Goiter

Goiter, or more specifically non-toxic goiter or euthyroid goiter, is an enlargement of the thyroid gland but without any evidence of thyroid dysfunction. Goiter is the most common cause of thyroid enlargement, seen more frequently during puberty, pregnancy, and menopause. The most prominent cause relates to an iodine deficiency, but other causes include the excess consumption of goitrogens (e.g. cruciferous vegetables), and drugs, including aminosalicylic acid and lithium. Somewhat paradoxically, high amounts of iodine may decrease the synthesis of thyroid hormone. (Rubin 2001, 600-01; Berkow 1992, 1080)

Gross iodine deficiency is very uncommon in the West but is the most common cause of goiter worldwide.(1)  Iodine is ingested in food and water, and is actively taken up by the follicular cells of the thyroid gland, which under the influence of thyroid stimulating hormone (TSH), uses it and the amino acid tyrosine to form thyroxine, of which the are two primary forms: T3 (triiodothyronine, comprised of three iodine atoms) and T4 (tetraiodothyronine, comprised of four iodine atoms). These hormones are then released by the thyroid where they are bound to thyroid hormone-binding serum proteins for transport. Thyroxine-binding globulin (TBG) accounts for 75% of thyroid hormone-binding proteins, and has high affinity but low capacity for T4 and T3. Other thyroid hormone-binding proteins include transthyretin (prealbumin), which has high affinity but low capacity for T4, and albumin, which has low affinity but high capacity for T4 and T3. Approximately 0.03% of the total serum T4 and 0.3% of the total serum T3 are free from carrier proteins. (Berkow 1992, 1071-72)

Increased levels of free thyroid hormones T3 inhibit TSH secretion from the pituitary, whereas decreased levels of T4 and T3 result in an increased TSH release from the pituitary. TSH secretion however is also influenced by thyrotropin-releasing hormone (TRH), an amino acid peptide synthesized in the hypothalamus, which binds to a specific TRH receptor on the thyrotropic cells of the anterior pituitary and causes the subsequent release of TSH. (Berkow 1992, 1071)

The thyroid hormones act to increase protein synthesis and O2 consumption in virtually every body tissue, increasing or enhancing the metabolic rate. Although T4 is much more abundant among the thyroid hormones, only T3 is thought to be metabolically active. Once taken up by a cell however, T4 can be deiodinated into T3. (Berkow 1992, 1071)

About 20% of the circulating T3 is produced by the thyroid and the remaining 80% is produced by the monodeiodination (removal of one iodine atom) in the outer ring of T4. The monodeiodination of the inner ring of T4 results in reverse T3 or rT3, mostly occurring in peripheral tissues. Unlike normal T3, rT3 has minimal metabolic activity and increases in certain diseases, e.g. chronic liver and renal disease, acute and chronic illness, starvation, and carbohydrate-deficient diets. Reverse T3 may also act to inhibit T4 conversion into the metabolically active T3, and is used as marker to rule out hypothyroidism (in which T3 levels are decreased). Some researchers speculate that rT3 may block T3 receptor sites, competitively inhibiting the activity of T3. (Berkow 1992, 1071)

Goiter is evidenced by a soft, symmetric, smooth mass in the neck. Goiter can range in size from a doubling of the thyroid gland to a massive enlargement that weigh several hundred grams. The early indications of the disease include follicular hypertyrophy and hyperplasia, and as the condition progresses this is followed by an increasingly nodular configuration. Serum TSH may be slightly elevated and serum T4 may be low-normal or slightly low, but serum T3 is normal or slightly elevated. Thyroid antibodies are typically measured to rule out Hashimoto's thyroiditis as the cause. (Berkow 1992, 1084-85; Rubin 2001, 600-01)

Holistic treatment

Given that gross iodine deficiencies are relatively uncommon in the Western world goiter is unlikely to be seen all that often in clinical practice, despite the fact that it affects upwards of 500 million people worldwide. Iodine is found abundantly in the ocean and coastal regions, but is sparsely distributed in the earth's crust, and those that live in the middle of continents and do not eat an iodine-supplemented diet (e.g. iodized salt) are particularly susceptible to goiter. Furthermore, it has been suggested that those whose ancestors come from coastal areas have a higher requirement for iodine than those whose ancestry is from inland regions (Fallon 1999, 44).

Some commentators have also debated the bioavailability of organic (e.g. kelp, seafood) versus inorganic (e.g. iodized salt, iodophore antiseptics in dairy) sources of iodine, suggesting that organic sources are better absorbed and stored by the thyroid. Certain foods can inhibit iodine absorption including legumes and cruciferous vegetables, as can a deficiency of vitamin A. Thus vegetarians eating an unrefined diet (w/o iodization), with an emphasis upon legumes (e.g. soy) and cruciferous vegetables, especially in in-land regions, are at a dramatically higher risk for iodine deficiencies and goiter (Ikeda et al 2000). Iodine deficiencies cause a decrease in the basal metabolic rate, promote goiter, and in pregnant and lactating women cause cretinism in infants, a condition marked by irreversible mental retardation. Supplementing with 5-10 grams of seaweed on a daily basis would provide enough iodine in an otherwise iodine deficient diet, taken with a daily consumption of between 5-10,000 IU of vitamin A.

Some commentators feel that the increasing prevalence of thyroid disorders could be related to something as simple as a dysfunction in iodine metabolism. Herbalist Ryan Drum postulates that the relatively large amount of active halides, fluorides, chlorides and bromides present in our food and water displaces iodine from the thyroid, promoting iodine deficiencies. Furthermore, environmental exposure to iodine 131 from nuclear testing, nuclear facilities, power plants and weapons facilities makes the thyroid particularly susceptible to the effects of ionizing radiation. Once again, supplementing with seaweed appears to protect against iodine 131, and reducing exposure to halides, fluorides, chlorides and bromides primarily in contaminated municipal water, appears to be an effective strategy to maintain thyroid health.

Another increasing problem associated with iodine is its overconsumption, particularly with highly refined foods that contain an abundance of refined, iodized salt. Similar to iodine deficiencies, an iodine excess can also suppress thyroid function and cause goiter. Other symptoms of iodine excess include a rash, depression, aggravation of acne, nausea, fatigue, numbness and tingling, swelling of the saliva glands, a metallic taste in the mouth, and salivation.

Footnotes