Dietary and Lifestyle Interventions to Support Functional Hypothyroidism

Introduction

Hypothyroidism is an unsuspected illness of epidemic proportions in western civilization unrecognized by the modern medical community (Starr xix). The affects are far-reaching and pervasive. The purpose of this research is to demonstrate that addressing nutrient deficiencies, mitigating the damaging effects of the environment, and changing certain lifestyle practices can boost thyroid hormone production naturally.

Research methodology includes a review of the current peer-reviewed publications by both conventional and alternative medicine practitioners, live presentations and personal interviews. Findings include a specific dietary, supplement, and lifestyle protocol or healing functional hypothyroidism developed based on the research and personal experience.

Normal Thyroid Function

Figure 1. Reprinted from Hormones, 2nd Ed., Norman, Anthony and Gerald Litwak, Chapter 6, Page171, Copyright 1997, with permission from Elsevier.

Thryoid hormones are chemical messengers made of proteins that interact with internalized hormone receptors at the cellular level to sustain a specific biological. Thyroid hormones are synthesized as a result of a negative feedback loop that involves the pituitary gland and thyroid-stimulating hormone (TSH) or thyrotropin, and the hypothalamus and thyrotropin-releasing hormone (TRH) (Figure 2). The biosynthesis of thyroid hormones requires thyroglobulin (Tg) the most abundant protein in thyroid tissue, thyroid peroxidase (TPO), the key enzyme in the synthesis of organically bound iodine, H₂O₂ (peroxide), and iodine from the diet (Norman et al. 172, 177). This negative feedback loop governs iodine uptake and the synthesis of Thyroxine (T4) by the thyroid gland. TSH is the most critical hormone affecting iodine uptake (Liska et al. 175, Norman Litwack 177).

Figure 2. Reprinted from The Endocrine System at a Glance, 2nd Ed., Greenstein, Ben and Diana Wood, Chapter 12, Page 32, Copyright 2006, with permission from Wiley.

The physiological regulation of the secretion of thyroid hormones by the thyroid gland via this negative feedback loop depends on blood concentration of T4 and triiodothyronine (T3), the two primary thyroid hormones which regulate the pituitary secretion of TSH. Thyroid hormones are released into the blood by hormone-producing cells in the follicles in response to a change in the concentration of thyroid hormones in the blood. These actions are orchestrated by polypeptide TSH receptors located in the cell membranes of the thyroid follicle cells. T4 is the chief thyroid hormone secreted by the thyroid gland. Approximately 80% of the T4 secreted by the thyroid gland is converted to equal amount of T3 and reverse T3 (rT3) in peripheral target cells, in the liver and in the kidneys, but the concentration of T4 in the blood is 40 to 100 times greater than that of T3 (ATA 24 May 2005, Hedberg June 2009, Liska et al. 175, Norman and Litwack. 180-1, Milner 2, Paoletti 4). T3 is the principal source of energy for our cells. rT3, the inactive form of T3, can bind to T3 receptor cells and as an antagonist of T3, can inhibit the activity of T3, even when T3 levels are optimal – rT3 needs to be displaced by the biologically active T3 to normalize metabolism (Milner 2, Paoletti 4).

The actions of various T3 receptors located in the nucleus of peripheral cells throughout the body mediate a wide variety of biological responses (Norman and Litwack 185, 187). (Table 1). (No T4 receptors have been identified in the body (Paoletti 4).) Approximately 90% of T3 binds with these intracellular thyroid receptors (Starr, 243). When peripheral cell receptors capture these “messages” (the mechanism is analogous to a key fitting into a lock) the cell responds to the presence of the hormone.

Table 1. Reprinted from Hormones, 2nd Ed., Norman, Anthony and Gerald Litwak, Chapter 6, Page 185, Copyright 1997, with permission from Elsevier.

Thyroid hormones regulate all metabolic activities – growth rate, sodium/potassium pump, cholesterol secretion in the bile, heart rate, heart strength, blood pressure, respiration, oxygen consumption (basal metabolic rate (BMR)), digestion, lipid, carbohydrate and protein metabolism, central nervous system function, and the actions of other endocrine glands. Normal sexual function is dependent on normal thyroid secretion. Low levels of thyroid hormones can have effects on behavior, growth, cardiac output, GI function, tissue oxygen consumption, muscle strength, and immune function. (Liska et al. 175, Norman and Litwack 169, 171, Starr, 243, 247-8).

Characteristics of Hypothyroidism

Hypothyroidism (type 1) is defined as “. . . failure of the thyroid gland to produce sufficient amounts of thyroid hormones necessary to maintain ‘normal’ blood levels of thyroid stimulating hormone (TSH). . . marked by lowered basal metabolism, subnormal body temperature, and myxedema . . .” (edema resulting from the abnormal accumulation of mucin)(Starr 255-7). Major symptoms include enlarged heart, lowered cardiac output, cool skin, reduced sweating, poor appetite, reduced GI activity, enlarged skeletal muscles with myopathy (weakness), and a drooping upper eyelid (Norman and Litwack 172, 189). Below normal thyroid hormone levels can have dramatic effects and may be life threatening (Standard in Natural Solutions).

In 2007 it was estimated that approximately two percent of the U.S. population, or 5.8 million people, are hypothyroid. Women are more likely to develop hypothyroidism than men and the incidence increases with age. As many as 24% of women over sixty are hypothyroid. The Colorado Thyroid Disease Prevalence Study (1995) found that approximately 10% of the general population suffered from untreated (functional or subclinical) hypothyroidism. As many as 10 to 15% of Americans have mild or subclinical hypothyroidism and may not know it. Even with the more narrow range of the standard TSH test, approximately 13 million Americans with thyroid disease remain undiagnosed today. (ATA 2003, 7, Brady 2, Milner 2, Murray “Hair Loss in Women” 1712, Paoletti 3,Teitelbaum 121-2).

Family history is the greatest risk factor for hypothyroidism, according to the American Thyroid Association (ATA), but others include those of older age, especially women whose risk increases if they are white or Asian and have reached menopause, having another autoimmune disorder, Down syndrome, Turner’s syndrome, or bipolar disorder. Conditions that increase risk include thyroid surgery, radiation to the neck area, and medicines that can cause hypothyroidism, including amiodarone, lithium, interferon alpha, interleukin-2, and thalidomide. (2003 at 7,8).

Definition of Functional Hypothyroidism

Functional hypothyroidism has been defined as a state where blood levels of thyroid hormone fall within normal range, but where temperature tests and other indicators show mild thyroid hormone deficiency (Standard in Natural Solutions). Even mild thyroid hormone deficiency can have far-reaching effects.

Sometimes referred to as subclinical hypothyroidism, functional hypothyroidism has been characterized by optimal levels of TSH and T4 with the presence of symptoms (Paoletti 4), or by slight to moderately elevated TSH levels with normal levels of T4 (Murray and Bongiorno “Hypothyroidism” 1795, Nadeau 90). The ATA defines subclinical hypothyroidism as mild subclinical hypothyroidism with normal T4 and slightly high TSH (TSH in the range of 4-10 mU/L) and subclinical hypothyroidism (TSH >10 mU/L) that may cause mild symptoms or none at all (2003 at 3, 2004).

In comparison, clinical hypothyroidism is characterized by abnormal levels of thyroid hormones due to failure of the thyroid gland. Causes include loss of functional thyroid tissue1, mild to severe autoimmune conditions, genetics and congenital factors, nutrient deficiencies2, exposure to toxins, failure in the hypothalamus-pituitary-thyroid (HPT) axis, and stress (Murray and Bongiorno “Hypothyroidism” 1794-5, Norman and Litwack 189, Paoletti 3, Fisher et al. 2722). Persons with breast cancer may develop hypothyroidism as a result of radiation treatments (ATA 2008, 2009). The ATA defines hypothyroidism as either primary, a failure of the thyroid gland because of a condition directly affecting the thyroid gland, or secondary hypothyroidism, a rare condition resulting from an abnormality in the pituitary gland (ATA 2005). In either case it is a permanent condition.