Broda Otto Barnes
Born	April 14, 1906(1906-04-14) Missouri
Died	November 1, 1988 (aged 82) Bend, Oregon
Education	University of Denver BS Western Reserve University MS University of Chicago PhD (1931) Rush Medical College MD (1937)
Occupation	Physician
Employer	University of Illinois Research Hospital[1]
Known for	Hypothyroidism
Spouse(s)	Helen Tucker Morgan (1905-2002) (m. 1981–1988) «start: (1981)–end+1: (1989)»"Marriage: Helen Tucker Morgan (1905-2002) to Broda Otto Barnes" Location: (linkback:http://en.wikipedia.org/wiki/Broda_Otto_Barnes) 2nd wife[2][3]
Parents	Addie and Robert B. Barnes

Broda Otto Barnes (April 14, 1906 – November 1, 1988) was an American physician who studied endocrine dysfunction, particularly hypothyroidism.^[4][5][6] In the 1970s, Barnes published several books proposing that hypothyroidism was more prevalent in the U.S. than standard measurements were predicting. He believed that standard assays of thyroid function were inadequate, and that undiagnosed thyroid dysfunction was responsible for a wide range of health problems. Barnes' views on the prevalence of hypothyroidism were never widely adopted in mainstream medicine and run counter to the current medical understanding of thyroid function, but they have been embraced by some elements of the alternative medicine community.^{[5][7][8][9][10]}

[edit] Career

Barnes was born on April 14, 1906 in a log cabin in Missouri,^[5][11] the son of Addie and Robert B. Barnes.^[12] Barnes studied chemistry at the University of Denver, and became an instructor of physiological chemistry at Western Reserve University for two years and received his MS in 1930 from there. Barnes received his PhD at University of Chicago in 1931 and taught physiology there from 1931 to 1936.^[5][13] He completed his MD in 1937 at Rush Medical College, and for two years he was an Assistant Professor of Medicine at the University of Illinois.^[1] He was named chairman of the Health Education Department at the University of Denver. He became professor affiliate in the department of physiology at Colorado State University from 1963 to 1968.^[5] On 13 September 1981 he married Helen Tucker Morgan (1905-2002) in California. She was his second wife.^[2]

In 1984, Barnes established a not-for-profit foundation to continue the legacy of his research, The Broda O. Barnes Research MD, Research Foundation, Inc.^[6][13] Barnes and his wife also established a program of interest-free student loans to aid "worthy and needy chemistry students" at the University of Denver.^[14] The University of Chicago library retains a collection of memorabilia, consisting largely of photographs related to Barnes' time there.^[13]

[edit] Hypothyroidism perspective

Diagnosis

Barnes developed and promoted a diagnostic test for thyroid function that became known as the "Barnes Basal Temperature Test". This test is performed by placing a thermometer in the armpit for 10 minutes immediately upon waking.^[15] A measurement of 97.8 °F (36.6 °C) or below was considered by him to be highly indicative of hypothyroidism, especially when hypothyroid symptoms are present. A reading over 98.2 °F (36.8 °C) was indicative of hyperthyroidism, unless a patient had advanced arthritis, which Barnes claimed would falsely elevate the temperature due to muscle contractions.^[3]

The details of the test were published in the Journal of the American Medical Association (JAMA) in August 1942, and again in The Lancet in 1945.^[3][7] The test has never been adopted by the medical profession; however it is currently advocated by some alternative practitioners.^[8] In modern medical practice, the most accurate means of assessing thyroid function is through specific biochemical tests which measure blood levels of thyroid gland hormones and regulators.^[16]

Barnes didn't consider his Basal Temperature Test to be 100% conclusive, and acknowledged there were other causes of lowered basal temperature. Nevertheless, he maintained that it was the most useful diagnostic test in the diagnosis of hypothyroidism, superior to blood tests of thyroid function.^[6] In his books, Barnes argued that hypothyroidism affected more than 40% of the American population,^[3][6] significantly higher than the prevalence of approximately 5% reported in the peer-reviewed medical literature.^[17] Barnes attributed this difference to the failure of diagnostic tests to correlate with the clinical signs and symptoms of hypothyroidism in all cases.^[3]

Diseases attributed to hypothyroidism

Barnes believed that many common diseases, including heart disease, cancer, depression, arthritis, diabetes, the common cold, tonsillitis, ear infections, apparent laziness in children, various menstrual disorders, and skin disorders, were caused or exacerbated by hypothyroidism.^[3][6]

Treatment

Barnes treated hypothyroidism by prescribing patients a daily dose of thyroid hormone. He recommended starting with a small dose, and then slowly increasing the dosage in monthly intervals until symptoms resolved. For most patients, he recommended continuing thyroid medication for life at that optimal dose, though some could be slowly weened off. He advised patients to take the thyroid medication first thing in the morning on an empty stomach, at least 20 minutes before food.^[6]

Barnes used a desiccated thyroid extract from Armour Thyroid almost exclusively, stating anecdotally that patients experienced much better improvement of symptoms with the natural extract rather than synthetic drugs.^[6] He claimed that the even with synthetic combination drugs containing T4 and T3, patients were left with symptoms (dry skin & fluid retention), that upon switching to desiccated thyroid extract would resolve.

During his years of practice, Barnes also began to conclude that virtually all his hypothyroid patients had a concomitant adrenal insufficiency. Following this speculation, he routinely gave an accompanying physiological dose of the synthetic corticosteroid prednisone together with desiccated thyroid extract. Barnes wrote that this was mandatory in patients showing more severe adrenal insufficiency exhibited by systolic blood pressure below 100.^[3][6]

[edit] Pregnancy mistest hormone research

In 1932, W. Fleischmann and S. Kann reported in a German gestational physiology journal^[18] that female bitterings, small carp-like fish, "...show an enlargement of the ovipositor following injection of an estrogenic preparation...".^[19]

Since human pregnancy urine contains estrogen, Drs. Aaron E. Kanter, Carl P. Bauer and Arthur H. Klawans of the University of Chicago added a teaspoon of urine from a pregnant woman to a bowl in which a bitterling was swimming. This experiment produced ovipositor lengthening, as expected by reasoning from the earlier results of Fleischmann. In 1935, TIME Magazine nationally reported their announcement of this potentially useful new test for human pregnancy, which was then currently determined by rabbit and mouse tests. But subsequent to the announcement, Kanter, et al., found that urine from non-pregnant women or men had the same effect.^[20]

Barnes was the principal investigator, with obstetricians Kanter and Klawans, in an experiment reported in 1936. They sought to determine the source organ of whatever non-pregnant urine substance was causing the same bitterling ovipositor response as Fleischmann's estrogenic preparation.^[20] Barnes, et al., extracted juice from 14 different organs of seven species (including both genders of humans) and exposed bitterlings to them. The organ they found responsible was the adrenal cortex.^[21] The Barnes, et al., 1936, publication in Science was also reported in TIME.^[20]

In 1938, Fleischmann and Kann determined that in addition to estrogen, a specific adrenal hormone, corticosterone, could cause the observed bitterling ovipositor reaction.^[19] This additional non-pregnant hormone reaction made the bitterling test not useful for its originally announced purpose, though it did open the door to an investigation of why corticosterone is significant in urine.^[20]

[edit] Publications

[edit] Books

[edit] References