Courtesy Dee Breger, Drexel University.

Hypothyroidism is very common, and it has serious health consequences, including cardiovascular disease, obesity, menorrhagia, infertility, polycystic ovarian syndrome, depression, psoriasis, and urticaria. But you’ll often miss it if you rely solely on conventional diagnostic criteria.

In the past, the most common cause of hypothyroidism was iodine deficiency, which is now relatively rare in developed countries thanks to iodized salt. By far, the more frequent cause is autoimmune thyroiditis, in which antibodies form and bind to thyroid peroxidase enzyme, thyroglobulin, and thyroid-stimulating hormone (TSH) receptors. This arises from a complex interaction of predisposing genes and non-genetic factors. A recent study shows an association between autoimmune thyroiditis and levels of organochlorine pollutants (Langer P, et al. Chemosphere. 2007 Aug; 69(1): 118–127).

Conventional diagnosis of hypothyroidism is based on serum concentrations of total and free thyroxine (T4), triiodothyronine (T3), and TSH. If the first two are low, and the latter is high, a patient is deemed hypothyroid. But these criteria may not reflect physiologic reality for a lot of our patients.

A person can have normal T4 and TSH levels, but if the autoimmune process interferes with conversion of the prohormone T4 to active T3 in peripheral tissues, he or she will show signs and symptoms of hypothyroidism despite “normal” serum hormone levels. Dr. Alan Gaby has humorously called this, “Sub-Laboratory Hypothyroidism” (Gaby A. Alt Med Rev. 2004; 9(2): 157–179). In the early 1990s, Dr. E. Denis Wilson described this clinical picture, suggesting that it underlies a host of common conditions, and named it, “Wilson’s syndrome,” though there is still debate whether this is a legitimate medical syndrome (Friedman M, et al. PR Health Sci J. 2006 Mar; 25(1): 23–29).

Measuring thyroid activity by functional methods rather than by serum thyroid hormone levels alone, will give a much more clear picture of what’s going on with an individual patient. Gaby and others advocate assessment of a person’s resting metabolic rate, as measured by basal body temperature, although they acknowledge that this method is limited by the fact that body temperature is highly variable. Some physicians look for a high reverse T3:T3 ratio as evidence of Wilson’s syndrome.

Another valuable method is reflexometry. A device like the Thyroflex (www.nitekmedical.com) accurately detects delays in the brachioradialis (BR) reflex. This is a relatively reliable physical sign of hypothyroidism. My experience is that, as indicated by the Thyroflex, a slow BR strongly suggests hypothyroidism, though a normal reflex does not necessarily rule it out.

Subclinical hypothyroidism (SCH), defined as elevated serum TSH with normal free thyroid hormones, affects 4–8% of the US general population, and up to 18% of women over age 60 (Evans TC. Prim Care. 2003; 30: 625–640). There’s still controversy over the clinical significance, morbidity, and optimal treatment of these patients. A recent Cochrane review concluded that levothyroxine therapy for SCH does not improve survival, cut CV morbidity nor improve quality of life, but may improve lipid profiles and left ventricular function (Villar H, et al. Cochrane Database Syst Rev. 2007; (3): CD003419).

It seems that many patients respond better to desiccated thyroid (derived from bovine or porcine thyroid) than to conventional levothyroxine, which might account for the relatively lack-luster outcomes observed by the Cochrane Collaboration. Desiccated thyroid is thought to stimulate blocking antibodies to the autoimmune antithyroid antibodies; it may also act as a decoy for the patient’s abnormal anti-thyroid antibodies.

My own clinical experience parallels that of Dr. Gaby, who reports that at least 60% of patients treated with natural thyroid will improve. I’ve had patients experience dramatic symptom relief after being told by other physicians for years that they did not have hypothyroidism because their TSH and/or T4 were normal.

In most cases, I begin with a 60 mg (one grain) daily dose of natural thyroid, taken on an empty stomach in the morning. I then re-evaluate in one month, increasing the dose gradually until we see improvement in symptoms and normalization of the brachioradial reflex. In patients who are highly sensitive to medications, I may start with 30 mg (one-half grain), and increase very slowly.

Though many clinicians have observed the superiority of natural versus synthetic thyroid, published studies are conflicting, making it difficult to draw a firm scientific conclusion. More definitive is the importance of T3. In one crossover study of 33 hypothyroid patients, reduction of standard levothyroxine by 50 mcg with concomitant addition of 12.5 mcg T3 significantly improved measures of mood and cognitive function, compared to levothyroxine alone (Bunevicius R, et al. N Engl J Med. 1999; 340: 424–429).

Side effects of excessive thyroid therapy are anxiety, insomnia, and palpitations. They occur infrequently and subside quickly on dose reduction. Although TSH is often suppressed with natural thyroid therapy, it is not reason to reduce the dose unless the patient has atrial fibrillation. The cardinal rule in hypothyroid treatment is to treat the patient, not the numbers.

A compounded, sustained-release preparation of T3 and T4 is sometimes better-tolerated and may be more effective than natural thyroid. Selenium at 200 mcg/day is a big help for some patients with autoimmune thyroiditis; it has been shown repeatedly to decrease the thyroid autoantibodies (Mazokopakis EE, et al. Thyroid. 2007 Jul; 17(7): 609–612).

Dr. Wilson advocates supraphysiologic cyclic dosing of sustained release T3 in order to reset low basal body temperature. To date, there are no published controlled trials to support this controversial approach.

Since subclinical iodine/iodide deficiency is associated with hypothyroidism, it is important to rule it out before jumping into hormone-based therapies. This can be assessed by analysis of urinary iodide excretion; if levels are low, they can usually be boosted with high-dose iodine supplementation (Abraham GE. The Original Internist. 2004; 11: 17–36).

Keep in mind that the endocrine glands are interconnected; they do not work in isolation. Correcting hypothyroidism may ameliorate hypoadrenalism, which is common in these patients. Conversely, correcting hypoadrenalism may ameliorate hypothyroidism (Gharib H, et al. Lancet. 1972; 2: 734–736). Consequently, adrenal support with adrenal extract and botanical medicines such as licorice root can help optimize outcomes in patients with hypothyroidism.

Michael Traub, ND, past-president of the American Association of Naturopathic Physicians, practices on the Big Island of Hawaii with Monica Scheel, MD. They are the authors of Essentials of Dermatological Diagnosis and Natural Therapeutics.