Hypothyroid

Dr. Weyrich's Naturopathic Functional Medicine Notebook

Overview

Low thyroid function, called hypothyroidism, is associated with a wide variety of disorders, including:

• Dyslipidemia (High Cholesterol/Triglycerides),
• Diabetes Mellitus Type I (Insulin Dependent),
• Diabetes Mellitus Type II (Insulin Resistance),
• Hypertension (High Blood Pressure),
• Congestive Heart Failure,
• Myocardial Infarction (heart attack),
• Chronic Fatigue Syndrome,
• Fibromyalgia,
• Alzheimer's Disease,
• Attention Deficit (Hyperactivity) Disorder (ADD/ADHD),
• Constipation,
• Multiple Sclerosis,
• Functional Immune Deficiency,
• Osteoporosis,
• Sleep Apnea,
• Muscle Weakness [Starr2005, pg 7],
• Autoimmune disorders such as Systemic Lupus Erythematosus (SLE),
• Skin and hair disorders such as Acne Eczema, Psoriasis, Alopecia.

Often these disorders resolve when hypothyroidism is treated [Starr2005].

Far more people in the United States have hypothyroidism than is commonly diagnosed, due to over-reliance on the TSH blood test as the definitive diagnostic tool in mainstream medicine [Starr2005]. Basal body temperature appears to be the most reliable indicator of functional thyroid capacity.

Etiology

Hypothyroid disease may be due to a number of causes, including poor adrenal function, environmental toxicity, inadequate nutrition, autoimmune disease, and genetic predisposition.

Prolonged treatment with superphysiological doses of corticosteroids such as prednisone can also lower thyroid function [Starr2005, pg 158].

Starr has identified two types of hypothyroid disease, which he refers to as Type I and Type II. In analogy with Diabetes Types I and II, Hypothyroidism Type I is due to a failure of the thyroid gland to produce adequate thyroid hormone, while Hypothyroidism Type II is attributed to cellular resistance to circulating thyroid hormone [Starr2005].

There are many causes for inadequate thyroid hormone being produced, which may result from a failure of the hypothalamus to produce Thyroid Releasing Hormone (TRH), failure of the pituitary to produce Thyroid Stimulating Hormone (TSH), failure of the thyroid gland to produce T4, or failure of the liver and kidneys to convert the T4 to the most active form of the thyroid hormone, T3. In some cases the peripheral tissues convert T4 to an inactive form called reverse-T3. Blood tests can help identify the nature of these failures in Type I Hypothyroidism.

On the other hand, when hypothyroidism is due to lack of cellular response to adequate levels of T3 (i.e. Type II Hypothyroidism), blood tests may appear to be normal and the diagnosis must be made based on signs and symptoms [Starr2005].

Diagnosis

One study has shown that patient medical history (signs and symptoms) was more reliable (76%) than either physical examination (12%) or lab tests (11%) in diagnosing hypothyroidism [Starr2005, pg 72; Peterson1992].

• Clinical sign/symptom picture [Starr2005 pp 80-81; Barnes; Braverman2000] (frequencies are estimates from particular populations and are included as a general indicator):
  • Low basal body temperature (almost all). Normal axillary temperature is 97.8 to 98.2 degrees Farenheit. Normal rectal temperature is 98.6 to 99.2 degrees Farenheit. Oral temperatures may be elevated above axillary temperatures by chronic sinusitis and hence are less reliable measures of basal body temperature. Menstruating women should measure their basal body temperature the second and third mornings after onset of menstrual flow. The basal temperature should be taken after a good night's rest before arising in the morning, with no food, exercise, nor excitement in the preceding 12 hour period. Electric blankets, heated water beds, excessive layers of bed-clothes, etc. may falsely elevate basal body temperature measurements. Use a reliable thermometer and place snuggly in the arm-pit for 10 minutes before reading [Starr2005, pg 17]. Note that in cases of chronic inflammation, a basal body temperature above 98.2 F may be observed along with other symptoms of hypothyroid [Starr2005, pg 137].
  • Dry skin (85%) [Starr2005].
  • Chronic fatigue (84%) [Barnes; Starr2005].
  • Brittle, soft, yellow, ridged, or striated nails (81%) [Barnes; Starr2005].
  • Menstrual disturbances and PMS (68% of females) [Barnes; Starr2005].
  • Cold intolerance (59%) [Starr2005].
  • Depression & mental disorders (58%) [Barnes; Starr2005].
  • Myxedema (non-pitting edema), especially around eyes and jaw-line (55%, pathognomonic) [Starr2005].
  • Hyporeflexia (diminished reflexes) and delayed relaxation of deep tendon reflexes, especially Achilles tendon (53%) [DeGroot1996; Starr2005].
  • Chronic pain (50%) [Ramsey1974; Barnes; Starr2005].
  • Cold, clammy extremities, pale nail beds, peripheral cyanosis and mottling (44%) [Starr2005; Braverman2000].
  • Allergies (44%) [Starr2005].
  • Weight gain (40%) [Starr2005].
  • Hair loss, especailly lateral eyebrows, arms, legs (38%) [Barnes; Starr2005].
  • Hysterectomy (32% females) [Starr2005].
  • Slow movements, slow speech, lethargy, general indolence and inertia, lassitude, apathy, listlessness (32%) [Starr2005, pg 19; Zondek1944a; DeGroot1996, pg 559].
  • Umbilical hernia (29%, infants) [Braverman2000; Starr2005, pg 95; DeGroot1996, pg 559].
  • Prolonged neonatal jaundice (29%) [Starr2005, pg 96; DeGroot1996, pg 559].
  • Constipation (26%) [Starr2005].
  • Paresthesias (abnormal sensations such as tingling, burning, etc.) (25%) [Starr2005].
  • Headaches (23%) [Barnes; Starr2005].
  • Poor suckling, failure to thrive (23%, infants) [Braverman2000; Starr2005, pg 94].
  • Delayed closing or enlarged fontanels (22%, infants) [DeGroot1996, pg 559; Starr2005, pg 87].
  • Elevated TSH (before treatment with T4) (21%) [Starr2005].
  • Diabetes (21%) [Starr2005].
  • Hypotonia (decreased muscle tone) (33%, infants) [DeGroot1996, pg 559; Starr2005, pg 96].
  • Enlarged tongue (macroglossia) and scalloping (19%, infants) [Zondek1944a; DeGroot1996, pg 559].
  • Heart disease (16%) [Starr2005].
  • Cancer (11%) [Starr2005].
  • Autoimmune disease (7%) [Starr2005].
  • Hypoglycemia, hyperinsuinemia (7%) [Barnes; Starr2005].
  • Emphysema (7%) [Starr2005].
  • Ligamental laxity, e.g. flat feet, hyper-flexibility, scoliosis (3%, more common females), stooped posture, knock-kneed, tendency to sprain or strain, dislocated kneecaps [Starr2005, pg 88, 97; Hertoghe1915].
  • Dyslipidemia (high cholesterol) (hallmark sign) [Barnes; Starr2005, pg 10].
  • Low immune function: Candida and other frequent infections, cancer (cardinal sign) [Barnes1972; Starr2005, pg 84, 90].
  • Crepitus felt in joints ("resembling the crackling of crushed snow"), especially at the knee (almost pathognomonic) [Hertogue1914; Starr2005, pg 158].
  • Decreased appetite, anorexia (common) [Starr2005, pg 19; Zondek1944a].
  • Tendency to fat deposits, especially around the hips, above the pubic bone, and above clavicles (common) [Zondek1944a; Starr2005, pg 19].
  • Joint pain, arthritis, rheumatoid pains (common) [Zondek1944a; Barnes; Starr2005, pg 19].
  • Deep depression of the root of the nose (where the nose meets the ridge between the eyebrows) and deep-set eyes due to faulty growth of the sphenoid bone [Zondek1944a; Starr2005, pg 91].
  • Delayed dentition, tooth decay, and mis-spacing of teeth (common) [Zondek1944a; tarr2005, pg 94].
  • Abnormalities in the shape of the pinna of the ear (common) [Zondek1944a; Brucker1995].
  • Swelling and and pallor of the mucus membranes (common) [Zondek1944a].
  • Oppressive feelings and convulsive pains in the cardiac region (common) [Zondek1944a].
  • Skeletal changes such as scoliosis and general contraction of the pelvis (narrow hips), (common) [Zondek1944a; Starr2005, pg 84].
  • Chronic deforming changes in the joints (common) [Zondek1944a].
  • Protuberent abdomen (common in infants) [Hertoghe1914; Starr2005, pg 94].
  • Other Cardiovascular and Blood Signs/Symptoms:
    • Bradycardia (slow heart rate) [Starr2005, pg 19].
    • Low blood pressure [Barnes].
    • Heart attack/Stroke [Barnes].
    • Heart palpitations, irregular heart beat [Barnes; Starr2005 pg 6].
    • Hypoglycemia [Starr2005, pg 101; Barnes1999].
  • Other Urogenital and Sexual Signs/Symptoms:
    • Delayed puberty or hypoplasia of breasts and genitals [Starr2005 pg 100; Zondek1944a].
    • Endometriosis [Barnes].
    • Cystic breast/ovaries [Barnes].
    • Loss of libido [Barnes].
    • Infertility, birth defects [Barnes].
    • Premature or delayed menopause [Starr2005 pg xx].
    • Disturbances in pregnancy: premature or long gestations, babies over 9 pounds at birth [Starr2005, pg 91].
    • Retroflexion of uterus [Starr2005, pg 100].
  • Other Musculo-Skeletal and Skin Signs/Symptoms:
    • Muscle weakness [Barnes].
    • Gout [Barnes; Starr2005, pg 19].
    • Osteoporosis [Barnes].
    • Short stature (DDX growth hormone deficiency, treat hypothyroid first) [Starr2005, pg 98].
    • Disproportionate development (early or premature closure of growth plates) [Starr2005, pg 98].
    • Decreased perspiration [Starr2005, pg 19].
    • Malar flush [Starr2005, pg 104]
    • Sallow (carotinemia, yellow due to failure of liver to convert beta-carotene to vitamin A) [Starr2005, pg 109].
  • Other Gastrointestinal Tract Signs/Symptoms:
    • Nutritional imbalances [Barnes].
    • Scant intestinal secretions [Hertoghe1914; Starr2005, pg 94].
    • Enlarged or irritated gums, gingivitis, hyperplasia [Starr2005, pg 94, 119].
    • Thickened lips [Starr2005, pg 100].
    • Downturned corners of the mouth [Starr2005, pg 104].
    • Difficulty swallowing [Starr2005, pg 121].
  • Other Neurological Signs/Symptoms:
    • Sleepiness [Starr2005, pg 19].
    • Mental/memory impairment [Barnes; Starr2005, pg 19].
    • Mutiple Sclerosis (MS) [Barnes].
    • Cataracts (infants) [Starr2005, pg 91].
    • Deaf-mutism [Zondek1944a; Starr2005, pg 91].
    • Cretinism [Starr2005, pg 89; Zondek1944a].
    • Alcoholism [Starr2005, pg 101; Barnes1999].
    • Various derangements and psychoses, including depression, mania, obsesions, delusion, halucinations, and frank insanity [Starr2005, pg 101; Zondek1944a].
    • Diminished amplitude of EEG theta and delta waves [DeGroot1996; Starr2005, pg 126].
    • Prolonged evoked potentials [DeGroot1996; Starr2005, pg 126].
  • Other Respiratory Signs/Symptoms:
    • Hoarsening or deepening of voice [Starr2005, pg 19, 75].
    • Mouth breathing and noisy respiration due to swollen nasal passages, respiratory distress [Starr2005, pg 94; Braverman2000].
  • Premature aging [Barnes; Starr2005, pg 109].
  • Excess cerumen in the ears [Starr2005, pg 1118].
  • Internal myxedema [Lisser1957; Starr2005, pg 145].

  Possible paradoxical signs and symptoms exhibited by some patients with low body temperature who respond well to treatment of hypothyroid condition include [Starr2005; Barnes]:

  • ADHD (72% of males, 43% of females) [Brucker1995; Starr2005 pg 89].
  • Insomnia (52%) [Starr2005].
  • Anxiety, nervousness, irritabity (35%) [Barnes; Starr2005 pg xx].
  • Hypertension (30%) [Barnes; Starr2005].
  • TMJ (due to muscle dysfunction), teeth clenching (23%) [Starr2005, pg 120].
  • Heat intolerance (20%) [Barnes; Starr2005].
  • Tremor (20%) [Starr2005].
  • Elevated basal metabolic rate [Starr2005, pg 14].
  • Elevated heart rate [Starr2005, pg 15].
  • Underweight [Starr2005, pg 14].
  • Tall stature, prolonged growth period [Starr2005, pg 85].
  • Precocious (premature) puberty or hyperplasia of breasts and genitals [Starr2005 pg 88, 100; Zondek1944a].
  • Abnormal muscle enlargement [Braverman2000; Starr2005, pg 95].
  • Excessive perspiration [Starr2005, pg 109].
• Thyroid panel (TSH, T4, free-T3, reverse-T3, etc.)
• Adrenal stress test.

Differential Diagnosis

• Iodine deficiency [Brownstein2008].
• Selenium deficiency [Peter1999].
• Magnesium deficiency [Starr2005, pg 183].
• Iron deficiency [Barnes; Starr2005, pg 182].
• Hashimoto's Thyroiditis
• Adrenal Deficiency (leads to intolerance of thyroid supplements)[Starr2005, pg 184].
• Adrenal Excess (shyts down thyroid) [Hill1950; Starr2005, pg 184].
• Myxedema (hydrated mucin) must be distinguished by palpable texture from subcutaneous fat in skinfold measurements, e.g. on the lateral arm.

Treatment

It is important to treat the patient's symptoms rather than their labs. Resolution of symptoms is more important than "normalization" of lab values.

Some symptoms of hypothyroidism will respond to treatment within a few months (thyroid replacement must be titrated up slowly), while it may take years for other symptoms (such as symptoms due to mucin deposition) to respond fully.

• When treating hypothyroidism, it is important to also adress adrenal dysfunction if present, due to the interaction between thyroid hormones and cortisol. Boosting thyroid function function in a patient with hypoadrenal function can further stress the adrenals, and contrariwise, poor adrenal function can impact thyroid function. This requires a careful balancing of thyroid and adrenal aspects of the treatment with frequent evaluation and adjustments to the treatment protocol.
• While Dr. Barnes typically started thryroid hormone first and then addressed adrenal insufficiency if necessary, Dr. Starr suggests starting with a course of iodine/iodide supplementation for one to four weeks to boost adrenal function before beginning thyroid hormone. Other doctors start with a 4 to 7 day course of low dose corticosteroids before beginning thyroid hormone [Starr2005, pg 186].
• Provide nutritional support to the thyroid as indicated by testing.
• Conventional medicine tends to prescribe only T4 (levothyroxine, Synthroid, Levoxyl, Unithroid), and occasionally T3 (Cytomel). There is also a product named Thyrolar that contains both T4 and T3.
• Dr. Sonkin suggests starting with a dose of 50 mcg T4 and titrating dose up to 150 mcg T4 over several weeks, and then adding 5 mcg T3 and titriating T3 up to 25 mcg in 5 mcg increments until symptomatic picture resolves [Sonkin1997; Starr2005, pg 172].
• Naturopaths more often supplement with a bioequivalent blend of T4 and T3 hormones in a sustained release formulation from a compounding pharmacy (the FDA frowns on using the word bio-identical).
• Dr. Barnes and others argue that the most effective approach is a natural product such as desiccated pork thyroid gland (Armour Thyroid) [Barnes; Barnes1972; Barnes1976b; Hertoghe2001; Barnes1999; Starr2005, pg 174].
• Dr. Barnes recommended starting a relatively healthy adult with 1 grain dessicated thyroid and titrating up to 5 grains in increments of 0.5 grain/month until symptomatic relief is obtained or side effects develop. When treating children, start with one quarter grain for children under three, or one-half grain in children over six, and titrate up more slowly by increments of one-quarter grain per two months. Dr. Barnes suggests a very slow rate of increase for persons with existing heart disease with a maximum of 2 grains for persons with a history of heart attack (other practitioners will go up to 2.5 grains). Dr. Barnes recommended not starting thryoid treatment until 2 months after a heart attack.
• Dr. Starr suggests starting all patients with one-quarter grain of dessicated thyroid [Starr2005, pg 178].
• When converting a patient from T4 to dessicated thyroid, Dr. Starr recommends maintaining the existing level of T4 and titrating dessicated thyroid up, and then titrating the T4 down [Starr2005, pg 178].
• Generally speaking, stop titrating up when the patient's heart rate rises 10-15 bpm above baseline [Starr2005, pg 179].
• Response to thyroid replacement therapy is slow - typically 6 to 12 months [Starr2005, pg 178].
• Drs. Sonkin, Cohen, and Rawson also used T3-propionate, which is no longer commercially avaiable in the United States. T3-propionate is slowly released into the blood stream and is better tolerated by some individuals. Apparently, since this product is not patentable, pharmaceutical companies have no interest in developing this product [Starr2005, pg 173].
• Note that 100 mcg T4 is equivalent to 1 grain of dessicated thyroid (1 grain = 64.8 mg).
• When titrating a patient up, if symptoms worsen, this is a signal that there may be an adrenal deficiency, iodine deficiency, or environmental toxicity that needs to be dealt with before increasing thyroid supplementation [Starr2005, pg 179].
• Overdosing thyroid supplements tends to elevate heart rate, but not affect blood pressure much [Starr 2005, pg 190].
• Regardless of the type, thyroid supplements are best taken on an empty stomach, first thing in the morning at least 20-30 minutes before eating.
• When treating hypothyroid conditions, onset of any of the following symptoms may be a signal that too much thyroid hormone has been administered, and the patient should discontinue taking the medication and contact the prescribing physician immediately [Starr2005, pg 181]:
  • Increase of basal body temperature above 98.2 degrees F.
  • Increase of heart rate above age/gender norms or 15 bpm above baseline.
  • Nervousness, tremor, or increased problems sleeping.
  • Weight loss.
  • Excessive sweating.
• Treat iodine deficiency if present.
• Treat selenium deficiency if present (200-400 mcg/day) [Peter1999].
• Treat iron deficiency if present (ferrous glycine is well tolerated) [Barnes; Starr2005, pg 182].
• Treat magnesium deficiency if present.

Pathophysiology

Myxedema results from an accumulation in the tissues of a substance called mucin. Mucin is a jelly-like substance that absorbs water, resulting in a boggy swelling of the tissues. This is unlike the pitting edema seen in congestive heart failure, in that the water is bound to the mucin instead of being mobile. Other tissues throughout the body are also affected, which results in impaired function of many organ systems [Starr2005, pp 2-3].

Hypotheses

In some cases, patients exhibit a paradoxical sign/symptom picture that is often associated with hyperthyroidism, except that these patients also have low body temperature and respond well to treatment of hypothyroid. It has been proposed that in these cases, the body is compensating for low thyroid status by increasing sympathetic tone (adrenaline or other adrenal hormones) [Starr2005, pg 15].

Armour Thyroid may give better results with fewer side-effects because the glandular product contains a mixture of T4, T3, T2, and T1 [Starr2005, pg 174]. It is known that T1 slows the heart rate and induces hypothermia [Scanlan2004], so it may moderate side effects by balancing the effects of T3. Note however that some studies show that T3 is converted to T2 and T1 primarily in the peripheral tissues, which raises questions regarding how much T2 or T1 is found in dessicated thryoid [Kelly2000].

Dr. Weyrich notes published data shows hypothyroid patients treated with T4 only have symptom scores and urinary T3 levels comparable to controls, whereas when these same patients are treated with natural dessicated thyroid, their symptom scores drop dramatically and their urinary T3 levels rise dramatically [Hertoghe2001]. This suggests that the "peripheral resistance to thyroid hormone" that [Starr2005] refers to as "type-II hypothyroidism" is at least in large part due to the inability of these patients to convert T4 to the more active T3 form.

ICD-9 Codes

ICD9-Code	Description	Comments
244.0	Post-surgical
244.1	Other postablative
244.2	Iodine
244.8	Other acquired (specify)
244.9	Unspecified

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References

Unless specifically noted above, references used in the construction of this web page include the following:

[FDM] Lecture notes from Functional Medicine University.

[SCNM] Lecture notes from Southwest College of Naturopathic Medicine.

[UT] Lecture notes from the University of Tennessee graduate programs in Chemistry and Biochemistry.

[Anderson1955] Anderson H, et al. Histopathologic examination of the skin in the diagnosis of myxedema in children. J Clinical Endocrinology 15:459 (1955). Cited by [Starr2005].

[Barnes] Broda O. Barnes M.D. Research Foundation at http://www.brodaobarnes.org. Of particular note are the audio tapes Thyroid Therapy I, II, III available from this source. Cited by [Starr2005].

[Barnes1942] Barnes BO. Basal temperature versus basal metabolism. JAMA 119:1072-3 (1942). Cited by [Starr2005].

[Barnes1972] B.O. Barnes. Heart Attack Rareness in Thyroid-Treated Patients. Springfield, IL: Charles C. Thomas (1972). Cited by [Starr2005].

[Barnes1976a] B. Barnes & L. Galton. Hypothyroidism: The Unsuspected Illness. New York: Harper and Row (1976). Cited by [Starr2005].

[Barnes1976b] B.O. Barnes. Solved: The Riddle of Heart Attacks. Trumbull, CT: The Broda O. Barnes M.D. Research Foundation (1976). [Cited by Starr2005].

[Barnes1999] B.O. Barnes & C.W. Barnes. Hope for Hypoglycemia, Revised Edition. America Book Company (1999). Cited by [Starr2005].

[Braverman2000] Braverman LE, et al. Warner's & Ingbar's The Thyroid: A Fundamental and Clinical Text, 8th Edition. Philadelphia: Lippincott Williams & Wilkins (2000). Cited by [Starr2005].

[Brownstein2008] Brownstein D. Iodine: Why You Need It, Why You Can't Live Without It, Third Edition. Medical Alternatives Press (2008). See also http://www.drbrownstein.com [Cited by Starr2005].

[Brucker1995] Brucker-Davis F, et al. Genetic and clinical features of 42 kindreds with resistance to thyroid hormone. The National Institutes of Health prospective survey Annals of Internal Medicine 123(8):572-583. [Cited by Starr2005].

[Brucker1998] Brucker-Davis F. Effects of environmental synthetic chemicals on thyroid function. Thyroid. 8(9):827-856 (1998).

[CSL1888]. Clinical Society of London. Report of a Committee of The Clinical Society of London to Investigate the Subject of Myxedema. Transactions Clinical Society London. Vol 21 (suppl) (1888). [Cited by Starr2005].

[DeGroot1996] L.J. DeGroot et al. The Thyroid and Its Diseases, Sixth Edition. New York: Churchill Livingston (1996). Cited by [Starr2005].

[Eggertsen1988] Eggertsen R, et al. Screening for thyroid disease in a primary care unit with a thyroid stimulating hormone assay with a low detection limit. BMJ. 297:1586 (1988). [Cited by Starr2005].

[Hertoghe1914] E. Hertoghe. Thyroid Deficiency. Lecture presented to the International Surgical Congress at the New York Polyclinic School and Hospital (April 1914). Copy availaible from Broda O. Barnes M.D. Research Foundation at http://www.brodaobarnes.org [Cited by Starr2005].

[Hertoghe1915] E. Hertoghe. The Practitioner Vol XCIV, No. 1 (January), 26-69 (1915). [Cited by Starr2005].

[Hertoghe2001] Hertoghe J, et al. Thyroid insufficiency. Is thyroxine the only valuable drug? Journal of Nutritional & Environmental Medicine. 11:159-166 (2001). [Cited by Starr2005].

[Hill1950] Hill SR, et al. The effect of adrenocorticotropin and cortisone on thyroid function, thyroid-adrenocortical interrelationships. Journal Clinical Endocrinology 10:1375 (1950). [Cited by Starr2005].

[Jackson1978] Jackson I, et al. Why does anyone still use dessicated thyroid USP?. American Journal of Medicine. 64:284-288 (1978). [Cited by Starr2005].

[Jarov1998]. Jarlov AE, et al. Observer variations in the clinical and laboratory evaluation of patients with thyroid dysfunction and goiter. Thyroid 8(5):393-398 (1998). [Cited by Starr2005].

[Kelly2000] Kelly G. Peripheral metabolism of thyroid hormones: A review. Alternative Medicine Review 5(4):306-333 (2000). [Cited by Starr2005].

[Lisser1957] Lisser H & Escamilla RF. Atlas of Clinical Endocrinology Including Text of Diagnosis and Treatment. St. Louis: C.V. Mosby (1957). [Cited by Starr2005].

[Ord1878] Ord WM. On myoxoedema, a term proposed to be applied to an essential condition in the creatinoid infection occasionally observed in middle-aged women. Trans. Med-Churg Society London 1877-1888; 60-1:57-78 (1878).

[Pelter1999] Pelter R. Selenium's got the power. American Druggist. 216(11):48-49 (1999). [Cited by Starr2005].

[Peter1999] Peter R. Selenium's Got the Power. American Druggist 216(11):48-49 (1999). [Cited by Starr2005].

[Peterson1992] M.C. Peterson et al. Contributions of the history, physical examination, and laboratory investigations in making medical diagnosis. West J Med. 156:163-65 (1992). [Cited by Starr2005].

[Ramsey1974] Ian Ramsey. Thyroid disease and muscle dysfunction. William Heinemann Medical Books (1974). [Cited by Starr2005].

[Scanlan2004] Scanlan TS, et al. 3-Iodothyronamine is an endogenous rapid-acting derivative of thyroid hormone Nature Medicine 10(6):638-642 (2004). [Cited by Starr2005].

[Silenkow1967] Silenkow HR & Refetoff S. Common tests of thyroid function in serum. JAMA 202:135 (1967).

[Sonkin1997] Sonkin L. Therapeutic trials with thyroid hormones in chemically normal thyroid patients with myofascial pain and complaints suggesting mild thyroid insufficiency. Journal of Back and Musculoskeletoan Rehabilitation 8(83):85 (1997). [Cited by Starr2005].

[Starr1954] Starr P. Hypothyroidism:An Essay on Modern Medicine. Springfield, IL: Charles C. Thomas (1954). Cited by [Starr2005].

[Starr2005] Mark Starr. Hypothyroidism Type 2: The Epidemic. Columbia, MO: Mark Starr Trust (2005).

[Weiss1996] Weiss RE, et al. Dominant inheritance of resistance to thyroid hormone not linked to defects in they thyroid hormone receptor alpha or beta genes may be due to a defective cofactor. J Clinical Endocrinology and Metabolism 81(12):4196-4203 (1996). Cited by [Starr2005].

[Wondisford1996] Wondisford FE. Editorial: Thyroid hormone action beyond the receptor. J Clinical Endocrinology and Metabolism 81(12):4194-4195 (1996). Cited by [Starr2005].

[Zondek1944a] H. Zondek. Diseases of the Endocrine Glands, Fourth Edition. Baltimore: Williams & Wilkins (1944). [Cited by Starr2005].

[Zulewski1997] Zulewski H, et al. Estimation of tissue hypothroidism by a new clinical score: Evaluation of patients with various grades of hypothyroidism and controls. J of Clinical Endocrinology and metabolism 82(3):771-776 (1997). [Cited by Starr2005].

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