In response to this question, I always forthrightly concede my lack of personal clinical experience with manipulation of the gland, then provide information practical for any DCs in the audience interested in this form of glandular manipulative therapy. In this article, I present the practical information I always give to inquiring DCs. My hope is that some will use the therapy, keep detailed records on their clinical results, then share their records with me. Accumulating a bank of careful clinical observations from several DCs will help those of us at the Fibromyalgia Research Foundation decide whether the time and expense of a systematic clinical trial of thyroid gland manipulation is worthwhile.
Primary Hypothyroidism: Patients Who Might Not Benefit
The DC should be discrete in selecting patients for whom manipulative therapy will be the primary form of therapy. Patients with autoimmune thyroiditis should be excluded.
The most common causes of primary hypothyroidism are autoimmune thyroid diseases; silent and subacute thyroiditis; antithyroid treatments; iodine deficiency or excess; lithium use; bromide use; growth hormone injections; viral infections; and thyroid gland trauma.1 Among these causes, chronic autoimmune thyroiditis is the most common mechanism.2
Patients with primary hypothyroidism caused by autoimmune thyroiditis should use exogenous thyroid hormone for life.9,10 For these patients, thyroid hormone therapy is almost always effective. While thyroxine (T4) alone (as in Synthroid) seldom provides satisfactory results, desiccated thyroid is especially effective. Thyroid hormone therapy suppresses antithyroid antibody levels and decreases (and may stop) the autoimmune process. Effective thyroid hormone therapy also relieves patients' hypothyroid symptoms.
Thanks to the Dietary Supplement Health and Education Act, one brand of desiccated thyroid is now available over the counter (OTC). Chiropractors practicing in states which permit them to advise patients in the use of OTC products can now treat hypothyroid patients with desiccated thyroid, just as they can treat patients with other food-derived products. This is a boon to hypothyroid patients who prefer DCs as their primary doctors. Chiropractic treatment of hypothyroid patients almost certainly excels over that of conventional doctors, because conventional medicine's treatment protocol for hypothyroidism leaves most patients chronically ill and tragically susceptible to avoidable early death.
Primary Hypothyroidism:Patients Who Might Benefit
While patients with autoimmune thyroid disease benefit most from thyroid hormone therapy, patients with primary hypothyroidism from other causes may benefit from manipulation of the gland. If manipulation restores normal function of the gland, patients may not need thyroid hormone therapy. That manipulation can improve thyroid gland function is conjecture. I can find no studies in which researchers have assessed the safety and effectiveness of the treatment procedure. However, a conjecture that a therapy will benefit patients, followed by careful clinical observation, almost always precedes systematic scientific evaluation of the therapy.
Patients who develop primary hypothyroidism following whiplash injuries may be among those who can benefit from thyroid gland manipulation. Whiplash-type injuries of the neck can cause hemorrhage of the thyroid gland.6 Impaired thyroid gland function from such injuries appears to account for some patients' posttraumatic chronic pain and fatigue, often leading to a diagnosis of fibromyalgia. The DC should exercise astute judgment in deciding whether to manipulate the thyroid gland in such cases; however, for some patients, gentle manipulation of the gland and the cervical spine and myofascia may prove therapeutic.
The only description of manipulative treatment of the thyroid gland I have found is attributed to A.C. Johnson, DC.5 Unfortunately, Dr. Johnson died many years ago, and we do not have the benefit of details of his clinical experiences.
Describing his technique, Johnson wrote, "Get the fingers underneath the mass and stretch the tissues upward so that there will be an increased drainage, loosening up all the muscles and ligaments in relation to the gland." He also advised the DC, as part of the treatment, to relax all the muscles of the patient's neck and shoulders, down to the 7th thoracic vertebra. He suggested that the patient participate by leaning back and extending the head up and back for three minutes to drain the gland.5
Johnson also cautioned the DC not to manipulate the delicate gland too forcefully. He warned that overtreatment may cause the gland to secrete excess thyroid hormones, leaving the patient tremulous.5
Other clinicians warn that manipulation of the thyroid gland, and the parathyroid glands attached to it, may cause excess calcitonin to exude from the glands.7,8 (Calcitonin is a hormone synthesized in the thyroid gland, parathyroid glands, and the thymus. The glands secrete the hormone when the blood calcium level rises, as after a meal. The hormone induces bone uptake of calcium.) These clinicians speculate that manipulation-induced excess blood calcitonin will cause an exodus of calcium from the blood to bone, and inhibit the release of calcium from bone. This chain of events, they argue, will lower the blood calcium level enough to cause spasm and tetany (a mineral imbalance in the body that results in severe muscle spasms).3,4 These descriptions of potential adverse effects highlight the prudence of a cautious approach to thyroid gland manipulation.
As mentioned previously, I have no clinical experience manipulating the thyroid glands of primary hypothyroid patients; I provide the information in this column for those DCs who have an interest in doing so. I am interested in hearing from those who do have experience with thyroid gland manipulation, and will be happy to pass along any of their clinically useful insights to others who are, as I am, interested in this method of thyroid gland treatment, but lack relevant experience. If well-documented outcomes of DCs' clinical experiences appear promising, our research foundation will consider designing and conducting a clinical trial of this method of glandular manipulation.
- Lowe JC. The Metabolic Treatment of Fibromyalgia. McDowell Publishing Co., Boulder, 2000.
- Braverman LE, Utiger RD. Introduction to hypothyroidism. In Werner and Ingbar's The Thyroid: A Fundamental and Clinical Text, 6th edition. LE Braverman, RD Utiger, editors. JB Lippincott Co., New York, N.Y., 1991, pp.919-920.
- Percival RC, Hargreaves AW, Kanis JA. The mechanism of hypocalcaemia following thyroidectomy. Acta Endocrinologica, 1985;109:220-226.
- Sonkin LS. Myofascial pain due to metabolic disorders: diagnosis and treatment. In Myofascial Pain and Fibromyalgia: Trigger Point Management. Edited by ES Rachlin, Mosby, St. Louis, Mo., 1994, pp.45-60.
- Johnson AC. Chiropractic Physiological Therapeutics, 5th edition. Palm Springs, Calif., self-published, 1977.
- Schutt CH, Dohan FC. Neck injury to women in auto accidents: a metropolitan plague. JAMA 1968;206:2692.
- Rasmusson B, Borgestov S, Holme-Hanson B. Changes in serum calcitonin in patients undergoing thyroid surgery. Acta Chiro. Scand 1980;146:15-17.
- Watson CG, Steed DI, Robinson AG, Deftos LJ. The role of calcitonin and parathyroid hormone in the pathogenesis of post-thyroidectomy hypocalcemia. Metabolism 1981;30:588-589.
- Volpˇ R. Autoimmune thyroiditis. In Thyroid Function and Disease. Edited by GW Burrow, JH Oppenheimer, R Volpˇ, W.B. Saunders, Philadelphia, 1989, pp.921-933.
- LiVolsi JA, LoGerfo P. Thyroiditis. CRC Press, Boca Raton, Fla., 1981.
John Lowe, MA, DC