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Resource Network of The Iodine Movement
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
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.
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
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 reticulum.
Subclinical Hypothyroidism & LAF [Lone Atrial Fibrilation]
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
Cardiovasc Res. 2005 Jan 1;65(1):195-202.
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.
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
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.
Iodine status and its correlations with age, blood pressure, and thyroid volume in South Indian
women above 35 years of age (Amrita Thyroid Survey).
Menon VU, Chellan G, Sundaram KR, Murthy S, Kumar H, Unnikrishnan AG, Jayakumar RV.
Department of Endocrinology, Diabetes and Podiatric Surgery, Amrita Institute of Medical
Sciences, Amrita Vishwa Vidyapeetham University, Kochi, Kerala, India.
Thyroid disorders are more commonly seen among females and the prevalence increases with
age. There is no population data from India focusing on iodine levels and their correlations with
thyroid volume and other factors in adult women.
This study was designed to establish the iodine status and its relation with various factors
including thyroid volume measured by ultrasound among the females of Kerala.
MATERIALS AND METHODS:
This was a cross sectional house to house survey among the females above 35 years of age in
a randomly selected urban area in Cochin Corporation, Kerala State, India. Selected subjects
were interviewed, examined and blood and urine tests were done. Thyroid volume was
calculated using ultrasound.
Among the 508 subjects who participated in the checkup, 471 subjects were included for
analysis. Mean age was 50.3 + 10.7 years and 53.2% were postmenopausal. A total of 98% of
the subjects were using iodized salt and median urinary iodine excretion (UIE) was 162.6 mcg/l.
UIE had negative correlation with age and systolic blood pressure (BP), but had no correlation
with thyroid volume (TV), thyroid nodularity, free thyroxine 4 (FT4), thyroid stimulating hormone
(TSH) or anti thyroid peroxidase (TPO) levels. Iodine deficiency was more commonly seen in
subjects with hypertension and also among postmenopausal females.
This study showed that females > 35 years were iodine sufficient, though one third of the
subjects had UIE levels less than the recommended level. Iodine levels had significant negative
correlation with age and systolic BP and no correlation with thyroid volume or biochemical
parameters. Iodine deficiency was significantly higher in subjects with new and known
hypertension and this relation merits further evaluation