Five Thyroid Patterns That Won’t Show Up on Standard Lab Tests
The five thyroid patterns
Thyroid physiology is complex and regulated by input from multiple endocrine glands, the immune system, the gut, and many cell-signaling molecules. Malfunctions in any one of these components can cause hypothyroid symptoms. However, these malfunctions are not revealed by a standard thyroid panel. Patients with hypothyroid symptoms but “normal” TSH and T4 according to the standard thyroid panel may be told that nothing is wrong with their thyroid glands and sent on their way. Some are handed prescriptions for thyroid hormone replacement. This one-size-fits-all approach to managing hypothyroidism ignores the multitude of factors that influence thyroid function and may even worsen symptoms in some patients. At best, it does our patients a disservice, and at worst it could be considered sheer negligence.
1.) Hypothyroidism caused by pituitary dysfunction
This pattern is caused by high cortisol. Cortisol, in turn, is elevated in response to active infection; (1) blood sugar dysregulation, hypoglycemia, insulin resistance, or chronic stress; (2) or pregnancy. These stressors fatigue the pituitary gland; as a result, it can’t release enough thyroid-stimulating hormone (TSH) to stimulate the thyroid gland to produce T4 and T3. In other words, there is nothing wrong with the thyroid gland itself; the problem lies with the pituitary gland. The key to correcting this pattern is to resolve the underlying causes of pituitary dysfunction by treating infection, balancing blood sugar, improving insulin sensitivity, and helping patients find ways to reduce their stress levels.
Patients with this pattern will present with hypothyroid symptoms, TSH below the functional range (1.8–3.0) but within the standard range (0.5–5.0), and T4 that is low in the functional range and possibly the standard range as well.
2.) Under-conversion of T4 to T3
T4 is the inactive form of thyroid hormone. It comprises 90 percent of thyroid hormone produced by the thyroid gland and must be converted to T3 before the body can utilize it. When T4 is not converted into T3 in adequate amounts, symptoms of hypothyroidism result. This pattern of thyroid dysfunction characterized by under-conversion of T4 to T3 has many potential causes, including inflammation, elevated cortisol, nutrient deficiencies, and intestinal dysbiosis. Patients with this pattern present with hypothyroid symptoms, normal TSH and T4, and low T3.
Twenty percent of thyroid hormone activation is initiated in the gastrointestinal tract by gut microbes, which produce deiodinase enzymes that convert T4 into T3. Disruption of the normal gut microbiota may reduce levels of beneficial bacteria that perform this crucial conversion, resulting in a decreased amount of T3 and symptoms of hypothyroidism. Lipopolysaccharides produced by pathogenic bacteria also impair T4 to T3 conversion by inhibiting thyroxine 5′-deiodinase, an enzyme that catalyzes the conversion.
T4 to T3 conversion occurs in cell membranes. Chronic inflammation involves the production of inflammatory cytokines, which damage cell membranes and impair thyroid hormone conversion. (7) Chronic fatigue syndrome and Crohn’s disease patients are two examples of patient subsets who may present with “low T3” syndrome due to chronic inflammation. (8, 9) High cortisol, which can become elevated due to chronic inflammation and stress, also suppresses the conversion of T4 to T3.
Nutrient status is essential in the pathogenesis of thyroid disorders. Nutrients such as iron and selenium serve as cofactors for enzymes involved in the conversion of