Thyroid: Therapy, Confusion and Fraud (3)

[Guest guest]

In the absence of commercial

techniques that reflect thyroid physiology realistically, there is no valid

alternative to diagnosis based on the known physiological indicators of

hypothyroidism and hyperthyroidism. The failure to treat sick people because of

one or another blood test that indicates " normal thyroid function, "

or the destruction of patients' healthy thyroid glands because one of the tests

indicates hyperthyroidism, isn't acceptable just because it's the professional

standard, and is enforced by benighted state licensing boards.

Toward the end of the twentieth century, there has been considerable discussion

of " evidence-based medicine. " Good judgment requires good

information, but there are forces that would over-rule individual judgment as

to whether published information is applicable to certain patients. In an

atmosphere that sanctions prescribing estrogen or insulin without evidence of

an estrogen deficiency or insulin deficiency, but that penalizes practitioners

who prescribe thyroid to correct symptoms, the published " evidence "

is necessarily heavily biased. In this context, " meta-analysis "

becomes a tool of authoritarianism, replacing the use of judgment with the

improper use of statistical analysis.

Unless someone can demonstrate the scientific invalidity of the methods used to

diagnose hypothyroidism up to 1945, then they constitute the best present

evidence for evaluating hypothyroidism, because all of the blood tests that

have been used since 1950 have been.shown to be, at best, very crude and

conceptually inappropriate methods.

H. McGavack's 1951 book, The Thyroid, was representative of the earlier

approach to the study of thyroid physiology. Familiarity with the different

effects of abnormal thyroid function under different conditions, at different

ages, and the effects of gender, were standard parts of medical education that

had disappeared by the end of the century. Arthritis, irregularities of growth,

wasting, obesity, a variety of abnormalities of the hair and skin, carotenemia,

amenorrhea, tendency to miscarry, infertility in males and females, insomnia or

somnolence, emphysema, various heart diseases, psychosis, dementia, poor

memory, anxiety, cold extremities, anemia, and many other problems were known

reasons to suspect hypothyroidism. If the physician didn't have a device for

measuring oxygen consumption, estimated calorie intake could provide supporting

evidence. The Achilles' tendon reflex was another simple objective measurement

with a very strong correlation to the basal metabolic rate. Skin electrical

resistance, or whole body impedance wasn't widely accepted, though it had

considerable scientific validity.

A therapeutic trial was the final test of the validity of the diagnosis: If the

patient's symptoms disappeared as his temperature and pulse rate and food

intake were normalized, the diagnostic hypothesis was confirmed. It was common

to begin therapy with one or two grains of thyroid, and to adjust the dose

according to the patient's response. Whatever objective indicator was used,

whether it was basal metabolic rate, or serum cholesterol. or core temperature,

or reflex relaxation rate, a simple chart would graphically indicate the rate

of recovery toward normal health.

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REFERENCES

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ill.Several chapters contributed by various authors.Call Numbers WK200 M145t

1951 (Rare Book).

Endocrinology 1979 Sep; 105(3): 605-12. r-mediated transport of thyroid

hormones through the rat blood-brain barrier: primary role of albumin-bound

hormone. Pardridge WM.

Endocrinology 1987 Apr;120(4):1590-6. Brain cortex reverse triiodothyronine

(rT3) and triiodothyronine concentrations under steady state infusions of

thyroxine and rT3. Goumaz MO, Kaiser CA, Burger A.G.

J Clin Invest 1984 Sep;74(3):745-52. Tracer kinetic model of blood-brain

barrier transport of plasma protein-bound ligands. Empiric testing of the free

hormone hypothesis. Pardridge WM, Landaw EM. Previous studies have shown that

the fraction of hormone or drug that is plasma protein bound is readily

available for transport through the brain endothelial wall, i.e., the

blood-brain barrier (BBB). To test whether these observations are reconcilable

with the free-hormone hypothesis, a tracer-kinetic model is used Endocrinology

113(1), 391-8, 1983, Stimulation of sugar transport in cultured heart cells by

triiodothyronine (T2) covalently bound to red blood cells and by T3 in the

presence of serum, Dickstein Y, Schwartz H, Gross J, Gordon A.

Endocrinology 1987 Sep; 121(3): 1185-91. Stereospecificity of triiodothyronine

transport into brain, liver, and salivary gland: role of carrier- and plasma

protein-mediated transport. Terasaki T, Pardridge WM. J. Neurophysiol 1994

Jul;72(1):380-91. Film autoradiography identifies unique features of

[125I]3,3'5'-(reverse) triiodothyronine transport from blood to brain. Cheng

LY, Outterbridge LV, Covatta ND, Martens DA, Gordon JT, Dratman MB

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bloodstream to brain: contributions by blood:brain and choroid

plexus:cerebrospinal fluid barriers. Dratman MB, Crutchfield FL, Schoenhoff

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Mech Ageing Dev 1990 Mar 15;52(2-3):141-7. Blood-brain transport of

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Endocrinology 1987 Sep;121(3):1185-91. Stereospecificity of triiodothyronine

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protein-mediated transport. Terasaki T, Pardridge WM. J Clin Invest 1984

Sep;74(3):745-52. Tracer kinetic model of blood-brain barrier transport of

plasma protein-bound ligands. Empiric testing of the free hormone hypothesis.

Pardridge WM, Landaw EM.

Endocrinology 1980 Dec;107(6):1705-10. Transport of thyroid and steroid

hormones through the blood-brain barrier of the newborn rabbit: primary role of

protein-bound hormone. Pardridge WM, Mietus LJ. Endocrinology 1979 Sep; 105(3):

605-12. r-mediated transport of thyroid hormones through the rat

blood-brain barrier: primary role of albumin-bound hormone. Pardridge WM.

Endocrinology 1975 Jun;96(6):1357-65. Triiodothyronine binding in rat anterior

pituitary, posterior pituitary, median eminence and brain. Gordon A, Spira O.

Endocr Rev 1989 Aug;10(3):232-74. The free hormone hypothesis: a

physiologically based mathematical model. Mendel CM. Biochim Biophys Acta 1991

Mar 4;1073(2):275-84. Transport of steroid hormones facilitated by serum

proteins. Watanabe S, Tani T, Watanabe S, Seno M Kanagawa.

D Novitzky, H Fontanet, M Snyder, N Coblio, D , V Parsonnet, Impact of

triiodothyronine on the survival of high-risk patients undergoing open heart

surgery, Cardiology, 1996, Vol 87, Iss 6, pp 509-515. Biochim Biophys Acta

1997. Jan 16;1318(1-2):173-83 Regulation of the energy coupling in mitochondria

by some steroid and thyroid hormones. Starkov AA, Simonyan RA, Dedukhova VI,

Mansurova SE, Palamarchuk LA, Skulachev VP

Thyroid 1996 Oct;6(5):531-6. Novel actions of thyroid hormone: the role of

triiodothyronine in cardiac transplantation. Novitzky D. Rev Med Chil 1996

Oct;124(10):1248-50. [severe cardiac failure as complication of primary

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Cardiology 1996 Nov-Dec;87(6):509-15. Impact of triiodothyronine on the

survival of high-risk patients undergoing open heart surgery. Novitzky D,

Fontanet H, Snyder M, Coblio N, D, Parsonnet V Curr Opin Cardiol 1996

Nov;11(6):603-9. The use of thyroid hormone in cardiac surgery. Dyke C

N Koibuchi, S Matsuzaki, K Ichimura, H Ohtake, S Yamaoka. Ontogenic changes in

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Biokhimiia 1984 Aug;49(8):1350-6. [The nature of thyroid hormone receptors.

Translocation of thyroid hormones through plasma membranes]. [Article in

Russian] Azimova ShS, Umarova GD, Petrova OS, Tukhtaev KR, Abdukarimov A. The

in vivo translocation of thyroxine-binding blood serum prealbumin (TBPA) was

studied. It was found that the TBPA-hormone complex penetrates-through the

plasma membrane into the cytoplasm of target cells. Electron microscopic

autoradiography revealed that blood serum TBPA is localized in ribosomes of

target cells as well as in mitochondria, lipid droplets and Golgi complex.

Negligible amounts of the translocated TBPA is localized in lysosomes of the

cells insensitive to thyroid hormones (spleen macrophages). Study of T4- and

T3-binding proteins from rat liver cytoplasm demonstrated that one of them has

the antigenic determinants common with those of TBPA. It was shown

autoimmunoradiographically that the structure of TBPA is not altered during its

translocation.

Am J Physiol 1997 Sep;273(3 Pt 1):C859-67. Cytoplasmic codiffusion of fatty

acids is not specific for fatty acid binding protein. Luxon BA, Milliano MT

[The nature of thyroid hormone receptors. Intracellular functions of

thyroxine-binding prealbumin] Azimova ShS; Normatov K; Umarova GD; Kalontarov

AI; Makhmudova AA, Biokhimiia 1985 Nov;50(11):1926-32. The effect of

tyroxin-binding prealbumin (TBPA) of blood serum on the template activity of

chromatin was studied. It was found that the values of binding constants of

TBPA for T3 and T4 are 2 X 10(-11) M and 5 X 10(-10) M, respectively. The

receptors isolated from 0.4 M KCl extract of chromatin and mitochondria as well

as hormone-bound TBPA cause similar effects on the template activity of

chromatin. Based on experimental results and the previously published

comparative data on the structure of TBPA, nuclear, cytoplasmic and

mitochondrial receptors of thyroid hormones as well as on translocation across

the plasma membrane and intracellular transport of TBPA, a conclusion was

drawn, which suggested that TBPA is the " core " of the true thyroid

hormone receptor. It was shown that T3-bound TBPA caused histone H1-dependent

conformational changes in chromatin. Based on the studies with the interaction

of the TBPA-T3 complex with spin-labeled chromatin, a scheme of functioning of the

thyroid hormone nuclear receptor was proposed.

[The nature of thyroid hormone receptors. Thyroxine- and

triiodothyronine-binding proteins of mitochondria] Azimova ShS; Umarova GD;

Petrova OS; Tukhtaev KR; Abdukarimov A. Biokhimiia 1984 Sep;49(9):1478-85. T4-

and T3-binding proteins of rat liver were studied. It was found that the

external mitochondrial membranes and matrix contain a protein whose

electrophoretic mobility is similar to that of thyroxine-binding blood serum

prealbumin (TBPA) and which binds either T4 or T3. This protein is precipitated

by monospecific antibodies against TBPA. The internal mitochondrial membrane

has two proteins able to bind thyroid hormones, one of which is localized in

the cathode part of the gel and binds only T3, while the second one capable of

binding T4 rather than T3 and possessing the electrophoretic mobility similar

to that of TBPA

Radioimmunoprecipitation with monospecific antibodies against TBPA revealed

that this protein also the antigenic determinants common with those of TBPA.

The in vivo translocation of 125I-TBPA into submitochondrial fractions was

studied. The analysis of densitograms of submitochondrial protein fraction

showed that both TBPA and hormones are localized in the same protein fractions.

Electron microscopic autoradiography demonstrated that 125I-TBPA enters the

cytoplasm through the external membrane and is localized on the internal

mitochondrial membrane and matrix.

[The nature of thyroid hormone receptors. Translocation of thyroid hormones through

plasma membranes]. Azimova ShS; Umarova GD; Petrova OS; Tukhtaev KR;

Abdukarimov A. Biokhimiia 1984 Aug;49(8):1350-6.. The in vivo translocation of

thyroxine- binding blood serum prealbumin (TBPA) was studied. It was found that

the TBPA-hormone complex penetrates-through the plasma membrane into the

cytoplasm of target cells. Electron microscopic autoradiography revealed that

blood serum TBPA is localized in ribosomes of target cells as well as in

mitochondria, lipid droplets and Golgi complex. Negligible amounts of the

translocated TBPA is localized in lysosomes of the cells insensitive to thyroid

hormones (spleen macrophages). Study of T4- and T3-binding proteins from rat

liver cytoplasm demonstrated that one of them has the antigenic determinants common

with those of TBPA. It was shown autoimmunoradiographically that the structure

of TBPA is not altered during its translocation. Endocrinology 1987

Apr;120(4):1590-6 Brain cortex reverse triiodothyronine (rT3) and

triiodothyronine concentrations under steady state infusions of thyroxine and

rT3. Goumaz MO, Kaiser CA, Burger AG.

Gen Comp Endocrinol 1996 Aug;103(2):200-8 Characteristics of the uptake of

3,5,3'-triiodo-L-thyronine and L-thyroxine into red blood cells of rainbow

trout (Oncorhynchus mykiss). McLeese JM, Eales JG.

Prog Neuropsychopharmacol Biol Psychiatry 1998 Feb;22(2):293-310. Increase in

red blood cell triiodothyronine uptake in untreated unipolar major depressed

patients compared to healthy volunteers. Moreau X, Azorin JM, Maurel M, Jeanningros

R.

Prog Neuropsychopharmacol Biol Psychiatry 1998 Feb;22(2):293-310. Increase in

red blood cell triiodothyronine uptake in untreated unipolar major depressed

patients compared to healthy volunteers. Moreau X, Azorin JM, Maurel M,

Jeanningros R.

Biochem J 1982 Oct 15;208(1):27-34. Evidence that the uptake of

tri-iodo-L-thyronine by human erythrocytes is carrier-mediated but not

energy-dependent. Docter R, Krenning EP, Bos G, Fekkes DF, Hennemann G. J Clin

Endocrinol Metab 1990 Dec;71(6):1589-95. Transport of thyroid hormones by human

erythrocytes: kinetic characterization in adults and newborns. Osty J, Valensi

P, Samson M, Francon J, Blondeau JP. J Endocrinol Invest 1999 Apr;22(4):257-61.

Kinetics of red blood cell T3 uptake in hypothyroidism with or without hormonal

replacement, in the rat. Moreau X, Lejeune PJ, Jeanningros R.