The thyroid gland is a small butterfly shaped gland in the neck on either side of the windpipe.  It is responsible for the secretion of thyroid hormone which speeds up the body's metabolism by increasing the number and size of the mitochondria.  The mitochondria are the little microscopic factories which make energy and heat for the cell functions. 

The thyroid tissue is made up of two types of cells: follicular cells and parafollicular cells. Most of the thyroid tissue consists of the follicular cells, which secrete iodine-containing hormones called thyroxine (T4) and triiodothyronine (T3). The parafollicular cells secrete the hormone calcitonin. The thyroid needs iodine to produce the hormones.

Functions of the Thyroid Gland
The thyroid gland controls how quickly the body uses energy, makes proteins, and controls how sensitive the body should be to other hormones. It participates in these processes by producing thyroid hormones, the principal ones being triiodothyronine (T3) and thyroxine (T4).

The T4 and T3 hormones stimulate every tissue in the body to produce proteins and increase the amount of oxygen used by cells. The harder the cells work, the harder the organs work. The calcitonin hormone works together with the parathyroid hormone to regulate calcium levels in the body.

The T4 and T3 hormones regulate the rate of metabolism and affect the growth and rate of function of many other systems in the body. T3 and T4 are synthesized from both iodine and tyrosine. The thyroid also produces calcitonin, which plays a role in calcium homeostasis.

Levels of hormones secreted by the thyroid are controlled by the pituitary gland's thyroid-stimulating hormone, which in turn is controlled by the hypothalamus.

Note: Metabolism is the chemical activity that occurs in cells, releasing energy from nutrients or using energy to create other substances, such as proteins. The basal metabolic rate (BMR) is a measurement of energy required to keep the body functioning at rest. Measured in calories, metabolic rates increase with exertion, stress, fear, and illness.

Thyroid Function Tests
Thyroid function tests are common procedures performed to determine how well the thyroid is functioning. Some of the most common thyroid function tests include the following:

• Blood tests:
  
  • to measure the level of thyroid-stimulating hormone in the blood which helps determine thyroid function. High levels of the hormone indicate an underactive thyroid.
  • to measure levels of hormones thyroxine (T4) and triiodothyroxine (T3), and to measure a protein called thyroxine-binding globulin.

• Ultrasound exam of the thyroid gland - to detect signs of growth and other irregularities. (An ultrasound scan is a diagnostic technique which uses high-frequency sound waves to create an image of the internal organs.)

• Thyroid scans using radioactive iodine or technetium (a radioactive metallic element) - to reveal any physical abnormalities of the thyroid.

• Functional stimulation tests - tests that help differentiate whether the problem lies with the pituitary gland or the thyroid gland. One such test includes injecting thyrotropin-releasing hormone and measuring the pituitary's response.

TSH Testing
A test for thyroid-stimulating hormone (TSH) is done to determine whether the thyroid gland is functioning properly.

An underactive thyroid gland (hypothyroidism) can cause symptoms such as weight gain, tiredness, dry skin, constipation, a feeling of being too cold, or frequent menstrual periods.

An overactive thyroid (hyperthyroidism) can cause symptoms such as weight loss, rapid heart rate, nervousness, diarrhea, a feeling of being too hot, or irregular menstrual periods.

Note: TSH levels can help determine whether hypothyroidism is due to a damaged thyroid gland or some other cause (such as a problem with the pituitary gland or the hypothalamus).

Please Note: The basic problem that traditional medicine has with diagnosing hypothyroidism is the so called "normal range" of TSH is far too high: Many patients with TSH's of greater than 1.5 (not 4.5) have classic symptoms and signs of hypothyroidism.

The alternative to monitor thyroid disease is to use the Free T3 and Free T4 and TSH levels and interpret them with new reference ranges. If one measures the Free T3 and Free T4 levels the only accurate measure of the actual active thyroid hormone levels in the blood, as well as the TSH, one will find out how often a low normal TSH does NOT exclude hypothyroidism. It is relatively common to find the Free T4 and Free T3 hormone levels below normal when TSH is in its normal range, even in the low end of its normal range. When patients with these lab values are treated, one typically finds tremendous improvement in the patient, and a reduction of the classic hypothyroid symptoms.
 
Normal Results
Adults:   0.4–4.5 mIU/L
Note: The normal ranges for the results of this test may vary from laboratory to laboratory.

High TSH values

• High thyroid-stimulating hormone (TSH) test result often indicates an underactive thyroid gland caused by failure of the thyroid gland (primary hypothyroidism). Hashimoto's thyroiditis is the most common cause of primary hypothyroidism.
• On rare occasions, a high TSH value can occur from a pituitary gland tumor that is producing excess amounts of TSH. In this case, the person usually has symptoms of hyperthyroidism such as weight loss, rapid heart rate, nervousness, diarrhea, a feeling of being too hot, or irregular menstrual periods. Other thyroid hormone test results will likely be high as well.
• A high TSH value can also occur in people who have an underactive thyroid gland and are receiving too little thyroid hormone medication.

Low TSH values

• Low thyroid-stimulating hormone (TSH) value can indicate an overactive thyroid gland (hyperthyroidism). Causes of hyperthyroidism include Graves' disease, a type of goiter (multinodular goiter), or a noncancerous (benign) tumor called a toxic nodule.
• A low TSH value can also indicate damage to the pituitary gland that prevents it from producing TSH (secondary hypothyroidism). In this case, the person usually has symptoms of hypothyroidism such as weight gain, tiredness, dry skin, constipation, a feeling of being too cold, or frequent menstrual periods.
• A low TSH value can occur in people who have an underactive thyroid gland and are receiving too much thyroid hormone medication.

What Affects the TSH Test
Factors that can interfere with your test and the accuracy of the results include:

• Medications, such as corticosteroids, levodopa, aspirin, heparin, dopamine, lithium (such as Carbolith, Duralith, Lithane), methimazole (Tapazole), and propylthiouracil.
• Recent X-rays with iodine dye or tests using radioactive materials.
• Severe stress or long-term (chronic) illness.
• The first trimester of pregnancy.

High TSH Levels Symptoms
The symptoms usually vary from one person to another, however, let us have a look at some of the common symptoms of high TSH levels in the blood. In the earlier stages of hypothyroidism, the person may undergo symptoms like:

• Fatigue
• Stress
• Mild depression
• Difficulty in waking up
• Weight gain and weight loss issues
• Brittle nails
• Intolerance to cold
• Decrease sex drive
• Abnormal periods
• Roughening of hair and skin
• Hair loss
• Constipation
• Memory loss

Normal TSH Levels
First, what does "normal" mean. A few years ago, the medical community went by the standard that .5 to 5.0 on the Thyroid Stimulating Hormone (TSH) blood test was the normal range. If your TSH was below .5, you were hyperthyroid/overactive. If your TSH was above 5.0, you were hypothyroid/underactive.

More recently, however, both the American Association of Clinical Endocrinologists and the The National Academy of Clinical Biochemistry's "Laboratory Medicine Practice Guidelines," have recommended that the normal range be revised, so that it is instead .3, to 3.0.

Many doctors and labs still haven't switched over to the new, narrower standards and range yet, so many people who are testing in the 3.0 to 5.0 range may be told they have "normal" thyroid function by some practitioners, and diagnosed as "hypothyroid" by others. So when a doctor tells you your levels are "normal" -- ask what "normal range" he/she is actually using to make that determination.

Interpretation of TSH Testing
The thyroid gland produces thyroid hormone. When it functions properly, the thyroid is part of a feedback loop with your pituitary gland. First, the pituitary senses the level of thyroid hormone that the thyroid has released into the bloodstream. The pituitary then releases a special messenger hormone, known as "Thyroid Stimulating Hormone" (TSH). TSH stimulates the thyroid to release more thyroid hormone.

When the thyroid, for whatever reason -- illness, stress, surgery, obstruction, for example -- does not produce enough thyroid hormone, the pituitary detects this reduction in thyroid hormone, and it moves into action. The pituitary then makes MORE TSH, to help trigger the thyroid to produce more thyroid hormone. This is the pituitary's effort to return the system to "normal" and normalize thyroid function.

There, a TSH that is higher than normal suggests a thyroid that is underactive and not doing its job of producing thyroid hormone. So, in general, HIGHER TSH = UNDERACTIVE THYROID / HYPOTHYROIDISM.

If the thyroid is overactive and producing too much thyroid hormone -- due to disease, or taking too high a dose of thyroid hormone replacement drugs -- the pituitary senses that there is too much thyroid hormone circulating. The pituitary then usually slows or shuts down TSH production, so that the thyroid will slow down its production of hormone. This drop in TSH is an attempt to return circulating thyroid hormone levels to normal.

So, a test to measure the amount of TSH in your system will usually show lower than normal TSH when the thyroid is overactive.

So, in general, LOWER TSH = OVERACTIVE THYROID / HYPERTHYROIDISM.

During diagnosis, most doctors use the TSH test to evaluate your thyroid function and determine the optimal course of treatment.

[NOTE: However, that some practitioners feel that relying solely on TSH -- a pituitary hormone -- without also evaluating the circulating levels of actual thyroid hormones T4 and T3 -- may not be able to detect more subtle thyroid problems, or conditions that are resulting from improper conversion of thyroid hormones. TSH is also not necessarily sufficient to monitor hypothyroidism during pregnancy. For these reasons, some practitioners also include other valuable blood tests, including T4, T3, Free T4, Free T3, Reverse T3, and antibodies tests.]

A major hitch in this connection of TSH to hypothyroidism and hyperthyroidism is an ongoing disagreement in the medical world. As of 2008, at most labs in the U.S., the normal reference range is approximately 0.5 to 5.0. So levels below 0.5 are considered possible evidence of hyperthyroidism, and levels above 5.0 would be considered possible evidence of hypothyroidism. There is, however, an ongoing, five-year dispute among thyroid experts, because as of late 2002, some endocrinologists believed that the range should be narrowed significantly, to 0.3 to 3.0. Endocrinologists have not yet reached agreement about a standardized normal reference range for the TSH thyroid test, despite the fact that they consider this test the gold standard test to use in diagnosing and treating many thyroid problems.

When you are being treated for hypothyroidism with thyroid hormone replacement drugs, doctors will typically attempt to medicate you into this so-called "normal" reference range -- of a TSH of .3/.5 to 3.0/5.0 (Patients who have had thyroid cancer, however, are often given suppressive doses that maintain TSH near to 0 in order to prevent cancer recurrence).

So, when you've gone for a checkup, and your TSH comes in below normal (and your doctor does not have you on a suppressive dose of thyroid hormone), they may want to REDUCE your dosage of thyroid hormone, because levels below normal are considered potentialy "hyperthyroid" (overactive.)

[Another point of controversy: Once on medication, some patients may find relief from hypothyroidism symptoms only when the TSH level drops below the normal range. In that case, some doctors will also check Free T4 and Free T3 levels, believing that it's acceptable for a patient to have a below-normal TSH, as long as Free T4 and Free T3 levels are normal.]

And if your TSH test comes in above normal, some doctors will want to INCREASE your dosage of thyroid hormone, because levels above normal are considered potentially "hypothyroid" (underactive.)

To summarize:
LOW TSH suggests you are closer to HYPERthyroidism (overactive), and have too much thyroid hormone circulating.

HIGH TSH suggests you are closer to HYPOthyroidism (underactive), and you don't have enough thyroid hormone circulating.

If you're being treated with thyroid hormone drugs (such as Synthroid, Levoxyl, Armour, Thyrolar, etc.), and your TSH comes back as too low, your doctor may suggest lowering your dose, or running other tests such as Free T4 and Free T3.

When TSH tests come back as higher, that suggests HYPOthyroidism (underactive), and doctors may suggest an INCREASE in your medication dosage.

Hypothyroidism Diagnosis

Hypothyroidism is a relatively common disorder. It affects more women then men. Symptoms of hypothyroidism include fatigue, gradual weight gain, constipation, muscle aches, joint pain, feeling cold, menstrual irregularities, weakness, hair loss, dry, cold skin and slow reaction time. Many patients will have a goiter (enlarged thyroid).

The incidence of hypothyroidism increases with increasing age. In other words, the older we get, the more likely a thyroid deficiency will show up. The most common cause of primary hypothyroidism (hypothyroidism originating in the thyroid gland itself), is Hashimoto’s Thyroiditis. Hashimoto's is an autoimmune condition. The body's own antibodies attack the thyroid gland and destroy it, leading to hypothyroidism. Hashimoto’s Thyroiditis may be a manifestation of multiple autoimmune syndromes and may occur in families. Hypothyroidism can also be due to a pituitary problem (central hypothyroidism).

Diagnosing all types of hypothyroidism is important, because treatment with thyroid hormone will improve symptoms in patients with hypothyroidism, but is unlikely to help those who do not have hypothyroidism. In primary hypothyroidism, the thyroid gland, located in the neck, is less able to produce the thyroid hormones, T4 and T3. The pituitary gland, located in the head, responds to this deficiency by secreting more TSH. Thus, in more mild cases of primary hypothyroidism, T4 and T3 levels are normal, but the TSH is high. In more severe cases, T4 and T3 levels drop. Although the normal range for TSH is often between 0.5 and 5 mU/mL, values at the high end of the normal range may be abnormal. T3 is the more bioactive hormone compared to T4, but T4 is more stable in the circulation.

A better approach to diagnosing hypothyroidism is to start with a careful history and physical. Then an Endocrinologist should perform a hands-on thyroid examination to determine if the patient has a goiter. Blood TSH, free T4, free T3 and anti-TPO antibodies should be tested. Patients with an enlarged thyroid and/or a positive anti-TPO antibody test AND a TSH greater than 4.0 mU/mL should be considered to have primary hypothyroidism. Patients without an enlarged thyroid and without a positive anti-TPO antibody test but WITH a TSH greater than 7.5 mU/mL should also be considered to have primary hypothyroidism. Patients with a free T4 of less than 0.9 mg/dL and a TSH less than 1.0 mU/mL are likely to have central hypothyroidism. Patients with symptoms of hypothyroidism but who do not meet these criteria should be watched and retested in 6 months.

High TSH Levels Treatment
Treating high TSH levels after the diagnosis has been made is the next important step. Usually a thyroid replacement therapy is conduced, wherein synthetic thyroid hormone medications like Unithroid, Synthroid, Levothroid and Levoxyl are used. These medications are taken orally and they reset the hormonal imbalance to the right balance. One may experience full effect of the medication, one or two weeks after the medicine has been taken. Conditions of weight gain, high cholesterol levels, etc. can also get reversed by using these medications.

Hypothyroidism Treatment
Once hypothyroidism is diagnosed, there are many treatment options, including synthetic L-thyroxine (T4) preparations (Synthroid, Levoxyl and Unithroid), synthetic L-triiodothyronine (T3) preparations (Cytomel), synthetic T4/T3 combinations (Thyrolar) and dessicated thyroid preparations (Armour, Naturethroid, Bio-Throid, and Westhroid).

The traditional approach is to use Synthroid/ Levoxyl/Levothroid (levothyroxine) which is only T4. Natural medicine doctors tend to use Armour thyroid which is a mixture of mono and di-iodothryonine and T3 and T4, the entire range of thyroid hormones.

All of the L-thyroxine preparations contain the same active ingredient, but contain different fillers and have different quality control. Until recently, Synthroid did not have FDA approval, but now all L-thyroxine preparations have FDA approval. Thyrolar and the dessicated thyroid preparations probably have a higher T3/T4 ratio than desirable and thus,  a lower amounts of these preparations supplemented with T4 are usually given.

Most endocrinologists use L-thyroxine preparations for the initial treatment of all forms of hypothyroidism. Although the use of L-thyroxine (T4) compared to L-triiodothyronine (T3) may be surprising as T3 is the more bioactive thyroid hormone, T4 is most frequently used. This is because tissues convert T4 to T3 to maintain physiologic levels of the T3. Thus, administration of T4 results in bioavailable T3 and T4. As T4 is more stable than T3, T4 therapy gives even blood levels, while T3 therapy leads to high levels after taking the medicine and low levels before the next dose. Armour thyroid is the least expensive preparation. Because Armour thyroid comes form pig thyroids, some Endocrinologists feel that there is high pill to pill variability, but this is unlikely to be true.

Hypothyroidism Reaching Epidemic Proportions

Why are so many people being diagnosed with hypothyroidism? Why do women seem to be more susceptible to this disease? What is the connection to diabetes?

In 1995, researchers studied 25,862 participants at the Colorado statewide health fair.  They discovered that among patients not taking thyroid medication, 8.9 percent were hypothyroid (under-active thyroid) and 1.1 percent were hyperthyroid (over-active thyroid). This indicates 9.9 percent of the population had a thyroid problem that had most likely gone unrecognized. These figures suggest that nationally, there may be as many as 13 million Americans with an undiagnosed thyroid problem.

In her book Living Well With Hypothyroidism: What Your Doctor Doesn't Tell You. . . That You Need to Know, Mary Shomon quotes endocrinologist Kenneth Blanchard, M.D., of Lower Newton Falls, Massachusetts as saying, “The key thing is . . . doctors are always told that TSH is the test that gives us a yes or no answer. And, in fact, I think that's fundamentally wrong. The pituitary TSH is controlled not just by how much T4 and T3 is in circulation, but T4 is getting converted to T3 at the pituitary level. Excess T3 generated at the pituitary level can falsely suppress TSH.”  Hence, many people who are simply tested for TSH levels and are found to be within “normal” range are, in fact, suffering from thyroid problems that are going undetected.

Ridha Arem, MD, Associate Professor of Medicine in the Division of Endocrinology and Metabolism at Baylor College of Medicine, agrees. He says that hypothyroidism may exist despite "normal range" TSH levels.  In his book The Thyroid Solution he says:

Many people may be suffering from minute imbalances that have not yet resulted in abnormal blood tests. If we included people with low-grade hypothyroidism whose blood tests are normal, the frequency of hypothyroidism would no doubt exceed 10 percent of the population. What is of special concern, though, is that many people whose test results are dismissed as normal could continue to have symptoms of an under active thyroid. Their moods, emotions, and overall well-being are affected by this imbalance, yet they are not receiving the care they need to get to the root of their problems.  Even if the TSH level is in the lower segment of normal range, a person may still be suffering from low-grade hypothyroidism.

Thus, if we were to include those who may be suffering from “low-grade hypothyroidism,” the number could well be double the 13 million estimate from the Colorado study.

What is Causing This Epidemic of Hypothyroidism?
While more research needs to be done, it is generally accepted that diet plays a major role in thyroid health.  For decades we have known that low iodine intake leads to low thyroid function and eventually to goiter.  Iodized salt was intended to solve this problem, but it has not been the answer.  There are a number of foods known as goitrogens that block iodine. Two goitrogens are quite prevalent in the American diet—peanuts and peanut butter and soybeans used most often in prepared foods as textured vegetable protein (a refined soy food) and soybean oil.

The rise of industrialization, corporate farming, and mass production of food has drastically changed our food supply from what our ancestors ate. Many studies show the detrimental effects of refined sugars and grains on our health. These foods are very taxing on the thyroid gland, and we consume them in large quantities.

Environmental stress such as chemical pollutants, pesticides, mercury, and fluoride are also tough on the thyroid.  A growing body of evidence suggests that fluoride, which is prevalent in toothpaste and water treatment, may inhibit the functioning of the thyroid gland.  Additionally, mercury may diminish thyroid function because it displaces the trace mineral selenium, and selenium is involved in conversion of thyroid hormones T4 to T3.

The Ugly Truth About Fats and Oils
In addition, many vegetable oils can negatively affect thyroid health. We cook with them almost every day and they are plentiful in commercially prepared foods. Expeller-pressed or solvent-extracted oils only became a major part of the American diet in the last century.  It is possible they are among the worst offenders when it comes to the thyroid.  The most common source of these vegetable oils used in commercially prepared foods is the soybean.

Large-scale cultivation of soybeans in the United States began after World War II and quickly increased to 140 billion pounds per year.  Most of the crops are produced for animal feed and soy oil for hydrogenated fats such as margarine and shortening. Today, it is nearly impossible to eat at restaurants or buy packaged foods that don’t have soy oil in the ingredients.  Often labels simply state “vegetable oil.”

Ray Peat Ph.D., a physiologist who has worked with progesterone and related hormones since 1968, says that the sudden surge of polyunsaturated oils into the food chain post World War II has caused many changes in hormones that especially affect women.

There is a growing body of research concerning soy’s detrimental affect on the thyroid gland. Much of this research centers on the phytoestrogens ("phyto" means plant) that are found in soy.  In the 1960s when soy was introduced into infant formulas, it was shown that soy was goitrogenic and caused goiters in babies. When iodine was supplemented, the incidence of goiter reduced dramatically. However, a retrospective epidemiological study by Fort, et al. showed that teenaged children with a diagnosis of autoimmune thyroid disease were significantly more likely to have received soy formula as infants (18 out of 59 children; 31 percent) when compared to healthy siblings (nine out of 76, 12 percent) or control group children (seven out of 54; 13 percent).

When healthy individuals without any previous thyroid disease were fed 30 grams of pickled soybeans per day for one month, Ishizuki, et al. reported goiter and elevated individual thyroid stimulating hormone (TSH) levels (although still within the normal range) in thirty-seven healthy, iodine-sufficient adults.  One month after stopping soybean consumption, individual TSH values decreased to the original levels and goiters were reduced in size.

Traditionally, polyunsaturated oils such as soybean oil have been used for livestock feed because they cause the animals to gain weight.  These oils are made up of what is known as long chain fatty acids—the kind of fatty acids that promote weight gain. In the North Carolina State University's Extension Swine Husbandry 1998-2000 Departmental report, for example, was a study entitled “EFFECT OF DIETARY FAT SOURCE, LEVEL, AND FEEDING INTERVAL ON PORK FATTY ACID COMPOSITION” by M.T. See and J. Odle. Ironically, since the market in its low-fat dogma of recent years is demanding leaner meats, this study showed that one could produce leaner meat and reduce the weight on swine by reducing their intake of soy oil and substituting it with saturated animal fat!7

According to Dr. Ray Peat, the fattening effect of polyunsaturated oils (primarily soy and corn) is due to the presence of Linoleic and linolenic acids, long-chain fatty acids, which have an anti-thyroid effect. Peat says:

Linoleic and linolenic acids, the "essential fatty acids," and other polyunsaturated fatty acids, which are now fed to pigs to fatten them, in the form of corn and soy beans, cause the animals' fat to be chemically equivalent to vegetable oil.  In the late 1940s, chemical toxins were used to suppress the thyroid function of pigs, to make them get fatter while consuming less food.  When that was found to be carcinogenic, it was then found that corn and soy beans had the same antithyroid effect, causing the animals to be fattened at low cost.  The animals' fat becomes chemically similar to the fats in their food, causing it to be equally toxic, and equally fattening.8

Of course in the 1940s the fat from pigs (lard) was highly desirable, as were most saturated fats. Today, saturated fats are fed to pigs to keep them lean, while most people buy polyunsaturated soy and corn oils in the grocery stores as their primary cooking oil! So we have a population now characterized by lean pigs and obese people.

Hypothyroidism and Insulin Resistance
Another cause of weight gain that is often associated with hypothyroidism is insulin resistance.  Insulin resistance prevents the body from using its own insulin efficiently. Those who are insulin resistant become immune to the insulin's effect on cells. This means that more insulin is being produced with fewer results. This causes the pancreas to work overtime and the body ends up storing more fat.

Insulin resistance also prevents the body from using this fat as energy stores. Because of this, the insulin responds to things such as carbohydrates and causes a person afflicted with the condition to gain weight, or not be able to lose weight. Hypothyroidism, which will already cause everything in the body to slow down, can often lead to, or cause, insulin resistance.

These two conditions make weight gain inevitable. But the importance of losing weight and maintaining a healthy weight is imperative for someone with hypothyroidism and insulin resistance. Ironically, the more necessary it becomes to attain a healthy weight, the more important it is. However, it is not impossible. Through a plant-based diet of low-carb, low-fat, and high protein, the person is able to maintain a healthy weight. This combined with regular exercise is the best way to treat hypothyroidism and insulin resistance.

Alternative Health Strategies for the Thyroid                         
The following section will discuss several alternative (non-drug) strategies to support a healthy thyroid, including: proper nutrition, detox, stress, sleep, and cardiovascular support.

Nutrition
Key nutritional strategies include a periodic detox and an organic plant-based diet, with minimum processed food and no tap water (because of the chlorine and fluoride). This is necessary to prevent any major nutrient deficiencies that may trigger diseases such as heart disease, diabetes, and cancer.

Without proper nutrition, your thyroid lacks nutrients to make basic thyroid hormone, known as T4 (thyroxin), or you may lack key nutrients that help convert T4 to the biologically active T3. Your thyroid can be inflamed or stressed, which gets in the way of making T4 at an optimal rate. And your liver can be inflamed or stressed, which gets in the way of converting T4 to T3 at an optimal rate. Cells around your body require basic nutrition to carry out the metabolic instructions that T3 is giving them; otherwise it is no different than not having enough T3.

Any or all of these simple-case thyroid problems can be addressed with nutrition. Optimal nutrition can enhance the formation of thyroid hormone in the thyroid gland, enhance the activation of T4 to the biologically active T3, and enhance the nutritional ability of cells to utilize thyroid hormone.  Various  wholefood-based dietary supplements  have been designed to fill these specific needs.

Some supplements provide the selenium needed by your liver to convert T4 to T3. As an example, the selenium containing enzyme type-I-iodothyronine-deiodinase is important for the conversion of T4 to T3. So selenium deficiency can reduce the activity of the thyroid hormones.

Manganese is also needed to boost specific antioxidant enzymes inside your thyroid gland and in your liver, so that both organs can function in a less stressed and inflamed manner.

Tyrosine is is an amino acid that is needed to boost dopamine and nerve related thyroid formation, as well as providing the core molecule of thyroid hormone (T4 is one molecule of tyrosine surrounded by four molecules of iodine). And so the use of tyrosine as a dietary supplement increases production of thyroid hormones.

It appears that a water-soluble and biologically active form of iodine called Iosol Iodine has proven to be very effective. It is one of the most popular supplements to help individuals warm up. Iodine is needed for thyroid hormone formation. Unlike potassium iodide which can clog the thyroid gland due to its poor solubility, Iosol readily washes away if it is not needed. It is hands down the best iodine on the market today. There used to be plenty of iodine in vegetables and fruits but the soil is very iodine depleted in most areas today. Kelp is rich in iodine. Other foods that contain iodine are yogurt, eggs, meat, fish and other seafood, radish, parsley, potatoes, oatmeal and bananas.

Thyroid glandular supplements have been used for some thyroid treatments. Usually it is only sold through your practitioner or by prescription (like Armour) but there are some over-the-counter thyroid glandular supplements available.

Bladderwrack is a seaweed that is a rich source of iodine. Traditionally it has been used for weight loss and hypothyroidism. The low incidence of goiter in maritime people has been attributed to the iodine in bladderwrack. It also contains the minerals potassium, magnesium, calcium, iron, zinc, etc. Bladderwrack is thought to stimulate the thyroid gland increasing metabolism.

Extra virgin coconut oil helps to promote your metabolism by providing thyroid support. It acts in tandem with the thyroid to produce an effect greater than the sum of their individual effects. Moreover, it is a highly recommended source of fats, as it improves sensitivity of tissues to thyroid hormones.

The fusion of the two work to the benefit of the body and help in maintaining optimum metabolic rate. To explain it in simple words, coconut oil serves as high octane fuel for the internal combustion engine in the car. An efficient fuel (coconut oil) makes the car (thyroid) perform better and last longer. Coconut oil is also considered to be the best cooking oil, as it does not add to your weight. More importantly, you should avoid most of the oils that we use to cook food and those used in commercially-prepared foods. These polyunsaturated vegetable oils have a negative affect on the thyroid and may in fact be the worst villains in the spread of thyroid diseases.

Alfalfa and wheat sprouts help to nourish the pituitary gland (especially if developing white skin blotches). Ginseng also helps to nourish the pituitary. Gotu Kola contains nutrients needed by the pituitary.

A wholefood multivitamin can be helpful if it contains all  the co-enzyme B vitamins and mineral transporters. Avoid the cheap cyanide-producing form of B12 known as cyanocobalamin. Cyanide metabolites are very hard on the thyroid -- only cheap vitamin companies put this low grade B12 in their products. Vitamin B12 and folic acid are especially important for the enzymes that make thyroid hormone. A lack of B12 is commonly found in those struggling with thyroid function (along with poor mood).

A variety of other nutrients, if lacking, can impede healthy thyroid function. At the top of this list are quercetin, Vitamin D, iron, and zinc. Ensure you are not lacking in these, as anyone of them can be responsible for the symptoms of a sluggish thyroid.

Quercetin is a bioflavonoid common in the plant kingdom, a potent polyphenol antioxidant and immune system modulator found in onions. It has a stabilizing affect on the immune system, helping various types of immune cells maintain their composure under stress. It has a modulating effect on immune system signals, helping to calm down inappropriate excess. This helps the tissues and cells in your thyroid gland better tolerate common irritants such as pollution and stress.

Researchers recently demonstrated that a lack of Vitamin D was associated with lower levels of T4 and that irritation of the thyroid gland was more pronounced if vitamin D is lacking. It should be noted that cold weather itself is a temperature stress that makes your thyroid work harder, and the lack of sun in winter months makes it more likely you could be deficient. Most people need 2000 IU of Vitamin D per day in the winter months for a variety of health needs, which includes thyroid support. Cod liver oil is a good source of Vitamin D.

When thyroid instructions reach the DNA of your cells it tells them how to set the metabolic pace of the cells activities, in turn setting into motion a number of different genes that carry out these instructions. It has now been discovered that iron is required for up to 80 of these vital gene signals, otherwise thyroid instructions dont get implemented. A lack of iron also impedes proper oxygenation of blood. A lack of iron can cause fatigue, especially muscle weakness, which can readily be confused with thyroid-related fatigue. Vegetarians, menstruating women, and heavy exercisers are most at risk for a lack of iron. Clams, oysters, beef liver, grains, pumpkin seeds, lentils, spinach,  and blackstrap molasses are good sources of iron.

Zinc is another cofactor mineral that needs to be adequate for thyroid hormone to perform at an optimal pace. A lack of zinc is known to reduce the activity of TRH (thyroid releasing hormone in the hypothalamus), in turn tending to depress thyroid hormone levels. Zinc participates in the conversion of T4 to T3, and zinc is needed to bind active thyroid hormone to the DNA of cells. Zinc is needed for immunity, sex drive, and maintaining leptin status while on a diet. It is lost in sweat and by stress. Beef, nuts, whole grains, legumes, and yeast are good sources of zinc.

Note: A number of homeopathic treatments for the pituitary gland are available these days. Much like the homeopathic tinnitus treatment remedies for ringing ears, the homeopathic treatment modes for pituitary gland disorders are basically derived from a wide array of natural ingredients and substances like herbs, animal extracts, plants and vegetables, which are taken in quite extremely minute doses. The homeopathic treatment therapies are usually chosen based on the patient’s symptoms, which also include the person’s physical, mental and emotional states, as well as their family history. Such treatment course is aimed to properly stimulate the body's own immune system, as well as lead to a long-term cure rather than simply offer temporary relief.

Note: Refer to the Nutritional Supplements ebook for more details about wholefood-based supplements.

Toxins that Affect the Thyroid

One of the key factors that helps induce weight gain and reduces the ease with which you can lose weight is the issue of environmental chemicals, chemicals in food and water, and toxins from low grade infections (like Candida or bacterial overgrowth). This issue is always made worse if your internal plumbing systems arent up to the challenge (constipation, irritable bowel, liver issues, lymph stagnation, chemical sensitivity, fibromyalgia, etc.)

Some chemicals like perchlorate, chlorine, and fluoride can directly bind to your thyroid gland and reduce iodine uptake. Many other chemicals, especially the fat-soluble ones, can bind to thyroid cell membranes and participate in thyroid inflammation and thyroid autoantibody production.

Fat-soluble chemicals can readily cross your blood brain barrier and interfere with how your brain senses any hormone level, including thyroid. Endotoxins from infections (lipopolysaccharides or LPS) directly interact in the Thyroid Releasing Hormone (TRH) region of your hypothalamus gland and intentionally turn down TRH production interfering with thyroid hormone production. Endotoxins also make you hungry by elevating your stomachs hunger signal, ghrelin.

Your liver, which is your main detoxification organ, is particularly sensitive to toxic excess. Because T4 is converted to T3 on cell membranes of your liver, fat-soluble toxins readily interfere with thyroid hormone activation by your liver.  Liver detox may be needed to help your liver specifically clear toxins more efficiently while simultaneously protecting liver cells. Refer to the Cleanse/Detox ebook for more details.

If you are trying to lose weight, you must keep detox systems working well as toxins will be released from stored fat as weight is lost. This toxins can crash your thyroid long before you get to your goal weight, if you dont take care to ensure they are smoothly flowing out of your body.

Soluble fiber (in vegetables) is needed to bind on to these toxins as they are excreted in your bile. Such fiber also helps regularity and reduce cravings for food. 

Other supplements that are helpful for those in a toxic rut include chlorella (a geat binder of fat-soluble toxic waste), and herbal tinctures (for congested lymph - excess mucous, shoulder stiffness, etc.).

In order to make sustained thyroid improvement it is vital to keep internal plumbing flowing along in a healthy way.

Stress and the Thyroid

Your stress management system is rooted in the function of your adrenal glands, which operate in an interdependent fashion with your overall thyroid system. Many books on adrenals list all the symptoms of low thyroid as adrenal problems and vice versa. There are differences. Morning energy, stress tolerance, and aerobic fitness are primarily adrenal issues. Thyroid issues are more about afternoon energy level, being too cold, and feeling mentally sluggish or heavy headed (adrenals issues go more with brain fog).

Thyroid sets your basic supply of energy for your body to use. Not having enough automatically stresses your adrenals if there is an increased demand for needed energy. Conversely, tired adrenals make it so your body gets too inflamed from even normal activities forcing your thyroid to go slower than it would like so that you dont overheat and burn up. Ongoing stress can wreak havoc with these problems.

If you are someone who struggles with a long list of adrenal and thyroid symptoms then you have to nurse both systems back on at the same time. A good way to do this is to use basic thyroid support along with basic adrenal support.

In order to get these systems back into good condition you must find an amount of exercise you can do on a consistent basis and then gradually increase the amount. When you can get a refreshing response to aerobic type exercise that is done at least three times a week, then both your adrenal and thyroid system will be working better. Dont push too hard with exercise, be consistent and gradually improve what you can do.

Key nutrients for stress management can be plugged into a thyroid support program, enabling you to have better stress tolerance, i.e. B-Complex vitamins, phosphatidyl serine (PS), quercetin and Vitamin C.

Sleep and the Thyroid

When stress is either extremely intense or has been going on too long, then the relaxed reserves in your nervous system tend to deplete. This gives your brain a wired feeling, meaning you are likely to be more anxious or irritable during the day and have poorer quality sleep at night. This has a major bearing on how your subconscious brain (hypothalamus gland) processes thyroid-related information, directly interfering with the normal production of TRH (thyroid releasing hormone), which in turn regulates your pituitary gland (TSH), and those overall regulation of your thyroid system. This will leave you with a mixture of hyper and hypo symptoms, and unless you cool this off these symptoms, including the lack of quality sleep, remain problematic and induce ongoing thyroid wear and tear.

This combination of symptoms causes you to be tired, irritable/anxious, and hungry during the day and you typically eat more because it brings temporary relief to these feelings. At night, your subconscious brain is set to hyper-vigilant, left over circuitry from evolution so that you do not miss a hunting opportunity. In this inappropriate metabolic pattern thyroid hormone levels are set very slow by your subconscious brain (TRH-related control) so that your body can conserve energy during this misperceived famine. The only way out of this is to relax and un-inflame your system so that it can calm down.

On an exercise basis this is stretching, walking, prayer/medication, stress management, etc. towards the goal of you feeling calmer and more in control of your life.

You are not just trying to knock yourself out at bed. You are trying to get a smoother energy production during the day and replenish depleted relaxed reserves. If this problem is locked in, then relaxing lifestyle adjustments are also mandatory. It can take a month or two to unwind a wound up system and thyroid wont work right until you do.  Refer to Chapter 13 of Death to Diabetes or the Stress Reduction ebook for more details about stress, sleep, and relaxation.

Cardiovascular Health and the Thyroid

Thyroid hormone controls the rate that oxygen is used at the cellular level to make energy. Your circulatory system is how oxygen is transported to cells. Thus, there is tremendous overlap between a healthy thyroid and cardiovascular system, and conversely, between a stressed thyroid and cardiovascular system.

Indicators of good health include a sense of feeling well oxygenated, reflected in very easy breathing and a head that feels quite awake. Numerous studies in the past year show the extreme importance of maintaining optimal thyroid function so as to support cardiovascular well being with the use of oxygen being a common theme. Additionally, stressed nerves directly irritate both systems, pushing them in the wrong direction (felt as a lack of stress tolerance, irritation, anxiety, racing heart, trouble sleeping, etc.)

Therefore, a relaxed and smooth feeling in your body, accompanied by easy breathing and an awake head, along with plenty of oxygen during exercise, are all signs of a good foundation of oxygen that enhances both thyroid and cardiovascular health.

High quality iron is vital for the transport of oxygen in your blood. Proper function of your hemoglobin also requires Vitamin E. The other best nutrient that supports oxygen status is CoQ10 (cellular and heart support). Refer to Chapter 15 of Death to Diabetes or  the How to Prevent a Heart Attack ebook for more details.

Other Treatment Options
Natural health practitioners who don't truly understand thyroid function are often quick to tell you that "thyroid problems mean you need iodine" or iodine-containing herbs or supplements, such as kelp.

If you are truly iodine deficient, iodine may be able to help your thyroid. One study done in 1998 found that over the past twenty years, the percentage of Americans with low intake of iodine has more than quadrupled. Currently about 12 percent of the U.S. population is iodine deficient, up from less than 3 percent in the early 1970s. So, for some people, iodine deficiency may be a factor in their thyroid problem.

But for some people, iodine or iodine-containing products make worsen autoimmune thyroid problems, both Hashimoto's and Graves' disease, and cause enlargement of the thyroid (goiter). Before you start iodine, consider having urinary iodine measured to see if you have an actual deficiency, and pay close attention to any symptoms that develop after you start to take iodine.

Perhaps one of the most common fallacies doctors regularly repeat is that Synthroid is the only treatment for hypothyroidism. Actually, Synthroid is a brand name for the drug "levothyroxine" -- a synthetic form of the thyroid hormone thyroxine, also known as T4.

Synthroid happens to be the top-selling levothyroxine drug -- primarily due to its marketing influence on physicians and their organizations, as well as relationships with distributors and insurers. Synthroid, however, is almost always the most expensive levothyroxine. Other brands, considered equally effective by many practitioners, and almost always less expensive, include Levoxyl, Levothroid, and Unithroid. Some patients find that they respond best to a one brand -- not necessarily Synthroid -- due to the way that brand dissolves and is absorbed, or the fillers and dyes used by the different manufacturers.

In addition to the levothyroxine drugs, there is also liotrix, the generic name for the brand name drug Thyrolar. Thyrolar is levothyroxine and liothyronine (the synthetic form of the thyroid hormone triiodothyronine, or T3). The addition of the T3 to this drug makes it an optimal drug for some thyroid patients who need that additional hormone in order to resolve symptoms and feel well. Liothyronine is also available as a separate prescription pill, known by its brand name Cytomel.

Finally, there is the category of prescription drugs known as natural thyroid. Don't mistake these with over-the-counter glandular thyroid supplements -- they are not the same. Prescription natural desiccated thyroid -- the primary brand being Armour Thyroid, but also available are Biotech and Nature-throid -- is made from the dried thyroid gland of pigs. It includes natural T4 and T3, plus other less understood thyroid hormones including T2, T1. Some practitioners, and in particular holistic, integrative and natural health experts, find that natural thyroid is optimal for some patients.

Warning! Try one or more of the non-drug alternative strategies before you succumb to any drug therapy! Once your body becomes "addicted" to the drugs, it's very difficult to wean off the drugs.

Additional Information about Treatment

If the Free T3 level is significantly lower than the Free T4 level, it is next to useless to treat with Synthroid/ Levoxyl/Levothroid (T4) only replacements. If the patient could not muster sufficient T3 from their gland (which produces some T3 directly), then they are certainly not going to convert enough T3 from T4 only. Traditional medicine assumes that preparations like Synthroid which are T4 only converts peripherally in the body to T3 in fairly standard amounts and at fairly standard rates.

Unfortunately, clinical experience shows this is not true for the majority of patients. Consistent measuring of both free T3 and free T4 blood levels in hypothyroid patients who are on T4 only therapy will very rapidly dispel this myth. A certain percentage of hypothyroid patients do convert enough T4 to T3 at a sufficient rate for T4 treatment to be adequate as a source of T3; but a substantial proportion of patients require some combination of both exogenous T3 and T4.

Once on hormone replacement, the TSH remains useful until it goes BELOW 0.4. Then one has optimized thyroid function by the TSH yardstick; it then remains to optimize thyroid function by the yardstick of the accurate measures of the 2 thyroid hormones, the Free T4 and Free T3 levels.

So one should use a combination of T4 and T3 which compensates for the inability to convert T4 to T3. This is most frequently done with Armour thyroid. However, Cytomel, which is T3 only, can be used in combination with one of the T4 only preparations. It is important to recognize that T3 should always be prescribed twice daily due to its shorter half life. This is typically after breakfast AND supper for compliance reasons.

Taking the dose at these times overcomes traditional medicine's major objection and resistance to using natural thyroid preparations - its variability in its blood levels. Armour thyroid is desiccated thyroid and has both T3 and T4. Most doctors using Armour thyroid are not aware that Armour thyroid should be used twice daily and NOT once a day. The major reason is that the T3 component has such a short half life and needs to be taken twice daily to achieve consistent blood levels.

Once or twice daily dosing one can then optimize both the T4 and T3 levels, with whatever thyroid preparation is required. This is not possible in most hypothyroid patients with T4 only preparations. It is important to use a preparation with T3 because T3 does 90% of the work of the thyroid in the body. The only exception to pursue optimization of the T3 level without using Armour thyroid is in severe acute cardio-pulmonary conditions, when the metabolic slowing effect of a low FT3 level can actually be life-saving. However, the vast majority of hypothyroid patients do not have acute cardio-pulmonary conditions, such as congestive heart failure.

The most common starting dose for patients with hypothyroidism is Armour thyroid, 90 mg which is cut in half with a razor blade and half is taken after breakfast and the other half after dinner. Taking it after meals also helps to reduce volatility of the blood-level of T3. If the patient has any problem breaking or cutting the pill, they should purchase a pill-cutter at the pharmacy. The TSH, Free T3 and Free T4 are then repeated in one month and the dose is adjusted.

In order to optimize the hormone replacement, the Free T3 and Free T4 should be above the median but below the upper end of the laboratory normal reference range. The goal for healthy young adults would be to have numbers close to the upper part of the range, and for cardiace and/or elderly patients, the numbers should be in the middle of its range. The Free T3 and Free T4 levels should be checked every month and the hormone therapy readjusted until the FT3 and FT4 levels are in the therapeutic range described. A small number of large, overweight, thyroid-resistant women may need 6-8 grains of Armour Thyroid or the equivalent of thyroxine per day (counting 0.1mg of T4 as 1 grain of Armour Thyroid).

If the patient is currently taking Synthroid (thyroxine), their Free T4 level is usually at or above the high end of its normal range and the Free T3 level is below. In this situation, or if a patient is allergic to Armour thyroid or is resistant to taking Armour thyroid, one may then add 5-12.5 mcg Cytomel (pure-T3) after breakfast and supper daily, rather than Armour Thyroid or Thyrolar (synthetic T4/T3 combo). It is important to remember that if the FT4 is being raised by a still-high TSH, the FT4 level will drop some when the TSH drops when adequate T3 is added to the hormone replacement.

Patients need to be warned about the overdosage symptoms which are frequently only temporary during the adaptation stage. The symptoms may include: palpitations, nervousness, feeling hot and sweaty, rapid weight-loss, fine tremor, and clammy skin. There is one exception to the 1.5 level of TSH as the cutoff for treatment. Overweight patients who have classic symptoms of hypothyroidism and have made heroic unsuccessful attempts to lose weight may benefit from thyroid hormone replacement even if their TSH slightly below 1.5 and FT4 and FT3 are not below their normal ranges

Patients who are already on once daily Armour thyroid should split their doses immediately and take half after breakfast and half after dinner. Since the only change will be in the FT3 level, which has a short half-life, the serum FT4 and FT3 levels (and TSH, if indicated) can be measured 48-72 hrs after the splitting of the doses if the patient had been on the hormone for 4-6 weeks before the splitting of the doses. This is because the T4 fraction is the one that takes a number of weeks to build up to its steady-state serum level.

Thyroid Connection to Diabetes
Researchers have now found that even subtle changes in thyroid function increase the risk for metabolic syndrome and diabetes.

The link between overt hypothyroidism and an increased risk of heart disease has already been established. But research published in the February 2007 issue of the Journal of Clinical Endocrinology and Metabolism found a connection between thyroid function and metabolic syndrome in people who have normal thyroid stimulating hormone (TSH) levels.

What the researchers found was that in those with normal TSH levels, the thyroid hormone level known as free T4 was important. Free T4 levels that were slightly low, but still within the normal range, significantly increased the risk of many risk factors for metabolic syndrome.

Lower levels of another thyroid hormone, free T3, were linked to risk factors including higher total cholesterol, LDL cholesterol, and triglycerides.

The researchers concluded that for people who have normal TSH levels, even slight changes in free T4 and free T3 levels can have an effect on the risk of metabolic syndrome and heart disease.

The researchers recommend that a study be done to determine whether early treatment of thyroid dysfunction might reduce the risk.

What Does This Means for You?

If future research does find that early treatment helps, free T4 and free T3, and not just TSH, will become key measurements in thyroid diagnosis and treatment decisions.

This research also suggests that if you are being treated for hypothyroidism, you should be monitored for signs of metabolic syndrome. If you are hypothyroid, you'll want to make every effort to reduce your metabolic syndrome risk factors.

Addressing the risk factors can be complex, but generally, involves a combination of any or all of the following approaches:

• Overall efforts to lose weight, including diet and exercise
• Specialized dietary changes to combat insulin resistance and improve cholesterol levels
• Exercise
• Diet changes to lower triglycerides, raise HDL, lower blood pressure, lower/manage blood sugar

Note: Hypothyroidism can be treated before it develops into diabetes. One of the biggest treatments is simply changing lifestyle and habits. Eating a low carbohydrate, low-fat plant-based diet that is also high in plant protein can greatly help with the treatment of hypothyroidism.

Thyroid Disease and Diabetes

Thyroid disease is common in the general population, and the prevalence increases with age. The assessment of thyroid function by modern assays is both reliable and inexpensive. Screening for thyroid dysfunction is indicated in certain high-risk groups, such as neonates and the elderly.

Hypothyroidism is by far the most common thyroid disorder in the adult population and is more common in older women. It is usually autoimmune in origin, presenting as either primary atrophic hypothyroidism or Hashimoto's thyroiditis. Thyroid failure secondary to radioactive iodine therapy or thyroid surgery is also common. Rarely, pituitary or hypothalamic disorders can result in secondary hypothyroidism.

Approximately 4 million people in the United States are hypothyroid and receive thyroxine replacement therapy. By contrast, hyperthyroidism is much less common, with a female-to-male ratio of 9:1. Graves' disease is the most common cause and affects primarily young adults. Toxic multi-nodular goiters tend to affect the older age-groups.

Hypothyroidism, because it slows down the body’s processes, also affects insulin production. When a condition such as hypothyroidism is involved, the pancreas slows down its ability to turn blood sugar into energy. This is a complication that leads to diabetes.

Diabetic patients have a higher prevalence of thyroid disorders compared with the normal population. Because patients with one organ-specific autoimmune disease are at risk of developing other autoimmune disorders, and thyroid disorders are more common in females, it is not surprising that up to 30% of female type 1 diabetic patients have thyroid disease. The rate of postpartum thyroiditis in diabetic patients is three times that in normal women. A number of reports have also indicated a higher than normal prevalence of thyroid disorders in type 2 diabetic patients, with hypothyroidism being the most common disorder.

How Thyroid Dysfunction May Affect Diabetic Patients
The presence of thyroid dysfunction may affect diabetes control. Hyperthyroidism is typically associated with worsening glycemic control and increased insulin requirements. There is underlying increased hepatic gluconeogenesis, rapid gastrointestinal glucose absorption, and probably increased insulin resistance. Indeed, thyrotoxicosis may unmask latent diabetes.

In practice, there are several implications for patients with both diabetes and hyperthyroidism. First, in hyperthyroid patients, the diagnosis of glucose intolerance needs to be considered cautiously, since the hyperglycemia may improve with treatment of thyrotoxicosis. Second, underlying hyperthyroidism should be considered in diabetic patients with unexplained worsening hyperglycemia. Third, in diabetic patients with hyperthyroidism, physicians need to anticipate possible deterioration in glycemic control and adjust treatment accordingly. Restoration of euthyroidism will lower blood glucose level.

Although wide-ranging changes in carbohydrate metabolism are seen in hypothyroidism, clinical manifestation of these abnormalities is seldom conspicuous. However, the reduced rate of insulin degradation may lower the exogenous insulin requirement. The presence of hypoglycemia is uncommon in isolated thyroid hormone deficiency and should raise the possibility of hypopituitarism in a hypothyroid patient. More importantly, hypothyroidism is accompanied by a variety of abnormalities in plasma lipid metabolism, including elevated triglyceride and low-density lipoprotein (LDL) cholesterol concentrations. Even subclinical hypothyroidism can exacerbate the coexisting dyslipidemia commonly found in type 2 diabetes and further increase the risk of cardiovascular diseases. Adequate thyroxine replacement will reverse the lipid abnormalities.

In young women with type 1 diabetes, there is a high incidence of autoimmune thyroid disorders. Transient thyroid dysfunction is common in the postpartum period and warrants routine screening with serum thyroid-stimulating hormone (TSH) 6­8 weeks after delivery. Glucose control may fluctuate during the transient hyperthyroidism followed by hypothyroidism typical of the postpartum thyroiditis. It is important to monitor thyroid function tests in these women since approximately 30% will not recover from the hypothyroid phase and will require thyroxine replacement. Recurrent thyroiditis with subsequent pregnancies is common.

Diagnosis of Thyroid Dysfunction
The diagnosis of thyroid dysfunction in diabetic patients based solely on clinical manifestations can be difficult. Poor glycemic control can produce features similar to hyperthyroidism, such as weight loss despite increased appetite and fatigue. On the other hand, severe diabetic nephropathy can be mistaken for hypothyroidism because patients with this condition may have edema, fatigue, pallor, and weight gain.

To further complicate the diagnostic process, poorly controlled diabetes, with or without its complications, may produce changes in thyroid function tests that occur in nonthyroidal illnesses. Typical changes include a low serum T3 due to impaired extrathyroidal T4-to-T3 conversion, a low serum T4 due to decreased protein binding, and an inappropriately low serum TSH concentration.

The availability of the highly sensitive immunoassay for serum TSH (with detection limit of <0.1 mU/l) provides a major advance in the diagnosis of thyroid disorders. It is the most reliable and sensitive screening test for thyroid dysfunction and allows both hypothyroidism and hyperthyroidism to be diagnosed with certainty. In addition, subclinical thyroid dysfunction can only be diagnosed by an abnormal TSH because the serum T3 and T4 are normal and, by definition, the patients are usually asymptomatic.

However, the underlying thyroid dysfunction can produce clinically important physiological effects. Subclinical hypothyroidism can elevate serum LDL cholesterol and worsen pre-existing dyslipidemia, further increasing the risk of atherosclerosis. Subclinical hyperthyroidism may increase the risk of cardiac arrhythmias and exacerbate angina. Since diabetic patients are at high risk for cardiovascular diseases, the diagnosis and treatment of subclinical thyroid diseases is important.

The presence of anti-thyroid peroxidase (TPO) antibodies is helpful in predicting the development of autoimmune thyroid disorders, especially hypothyroidism. Patients who have anti-TPO antibodies should be screened for thyroid dysfunction on a regular basis, so early detection and treatment is possible.

Management of Thyroid Dysfunction
Hypothyroidism should be treated with thyroid hormone therapy. L-thyroxine is the most widely used thyroid hormone replacement. Natural thyroid extracts such as desiccated thyroid should no longer be used.

The usual full replacement dose is 1.6 µg L-thyroxine per kg of body weight. Often, patients with mild thyroid failure require less than a full replacement dose initially. The dose can be adjusted by measuring TSH every 2­3 months.

Once the TSH is normalized and the patient is established on a stable dose of L-thyroxine, TSH monitoring can be done annually. With progression to complete thyroid failure, there is usually a need to increase the thyroxine dose with time. In diabetic patients with underlying coronary artery disease, L-thyroxine therapy may exacerbate angina by increasing myocardial contractility and heart rate. Therefore, it is best to start with a low dose, such as 25 µg daily, and increase slowly by monthly increments of 25 µg while monitoring the patient's clinical status and serum TSH levels.

Treatment of subclinical hypothyroidism should be considered if 1) patients have elevated serum LDL cholesterol that is worsened by the hypothyroidism, or 2) they have detectable serum anti-TPO antibodies, because the progression to frank hypothyroidism is high in this group, or 3) they are symptomatic.

Because hyperthyroidism can cause serious adverse effects on glycemic control and possibly worsen pre-existing coronary artery disease, it is desirable to consider definitive treatment with radioactive iodine therapy whenever possible. There is no contraindication to the use of antithyroid medications in diabetic patients, but the long-term remission rate of Graves' disease is <40%. Patients with toxic multi-nodular goiters or an autonomously functioning thyroid nodule should be definitively treated by radioactive iodine or surgery.

Conclusion
Thyroid dysfunction is common in diabetic patients and can produce significant metabolic disturbances. Therefore, regular screening for thyroid abnormalities in all diabetic patients will allow early treatment of subclinical thyroid dysfunction. A sensitive serum TSH assay is the screening test of choice. In type 1 diabetic patients, it is helpful to determine whether anti-TPO antibodies are present. If these are present, then annual TSH screening is warranted. Otherwise, a TSH assay should be done every 2­3 years. In type 2 diabetic patients, a TSH assay should be done at diagnosis and then repeated at least every 5 years.


References

1. _{Roos, Annemieke, et. al. "Thyroid Function Is Associated with Components of the Metabolic Syndrome in Euthyroid Subjects," The Journal of Clinical Endocrinology & Metabolism Vol. 92, No. 2 491-496.}
2. _{Mayo Clinic, "Metabolic Syndrome," Mayo Foundation for Medical Education and Research, 1998-2007}
3. ^ Clinical Case - Anterior Triangle of the Neck.
4. ^ Yalçin B., Ozan H. (February 2006). "Detailed investigation of the relationship between the inferior laryngeal nerve including laryngeal branches and ligament of Berry". Journal of the American College of Surgeons 202 (2): 291–6. doi:10.1016/j.jamcollsurg.2005.09.025. PMID 16427555. 
5. ^ Lemaire, David (2005-05-27). "eMedicine - Thyroid anatomy". http://www.emedicine.com/ent/topic532.htm. Retrieved 2008-01-19. 
6. ^ Kamath, M. Aroon. "Are the ligaments of Berry the only reason why the thyroid moves up with deglutition?". Doctors Lounge Website. http://www.doctorslounge.com/index.php/blogs/page/13485. Retrieved August 24, 2010. 
7. ^ Venturi, S; Donati, FM; Venturi, A; Venturi, M (2000). "Environmental iodine deficiency: A challenge to the evolution of terrestrial life?". Thyroid : official journal of the American Thyroid Association 10 (8): 727–9. doi:10.1089/10507250050137851. PMID 11014322. 
8. ^ Küpper FC; Carpenter LJ; McFiggans GB et al. (2008). "Iodide accumulation provides kelp with an inorganic antioxidant impacting atmospheric chemistry" (Free full text). Proceedings of the National Academy of Sciences of the United States of America 105 (19): 6954–8. doi:10.1073/pnas.0709959105. PMC 2383960. PMID 18458346. http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=2383960. 
9. ^ Venturi, S; Bégin ME (2010). "Thyroid Hormone, Iodine and Human Brain Evolution". In Cunnane S; Stewart K. Environmental Influences on Human Brain Evolution. John Wiley & Sons. pp. 105–124. ISBN 978-0-470-45268-4. 
10. ^ Brown-Grant, K. (1961). "Extrathyroidal iodide concentrating mechanisms". Physiol Rev. 41 (1): 189. http://physrev.physiology.org/cgi/reprint/41/1/189.pdf. 
11. ^ Spitzweg, C., Joba, W., Eisenmenger, W. and Heufelder, A.E. (1998). "Analysis of human sodium iodide symporter gene expression in extrathyroidal tissues and cloning of its complementary deoxyribonucleic acid from salivary gland, mammary gland, and gastric mucosa". J Clin Endocrinol Metab. 83 (5): 1746. doi:10.1210/jc.83.5.1746. PMID 9589686. 
12. ^ Banerjee, R.K., Bose, A.K., Chakraborty, t.K., de, S.K. and datta, A.G. (1985). "Peroxidase catalysed iodotyrosine formation in dispersed cells of mouse extrathyroidal tissues". J Endocrinol. 2: 159. 
13. ^ ^{a b} Page 493 (Table 33-3) in: Eugster, Erica A.; Pescovitz, Ora Hirsch (2004). Pediatric endocrinology: mechanisms, manifestations and management. Hagerstwon, MD: Lippincott Williams & Wilkins. ISBN 0-7817-4059-2. 
14. ^ Zoeller RT (April 2003). "Transplacental thyroxine and fetal brain development". J. Clin. Invest. 111 (7): 954–7. doi:10.1172/JCI18236. PMC 152596. PMID 12671044. http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=152596. 
15. ^ Berbel P, Navarro D, Ausó E, Varea E, Rodríguez AE, Ballesta JJ, Salinas M, Flores E, Faura CC et al. (2010). "Role of late maternal thyroid hormones in cerebral cortex development: an experimental model for human prematurity". Cereb Cortex 20 (6): 1462–75. PMID 19812240. http://cercor.oxfordjournals.org.libproxy.ucl.ac.uk/cgi/reprint/20/6/1462. 
16. ^ Fawcett, Don; Jensh, Ronald (2002). Bloom & Fawcett's Concise Histology. New York: Arnold Publishers. pp. 257–258. ISBN 0-340-80677-X. 
17. ^ Thyroid Problems eMedicine Health. Retrieved on 2010-02-07
18. ^ Thyroid Disorders Information MedicineNet. Retrieved on 2010-02-07
19. ^ Treatment for Thyroid disease Retrieved on 2010-02-07
20. ^ Thyroid Disorders overview Merck Sharpe & Dohme. Retrieved on 2010-02-07
21. ^ Yamamoto M, Shibuya N, Chen LC, Ogata E (February 1988). "Seasonal recurrence of transient hypothyroidism in a patient with autoimmune thyroiditis". Endocrinol. Jpn. 35 (1): 135–42. PMID 3396511. 
22. ^ Hidaka Y, Amino N, Iwatani Y, Itoh E, Matsunaga M, Tamaki H (December 1993). "Recurrence of thyrotoxicosis after attack of allergic rhinitis in patients with Graves' disease". J. Clin. Endocrinol. Metab. 77 (6): 1667–70. doi:10.1210/jc.77.6.1667. PMID 8263157. http://jcem.endojournals.org/cgi/pmidlookup?view=long&pmid=8263157. 
23. ^ ^{a b} How Your Thyroid Works: A Delicate Feedback Mechanism. Updated 2009-05-21.
24. ^ ^{a b} The thyroid gland in Endocrinology: An Integrated Approach by Stephen Nussey and Saffron Whitehead (2001) Published by BIOS Scientific Publishers Ltd. ISBN 1-85996-252-1 .
25. ^ References used in image are found in image article in Commons:Commons:File:Thyroid_system.png#References.
26. ^ Boron WF, Boulpaep E (2003). "Chapter 48: "synthesis of thyroid hormones"". Medical Physiology: A Cellular And Molecular Approaoch. Elsevier/Saunders. pp. 1300. ISBN 1-4160-2328-3.
27. Gay J. Canaris, MD, MSPH; Neil R. Manowitz, PhD; Gilbert Mayor, MD; E. Chester Ridgway, MD The Colorado Thyroid Disease Prevalence Study Arch Intern Med. 2000;160:526-534.
28. Mary Shomon, Living Well With Hypothyroidism: What Your Doctor Doesn't Tell You. . . That You Need to Know (New York Harper Collins, 2002)
29. Ridha Arem,  The Thyroid Solution : A Mind-Body Program for Beating Depression and Regaining Your Emotional and Physical Health, (New York: Ballantine Books,1999)
30. Raymond Peat Newsletter "Unsaturated Vegetable Oils Toxic” 1996
31. P. Fort, N. Moses, M. Fasano, T. Goldberg and F. Lifshitz “Breast and soy –formula feeding in early infancy and the prevalence of autoimmune thyroid disease in children”’J. Am. Col. Nutr. 1990;(9):164-167.
32. Daniel R. Doerge, Hebron C. Chang, “Inactivation of thyroid peroxidase by soy isoflavones in vitro and in vivo” Journal of Chromatography B Vol. 777 (1, 2); 25; September 2002: 269-79
33. M.T. See and J. Odle, “EFFECT OF DIETARY FAT SOURCE, LEVEL, AND FEEDING INTERVAL ON PORK FATTY ACID COMPOSITION” 1998-2000 Departmental Report, Department of Animal Science, ANS Report No. 248 - North Carolina State University
34. Raymond Peat Newsletter "Unsaturated Vegetable Oils Toxic” 1996