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Iodine Research

Resource Network of The Iodine Movement

                                   Iodine and the Body


Iodine deficiency can have deleterious effects on the cardiovascular system.  Thus, a higher iodine
intake may benefit cardiovascular function.

In recent years, sodium restriction has been promoted as a means of reducing hypertension and the
risk of cardiovascular disease.

Since iodized salt is the primary source of iodine for many people, iodine deficiency has become
much more common in developed countries, especially among the elderly and others who are
restricting salt intake.

Adequate iodine is necessary for proper thyroid function.  The heart is a target organ for thyroid
hormones.  Marked changes occur in cardiac function in patients with hypo- or hyperthyroidism.

Cann considers the role iodine deficiency plays in the etiology of cardiovascular disease.

West discusses iodine and heart arrhythmia, especially atrial fibrillation.

Kahaly and Danzi discuss thyroid hormone action in the heart.

The historical background of the iodine project.
Abraham GE
The Original Internist, 12(2):57-66, 2005

Amiodarone is a toxic form of sustained release iodine. The author has previously discussed the
interesting observation that this antiarrhythmic drug becomes effective when the body has
accumulated approximately 1.5 gm of iodine. This is exactly the amount of iodine retained by the
human body when iodine sufficiency is achieved following orthoiodosupplementation. Whole body
sufficiency for inorganic non-radioactive iodine/iodide results in optimal cardiac functions. Inorganic
non-radioactive iodine was never tested in clinical conditions for which physicians prescribe
amiodarone. However, inorganic iodide is blamed for the severe side effects of this drug.

Hypothesis: dietary iodine intake in the etiology of cardiovascular disease.
Hoption Cann SA
J Am Coll Nutr. 2006 Feb;25(1):1-11.

This paper reviews evidence suggesting that iodine deficiency can have deleterious effects on the
cardiovascular system, and correspondingly, that a higher iodine intake may benefit cardiovascular
function. In recent years, public health bodies have aggressively promoted sodium restriction as a
means of reducing hypertension and the risk of cardiovascular disease. These inducements have
led to a general decline in iodine intake in many developed countries. For example, a United States
national health survey conducted in the early 1970s observed that 1 in 40 individuals had urinary
iodine levels suggestive of moderate or greater iodine deficiency; twenty years later, moderate to
severe iodine deficiency was observed in 1 in 9 participants. Regional iodine intake has been shown
to be associated with the prevalence of hypothyroidism and hyperthyroidism, where autoimmune
hypothyroidism is the more common of the two in regions with moderate to high iodine intake. Both of
these thyroid abnormalities have been shown to negatively affect cardiovascular function. Selenium,
an important antioxidant in the thyroid and involved in the metabolism of iodine-containing thyroid
hormones, may play an interactive role in the development of these thyroid irregularities, and in turn,
cardiovascular disease. Iodine and iodine-rich foods have long been used as a treatment for
hypertension and cardiovascular disease; yet, modern randomized studies examining the effects of
iodine on cardiovascular disease have not been carried out. The time has come for investigations of
sodium, hypertension, and cardiovascular disease to also consider the adverse effects that may
result from mild or greater iodine deficiency.

Thyroid hormone and the cardiovascular system.
Danzi S, Klein I.
Minerva Endocrinol. 2004 Sep;29(3):139-50. Review.

Thyroid hormone is an important regulator of cardiac function and cardiovascular hemodynamics.
Triiodothyronine, (T(3)), the physiologically active form of thyroid hormone, binds to nuclear receptor
proteins and mediates the expression of several important cardiac genes, inducing transcription of
the positively regulated genes including alpha-myosin heavy chain (MHC) and the sarcoplasmic
reticulum calcium ATPase. Negatively regulated genes include beta-MHC and phospholamban, which
are down regulated in the presence of normal serum levels of thyroid hormone. T(3) mediated
effects on the systemic vasculature include relaxation of vascular smooth muscle resulting in
decreased arterial resistance and diastolic blood pressure. In hyperthyroidism, cardiac contractility
and cardiac output are enhanced and systemic vascular resistance is decreased, while in
hypothyroidism, the opposite is true. Patients with subclinical hypothyroidism manifest many of the
same cardiovascular changes, but to a lesser degree than that which occurs in overt hypothyroidism.
Cardiac disease states are sometimes associated with the low T(3) syndrome. The phenotype of the
failing heart resembles that of the hypothyroid heart, both in cardiac physiology and in gene
expression. Changes in serum T(3) levels in patients with chronic congestive heart failure are
caused by alterations in thyroid hormone metabolism suggesting that patients may benefit from T(3)
replacement in this setting.

Thyroid hormone action in the heart.
Kahaly GJ, Dillmann WH.
Endocr Rev. 2005 Aug;26(5):704-28. Epub 2005 Jan 4. Review.

The heart is a major target organ for thyroid hormone action, and marked changes occur in cardiac
function in patients with hypo- or hyperthyroidism. T(3)-induced changes in cardiac function can
result from direct or indirect T(3) effects. Direct effects result from T(3) action in the heart itself and
are mediated by nuclear or extranuclear mechanisms. Extranuclear T(3) effects, which occur
independent of nuclear T(3) receptor binding and increases in protein synthesis, influence primarily
the transport of amino acids, sugars, and calcium across the cell membrane. Nuclear T(3) effects are
mediated by the binding of T(3) to specific nuclear receptor proteins, which results in increased
transcription of T(3)-responsive cardiac genes. The T(3) receptor is a member of the ligand-
activated transcription factor family and is encoded by cellular erythroblastosis A (c-erb A) genes. T
(3) also leads to an increase in the speed of diastolic relaxation, which is caused by the more
efficient pumping of the calcium ATPase of the sarcoplasmic reticulum. This T(3) effect results from T
(3)-induced increases in the level of the mRNA coding for the sarcoplasmic reticulum calcium
ATPase protein, leading to an increased number of calcium ATPase pump units in the sarcoplasmic

Subclinical Hypothyroidism & LAF [Lone Atrial Fibrilation]
Larsen HR

The reason why this topic is relevant to afibbers is the fact that both diagnosed and subclinical HT
can cause atrial fibrillation. (Subclinical means not diagnosed by laboratory tests.) Hypothyroidism
can result in reduced heart rate due to the slowing of metabolism…and this could set the AF stage
for many people. When the SN rate drops below that of the ectopically firing cells, the ectopics
become the drivers--that's how it works for some.... Patients with “normal” thyroid tests are frequently
prescribed Prozac for depression, amitriptyline for fibromyalgia, anti-inflammatories for
musculoskeletal pain; oral contraceptives for irregular menses; low levels of antibiotics for acne,
Viagra for loss of libido; Ritalin for ADD, allopurinol for gout and/or Lipitor for high cholesterol...

Cardiac reporter gene imaging using the human sodium/iodide symporter gene.
Miyagawa M, Beyer M, Wagner B, Anton M, Spitzweg C, Gansbacher B, Schwaiger M, Bengel FM.
Cardiovasc Res. 2005 Jan 1;65(1):195-202.
[abstract only]

OBJECTIVE: Imaging of reporter gene expression holds promise for noninvasive monitoring of
cardiovascular molecular therapy. We investigated the feasibility of myocardial gene expression
imaging in living rats using the human sodium/iodide symporter gene (hNIS) and widely available
scintigraphic techniques.

METHODS: We injected adenovirus expressing hNIS under control of cytomegalovirus promoter (Ad
(hNIS)) directly into left ventricular myocardium of Wistar rats. For detection of reporter gene
expression, dynamic gamma-camera imaging was performed following intravenous injection of (123)
Iodide or (99m)Technetium.

RESULTS: For both radiotracers, focal cardiac accumulation was identified as early as 10 min, and
remained detectable until 2 hrs after injection, while it was not present in animals injected with LacZ
control virus. Intensity of tracer accumulation gradually decreased when decreasing titers of Ad
(hNIS) were applied. Treatment with sodium perchlorate (a blocker of hNIS) abolished cardiac tracer
uptake after Ad(hNIS)-infection. Serial imaging after cardiac gene transfer demonstrated a peak of
tracer signal between days 1 and 3, and a subsequent decrease until day 12. Postmortem analysis
of hearts yielded significant correlation between in vivo radiotracer accumulation and ex vivo gamma-
counting. Autoradiography demonstrated specific regional radioactivity in Ad(hNIS)-infected
myocardial areas.

CONCLUSIONS: hNIS offers a practical and reliable approach for myocardial gene expression
imaging. Using suitable vectors, hNIS may be coexpressed with therapeutic genes or stably
expressed in stem cells for future monitoring of cardiovascular molecular therapy.

[Iodine deficiency in cardiovascular diseases]
Molnar I, Magyari M, Stief L.
Orv Hetil. 1998 Aug 30;139(35):2071-3. Hungarian.
[abstract only]

The thyroid hormone deficiency on cardiovascular function can be characterized with decreased
myocardial contractility and increased peripheral vascular resistance as well as with the changes in
lipid metabolism. 42 patients with cardiovascular disease (mean age 65 +/- 13 yr, 16 males) were
investigated if iodine insufficiency can play a role as a risk factor for the cardiovascular diseases.
The patients were divided in 5 subgroups on the ground of the presence of hypertension, congestive
heart failure, cardiomyopathy, coronary dysfunction and arrhythmia. Urine iodine concentration (5.29
+/- 4.52 micrograms/dl) was detected with Sandell-Kolthoff colorimetric reaction. The most decreased
urine iodine concentration was detected in the subgroups with arrhythmia and congestive heart
failure (4.7 +/- 4.94 micrograms/dl and 4.9 +/- 4.81 micrograms/dl, respectively). An elevated TSH
level was found by 3 patients (5.3 +/- 1.4 mlU/l). An elevation in lipid metabolism (cholesterol,
triglyceride) associated with all subgroups without arrhythmia. In conclusion, the occurrence of iodine
deficiency in cardiovascular disease is frequent. Iodine supplementation might prevent the worsening
effect of iodine deficiency on cardiovascular disease.

Atrial Fibrillation, Arrhythmias and Iodine
West B
Health Alert, June 2006, Volume 23, Issue 6

Iodine supplementation may be the missing link in a good percentage of heart arrhythmia cases,
especially atrial fibrillation.  The body needs adequate stores of iodine for the heart to beat
smoothly.  After close to a year now of using Iodine Fulfillment Therapy, I can attest to this fact.  Most
of the stubborn cases of cardiac arrhythmias and atrial fibrillation that we were unable to completely
correct with our cardiac protocols have now been resolved with adequate supplies of iodine added to
the protocol.