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Iodine in Cardiovascular Disease

17th September 2007 by Arrow Durfee Posted in Uncategorized

Hypothesis: Dietary Iodine Intake in the Etiology of
Cardiovascular Disease
Stephen A. Hoption Cann, PhD
Department of Health Care and Epidemiology, University of British Columbia, Vancouver, British Columbia, CANADA

Key words: atherosclerosis, coronary heart disease, iodine, selenium, thyroid hormones
This paper reviews evidence suggesting that iodine deficiency can have deleterious effects on the cardio-vascular 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.

Key teaching points:
€ Iodine deficiency can cause thyroid dysfunction including hypothyroidism, impaired mental and physical development, loss of energy, and increased prenatal and infant mortality.

€ In recent years, the prevalence of iodine deficiency has increased in many countries that use iodized salt as a dietary source of iodine.

€ The prevalence and incidence of hypothyroidism and hyperthyroidism has been shown to vary with regional iodine intake. Both thyroid diseases are known to adversely affect cardiovascular function.

€ Selenium interacts uniquely with iodine: selenium-containing antioxidants protect the thyroid against oxidative damage during thyroid hormone synthesis; whereas selenium-containing deiodinases are involved in both activation and inactivation of thyroid hormones.

Few public health interventions have produced the degree of
benefit as the addition of iodine to table salt. It is a well-
recognized intervention for the prevention of iodine deficiency
disorders such as thyroid dysfunction, impaired mental and
physical development, loss of energy, and prenatal and infant
mortality [1]. It is of concern that this successful intervention
may be compromised by the suggested link between cardio-
vascular disease and sodium, if emphasis is not placed on the
beneficial role iodine plays in human health, particularly with
respect to cardiovascular function [2].
Address reprint requests to: Stephen A. Hoption Cann, PhD, Department of Health Care and Epidemiology, University of British Columbia, 5804 Fairview Avenue,
Vancouver, BC, V6T 1Z3, CANADA. E-mail:
Journal of the American College of Nutrition, Vol. 25, No. 1, 1°©11 (2006)
Published by the American College of Nutrition
This manuscript reviews animal and human data on the
association between iodine and cardiovascular disease, includ-
ing: (1) recent trends in iodine intake; (2) the association
between iodine intake and cardiovascular disease in Finland;
(3) the association between iodine intake and thyroid disease;
(4) how hypothyroidism and hyperthyroidism affect the cardio-
vascular system; (5) animal and human studies examining the
influence of iodine and thyroid hormones on cardiovascular
disease; (6) the physiological interactions between iodine and
selenium and its relevance to cardiovascular health; and (7)
finally, some potential mechanisms through which iodine may
affect the cardiovascular system.

Current Trends in Iodine Intake

In the general United States (US) population, a declining
trend in urinary iodine levels has been observed as estimated
through the large National Health and Nutrition Examination
Surveys (NHANES I, 1971°©74; and NHANES III, 1988 °©94)
[3]. The proportion of the US population with moderate to
severe iodine deficiency ( than quadrupled in the last 20 years, 2.6% in NHANES I vs
11.7% in NHANES III [3]. This decline may be due to a
reduced intake of iodized salt. For example, Enstrom et al. [4]
compared data from nationally representative samples of the
American population from two time periods, 1980 °©1982 vs
1990 °©1992. Based on dietary intake studies from over 10,000
individuals, no change was observed in sodium intake from
food, while there was a 65% decline in sodium intake from
discretionary (iodized) salt. Adventitious sources of iodine
have also declined with reductions in the use of iodine in the
dairy industry and in commercial bread production [5]. Com-
parable trends have been observed in other countries that iodize
salt. For example, public health recommendations to reduce salt
intake have been implicated in the decreasing iodine status in
Australia and New Zealand [6]. Similarly, a recent decline in
median urinary iodine levels in Austria may be due to lower
salt intake as well as the availability of noniodized salt in
Austria after joining the European Union in 1995 [7]. In Green-
land, as imported foods have replaced consumption of tradi-
tional foods such as fish and sea mammals, there has been a
gradual decline in iodine status. Andersen et al. [8] found that
median urinary iodine excretion declined with the degree of
decrease in the traditional lifestyle. Evidence of iodine defi-
ciency was seen in non-inuit subjects, who had the lowest
levels. Thus, in countries where there are changing dietary
patterns, including those long established iodization programs,
significant declines in iodine intake may occur.
A segment of the population that may often experience a
decline in iodine intake includes individuals with hypertension
or other cardiovascular diseases. Sodium restriction has been
associated with improvement in intermediate physiological
variables such as reduced blood pressure. For example, a recent
meta-analysis reviewed randomised studies examining the ef-
fects of a low sodium vs high sodium diet in normotensive
individuals [9]. A small but significant decrease in systolic
0.0001) and diastolic 0.009) blood pressure was observed; however, there was a
simultaneous and significant increase in plasma lipids: choles-
terol, 5.4% (p 0.0001), LDL cholesterol, 4.6% (p 0.004),
and triglycerides, 5.9% (p 0.03) [9]. Whether some of these
effects were due to concomitant changes in iodine intake (from
iodized salt) was not considered in these studies. Overall iodine
intake has been shown to decline in subjects on sodium-re-
duced diets for cardiovascular disease. Simpson et al. [10]
conducted a one-year randomized study of hypertensive sub-
jects on sodium-restricted vs control (unrestricted) diets. De-
spite other dietary sources of iodine, urinary iodine excretion
was strongly correlated with sodium excretion (r 0.69, p
0.001) and was significantly lower in the sodium-restricted
group at one year (p 0.01). Grzesiuk et al. [11] monitored the
adequacy of a newly implemented iodization program in Po-
land. Thirty-six months after implementation of the program,
an overall rise in iodine status in the study cohort was observed;
yet for subjects placed on sodium-restricted diets due to car-
diovascular disease, their iodine status was half that of pre-
implementation values and indicative of mild to moderate
iodine deficiency. Fruhwald et al. [12] has recommended that
patients with cardiovascular disease on sodium-reduced diets
should be screened for the presence of thyroid disorders. They
investigated the prevalence of thyroid disorders in 61 patients
with idiopathic dilated cardiomyopathy. Only two patients
(3%) showed completely normal thyroid morphology and func-
tion. Moreover, the duration of cardiomyopathy was signifi-
cantly correlated with thyroid gland volume (r 0.44, p
0.001). Iodine intake was not determined, however, the authors
suggested that iodine deficiency (the most common cause of
goiter) secondary to sodium restriction was the underlying
cause. Although subjects with hypertension or other cardiovas-
cular conditions may benefit from a reduction in sodium intake,
a concomitant reduction in iodine intake may counter some of
these benefits. This latter point is a particular concern in light
of the increasing prevalence and incidence of chronic heart
failure. Improved treatment of acute coronary events resulting
in prolonged survival, an increased awareness of and ability to
diagnose heart failure, and the aging of the population, account
for the continuing increase in the incidence and prevalence of
this condition [13,14]. The burden of prolonged iodine defi-
ciency in such individuals placed on sodium-reduced diets is
At what level of iodine deficiency one would observe neg-
ative effects on cardiovascular function is not known. A one
year study conducted by Andersen et al. [15] examined the
relationship between thyroid hormone production and iodine
intake in subjects with mild to moderate iodine deficiency.
Iodine and Cardiovascular Disease
2 VOL. 25, NO. 1
Clear signs of substrate deficiency for thyroid hormone syn-
thesis were observed in subjects with moderate iodine defi-
ciency (20 °© 49
a declining intake of iodine in many developed countries and
declines have been observed in subjects with cardiovascular
disease on sodium-reduced diets. The costs of concurrently
reducing iodine intake with respect to the development of
cardiovascular disease or its adverse effects in subjects with
pre-existing cardiovascular disease need to be determined.
Cardiovascular disease in Finland
Before the establishment of an iodization program in Fin-
land in 1963, some early investigations suggested an inverse
association between iodine intake and cardiovascular disease.
Epidemiological studies in the 1950s revealed that Finland had
the highest rate of coronary heart disease mortality in Europe
[16]. These findings led to a series of studies examining pos-
sible causative factors. Keys et al. [16] demonstrated that
serum cholesterol levels in Finland were unusually high, par-
ticularly in the eastern part. This paralleled the fact that car-
diovascular disease was significantly more prevalent in eastern
than western Finland [16].
Roine et al. [17] comprehensively examined the dietary
differences between western and eastern Finland. A wide va-
riety of dietary components were examined in the summer and
winter, including: major foodstuffs, proteins, fats, carbohy-
drates, lipids, amino acids, vitamins and minerals. Among the
47 macro and micronutrients considered, iodine showed the
greatest difference statistically, being higher in the west in both
winter and summer. There was no significant difference in
cholesterol or saturated and unsaturated fat intake.
Uotila et al. [18] made the observation that subjects who
died from coronary sclerosis often had goitre. In order to
further examine this phenomenon, 250 Finnish subjects who
had died from coronary heart disease were age and sex-
matched to controls who died from other causes [19]. The risk
of death from coronary heart disease was found to be signifi-
cantly higher in individuals with goiter (odds ratio (OR)
3.53, 95% confidence interval (CI) 2.43°© 4.99). It was noted
that the average thyroid weight was higher in those dying from
coronary disease. Moreover, among the coronary disease cases
with goiter, there was a lower average age of death and a higher
average heart weight. Due to the low iodine content of foods
and lack of an iodization program at the time, endemic goiter
was common in Finland, particularly in the east.
In 1971, Hasanen [19] carried out a correlational study
comparing the levels of a variety of trace elements in drinking
water (i.e. calcium, chlorine, fluorine, bromine, and iodine) to
the prevalence of cardiovascular diseases in 21 Finnish cities.
The prevalence of such diseases for each city was estimated
from disability pensions, which included a spectrum of cardio-
vascular conditions, primarily: angina pectoris (26%), coronary
thrombosis (20%), hypertensive diseases (19%) and arterioscle-
rosis (7%). The strongest correlation was noted for iodine (r
the lowest rates of cardiovascular disease. It was estimated that
up to 23% of the average daily intake of iodine in Finland could
be obtained from drinking water [19]. Overall, while not de-
finitive, these studies were suggestive of a protective role for
iodine against the development of cardiovascular disease.
Geographical Variations in Hypothyroidism and
Population-based studies of adults have shown that the
prevalence and incidence of thyroid diseases differ from one
region to the next, varying with regional iodine intake [20,21].
In developing countries with moderate or greater iodine defi-
ciency, hypothyroidism due to iodine substrate insufficiency is
the more common of the two [22,23], and more common in
individuals from a lower socio-economic status [23]. In these
developing countries, human studies have demonstrated that
inadequate nutrition has been shown to exacerbate the adverse
effects of iodine deficiency [24 °©28].
In developed nations with moderate iodine deficiency, prev-
alence of hyperthyroidism tends to be higher than hypothyroid-
ism [29]; whereas in regions where iodine intake is sufficient or
high, hypothyroidism predominates [30,31]. In support of these
findings, it has been observed that in areas of moderate defi-
ciency, as regional iodine intake increases, the incidence of
hyperthyroidism gradually declines while hypothyroidism in-
creases [32°©35]. For example, following the initiation of iodine
supplementation in deficient regions, there is a marked rise in
the incidence of thyroglobulin and thyroperoxidase autoanti-
bodies [33,34]‹autoantibodies that are found in a form hypo-
thyroidism called autoimmune thyroiditis. The overall preva-
lence of hypothyroidism and hyperthyroidism, however, is
similar in regions of adequate iodine intake such as the USA
[31] and in regions where iodine intake may be excessive such
as Japan [30].

In addition to the variable prevalence of hyperthyroidism
and hypothyroidism, the underlying causes of these conditions
appear to vary with regional iodine intake. For example, in
regions of moderate iodine deficiency, such as Denmark and
Spain, toxic nodular goiter is the main cause of hyperthyroid-
ism [36,37]; whereas in regions of adequate or greater iodine
intake such as Iceland, USA or Japan, autoimmune Graves©ˆ
hyperthyroidism prevails [30,38,39]. In regions where io-
dine intake is high such as Japan, an autoantibody-negative
form of hypothyroidism is also observed, which is largely
reversible following iodine restriction [30,40]. What re-
mains undetermined is how an individual©ˆs underlying io-
dine intake in these conditions may influence its effects on
the cardiovascular system.

Iodine and Cardiovascular Disease
Thyroid Disease and the Cardiovascular System
Iodine-containing thyroid hormones, thyroxine (T4) and
triiodothyronine (T3), are important metabolic regulators of
cardiovascular activity with the ability to exert action on car-
diac myocytes, vascular smooth muscle, and endothelial cells
[41,42]. Numerous studies of patients with spontaneously oc-
curring hypothyroidism and hyperthyroidism have demon-
strated that thyroid hormones can have profound effects on the
heart and cardiovascular system [43,44].
Clinical cardiovascular features of hypothyroidism include:
bradycardia, reduced cardiac output, increased pericardial and
pleural effusions, increased diastolic blood pressure and periph-
eral vasoconstriction [43,44]. In addition, cardiovascular dis-
ease risk factors known to be more prevalent in hypothyroid
subjects include: elevated C-reactive protein (CRP), elevated
total cholesterol and LDL cholesterol, and reduced HDL cho-
lesterol [45]. T4 therapy generally leads to the normalization of
these parameters in hypothyroid subjects [46], with more mod-
est effects in subjects with subclinical hypothyroidism (normal
serum T3 or T4 with elevated thyroid stimulating hormone
(TSH)) [47,48]. A population-based cross-sectional study of
1149 randomly selected women by Hak et al. [49] found that
women with subclinical hypothyroidism were at an increased
risk of for atherosclerosis (OR 1.9, 95% CI 1.1°©3.6) and
myocardial infarction (OR 3.1, 95% CI 1.5°© 6.3).
Cardiovascular abnormalities seen in subjects with hyper-
thyroidism include: increased systolic blood pressure, venous
resistance, cardiac output and cardiac mass; tachycardia and
atrial arrhythmias such as atrial fibrillation; as well as symp-
toms such as palpitations, dyspnea and chest pain [43,44]. Most
cardiac abnormalities return to normal once a euthyroid state
has been achieved, although atrial fibrillation may persist in a
minority [51,52]. Long-term followup studies have demon-
strated an increased mortality (primarily from cardiovascular
disease) in those with past history of hyperthyroidism or overt
hyperthyroidism [53°©55], as well as those with subclinical
hyperthyroidism [56,57]. Thus, many cardiovascular features
of hypothyroidism are in diametric opposition to those of

Amongst the subtypes of hypothyroidism and hyperthyroid-
ism, there are often subtle differences in the prevalence of
cardiovascular signs and symptoms. For example, atrial fibril-
lation is more common in toxic nodular goiter than in Graves©ˆ
disease [51,58], however, Graves©ˆ disease tends to present at a
much younger age and therefore increasing age may increase
the frequency of disease manifestations.

Animal Studies of Iodine, Thyroid Hormones and
Cardiovascular Disease
In 1918, Murata and Kataoke [59] first demonstrated that
the feeding of iodine compounds could prevent the deposition
of cholesterol in the arteries, when the latter substance was fed
to rabbits. Further studies in rabbits elaborated upon and con-
firmed their findings [60 °© 64]. In 1933, Turner [62] conducted
the only study to compare the relative efficacy of T4, iodine,
and desiccated thyroid (a source of both iodine and thyroid
hormones) in preventing the development of atherosclerosis in
rabbits. Control rabbits fed a cholesterol-rich diet for over three
months exhibited moderate to marked aortic atherosclerosis.
Rabbits fed a cholesterol-rich diet and T4 showed slight to
moderate aortic atherosclerosis. Yet, rabbits fed cholesterol and
either desiccated thyroid or iodine similarly showed an absence
of atherosclerotic lesions. Average blood cholesterol levels of
animals on the three diets were: cholesterol (13.45 mmol/L),
cholesterol T4 (10.32 mmol/L), cholesterol desiccated
thyroid (4.60 mmol/L), and cholesterol iodine (4.73 mmol/
L). Thus, iodine appeared to have an effect independent of or
possibly synergistically with thyroid hormones.
Studies in rats [65,66] have suggested that a higher relative
dietary cholesterol intake may further exacerbate iodine defi-
ciency by enhancing thyroid hyperplasia. This was demon-
strated by Girard et al. [66] who examined the interaction
between iodine intake and cholesterol on the development of
goiter over a four and a half month period. Relative to rats on
a basal (iodine-reduced) diet, iodine supplementation was
found to lead to a lower average thyroid weight (43.4 vs 10.3
mg, respectively). In contrast, dietary cholesterol supplemen-
tation led to a significant increase in average thyroid weights
compared to combined cholesterol/iodine supplementation
(133.6 vs 12.1 mg, respectively). Using injections of I131-
labeled T4, increased fecal excretion of I131 was observed in
the cholesterol supplemented group relative to the group on the
basal diet; hence suggesting that cholesterol feeding enhanced
iodine depletion either by increasing biliary excretion of T4 or
interfering with intestinal reabsorption of T4.

Morreale de Escobar et al. [67] studied the effects of an
iodine-reduced diet on thyroid hormone levels in rats. The
iodine deficiency led to a condition analogous to subclinical
hypothyroidism‹that is while there was a rise in plasma TSH
levels, T3 and T4 levels remained unchanged. Yet despite
normal plasma thyroid hormone levels, T3 concentrations were

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4 Responses to “Iodine in Cardiovascular Disease”

  1. Arrow Durfee Says:

    Lugols loading dose = 8 drops daily for 3 months

    12.5mg is maintence dose (2 drops)

    15 mg is upper maximum daily dosage for safety

    Severe hypothryroid can require up to 20mg per day

    Another valuable iodine preparation is saturated solution of potassium iodide. This does not have the correct ratio of iodine iodide recommended by Dr.Abrahams for correcting iodine deficiency but it does have a multitude of valuable healing properties. Some people use it for replacement therapy and do well. Read all the information available on this website. Ultimatley the decision is up to you. My medical doctor recommends Lugols. It can help open up blocked arteries, disinfect water, cure bladder infections, reduce or eliminate ovarian cysts, diminish unsightly keloids, loosen thick bronchial secretions, reduce or eliminate Peyronie’s Disease and Dupuytron’s contracture.

    Lugols: 2 drops= 12.5mg
    4 drops=25 mg
    8 drops=50 mg
    16 drops=100 mg
    20 drops=125 mg

    ICK! your taste buds will do the tango!

  2. Rosalie Kroot Says:

    I am on warfarin (half a pink tablet @ 6 p.m. daily for eep vein thrombosis. In the morning I take 2 x Lasix and 2 x Plenish K as I have developed congestive heart failure. Please advise if I take two drops of Lugol’s iodine at 2.30 p.m. it will or will not have effect on the medications I am taking. Many thanks
    Rosalie Kroot
    Cape Town, South Africa

  3. Arrow Durfee Says:

    Hello Rasalie

    I don’t think iodine will affect your medicaitons. If you are on a thyroid medicine you should have your thyroid levels checked in about 6 weeks. If things are ok you can increase your iodine by one drop. Often people on thryoid who take iodine end up needing to decrease their thyroid medicine.

    I strongly suggest that you read on the cardiovascular thread on this blog. There is a series of posts that deal with heart disease. I have provided the link to the first one and you should be able to find the others from there. There are several very powerful things you can be doing for your condition.

    At the bottom of the article you will see links to the related posts to find the other articles.

  4. Rosalie Kroot Says:

    Dear Rett
    Thank you for your reply and the reference to the ultimate solutions to heart disease stroke etc. Note – I am not on any thyroid medication – just started on 2 drops of Lugol’s solution and did not want it to have an effect on my INR readings – the next reading is set down for October 15th. I am really grateful for posts such as Health Salon as we as for your so very prompt reply.
    Rosalie Kroot