Many of you know that the primary reason I am able to help others overcome health challenges is because I have experienced so many of them myself. Nothing encourages me to research an issue more intensely than a desire to restore my own health. Often I discover that conditions I believed to be independent of each other share a common cause. Many times I am forced to re-examine my beliefs about how disease develops and what is required to restore and maintain health.

Five years ago I discovered that my thyroid gland was not functioning properly. I had been waking up at night “cold to the bone” and had several other symptoms that suggested a hypothyroid condition. Standard thyroid blood tests failed to confirm a problem, but were suggestive that something was awry.

My TSH (thyroid stimulating hormone), which is produced by the pituitary gland to encourage the thyroid gland to produce thyroid hormones, was approaching the upper limit of normal while my T4 (thyroxine), the primary thyroid hormone, was just above the lower limit of the normal range. That, coupled with my hypothyroid symptoms, prompted me to look further.

I discovered that my body was producing anti-thyroid antibodies. As a result, my body was not receiving enough active thyroid hormone to function properly. The presence of thyroid auto-antibodies indicated that the thyroid gland had been inflamed at some point in the past.

If my TSH or T4 had been “abnormal” I would have been diagnosed as having a condition called Hashimoto’s thyroiditis. In our bizarre medical environment having thyroid antibodies and symptoms of hypothyroidism does not qualify for diagnosis and treatment of Hashimoto’s thyroiditis, even though the TSH or T4 will become abnormal at some future time in nearly all instances. I have had many people come to me with unrelenting weight gain, thinning hair, brittle nails, constipation, tiredness, and other hypothyroid symptoms who have thyroid antibodies, but who have been told that they do not qualify for treatment because their TSH and T4 are still within the “normal” range. Fortunately, an understanding colleague was willing to prescribe Armour Thyroid. My hypothyroid symptoms promptly resolved when I began taking the supplemental hormone.

I firmly believe that disease doesn’t “just happen”; that all disease has a root cause. While I have identified many underlying causes of disease there are instances in which I do not understand why an illness has occurred. That was the case with my thyroiditis – I knew that my thyroid had been inflamed at some time, but I had no idea why this had occurred. Without learning why I had developed thyroid antibodies I was unable to teach others how to prevent them.

Hashimoto’s thyroiditis is considered an “autoimmune” disease and it appears to be more common if another family member has had the disease. This suggests that some individuals have a genetic susceptibility to the condition, but as is often the case, something must occur environmentally to cause it to appear.

I have observed, and statistics confirm, that the incidence of Hashimoto’s thyroiditis has been increasing over the past two decades. At this point in time it is estimated that 1 out of every 10 women have thyroid antibodies. When I discover that a disease process is becoming more common I immediately ask what has changed to make this so.

The explanation that is commonly given is that physicians have better diagnostic skills today than they did back in the dark ages of the 1970s and 1980s. I take issue with the assumption. I was a physician in the 1970s and 1980s. I was taught about Hashimoto’s thyroiditis during my medical training, and I feel that the diagnostic skills of my colleagues and I were as good as those of today’s recent medical graduates. (I would argue that physicians did a better job of diagnosing illnesses thirty years ago simply because they had more time available to listen to patients and develop a plan of diagnosis and treatment.) No, there must be a reason that more people are presenting with thyroid antibodies today than in the past.

Approximately a year after I discovered that I had thyroid antibodies I experienced an episode of an irregular heartbeat. It occurred after I had been repeatedly bending over to pick up leaves I was raking in my yard. The episode was unsettling, but it passed within two hours and I appeared to be back to normal.

Six months later, however, I awoke with a similar episode, which lasted a bit longer. Another attack hit three or four months after the second. The arrhythmia, which I found to be atrial fibrillation, began occurring with increasing frequency and having a longer duration. By the fall of 2005 the episodes were appearing weekly and lasting for up to 36 hours. At its peak, from December 2005 to June 2006, the arrhythmia was present over forty percent of the time.

When I was experiencing atrial fibrillation I felt that I was functioning at less than seventy percent of my normal capacity. It would take me a day to recover, I would feel relatively normal for a day, and then the fibrillation would return.

As is true for Hashimoto’s thyroiditis, the incidence of atrial fibrillation has increased significantly in recent years. Not only is the condition occurring more frequently, its character has changed dramatically.

When I entered medicine in the 1970s, atrial fibrillation was rare. When it did occur it was almost always due to an underlying heart abnormality, most commonly enlargement of one or both of the upper chambers of the heart. While atrial fibrillation still occurs when heart disease is present, many, perhaps most, instances today occur with no evidence of heart enlargement or disease. This is referred to as lone atrial fibrillation.

Lone atrial fibrillation typically comes on without warning, but it may be preceded by an increased frequency of early beats called PACs or PVCs. A number of triggers have been identified including emotional stress, physical overexertion, rest, alcohol, caffeine, a heavy meal, lying on one’s left side, acid reflux, cold foods or beverages, becoming chilled, coughing, taking a hot bath or shower, and flying. MSG and aspartame have been reported to trigger episodes, as have aged cheeses, sugar, various food additives, and chocolate. Some individuals report episodes in association with exposure to electromagnetic fields or changes in weather patterns. Once the pattern is established lone atrial fibrillation seems to occur without any obvious trigger.

A number of drugs are used to treat atrial fibrillation. Ablation, a surgical procedure in which an area of the heart is cauterized (burned) to eliminate signals that trigger fibrillation, is very popular. Episodes can be stopped by electrocardioversion (shocking the heart), and a device can be implanted to shock the heart whenever an episode begins.

Since treatment is available, it is reasonable to ask why I did not seek it. The answer is multifold. The drugs that are routinely used to control atrial fibrillation are associated not only with a number of undesirable side effects, but they are capable of turning an annoying, but not deadly arrhythmia (atrial fibrillation) into a fatal one. I would like to be around to support my family as long as possible, so I chose not to accept the risk of sudden death associated with the anti-arrhythmic drugs.

Physicians routinely prescribe warfarin (Coumadin) to anyone who has experienced an episode of atrial fibrillation. Numerous studies have shown, however, that the risk of experiencing a hemorrhage or other serious complication from the drug itself is far greater than the risk of having a stroke when lone atrial fibrillation exists. This is particularly true for individuals under the age of sixty.

The success rate of ablation therapy is said to be eighty-five percent, but I have had too many people consult me whose atrial fibrillation has returned after having ablation performed to feel confident in the procedure, which carries a price tag of $15,000.

The primary reason I did not pursue standard medical therapies, however, was my unwavering belief that the episodes of atrial fibrillation had appeared for a reason. Something had changed to cause me to be susceptible to them. I was committed to learning what that something was – not only for my own sake, but for that of others dealing with the condition.

I tried various levels of physical activity, but I did not notice any relationship between the degree of my activity and the frequency or duration of the attacks. Initially, magnesium supplementation seemed to be of benefit, but the episodes soon returned. Supplementing a combination of magnesium and potassium controlled them for a time, but again they appeared. Coenzyme Q10 and L-carnitine did not appreciably change the character of the episodes, nor did L-taurine and Hawthorne berry. The use of systemic enzymes to control inflammation brought some improvement in the duration of the episodes, but it did not stop them from occurring.

While attending a medical meeting in Oklahoma City I had a chance meeting with an individual who had consulted me about atrial fibrillation several years before. I had recommended various supplements, but his fibrillation had continued. He decided to undergo ablation treatment, which appeared to have been effective. The benefit was short-lived, however. His atrial fibrillation returned three months later.

I asked about his health. He reported that he was no longer experiencing any arrhythmia. He had spoken with another individual who had been struggling with atrial fibrillation and learned that the condition had been eliminated with iodine supplementation. Shortly after starting iodine supplementation my former patient’s fibrillation had also resolved.

I was happy for him, but I was not ready to begin iodine supplementation. I had been taught that iodine is highly toxic and that iodine supplements were to be avoided. I also believed that iodine allergy was common. I began to research the possible relationship between iodine and atrial fibrillation, but I also continued to look for what I believed would be a “less toxic” answer.

My iodine research led me to the work of Dr. Guy Abraham, a former professor of Obstetrics, Gynecology, and Endocrinology at UCLA, who had become interested in the role of iodine in the body. Dr. Abraham’s findings contrasted sharply against what I had been taught.

I had been taught that the body needed only a small amount of iodine to function properly and larger amounts were highly toxic. Dr. Abraham had, on the basis of his research, concluded that the recommended daily allowance of iodine was far too low to meet the body’s needs. He likened the body’s need for iodine to the body’s need for vitamin C.

The RDA of vitamin C is very low – 75 mg. daily for adult women and 90 mg. daily for adult men. This is enough to prevent the appearance of scurvy. The RDA of vitamin C is far below the body’s actual needs, however. A wealth of research has demonstrated that optimum levels of vitamin C intake in adults are in excess of 2000 mg. daily. In times of stress the need can easily rise to 10,000 mg daily. Many believe that scurvy is the result of a severe short-term vitamin C deficiency while atherosclerosis is the result of a less profound long-term vitamin C deficiency.

The RDA of iodine is similarly low – only 150 micrograms daily. Dr. Abraham’s findings suggest that while the RDA of iodine is sufficient to prevent the development of a goiter (an enlarged thyroid) it is woefully inadequate to meet the needs of the rest of the body. A goiter represents a severe short-term deficiency of iodine, but long-term iodine deficiency is associated with a wide range of disease states including many thyroid diseases, fibrocystic breast disease, polycystic ovary disease, autoimmune diseases, chronic fatigue, and an increased risk of cancer.

The optimum level of iodine intake appears to be between 12.5 mg. and 50 mg. rather than the RDA of 0.15 mg. It has been found that the mainland Japanese diet provides approximately 13.8 mg. of iodine daily – over 100 times that of the average United States’ diet. Japanese women have the lowest incidence of fibrocystic breast disease and breast cancer in the world. Thyroid problems are also much lower in Japan than in the United States.

I am unaware of any research that has shown a link between atrial fibrillation and iodine deficiency, but it is interesting to note that a drug employed in the treatment of arrhythmias is 37.5 % iodine. Amiodarone contains 75 mg. of iodine per 200 mg. tablet.

Amiodarone is an unusual drug in many ways. Its mechanism of action is poorly understood. It does not have a rapid onset of action, but takes up to two months to reach maximum effectiveness. Therefore a loading dose of up to 1600 mg. daily is often prescribed for the first few weeks. Dr. Abraham has calculated that the total of iodine administered in the form of amiodarone over seven week’s time is identical to the amount of iodine his research has found to result in restoration of the body’s iodine stores.

It is quite possible that amiodarone’s antiarrhythmic effect is achieved by restoring the body’s optimum iodine level. Unfortunately, the drug is quite toxic and can damage the cornea of the eye, generate a bluish discoloration of the skin, destroy the thyroid gland and trigger a life-threatening inflammation of the lungs. Inorganic iodine supplementation has not been associated with any serious adverse effects.

Given the many important roles iodine plays in the body it is important that individuals be able to determine if they, like most in our society, have an iodine deficiency. I have had many people tell me that they had done an iodine test by applying a two inch square of iodine tincture to the inner aspect of their upper arm and observing how quickly it faded. This test is not reliable, since the rate of fading of the iodine is more dependent upon factors such as the relative humidity of the surrounding air than it is on the body’s need for iodine.

Iodine is excreted by the kidneys and can be measured in the urine. A single measurement of urinary iodine is not helpful, however, since it says little about the body’s total iodine stores. To objectively determine the body’s need for iodine an iodine loading test must be performed.

Dr. Abraham’s research found that when an individual has an adequate supply of iodine he or she will excrete at least ninety percent of a single serving of iodine within 24 hours. He has demonstrated that individuals who are deficient in iodine will often release less than sixty percent of the amount of iodine administered within the following 24 hours. The iodine loading test, in which 50 mg. of iodine is administered and the urine collected for the following 24 hours, has been performed on tens of thousands of individuals and has been shown to accurately reflect the state of the body’s iodine stores.

When iodine stores are low they can be restored by taking 50 mg of iodine daily for approximately three months. The amount of iodine required to maintain the optimum level in the body varies between 12.5 and 37.5 mg. daily.

After studying the research of Dr. Abraham and others I concluded that the Hashimoto’s thyroiditis and atrial fibrillation I had developed had a common cause: Iodine deficiency. An iodine loading test confirmed my suspicions.

The frequency and duration of my atrial fibrillation episodes began to decrease shortly after I began taking an iodine supplement. Within a month I was able to lower my thyroid hormone replacement dosage by a third. While I have not completely eliminated the episodes of atrial fibrillation they are currently occurring at two to three month intervals rather than two or three day intervals. Rather than lasting for two to three days they are stopping within fourteen hours.

If the increasing incidence of conditions such as Hashimoto’s thyroiditis and atrial fibrillation are due to widespread iodine deficiency something must have happened two or three decades ago to create that deficiency. I discovered that something very significant had occurred.

Dietary iodine content declined dramatically over the last two decades of the twentieth century. A decrease in the iodine content of bread appears to have been a major factor. Prior to 1980, bread makers routinely used iodine in their recipes, as it made the bread easier to knead. In 1980 most commercial bakers abruptly discontinued this practice, apparently due to concerns about iodine toxicity. In subsequent years potassium bromate has been commonly used. Bromide and iodide are in the same chemical family and therefore compete with each other for absorption. This means that the changes in commercial bread recipes had a duel impact on iodine levels. Not only was one of the most significant sources of dietary iodine lost, but a competitor was introduced that limited the body’s ability to absorb iodine from other sources. It is worth noting that fluoride, which has been added to the water supplies of many cities, also reduces iodine absorption.

Iodine is not a “magic bullet” that will prevent or cure all diseases, but I am convinced it is another significant piece in the wellness puzzle. Some of the disease conditions that are reported to be prevented or significantly improved by iodine supplementation include goiter, Hashimoto’s thyroiditis, hypothyroidism, Grave’s disease, fibrocystic breast disease, breast cancer, polycystic ovarian syndrome, fibromyalgia, and chronic fatigue syndrome. Based upon my personal experience and that of others with whom I have spoken or consulted, I would add atrial fibrillation to the list.