Different tissue responses for iodine and iodide in rat thyroid and mammary glands. Biological Trace Element
Research. Vol. 49, 1995
3
 Eskin, B. IBID. 1995
4
 Aceves, C. Is Iodine a gatekeeper of the integrity of the mammary gland? J. of Mammary Gland Biol. and Neoplasia. Vol. 10, No. 2. April 2005.Chapter 4
Iodine and the Thyroid Gland 
CHAPTER 4: IODINE AND THE THYROID GLAND
Iodine is an essential ingredient in all of the thyroid hormones. T4 (thyroxine) contains four iodine atoms. T3 (triiodothyronine)
contains three iodine atoms. Without sufficient iodine supply, the thyroid gland is unable to make thyroid hormones in adequate
amounts. The thyroid gland cannot optimally function in an iodine-deficient state. One of the consequences of an iodine-deficient state
is goiter (swelling of the thyroid gland). Over a hundred years ago, it was shown that goiter could be avoided and often reversed
with iodine. In addition to goiter formation, iodine deficiency may also lead to other thyroid conditions including hypothyroidism,
autoimmune thyroid diseases such as Graves’ and Hashimoto’s disease, as well as thyroid cancer. Studies have shown that
iodine-deficient individuals have an increased incidence of anti-thyroid antibodies. 1
 
2
 This chapter will focus on the relationship
between low iodine levels and hypothyroidism. More information about iodine and autoimmune thyroid illnesses and thyroid
cancer can be found in the 
Chapter 6
. Iodine is found throughout the body, with approximately 15-20mg stored in the thyroid of the average adult. 3
 
4
 When body
iodine levels are sufficient, the thyroid gland can hold up to 50mg of iodine. The thyroid gland requires adequate iodine levels to
make thyroid hormone. The thyroid gland has developed a specialized system to concentrate a large amount of iodine as
compared to its size. This system is known as the sodium/iodide symporter (NIS). There are other tissues of the body that utilize
NIS to concentrate iodine including the breasts, kidneys, placenta, stomach, rectum, and salivary glands. 5
The thyroid gland is located in the lower part of the neck and produces thyroid hormone. It is regulated by the pituitary gland
which produces thyroid stimulating hormone—TSH. TSH stimulates the thyroid gland to release thyroxine (T4). Triiodothyronine
(T3) is converted from T4 in the periphery of the body. T3 is believed to be the active form of thyroid hormone that drives the
metabolic functions of the body. The Figure below illustrates how the thyroid gland produces thyroid hormone. T4 and T3 are the most common thyroid hormones produced. The ‘4’ in T4 and the ‘3’ in T3 refer to the number of iodine
atoms present. As previously stated, T4 has four iodine atoms present, while T3 has three iodine atoms present. The end result of
iodine deficiency is severe. It can include a poorly functioning thyroid gland, goiter, increased autoimmune thyroid problems, and
an increased risk of thyroid cancer. Thyroid hormone is essential for normal brain development of the newborn. Since iodine is necessary for the production of
thyroid hormone, an iodine-deficient state may predispose the newborn to abnormal brain development. In children, iodine
deficiency can result in mental retardation, goiter, lowered IQ, attention deficit hyperactivity disorder (ADHD), and autism. Furthermore, fetal iodine deficiency is associated with 
increased rates of stillbirth, abortion, and congenital anomaly. 6
 The World
Health Organization stated that iodine deficiency is the single greatest cause of preventable mental retardation. 7
 Research has
found almost a 50% increase in perinatal mortality due to iodine deficiency. 8
 When iodine deficiency is rectified, neonatal
mortality has been shown to decline by over 50%. 9
 
10
Many studies have shown that children who live in iodine-deficient areas have lower IQ’s as compared to children living in
iodine-sufficient areas. A large analysis comparing children in iodine-deficient and iodine-sufficient areas showed a 13.5 point
difference in IQ score. 11
Janet, age 57, had been treated for hypothyroidism for two years. She was found to be deficient in iodine and given a
therapeutic trial of a combination of iodine and iodide (Iodoral
®
). I asked her to write a letter to me about her
experience with iodine. She wrote the following letter:
“After taking Armour
®
 thyroid for over two years, I began to feel somewhat sluggish and felt that perhaps I needed
more thyroid hormone. Dr. Brownstein told me to take two tablets of iodine (Iodoral
®
–25mg) with my thyroid medicine. It
has been over five months since I began the iodine treatment and I still feel the perkiness everyday that I have been
looking for. In fact, I started to feel better the first day that I took the iodine. The 
iodine certainly was needed. I am just
thrilled about how much better I feel.”
WHAT ABOUT IODIZED SALT? As mentioned in 
Chapter 2
, iodine was added to iodized salt over 70 years ago to combat goiter and cretinism. The RDA to
combat these illnesses was established (150ug/day) with one goal in mind: prevent goiter and cretinism. The RDA for iodine has
been successful at combating goiter and cretinism; however, the RDA is woefully inadequate in preventing many other thyroid
disorders including hypothyroidism, Graves’ disease, Hashimoto’s disease, and thyroid cancer. Furthermore, the RDA for iodine
fails to provide optimal amounts of iodine for the rest of the body’s iodine needs. Finally, our increasing exposure to toxic
halogens—bromide, fluoride, and chlorine derivatives—have markedly increased our iodine requirements. Other illnesses
associated with iodine deficiency (e.g., breast cancer, fibrocystic breast disease) are covered in other chapters. HOW COMMON ARE THYROID PROBLEMS?Thyroid illnesses are found at ever increasing numbers. Recent studies have estimated that 10% of the adult population of the
United States (13 million) may have laboratory evidence of thyroid disease. 12
 I have written in my book, 
Overcoming Thyroid
Disorders, 3
rd
 Edition
, that I believe these numbers are too low and a more accurate estimate would probably approach 30-
40% 
of the population (up to 52 million adult Americans). 13
 Why the discrepancy? Conventional medicine diagnoses a thyroid
problem based solely on the blood tests. I feel that the blood tests are not sensitive enough to pick up thyroid abnormalities in the
vast majority of patients suffering from thyroid problems. Therefore, a holistic approach to diagnosing a thyroid issue, as I outline
in my book, is a much more comprehensive way to diagnose a problem that affects every single cell in the body. Why is adequate thyroid hormone so important? Every single cell, muscle, and organ in the body depends on adequate
thyroid hormone levels for optimal functioning. Thyroid hormone acts as the body’s major metabolic regulator. In a low thyroid
state, known as hypothyroidism, the thyroid gland is releasing inadequate amounts of thyroid hormone to meet the body’s
metabolic demands, and the metabolic rate is therefore reduced. In a hyperthyroid state, the thyroid gland is releasing excess
amounts of thyroid hormone that results in an elevated metabolic rate. Why do so many people across this country and the world have a serious problem like a thyroid disorder? Although the
etiology of thyroid illness can be varied, one common denominator that could explain this epidemic is iodine deficiency. As previously discussed in 
Chapter 2
, one-third of the world’s population lives in an iodine-deficient area by World 
Health
Organization (WHO) standards. This large number of people living in an iodine-deficient area closely correlates with the estimates
for the number of people who have thyroid disorders. All individuals with a thyroid disorder should be screened for iodine
deficiency. WHAT DOES IODINE DO IN THE THYROID GLAND? Iodine is responsible for maintaining the normal architecture of the glands of the body including the thyroid, ovaries, uterus,
breast, and prostate. When the cells of the glandular tissue have enough iodine, the tissue maintains a normal structure. When iodine is deficient, the architecture of the glandular tissue becomes disrupted and the tissue becomes cystic. Cysts are
fluid-filled sacs that have a distinct border from the surrounding normal tissue. When palpated, cysts are generally soft and
compressible. If iodine deficiency persists, the cysts become nodular—that is, they become more firm upon palpation. If iodine deficiency
continues, the nodules start to change their histological appearance to become hyperplastic. Hyperplasia literally means ‘over-
formation’. In a hyperplastic state, the cells start to multiply rapidly and take on an increasingly disordered appearance when
viewed microscopically. Eventually, if iodine deficiency is not corrected, the end stage of this continuum can be cancer. Chapter 8
 will discuss fibrocystic breast disease and iodine deficiency. Fibrocystic breast disease is a precursor to breast
cancer. I have successfully treated many fibrocystic breast disease patients with iodine. I feel that cysts on any glandular tissue
should prompt a physician to check the patient’s iodine status and to prescribe iodine, if indicated, to reverse the process. In the thyroid gland, iodine deficiency results in the formation of cysts, nodules, and goiter. The thyroid gland does not
function optimally when the normal architecture is disrupted. I have treated hundreds of patients for growths in their thyroid and
other glandular tissue that resolve or get significantly better with iodine therapy. Lexi is a 15-year-old girl who was diagnosed with thyroid cysts and nodules one year previously. Her thyroid was
two-times the normal size. At our first visit, I could see Lexi’s thyroid protruding out of her neck. Lexi had seen two
endocrinologists who both recommended surgery. Lexi’s mother commented, “I really don’t want her to have surgery, but
they are offering me nothing. We have been following her thyroid ultrasounds and it just keeps getting bigger. I have a
surgery date already scheduled for three weeks from now unless you tell me otherwise,” she said. At our first visit, I
asked Lexi how she was feeling. She did not 
have any major complaints. Her energy level was good and she was very
active in school activities. I told Lexi and her mother that surgery was not warranted yet; the enlarged thyroid had not
caused any problems. After my exam, I ordered a spot urine iodide level and a 24-hour urinary iodide loading test. Lexi’s
spot urine iodide was below the laboratory detectable limits. Her 24-hour loading test was also low at 50% excretion
(normal 95%). At this point I prescribed iodine—25mg/day, unrefined salt (1tsp/day of Redmond’s Real Salt), and a
multivitamin (Optivite). Two weeks later, Lexi had another ultrasound of her thyroid because both both she and her
mother–who is an ultrasound technician–felt the thyroid was visually smaller. The ultrasound showed a 50% reduction in
the overall size of her thyroid and all the cysts and nodules were shrinking. “The radiologist called in two other
colleagues to look at the ultrasound as he could not believe how much it had shrunk,” Lexi’s mother commented. I have seen countless patients with cysts, nodules, and disrupted architecture of glandular tissue—including the breasts,
ovaries, uterus, and prostate improve or dramatically reverse their condition with iodine supplementation. In many cases, iodine
supplementation results in a cure. How long does this process take? For most patients, three to six months is a reasonable time
period to see results. Severely ill patients may take years to see results. HYPOTHYROIDISM
The thyroid gland controls the metabolic activity of the body. When there is adequate thyroid hormone available for the cells
of the body, there is a normal metabolic activity present. By contrast, in a hypothyroid state, the metabolic activity of the body islowered. Table 4
, on the following page, lists some of the signs and symptoms related to hypothyroidism. The main thyroid hormones, T4 and T3, require sufficient iodine in order to be produced. In an iodine-deficient state,
hypothyroidism is the expected outcome as thyroid hormone will not be manufactured. My research has shown that iodine levels
need to be investigated in all hypothyroid individuals. If iodine is found to be deficient, many times, supplementing with iodine can
improve or even cure the hypothyroid condition without the use of exogenous thyroid hormone. Iodine and thyroid hormone have a synergistic action in the hypothyroid patient. When it is indicated, it is more effective to
use iodine along with thyroid hormone to achieve the best results. Karen, age 50, suffered with hypothyroidism for 15 years. Her symptoms included fatigue, mental confusion,
puffiness, and hair loss. I diagnosed Karen with hypothyroidism three years ago and began treating her with Armour
®
thyroid as well as a combination of vitamins, minerals, and herbs. She noticed a significant improvement in her
symptoms when she began taking Armour
®
 thyroid. “I feel like I got my life back. I could think much more clearly and
my energy level started to improve,” she said. Karen’s daughter, Lisa (22 years old) had similar symptoms and was
diagnosed with hypothyroidism two years ago. She had similar positive results with thyroid supplementation. Four
months ago, the laboratory tests showed both Karen and Lisa had iodine deficiency. Three months after starting iodine
supplementation, I received a letter from Karen that said in part, “Lisa and I take Armour
®
 thyroid and we have had
much success with that, but adding iodine really made a difference. We have 
more energy and it is much easier to get up
in the morning. The muscle stiffness I occasionally experienced is gone. As you know, I spent three weeks in California
with my mom who had undergone surgery for colon cancer. I was in a bed other than my own and I was on a different
time schedule. I wasn’t getting much sleep and the stress level was very high. In the past, a situation like that would have
exhausted my body and I would be aching all the time. Not this time! In spite of everything that was going on, I felt
great. I attribute that to the iodine, because it is the only change I have made since being in California. Lisa’s experience
has been similar. She is in college and has a very irregular schedule. Since she started taking iodine, I have a noticed a
big difference in her energy level. She actually wakes up on her own and has much more energy during the day and
night.” After two months of therapy, I had asked Karen and Lisa to reduce their iodine dosage slightly and they did not
feel as good. “When Lisa and I cut down our dosage of iodine, we gradually noticed we did not feel as well. At your
recommendation, we increased the dosage and began to feel as good as we were before,” Karen wrote. Karen and Lisa’s
experience is very common for many of my other patients. As is the case with Karen and Lisa, optimal thyroid function is
dependent on having adequate iodine ingestion. Table 4: Signs and Symptoms of Hypothyroidism
IODINE AND THYROID SUPPLEMENTATION
It has been over 20 years since I started studying and 
practicing holistic medicine. During this time, every new patient who
comes to see me receives a full thyroid and hormonal evaluation. Helping a patient balance their hormonal status has proven to be
one of the most rewarding things I do in the practice of medicine. I did not learn how to properly use iodine in treating these
patients until about ten years ago. Over the first ten years of my holistic practice, I diagnosed many patients with hypothyroidism. Needless to say, I treated many of these patients with thyroid hormone. During this time, I was frustrated. Although most patients were doing better, I could not believe that so many people weresuffering from thyroid problems. I did not want to treat every patient with thyroid hormone. I wanted to find an underlying reason
why so many patients were suffering from thyroid issues. At first I looked for nutritional deficiencies such as selenium, iodine, vitamin A, vitamin D, and vitamin C. Although I tried to
correct these deficiencies, my patients were not responding until I gave them thyroid hormone. Approximately 10 years into this practice I met my mentor on iodine—Dr. Guy Abraham. He showed me the form of iodine I
was using—iodide—was not the most efficacious form and he taught me how to measure iodine levels. Furthermore, Dr.
Abraham’s research was clear; whole-body iodine sufficiency was 
best achieved by using both iodine- and iodide-containing
products. Only when I started using the correct form of iodine—in combination with iodide—was I able to reduce my use of thyroid
hormone. My practice now is much different than it was 20 years ago. Hopefully, I have become a little wiser (some may disagree with
that). Now, every patient has their iodine levels assessed. If I diagnose a patient with hypothyroidism, I do not start thyroid
hormone therapy until they have sufficient iodine levels. This has allowed me to use much smaller thyroid hormone dosing. Twenty
years ago, my average thyroid dose was 120-180mg/day of desiccated thyroid hormone. Now, it is 30mg/day. WHAT TO DO IF YOU ARE ALREADY TAKING THYROID HORMONE: RULE OF THIRDS
If someone is already taking thyroid hormone and they are diagnosed with iodine deficiency, the ‘rule of thirds’ comes into
play. These patients may need to:
Maintain the same thyroid hormone dose
Reduce their thyroid hormone dose in half
Stop taking thyroid hormone
The problem is, when starting iodine therapy, I do not know which of the three groups an individual patient will fall into. I tell
my patients if, upon staring iodine therapy, they become 
nervous, anxious, or develop palpitations, they need to immediately cut
their thyroid hormone dose in half. If the above symptoms still persist, it is best to stop the thyroid hormone. Following patients closely can minimize complications. In addition, performing an appropriate exam and checking blood tests
can help guide the process. WHY DOES TSH INCREASE WHEN STARTING IODINE THERAPY? One of the most frequent e-mails I receive from physicians and laypeople is their concern about TSH levels elevating after
beginning iodine therapy. As previously mentioned, TSH is released by the pituitary gland to stimulate the thyroid gland to
produce thyroid hormone. However, TSH has another function besides stimulating thyroid hormone production. It also helps stimulate the body’s
production of the iodine transport molecules–the sodium-iodide symporter-NIS. Without adequate amounts of NIS, iodine would
not be able to enter the cells and be utilized. In other words, the NIS is like a taxi cab that shuttles the iodine from the blood stream into the thyroid cell in order for the
cell to use the iodine to make thyroid hormone. This concept is not hard to grasp. Let’s take the example of a patient who is iodine deficient. This iodine-deficient patient’s
body does not require a large amount of NIS since there is little 
iodine that needs to be transported into the cells. However, when
this individual begins to supplement with iodine, the extra iodine now needs to be transported into the cells. One way the body
will accomplish this is to increase the production of TSH to stimulate more NIS. In other words, when iodine supplementation is
started, the body will produce more “NIS taxi cabs” to shuttle the iodine into the thyroid cell in order to produce thyroid
hormone. My experience has shown, when iodine supplementation has begun, an elevated TSH without clinical signs of hypothyroidism
(i.e., fatigue, hair loss, headaches, etc.) as well as normal T3 and T4 levels does not indicate a hypothyroid condition. On the
contrary, the elevated TSH is the body’s appropriate and necessary response to produce more NIS or “taxi cabs” to increase the
transport of iodine into the thyroid cells. How long does TSH stay elevated? I have found that TSH may remain elevated for up
to 6 months before lowering to normal. How high do TSH levels rise? The normal TSH level ranges from 0.5-4.5mIU/L. I have witnessed TSH levels elevated to 5-
30mIU/L for a period of time–sometimes up to six months–before falling back to the normal range. Remember, if there are no
clinical symptoms of thyroid problems and T3 and T4 levels are normal, it is doubtful that TSH elevation is sign of
hypothyroidism. In this case, TSH elevation is normal and expected. The TSH will 
decline back to the reference range after the
thyroid gland is saturated with iodine. IODINE-INDUCED HYPOTHYROIDISM
I, and my partners, have treated thousands of patients, autoimmune thyroid (AIT) disease patients included, and we have not
seen an epidemic of iodine-induced hypothyroidism. In fact, as I was going to print with this book, I queried my partners on thisissue, and we came up with two cases of iodine-induced hypothyroidism. Keep in mind that is only two out of over thousands of
patients treated with iodine. Most doctors and some holistic doctors do not seem to understand the concept of how the TSH rises with the initiation of
iodine therapy. Allow me to repeat myself: Increasing TSH levels, without falling T3 and T4 levels and clinical signs and
symptoms, do not indicate iodine-induced hypothyroidism. Finally, it is worth repeating–TSH levels initially rise in nearly all who
start iodine therapy. This is a normal and expected response. IODINE-INDUCED HYPERTHYROIDISM
Does iodine therapy cause hyperthyroidism? I was taught in medical school that it did, especially in patients suffering from
autoimmune thyroid disorders such as Graves’ or Hashimoto’s disease. Young doctors-in-training are still taught this today. So, let
me answer the question: Very rarely. Between my partners and myself, we estimate that over 12 years, less than 10 patients 
out
of thousands treated became hyperthyroid when treated with iodine. When I lecture to doctors, I tell them one particular condition can predispose to iodine-induced hyperthyroidism. This
condition occurs in a patient who has an autonomously functioning nodule in their thyroid. Sometimes this is referred to as a hot
nodule on a thyroid scan. An autonomously functioning nodule is not under the feedback control of the pituitary and the hypothalamus. It functions
independently of the thyroid gland. When iodine is present, these nodules can take up the iodine and produce copious amounts of
thyroid hormone leading to hyperthyroidism. This condition can be diagnosed with a thyroid scan. However, it is most frequently
diagnosed after a trial of iodine therapy is given and the patient becomes hyperthyroid after taking the first couple of doses. How do you treat a patient with an autonomously functioning thyroid nodule? These patients must avoid iodine supplements
and food (such as seaweed) that is high in iodine until the nodule is surgically removed. Even less frequently, I see iodine cause hyperthyroidism in a patient without an autonomously functioning thyroid nodule. However, iodine can cause adverse effects, including symptoms of hyperthyroidism such as nervousness, jitteriness, palpitations,
etc., from a detoxification reaction. When this occurs, in most cases, it is due to iodine displacing the toxic halide bromine. Bromine toxicity can display all the symptoms I mentioned above. More about bromine toxicity can be found in 
Chapter 11
. BREAST CANCER: THE PROBLEM WITH TAKING THYROID HORMONE WHEN IODINE DEFICIENCY IS
PRESENT
One of the main jobs of thyroid hormone is to stimulate the metabolism of the body. In hypothyroidism, the metabolism of the
body is slowed down. Consequently, excess weight gain is common in hypothyroidism. Conversely, in hyperthyroidism, the
metabolism of the body is accelerated and weight loss is more common. Iodine is not only necessary for thyroid hormone production, it is necessary for the production of all the hormones of the
body. Every gland concentrates iodine and utilizes iodine to manufacture hormones. Furthermore, every cell depends on adequate
iodine stores for the cell machinery to run optimally. When thyroid hormone is taken, all the cells of the body are affected by it. In effect, thyroid hormone raises the metabolism of
every cell in the body. The elevated metabolic rate naturally increases the body’s need for iodine. Therefore, if iodine is deficient,
supplementing with thyroid hormone will exacerbate the iodine-deficient problem. Researchers have looked at the link between hypothyroidism and breast cancer for over 40 years. There are researchers
who feel that thyroid illnesses, including hypothyroidism and Hashimoto’s disease are associated with the development of breast
cancer. On the other hand, researchers have reported that women who take thyroid hormone for at least 15 years have an
increased risk for developing breast cancer. One study compared women taking thyroid hormone versus women not taking thyroid hormone. 14
 As compared to women
who never took thyroid hormone, the women taking thyroid hormone had a 50% increased incidence of breast cancer. This same
study found that breast cancer incidence was linearly increased the longer the time period that the women took thyroid hormone. This is illustrated in 
Figure 7
. Figure 7: Length of time taking thyroid hormone and incidence of breast cancer. What is the link between an increased breast cancer risk in both women who took thyroid hormone for a long time period
and women who had hypothyroidism? I think the common link is iodine deficiency. In an iodine-deficient state, taking thyroid
hormone elevates the metabolic rate of the body which also increases the body’s need for iodine. When iodine deficiency is
present, the longer that thyroid hormone is taken, the worse the iodine-deficiency problem will be. In women, this worsening
problem is reflected in an increased breast cancer rate. Presently, we are facing an epidemic of breast cancer where one in seven
U.S. women are suffering from it. It is my hypothesis that this epidemic will not be solved until the iodine connection is identified
and treated. More information about iodine and breast cancer can be found in 
Chapter 8
. FINAL THOUGHTS
The thyroid gland will not function optimally when iodine deficiency is present. Thyroid hormone production, like all the other
hormones of the body, requires iodine. Sadly, iodine deficiency is occurring at epidemic rates, whether by my own research or the
National Health and Nutrition Examination Survey. Hypothyroidism is occurring at epidemic rates. However, thyroid hormone supplementation should not be instituted without
measuring iodine status. Taking thyroid hormone when 
iodine deficiency is present can worsen the iodine deficiency problem by
increasing the body’s metabolic rate. The research is clear; taking thyroid hormone when iodine deficiency is present increases the risk for breast cancer and, I
believe, other glandular cancers including breast, ovary, uterine, and prostate. This increased risk could be predicted as the
glandular tissue requires iodine to maintain their normal architecture. Anything that lowers the body’s iodine stores or increases
the body’s need for it could be predicted to cause an increase in breast cancer—as well as cancer of the other glands. All individuals with a thyroid problem should have their iodine levels checked. If iodine levels are suboptimal, iodine
replacement with the correct form of iodine should be instituted. My experience has clearly shown that the appropriate use of
iodine in treating thyroid disorders, from hypothyroidism to Graves’ and Hashimoto’s disease, is not only safe, but effective and
inexpensive. What I have outlined for you is a holistic approach to search for and treat an underlying cause of thyroid problems. Iodine replacement is not the only therapy for thyroid illness. Nutritional supplementation, detoxification, drinking adequate
amounts of water, and dietary changes can also improve these conditions. For more information on a 
comprehensive holistic plan
to treat thyroid disorders, I refer the reader to my book, 
Overcoming Thyroid Disorders, 3rd Edition
. Keep in mind that an elevated TSH when starting iodine therapy does not necessarily mean that iodine is causing an adverse
effect. On the contrary, for most patients, this is a normal and expected response if the other thyroid hormone levels are normal
and there are no clinical signs of hypothyroidism. The next three chapters will expand on the concept that deficiency of iodine is one of the major causes of autoimmune thyroid
disorders. Remember, once you understand the cause of an illness you can formulate an effective treatment plan. These chapters
will identify the cause(s) of autoimmune thyroid illness and present a treatment plan designed to stop the progression as well as
reverse autoimmune thyroid disorders. 1
 Fenzi, F. Role of autoimmune and familial factors in goiter prevalence. Studies performed in moderately endemic area. J.
Endocrin. Invest. 9:131-164. 1986
2
 Eur. J. Endocr. 2000 Oct; 143(4):485-991
3
 Delange, F. Werner and Ingbar’s The Thyroid. Lippincott Williams and Wilkins. 2000. 4
 Herzel, B. Modern Nutrition in Health and Disease. 1998
5
 Endocrine Reviews February 1, 2003 vol. 24 no. 1 48-77
6
 J. Nutr. 127:574-8. 1997
7
 WHO. http://www.who.int/nutrition/topics/idd/en/
. Accessed 7.3.13
8
 Thilly, C.G. Bull. Acad. Med. Belg. 1981; 136:3899
 Lancet. 2003; 362:1859-60
10
 Lancet. Vol. 350. 9.13.97. p. 771-773
11
 Herzel, B. Modern Nutrition in Health and Disease. 1998
12
 Canaris, Gay, et al. The Colorado Thyroid Disease Prevalence Study. Arch. Intern. Med. Vol 160, Feb 28, 2000
13
 Brownstein, D. Overcoming Thyroid Disorders. Medical Alt. Press. 2002
14
 JAMA. Vol. 236. No. 10. 09.1976Chapter 5
The Oxidation and Organification of Iodine 
CHAPTER 5: THE OXIDATION AND ORGANIFICATION OF IODINE
Approximately seven years ago, after I gave a lecture about iodine to a group of doctors in Houston, TX, a physician from
Australia, Dr. John Lee, asked me a question. His question sounded simple enough: “David, what does iodine do in the cell?” At
that time, I answered the question to the best of my 
knowledge, but I knew the answer did not satisfy him or me. That started me
on a quest to better answer this question. Although we still don’t know everything that iodine does in the cell, there are many
more answers now. This chapter will discuss the oxidation and organification of iodine. I know this is a difficult concept to master. I feel it is
important to appreciate what happens to iodine inside the cell and what iodine does inside the cell in order to understand why it is
so important to ensure adequate iodine levels. WHAT HAPPENS TO IODINE AFTER IT IS INGESTED? After iodine and iodide are ingested, they are absorbed from the gastrointestinal tract by the halide channel. Iodine is
transferred inside the cell by facilitated diffusion. Iodide is transported into the cells via a transport molecule called the sodium-
iodide symporter (NIS). After iodide is transported into the cell, it undergoes two important processes: oxidation and
organification, which will be explained in this chapter. John, age 58, was diagnosed with fibromyalgia two years ago. “I don’t know what happened. One day I was okay
and the next day I ached all over and I was tired. John saw numerous doctors who prescribed various medications. “The
drugs did not 
help. I kept telling my doctors I wasn’t depressed but they kept prescribing antidepressants. I finally got
sick and tired of taking the drugs,” he said. When John saw me, I found his thyroid gland to be enlarged. I ordered an
ultrasound of his thyroid gland and blood work and diagnosed him with Hashimoto’s disease. “When I found out I had
Hashimoto’s disease, I couldn’t believe it. I had been seeing many different doctors and they couldn’t tell me what was
wrong. They kept telling me I needed to be on an antidepressant medication,” he said. As part of the initial exam, I
tested John’s iodine level. John’s iodine loading test was found to be low at 45% (normal >90%). John was placed on
75mg of iodine/day along with a complete nutritional program. After twelve weeks of taking iodine, a follow-up 24-hour
iodine loading test was now normal at 95% excretion. However, he did not feel better. John was still complaining of
fatigue and body aches. Furthermore, John’s TSH increased from a baseline of 4mIU/L to 12 mIU/L after taking 75mg of
Iodoral
®
 
for 30 days. At this time, John had normal T3 and T4 levels. John’s endocrinologist placed him on thyroid
hormone (Synthroid
®
) for the elevated TSH level. The Synthroid
®
 
had no effect on his symptoms. When I saw John, I
explained to him that the elevated TSH was a normal result of the body producing more iodine transport molecules
(NIS). Because he was not feeling better, I felt that he may be having an organification problem with the iodine. I
explained to him that his 
cells were unable to effectively utilize iodine. After placing him on Vitamins B2 (100mg) and B3
(500mg) two times per day, John noticed an immediate improvement. “It was a miracle. With the second dose of the B-
vitamins, my head cleared and all my fatigue went away. I felt 20 years younger. I have never taken anything that works
that quickly,” he said. John has continued to take iodine (now 50mg/day) in addition to vitamins B2 (200mg/day) and B3
(1,000mg/day). His thyroid antibody levels gradually lowered to normal levels over the next six months. Most
importantly, John now feels well. “I can’t believe how much energy I have. Everybody has noticed the difference,” he
claims. John’s story is not unique. Ensuring optimal oxidation and organification of iodine improves the immune system function and
energy production. Figure 8
 (next page) shows what happens to iodide once it enters the thyroid gland. Once iodide is transported into the
thyroid cell, it undergoes oxidation. This is the process whereby iodide (the reduced form of iodine) is oxidized to iodine. What
this means is that iodide is relieved of one electron which results in the production of iodine, as illustrated in 
Figure 8
. The oxidation process occurs through the interaction of hydrogen peroxide (H
2
0
2
) with thyroperoxidase (TPO). This step is a
very important process in the body’s ability to utilize iodide. Abnormalities of the oxidation of iodide can result in the production of anti-thyroperoxidase antibodies (anti-TPO). This leads
to a condition called Hashimoto’s disease. More about Hashimoto’s disease will be discussed near the end of this chapter. FIGURE 8: The Oxidation of Iodide
 
Hydrogen Peroxide: An Essential Element for Oxidation
Adequate hydrogen peroxide production is essential for facilitating the oxidation of iodide. Without adequate hydrogen
peroxide production, iodine will not be formed from iodide. Hydrogen peroxide is a potent oxidizing agent. In the thyroid cell, its
function is to oxidize iodide to iodine (
Figure 8
). Hydrogen peroxide along with TPO is essential for this step. If the production and utilization of hydrogen peroxide is not closely maintained, it can damage tissue and cause autoimmune
thyroid disorders such as Hashimoto’s disease. The immune system has developed defense mechanisms to keep H
2
0
2
 
from
harming tissues. This is primarily done with the selenium-containing enzyme glutathione peroxidase which functions to keep
hydrogen peroxide reduced to H
2
O after it oxidizes iodide. 1
 
2
 A deficiency of selenium can impair this defense mechanism. More
about selenium can be found in 
Chapter 7
. If the oxidation process occurs correctly, the next step in the utilization of iodine is called organification. THE ORGANIFICATION OF IODINE
Once iodine is formed, it undergoes organification and becomes part of cholesterol, lipids (fats), and proteins (
Figure 9
, next
page). Organification simply means being bound to an organic molecule. As can be seen from 
Figure 9
, iodine in RDA amounts–
150μg/day–can be bound to thyroglobulin and make thyroid hormones—T1, T2, T3, and T4. However, it takes larger doses of
iodine–at least 100x the RDA for iodine–to produce the important iodo-lipids such as δ-iodolactone. At 100x the RDA, iodine can be organified to lipids in order to produce δ-iodolactone and other iodo-lipids. δ-iodolactone,
as well as the other iodo-lipids will not be formed in any appreciable amounts when iodine is taken in RDA amounts. Simply put,
RDA 
amounts of iodine barely give the cell enough iodine to make thyroid hormone and prevent goiter. FIGURE 9: THE ORGANIFICATION OF IODINE
 
Rick, a 52-year-old physician was very active in his daily life. He played tennis twice per week and exercised daily. “I
feel good most of the time, but I still have my ups and downs,” he said. Rick was diagnosed with Hashimoto’s disease 15
years ago. Since that time, his main problem was maintaining his concentration. He claims, “Although I can still do
everything, my brain has never felt the same after Hashimoto’s disease came along.” Rick was on a holistic treatment
regimen of vitamins, minerals, and eating a good diet for years. When Rick added in iodine (75-100mg/day), he
immediately noticed the difference. Rick stated that, “Ninety percent of my complaints melted away with the iodine. It
was 
miraculous.” After two years of taking the iodine, Rick was tested via blood, urine, and saliva and we found that he
had an organification defect with iodine. That means his cells were not properly utilizing the iodine he was supplementing
with. Upon taking two doses of a supplement containing 100mg of Vitamin B2 and 500mg of Vitamin B3 (ATP
CoFactors
®
) he felt “fabulous”. “I have never felt that good with just starting a new supplement. This cleared up all my
nagging complaints. I now feel 100% healthy,” he said. Rick is my partner, Dr. Richard Ng. His story is not an isolated story. If there is an inability to organify or oxidize iodine, the
body will not receive the true benefits of it. It is important to keep searching for answers if you are not receiving the best results
with iodine therapy. Rick was not satisfied until he felt 100% well. AT THE RDA FOR IODINE: PRODUCTION OF THYROID HORMONE
When iodine is taken in amounts consistent with the RDA–approximately 150μg/day–iodine can be bound to thyroxine
molecules and become thyroid hormone. If there is insufficient iodine to accomplish this, it can lead to an inadequate production
of thyroid hormone and a hypothyroid state. The different thyroid hormones are shown in 
Figure 9
.AT 100X THE RDA FOR IODINE: PROTECTION FROM CANCER
When iodine is taken in amounts at least 100x the RDA (>15mg/day), iodine can now also bind to other molecules including
lipids (i.e., fats) and proteins. The binding of iodine to the fat molecule lactone results in a fat-like substance known as δ-
iodolactone. δ-iodolactone is a key regulator of apoptosis and cellular proliferation of the thyroid gland. 3
 
4
 In other words, δ-
iodolactone is an anti-cancer substance. Apoptosis refers to the programmed cell death that all of our normal cells have. IODINE AND APOPTOSIS: PROTECTION FROM CANCER
Apoptosis is a very important concept. All cells, like all living things, have a life cycle. All cell life cycles have a growth phase,
a division phase, and a death phase. After a cell dies, it is replaced by a new cell. We want our cells to undergo apoptosis or
programmed death. Without apoptosis, cells will continue to divide until they overwhelm the body. Cancer cells are examples of
cells that do not undergo apoptosis. One of the mysteries of cancer is why these cells do not undergo apoptosis. A potent
anticancer item would be one that would promote apoptosis of cancer cells, without toxicity to other cells. Iodine is one of these nutrients. We know that iodinated lipids such as δ-iodolactone have been shown to regulate and
promote apoptosis. Common sense would lead one to conclude that it is important to ensure adequate iodine intake in order to
promote the production of iodinated lipids such as δ-iodolactone. These iodinated proteins are not detected in human tissue when
iodine deficiency is present. However, they are detectable when iodine is taken well in excess of the RDA for iodine. It is important to emphasize that the apoptotic (i.e., anti-cancer) effect of iodine only occurs when iodine is ingested with
doses in excess–100x–of the RDA for iodine. Similar effects have also been shown to occur in animals (dogs) as well. 5
 I believe
one of the major reasons we are seeing a significant increase in cancer of the iodine dependent tissues (including the thyroid,
breasts, ovaries, and prostate) is due to a deficiency of iodine resulting in non-apoptotic cells as well as a suboptimal environment
for oxidation and organification. PUTTING IT ALL TOGETHER: WHAT DOSE OF IODINE IS THE BEST FOR PROTECTING AGAINST
CANCER? If we want to achieve the proper oxidation and organification of iodine, it becomes clear that the RDA for iodine 
is woefully
inadequate to provide the apoptotic (i.e., anti-cancer) effect. In fact, I believe the RDA for iodine is not only inadequate for
providing the apoptotic effect of cells throughout the body, it is also inadequate to provide for the total needs of even the thyroid
gland. As mentioned previously in this book, the exposure to toxic halides--bromine, fluoride, and the chlorine derivatives--have
been increasing over time. These items not only cause iodine deficiency, they can poison the enzymes responsible for organifying
iodine. THE UNDERLYING CAUSE OF AUTOIMMUNE THYROID ILLNESSES: IODINE DEFICIENCY AND
ANTIOXIDANT DEFICIENCY
I have already described the apoptotic (i.e., anticancer) effects of the iodinated form of lactone δ-iodolactone. δ-iodolactone
is not only important for preventing cancer, its production is also necessary to help regulate the oxidation of iodine. Figure 10
(next page) illustrates this regulatory step in the oxidation/organification of iodine. As previously mentioned, the oxidation of iodide to iodine occurs through the interaction of H
2
O
2
 and TPO. Iodine is a
necessary product in order to provide the correct molecule in the cell so that organification can occur. If organification does not
take place or is blocked, thyroid hormone and iodo-lipids will not be formed. As can be seen from 
Figure 10
, this reaction is
controlled by intracellular calcium levels and iodinated lipids—δ-iodolactone. FIGURE 10: ORGANIFICATION OF IODINE AT 100x RDA
 Intracellular calcium stimulates this pathway. 6
 On the other hand, δ-iodolactone and other iodinated lipids act as a brake on
the system. 7
 
8
 If there is not enough iodine in the cell to organify and produce adequate amounts of δ-iodolactone, it can set the
stage for damage to the thyroid cell and the development of an autoimmune thyroid disorder such as Hashimoto’s or Graves’
disease. A Proposed Mechanism For The Development Of Autoimmune Thyroid Disorders
The NADPH oxidase system is found in the mitochondria of our cells. The mitochondria are the energy-producing cells of
our body. The mitochondria produce energy (i.e., ATP) through a complex process called oxidative phosphorylation. All medical
students (and most physicians) are familiar with oxidative phosphorylation because we have to memorize the many steps
responsible for producing ATP. This production of ATP requires many items including: oxygen, magnesium, ADP, vitamins, and
amino acids. 9
 
10
Many people with chronic illnesses, such as fibromyalgia, chronic fatigue syndrome, and autoimmune disorders, complain
they have no energy. ATP is the molecule that stores energy for the body. The body is constantly producing and utilizing ATP. Its
production is a complex process that is beyond this book. However, there are two cofactors, vitamins B2 (riboflavin) and B3
(niacin), that are integral to stimulating oxidative phosphorylation and ATP production. Hydrogen peroxide is a byproduct of oxidative phosphorylation. 11
 It is this production of hydrogen peroxide that 
is so critical
to the oxidation process of iodine. Hydrogen peroxide and TPO help to oxidize iodide to form iodine. If there is a deficiency in iodine, which is common when ingesting the RDA for iodine, there will not be enough substrate (i.e.,
iodine) to produce iodinated lipids. As can be seen from 
Figure 10
, the lack of δ-iodolactone and other iodinated lipids results in
a loss of the ‘brake’ in the pathway to oxidize iodide. This may result in a temporary production of too much hydrogen peroxide. This excess hydrogen peroxide can damage the enzyme TPO. What Happens If TPO Is Damaged? Autoimmune Thyroid Illness
The body’s response to TPO damage is to produce antibodies against TPO or anti-TPO antibodies. A diagnosis of
Hashimoto’s disease requires the presence of anti-TPO antibodies. As the damage worsens, surrounding proteins can also be
damaged such as thyroglobulin. Damaged thyroglobulin will result in the body producing antibodies against thyroglobulin—anti-
thyroglobulin antibodies. In most cases of Hashimoto’s disease, there are antibodies to both TPO and thyroglobulin present. Although Graves’ disease
may also possess these same antibodies, antibody production is not necessary to make the diagnosis of Graves’ disease. However, 
my clinical experience has shown that the treatment for both Hashimoto’s and Graves’ disease can follow a similar
course with similar positive outcomes. EARLY AND LATE STAGES OF AUTOIMMUNE THYROID DISORDERS
It is well known that patients with autoimmune thyroid disorders can fluctuate symptomatically between overactive thyroid
symptoms (hyperthyroidism) and underactive thyroid symptoms (hypothyroidism). These patients can also suffer from a
combination of hypo- and hyper-thyroid symptoms. For those struggling with autoimmune thyroid disorders, it can be an
intolerable situation. Early Stages Autoimmune Thyroid Disorders
As previously explained, the early onset of the illness seems to be fueled by too much hydrogen peroxide damaging TPO and
causing oxidative damage. As the illness progresses, thyroid hormone production can become unbalanced. Thyroid hormone is
integral to stimulating the mitochondria to produce energy or ATP. If the mitochondria are not producing enough energy
molecules, fatigue will set in. This fatigue can be unrelenting. Patients with this type of fatigue cannot exercise, as exercise will
worsen their fatigue. These same patients will also complain of brain fog, as well as muscle aches and pains. Late Stages Autoimmune Thyroid Disorders
When the mitochondria are producing adequate energy molecules, we have enough energy to do as we please. When the
illness has progressed and energy levels have declined, the system may be ‘burning itself out’ due to excessive oxidative damage. It is almost as if an oxidative storm has overwhelmed the energy producing cells of the body. Now, the mitochondria are not
producing ATP (energy) in amounts necessary for health. So what can you do? As shown in 
Figure 10
, providing enough iodine to produce iodo-lipids (e.g., δ-iodolactone) is a start. Next, it becomes
necessary to stimulate the NADPH oxidase pathway. Remember, this pathway is integral to energy production. How do you
increase the production of ATP in the mitochondria? You can provide the correct co-factors in this pathway to increase the
production of ATP. Vitamins B2 (riboflavin) and B3 (niacin) are cofactors in the NADPH oxidase pathway and their use can help
stimulate the mitochondria to produce more energy as well as provide the thyroid cells with enough H
2
O
2
 to properly oxidize
iodide. The initial treatment in either early or late stage autoimmune thyroid disorders is to correct iodine deficiency. Concurrently, acomplete nutritional program, which includes the use of vitamins B2 and B3, vitamin C, magnesium, and unrefined 
salt, can be
instituted to correct mitochondrial dysfunction, oxidant stress and tissue damage as described in the next section. I diagnosed my nurse Angela with Hashimoto’s disease two years ago. Angela’s complaints included fatigue, difficulty
concentrating, and a general sense of not feeling well. “I am only 23 years old, I can’t imagine what I will feel like when
I am 50,” she said. Angela was treated with iodine (50mg/day) and a complete nutritional program including vitamins
and minerals. Angela did feel somewhat better (approximately 30%) but was not satisfied. When she walked into my
office one day, she saw a bottle of ‘ATP Co-Factors
®
’ 
(
www.Optimox.com
), which contains 100mg of B2 and 500mg of
B3. She asked me what this bottle was for and I told her that this therapy has been a big help for Hashimoto’s, Grave’s
disease, fibromyalgia, and chronic fatigue suffering patients. She said, “I have Hashimoto’s, how come I am not on it?” I
did not want to tell her that I forgot to tell her to take it, so I sheepishly told her that the next bottle was for her. Angela
took one pill (100mg of B2 and 500mg of B3) and felt her energy improve within two hours. “I have taken so many
supplements without having an effect, either positive or negative. This (ATP Co-Factors) was the greatest. I feel like I
have woken up,” she stated. Angela continues to take the supplement and continues to feel well. Update on Angela’s
case: Angela is still taking B2 and B3 along with iodine and continues to do well. “My antibodies are 
gone and I feel
better than I have ever felt. I feel healthy now,” she said. How to Treat Autoimmune Thyroid Disorders
1. Ingest enough iodine in order to provide adequate substrate to iodinate lipids. The first step to treating autoimmune thyroid disorders is to assess iodine status. Iodine levels can be measured by checking
blood, urine, and/or saliva. I routinely check every new patient in my office for their iodine levels primarily by measuring urinary
levels. Either a spot urine or 24-hour loading test for iodine can be performed. For more information on testing, please refer to
the Appendix. If iodine levels are low, I recommend taking enough iodine to ensure that there will be enough substrate to organify (iodinate)
lipids. As previously mentioned, it is impossible to achieve this with the RDA for iodine. My clinical experience has shown that
most people need from 12-50mg/day of a combination of iodine and iodide. Lugol’s solution or tableted Lugol’s solution have
both proven effective. More information on where to purchase iodine can be found in the Appendix. However, I suggest working
with a health care provider 
knowledgeable in how to dose iodine in order to get the best results. 2. Take Vitamins B2 and B3 in amounts necessary to stimulate the NADPH system to produce adequate
amounts of H
2
O
2
. The amounts of vitamins B2 and B3 must be sufficient to overcome deficiencies in the system. Dr. G. Abraham’s research has
shown that using 100mg of vitamin B2 (riboflavin) and 500mg of vitamin B3 (niacinamide) twice per day will help to stimulate
ATP production and provide adequate H
2
O
2
 for oxidation of iodide. 3. Correct oxidant stress in the thyroid gland and the mitochondria with antioxidants. I have used higher-dosed vitamin C in my practice for years with excellent results. My clinical experience has shown that
larger doses of vitamin C are needed when one is suffering an exacerbation of any illness. Generally, between 3-10,000 mg/day
of vitamin C provides the antioxidant protection necessary to overcome oxidative damage for most patients. Some people may
require more. If the illness is severe, intravenous vitamin C can be very helpful. The only major side effect of vitamin C is diarrhea,
which can easily be rectified by reducing the dose. 4. Ensure adequate magnesium levels. At the present time, my research has shown that magnesium deficiency is widespread. Magnesium levels can be ascertained
by a red blood cell magnesium test. Magnesium acts as an antagonist to excess intracellular calcium levels which can fuel the
oxidative pathways as shown in 
Figure 10
. 5. Minimize oxidative stress in the body. There are many ways to minimize oxidative stress in the body. Two of the most important ways are to drink adequate
amounts of pure water and to eat a healthy diet. Drinking adequate amounts of water keeps the body hydrated. Table 5
 (next
page) shows you how to calculate your water intake. Furthermore, eat a healthy diet that supplies the proper nutrients for your
body. For information on eating a healthy diet, I refer the reader to my book, 
The Guide to Healthy Eating. Ensuring an adequate intake of unrefined salt in the body is also essential to minimize oxidative stress. More information on
salt can be found in my book, 
Salt Your Way to Health. Finally, reduce stress in your daily life and make sure you get the rest
that you need. Table 5: How to Calculate Your Water Intake
1
. Take your weight in pounds2
. Divide by 2
3
. The calculated number is the amount of water you should ingest in ounces per day
FINAL THOUGHTS
My research and my clinical experience have been clear: the RDA dose for iodine is inadequate to prevent cancer. In fact, I
believe that lowered iodine levels will provide fertile ground for cancer to begin in many different hormonally sensitive tissues
including the thyroid, breasts, ovaries, uterus, and prostate gland. Optimal iodine supplementation varies in each individual;
however, average doses to achieve the best effects (including cancer prevention) occur with daily doses ranging from 12-
50mg/day for the vast majority of adults. A diagnosis of an autoimmune thyroid disorder does not have to be a prescription for life-long suffering. In fact, following the
principles outlined in this chapter has proven effective for many of my patients in helping them overcome an autoimmune thyroid
disorder. An autoimmune thyroid disorder (or any autoimmune disorder) is an example of excess oxidative stress in the body. Remember, oxidative stress in the body is similar to a fire burning. You can put out this fire by providing the body with what it
needs: adequate intake of water, unrefined salt, and healthy food full of nutrients. Finally, it is important to reduce your stress
levels. To achieve the best results, you should find a health care practitioner who can help guide you as well as monitor your
symptoms. The best results will be achieved with a comprehensive holistic approach. 1
 Farber, J. Mechanisms of cell injury by activated oxygen species. Lab. Invest. 62:670-79. 1990
2
 Kohrle, J., et al. Selenium, the thyroid, and the endocrine system. Endocrine Reviews. 26(7):944-84
3
 Eur. J. of Endocrin. 132. 735-43. 1995
4
 Horm. Metab. Res. 26. 465-69. 1994
5
 Rabinovitz, JL. Identification by nuclear magnetic resonance of iodinated lipids in the dog thyroid. Biochem and Biophy
Res. Com. 1976; 68:1161-8
6
 Bachi, N. Thyroid cell injury is an initial event in the induction of autoimmune thyroiditis by iodine in obese strain chickens. Endocrinology. 1995; 136:5054-60
7
 Krawiec, L. The inhibition of PB125I formation of calf thyroid caused by 14-iodo-15-hydroxy-eicosatrienoic acid is due to
decreased H2O2 availability. Horm. Metab. Res. 1988:20:86-90
8
 Pisarev, MA. Thyroid autoregulation. Inhibition of goiter growth and of cyclic AMP formation in rat thyroid by iodinated
derivatives of arachidonic acid. J. Endocrin. Invest. 1988; 11:669-74
9
 Abraham, G. Evidence of Defective Cellular Oxidation and Organification of Iodide in a Female with Fibromyalgia and
Chronic Fatigue. Original Internist. June, 2007. 10
 Abraham, GE, and Flechas, JD. Management of fibromyalgia rationale for the use of magnesium and malic acid. Journal of
Nutr. Med. 1992:3, 49-59
11
 Ohayon, R. Inhibition of thyroid NADPH-oxidase by 2-iodohexadecanal in a cell-free system. Molec. And Cell. Endocr. 1994; 99:133-41Chapter 6
Iodine and Autoimmune Thyroid Disorders 
CHAPTER 6: IODINE AND AUTOIMMUNE THYROID DISEASE
Graves’ disease is an autoimmune illness whereby the thyroid gland is attacked by the body’s production of antibodies. This
causes an inflammation and swelling of the thyroid gland. Hyperthyroidism–an overactive metabolic state–is common in 
Graves’
disease. However, the end-stage of Graves’ disease often results in a hypothyroid picture. Graves’ disease occurs in 0.25-1% of the population and the number of individuals diagnosed with Graves’ disease is
increasing. Graves’ is more common in females and usually occurs in middle age. In conventional medicine, there is no known
cause of Graves’ disease. Some causative factors reported in the literature include a genetic predisposition, infections, and stress. Hashimoto’s disease is also an autoimmune illness where the body produces antithyroid peroxidase antibodies (anti-TPO)
that cause an inflammation of the thyroid gland. Goiter is a common occurrence with Hashimoto’s disease. Both hyperthyroidism
and hypothyroidism can be associated with Hashimoto’s disease. Frequently, hypothyroidism is the end result of long-standing
Hashimoto’s disease. In conventional medicine, there is no known cause of Hashimoto’s disease. However, I have identified two
major causes of both Graves’ and Hashimoto’s disease: iodine deficiency and gluten sensitivity. More about these causes later. Hashimoto’s disease is more prevalent than Graves’ disease. The incidence of autoimmune thyroid disease is commonly
reported to occur in 0.1-5% of the population. The incidence of Hashimoto’s disease is also rising rapidly. However, I 
believe the
incidence of autoimmune thyroid disorders is much higher than the reported numbers. Over the last twenty years, I have been
checking every new patient for an autoimmune thyroid illness. My experience would lead me to believe that the incidence of
autoimmune thyroid disorders is much higher–in the range of 15-20% of the population. Part of this estimate is also based on
asking other doctors at my lectures around the country what their experience has been. Nearly 100% of these doctors have
reported finding similar (or sometimes higher) percentages of patients suffering from autoimmune thyroid disorders. Needless to
say, I feel that autoimmune thyroid disorders, particularly Hashimoto’s disease, are increasing at epidemic rates. FALLING IODINE LEVELS = INCREASED INCIDENCE OF AUTOIMMUNE THYROID DISORDERS
Over the last 40 years, the rising incidence of Hashimoto’s and Graves’ disease correlates with falling iodine levels. I believe
the increase in both Hashimoto’s and Graves’ disease, which are occurring at near epidemic rates, are due, in large part, to iodine
deficiency. In the U.S., every few years the government surveys vitamin, mineral, and toxicity levels from a cross section of the U.S.
population. It is reported as the National Health and 
Nutrition Examination Survey (NHANES). From 1970-2012 NHANES
reports iodine levels have fallen by over 50%. 1
Keep in mind that nearly all conventional doctors are under the misinformed opinion that iodine supplementation causes
autoimmune thyroid diseases. I was taught that concept in medical school and I can assure you that it is still taught today. However, the research does not support this hypothesis as, over the last 40 years, iodine levels have significantly fallen while
autoimmune thyroid disorders have markedly increased. This concept of falling iodine levels resulting in a rising incidence of autoimmune thyroid disorders was illustrated in a
European study. Researchers in Europe reported on the incidence of hyperthyroidism in two areas of Denmark (Aalborg and
Copenhagen). The two areas were chosen because Aalborg had slightly lower iodine levels (53μg/L—measured on urinary
excretion) as compared to Copenhagen (68μg/L). The results are shown in 
Figures 11
 and 
12
 (next page). For comparison to the Denmark results, the average iodide excretion in the U.S. is 134μg/L. 2
 In the U.S., nearly 60% of
women of pregnancy age are deficient in iodine and 16.5% of women in their reproductive age have a remarkably low iodide
excretion (below 50μg/L). 3
 
4
 The World Health Organization (WHO) claims iodide excretion below 50μg/L is classified as
moderate/severe iodide deficiency. 5
 
Figure 11: Iodine Excretion in Two Areas of Denmark
 Figure 12: Iodine Deficiency and the Relationship of Hyperthyroidism
If iodine caused autoimmune thyroid problems, you would expect the rate of hyperthyroidism to decline as iodine levels fall. As illustrated in the European study above, that is just not the case. This study clearly illustrates that lowered iodine levels in
Aalborg are associated with a 260% elevated incidence of 
autoimmune thyroid problems (hyperthyroidism) when compared to
an area with slightly higher iodine levels–Copenhagen. 6
X-RAY FLUORESCENCE SCANNING
If iodine was causing autoimmune thyroid (AIT) disorders, it is reasonable to expect that subjects with higher thyroid iodine
levels, when compared to a group with lower thyroid iodine levels, would have an increased incidence of AIT disease. However,
that is not what the research has found. The subjects who had AIT disorders had less iodine in their thyroid as compared to the
subjects without AIT disorders. Figure 13: Thyroid Iodine Levels and Autoimmune Disorders
 
X-ray fluorescence scanning measures the stable iodine content of the thyroid gland. A mean value of 10mg/thyroid was
reported in a normal population. Fifty-six subjects with 
autoimmune thyroiditis had a mean value of 4.7mg iodine/thyroid–these
subjects had normal thyroid levels. Thirteen subjects with autoimmune thyroiditis and hypothyroidism had a mean value of
2.3mg/thyroid. Figure 13
 (previous page) illustrates this study. 7
DOES IODINE TREAT AUTOIMMUNE THYROID DISORDERS? When I was in medical school, I was told that no one needed to supplement with iodine. I was also told that there was
enough iodine in salt. Furthermore, it was implied that iodine supplementation caused autoimmune thyroid disorders including
Graves’ and Hashimoto’s disease. Finally, I was taught that patients with AIT disorders need to avoid ingesting all sources of
iodine. At that point in my medical career, I did not question these statements. However, years later, when I did question those
ideas, I found the medical literature did not support those conclusions. In fact, the use of iodine to treat AIT disorders, including Graves’ disease, dates back hundreds of years. The first treatment
of toxic goiter (an earlier term for Graves’ disease) was reported in 1840 by Von Basedow and in 1854 by Sokes. 8
 
9
 In 1863,
the first double-blind cohort study was done with the use of iodine in a Graves’ disease patient. 10
 Dr. Armand Trousseau
inadvertently treated a Graves’ disease patient with iodine (75-
100mg of Lugol’s solution) instead of digitalis—which was the
treatment of choice for Graves’ disease at that time. Dr. Trousseau was surprised as his patient improved. Upon realizing his
mistake, he stopped the iodine and resumed the digitalis treatment. The patient worsened. Since Dr. Trousseau and the patient
were both unaware of what the patient was initially being treated with–iodine–this could be considered a “double-blind” study. Dr. Trousseau wrote, “In the course of October, 1853, I was consulted by a young married lady…She was suffering from sub-
acute exophthalmic goiter {i.e., Graves’ disease}…. I found her heart beating at the rate of 140-150 times in the minute…I
wished to administer at the same time tincture of digitalis, but preoccupied with the idea that there would be some danger in givingiodin (
sic)
, I wrote iodin (
sic)
 instead of digitalis, so that the patient took from 15-20drops of tincture of iodin (
sic)
 a day for a
fortnight. When she came back to me her pulse was only 90. I found out my mistake, and I substituted tincture of digitalis for that
of iodin (
sic
), but, after a fortnight, the pulse had again gone up to 150, so that I at once returned to the iodin (
sic
).” Keep in mind
that Dr. Trousseau’s dose of iodine was 94-131mg of iodine per day. In 1923, Dr. Henry Plummer was administering Lugol’s iodine pre-op (130-195mg) and post-op (62.5mg) to prevent 
thyroid
storm during surgery of Graves’ disease. He reported that mortality declined from ‘high’ to zero with the use of iodine. 11
 
12
There are many other older research articles touting the benefits of using iodine in treating Graves’ disease. 13
 
14
 
15
 As a
treatment for hyperthyroidism, iodine fell out of favor with the advent of radioactive iodine treatment. CONVENTIONAL APPROACHES TO AUTOIMMUNE THYROID DISEASE: RADIOACTIVE IODINE
The conventional approach to treating autoimmune thyroid disorders revolves primarily around alleviating the symptoms of the
autoimmune illness–mainly the symptoms of hyperthyroidism. This includes the use of antithyroid drugs (e.g., Propylthiouracil,
Methimazole) that block the production of thyroid hormone. Other conventional treatments include surgery and radioactive
iodine. Both of these destructive modalities work by reducing the volume of thyroid tissue. However, neither of these treatments
addresses the underlying causative factor of these illnesses.
Iodine_-_Why_You_Need_It_Why_You_Cant-Live_Without_It.txt
Summarize the following text section accurately and concisely. Maintain specific details and numerical information, and use anti-repetition mechanisms:

        Different tissue responses for iodine and iodide in rat thyroid and mammary glands. Biological Trace Element
Research. Vol. 49, 1995
3
 Eskin, B. IBID. 1995
4
 Aceves, C. Is Iodine a gatekeeper of the integrity of the mammary gland. J. of Mammary Gland Biol. and Neoplasia.
The thyroid gland produces thyroid hormones, including T4 and T3, which are essential for normal brain development in newborns and normal metabolic function in the body.
What is the primary function of the thyroid gland?
Iodine deficiency can lead to goiter, increased autoimmune thyroid problems, and an increased risk of thyroid cancer, as well as mental retardation, goiter, lowered IQ, and increased rates of stillbirth, abortion, and congenital anomalies.
What is the consequence of iodine deficiency?
The research suggests that iodine deficiency is associated with an increased risk of breast cancer, as it is necessary for the production of iodinated lipids, which are essential for maintaining the normal architecture of glandular tissue.
What is the relationship between iodine and breast cancer?
The NIS is a system that concentrates iodine in the thyroid gland, allowing it to produce thyroid hormone. The same system is also present in other tissues, including the breasts, kidneys, placenta, stomach, rectum, and salivary glands.
What is the purpose of the sodium/iodide symporter (NIS) in the body?
TSH is produced by the pituitary gland and stimulates the thyroid gland to release thyroxine (T4).
What is the main job of TSH?