenital defects
These are the symptoms most commonly associated with hypothyroidism:
- Weight gain
- Extreme fatigue
- Sensitivity to cold
- Thinning hair
- Dry skin
- Brittle Nails
- Low basal body temperature
- Muscle/joint aches
- Low libido
- Chronic yeast infections
- Labored breathing
- Difficulty concentrating/”brain fog”
- Irregular Menstrual Cycles
Conversely, hyperthyroidism is associated with the thyroid producing an excess of hormones, resulting in speedy or “overactive” thyroid. This ramp up in metabolism can lead to malnutrition because of how quickly the body burns through nutrients.
- Thyroiditis (inflammation of the thyroid)
- Graves’ disease
- Plummer’s disease
- Toxic multi-nodular goiter
- Thyroid nodules
- Benign thyroid tumors
- Dysregulation of the hypothalamus-pituitary-adrenal (HPA) axis or hypothalamus-pituitary-thyroid (HPT) axis
- Liver dysfunction
- Heavy metal toxicity
- Nutrient deficiencies
The most commonly reported symptoms of hyperthyroidism include:
- Sudden weight loss
- Change in appetite
- Heart palpitations
- Loose stools
- Hair loss
- Increase in sweating
- Irregular menstrual cycle
- Shortness of breath
- Vision problems
- Anxiety/panic attacks
- Blood sugar imbalances
- Protruding eyes
- Difficulty concentrating
Autoimmune Thyroid Conditions
Certain types of thyroid conditions are caused by an autoimmune process. Graves’ disease is the most common form of autoimmune hyperthyroidism and Hashimoto’s Thyroiditis is one of the most common form of autoimmune hypothyroidism. In Graves’ disease, antibodies against thyroid receptors (called Thyroid Stimulating Immunoglobulin or TSI) causing the thyroid to release too much T4. In Hashimoto’s, antibodies to thyroglobulin and thyroid peroxidase are produced. Anti-thyroglobulin (ATG) is found in 80% of Hashimoto’s patients and anti-thyroid peroxidase (TPO) is found in 90%. T-lymphocytes can also be involved, invading the thyroid and causing enlargement. Often an individual experiences symptoms that alternate between hypo and hyperthyroidism before the gland is damaged to a point where it stays underactive. Autoimmune thyroid conditions are generally multi-factorial and often involve the combination of genetic predisposition and environmental triggers.
Inadequacies of Current Testing & Treatment
So why are an estimated 13 million cases of thyroid dysfunction being missed every year? The main reason is thyroid doctors use an outdated standard of care for diagnosis and treatment. A growing body of research has revealed that a breakdown of the normal processes involved in thyroid hormone production, conversion of T4 to T3, and transportation of thyroid hormones into the cell occurs in many different chronic diseases and under certain circumstances. These findings clearly make current testing and diagnosis inadequate and yet many physicians are still practicing under the assumption of these old ideas. Dr. Claude Lenfant, who published an article called “Clinical Practice: Lost in Translation” in the New England Journal of Medicine, estimated that most physicians are practicing 10-20 years behind the current medical literature.
One example is this – the American Thyroid Association (ATA) acknowledges a genetic problem that affects the enzymes (deiodinases) that convert inactive thyroid hormone (T4) into active thyroid hormone (T3), yet they overlook the evidence showing that this same enzyme issue can be present in a multitude of chronic diseases as well. In addition, the ATA also overlooks studies showing that transport of thyroid hormones into the cell can be poor in these circumstances. It was previously thought that the transport of thyroid hormones into the cell happened via simple diffusion. Newer research has shown, however, that this is not the case. It is actually an energy-dependent, active transport process. So anyone with a reduction in energy production (mitochondrial dysfunction) as seen in a multitude of chronic diseases would have this issue with transport.
It should become evident in cases of poor transport into the cell, that blood levels of T3 and T4 would not appear low, and therefore are not an accurate assessment of tissue thyroid hormone activity. Interestingly, research shows that the pituitary is generally unaffected by this problem of reduced transport. And since TSH is related only to pituitary function, it is not an accurate assessment in these cases either. TSH could be normal, while many other tissues of the body (besides the pituitary) are not getting enough thyroid hormones. This is referred to as “tissue hypothyroidism.”
Chronic conditions associated with poor intracellular thyroid function due to poor transport and/or poor conversion of T4 to T3 include:
- Neurodegenerative disease
- Insulin resistance/diabetes
- Chronic Fatigue Syndrome
- Chronic inflammatory conditions
- Mitochondrial dysfunction
- Chronic dieters/calorie restricting
- Chronic infections
- Those with high cholesterol or triglycerides
- Those exposed to endocrine-disrupting chemicals
These are the patients who typically “fall through the cracks” and are told by their thyroid doctor that they have normal thyroid function despite ongoing symptoms of dysfunction. The old standard of care still followed by many physicians, even endocrinologists, is also inadequate due to:
- Reference ranges based on population averages, rather than optimal functioning (making the “normal” range wider and wider as the population gets sicker)
- Reference ranges varying from lab to lab
- Continued use of TSH and serum thyroid hormones as the “gold standard” of diagnosis
- Treatment with T4 (Synthroid/Levoxyl) only, despite research on better outcomes with combination T4 /T3 or T3-only treatment. (T4-only therapy would not help those with poor T4 to T3 conversion as discussed above)
Testing for More Accurate Diagnosis
A combination of the commonly used thyroid tests along with newer markers based on current research will more thoroughly and accurately assess thyroid function and activity of thyroid hormones within the cell. This includes:
- Free T3
- Free T4
- Reverse T3
- Free T3/Reverse T3 ratio
- Thyroid antibodies
- SHBG (Sex Hormone Binding Globulin)
- Basal body temperature
- Basal Metabolic Rate (BMR)
- Reflex Relaxation Phase
- Signs and Symptoms
Integrative Medicine: A Path To More Effective Treatment
With the mounting evidence supporting this phenomenon of “tissue hypothyroidism” and the large percentage of the population most likely affected by it, a growing minority of respected physicians are adapting their approach to treatment accordingly. Not only are they changing the way thyroid hormones are prescribed, but many of them are also addressing the underlying causes of the dysfunction, such as chronic infections, exposure to endocrine-disrupting chemicals, stress (and its effect on stress hormones), and nutritional deficiencies. Individualized nutrition and lifestyle recommendations, therefore, can be a crucial step in re-balancing hormones and optimizing thyroid function.
Several nutrients are essential to normal thyroid function. Iodine obtained from the diet and converted into iodide, is used to produced T4 and T3. Inadequate iodine intake or over-exposure to foods/substances that interfere with the iodination of thyroglobulin, such as bromine, fluoride, and goitrogens, can result in poor thyroid function. Good food sources of iodine include seaweed, kelp, fish (saltwater), organic potatoes, radishes, and cranberries.
Selenium also plays an important role in thyroid health, by acting as an antioxidant and aiding in the conversion of T4 to T3. Those with chronic infections, inflammation, or digestive disorders are at greater risk of deficiency. Good food sources of selenium are red meat, eggs, chicken, fish, brazil nuts, garlic, and wheat germ. Iron deficiency can also significantly reduce T4 to T3 conversion.
In cases of autoimmune thyroid diseases, molecular mimicry should also be considered. The likely dietary culprits are gluten and casein (protein in dairy), because these proteins closely resemble those of thyroid tissue. If these proteins “leak” into the bloodstream without adequate digestion because of poor intestinal integrity, the body’s immune response is activated and it cannot differentiate between these food-derived proteins and the body’s own thyroid tissue. Testing or a trial elimination should be conducted. Infectious agents may also cause an autoimmune response related to molecular mimicry.
Finding The Right Thyroid Doctor
Thankfully, there are physicians who are committed to staying up-to-date on all the latest thyroid research in order to effectively diagnose and treat even the most complicated thyroid issues. Look for a thyroid doctor who listens to your concerns, investigates thoroughly, addresses nutrition and lifestyle factors, and is educated on some of the topics discussed in this article. Since stress has been shown to negatively affect thyroid function, practicing a stress-reducing activity daily such as yoga, meditation, walking in nature, or deep-breathing techniques is one simple way you can jump-start your healing process as you search for the right health care provider.
10. Holtorf, K. Thyroid Hormone Transport into Cellular Tissue. Journal of Restorative Medicine. 2014; 3: 53-68.
10. Rakel, D. Integrative Medicine, 3rd Ed. Philadelphia, Pa: Elsevier Saunders; 2012: 312-20.