Thyroid Deficiency: The Great Masquerader

Welcome to my NETrageouz! Medical Hub...

So glad you could join me in my premier issue covering the subtle effects of aging on our hormones, especially that sneaky little thyroid gland!

A little disclaimer here, please understand that by offering the following information I am in NO WAY establishing a patient-physician relationship, I'm not making a diagnosis for YOU, and I'm not suggesting that you quit taking your meds just ‘cause I SAID SO online. Okey dokey?

In women, menopause is that well known condition whereby the ovaries sputter & falter over the course of around a decade (otherwise known as the perimenopausal stage) just before delivering their final farewell & drifting off into eternal hibernation.

In men, this fanfare and delayed 'good-bye' phase is far more subtle, yet every bit as clever in its masquerade. In effect, this waning away of testicular function is the major cause of a cascade of hormonally induced upheavals. We will talk much more about these sexual hormones in articles to come.

One of my favorite hormonal tricksters is the thyroid gland, a little bow-tie shaped gland located in the neck. Its main function is to produce thyroid hormones, which control the body's metabolism. This little gland, to this day, is the cause of major debates in the medical literature.

In fact, there is lots of evidence suggesting that the standard blood test reference ranges may cause many cases of hypothyroidism to be missed. Recently, many clinicians and scientists agree that the upper limit of the established "normal" range is too high to permit detection of people with significantly low thyroid function. In reality, a TSH reading of more than 2.0 may indicate lower-than-optimal thyroid hormone levels. Patients in this group have an increased chance of developing frank hypothyroidism (a TSH greater than 5.5) and may also suffer from symptoms such as depression and weight gain. One study found that TSH levels of more than 4.0 are associated with increased risk of heart disease. Based on the published clinical data, I always perform a more complete thyroid evaluation to rule out thyroid deficiency as a cause of common age-associated maladies such as depression, fatigue, and unwanted weight gain. For these reasons, I use the 2.0 - 2.5 TSH levels as my cut off for treating sub clinical thyroid deficiency.

As physicians we often find ourselves in a dilemma of whether to treat or not to treat, as we ask ourselves the following...

"What is the meaning of this lab result?"

"Where should I cut off the normal values & make the diagnosis of thyroid failure in this patient?"

"Should I treat sub clinical thyroid failure?" (The perimenopausal state, so to speak, of your thyroid)

"Shall I wait until the thyroid is totally shut down to treat this patient?"

Oftentimes we physicians are left working out the answers of what to do for the patients while the rest of the medical societies "duke It out" to decide when and how to change lab value cut-offs, medical guidelines, yada yada... You get my point.

In my practice I have chosen to the proactive approach and "listen to my patient" tell the story. It's the story that tells me when to begin offering treatment strategies even more than the labs do.

SO anyways, this thyroid gland uses iodine (mostly available from the diet in foods such as seafood, bread, and salt) to produce thyroid hormones. The two most important thyroid hormones are thyroxine (T4) and triiodothyronine (T3). While a small amount of T3 is actually made in the thyroid gland, most of it is converted in the tissues from the T4 released from the thyroid gland into the blood. T3 is the active hormone that affects the metabolism of cells.

Too much (hyperthyroidism) overstimulates the body, resulting in increased heart rate, anxiety, and weight loss. While too little (hypothryoidism) can cause depression, sluggishness, weight gain, and heart failure.

Hyperthyroidism is rare (affecting about 1 percent of the population), while mild, subclinical hypothyroidism may be much more common than most people think.

One side effect of thyroid deficiency that I see far too often in my office is high cholesterol. It is very possible that many people are being prescribed cholesterol-lowering statin drugs (Lipitor, Zocor, Crestor, etc) while their underlying problem-low thyroid function-goes unaddressed. That is one of the things I consider when I am on the fence about treating a patient with borderline deficiencies.

The most common cause of overt hypothyroidism in the United States is an autoimmune disorder known as Hashimoto's thyroiditis. This condition is characterized by an overactive immune system response that floods the thyroid gland with white blood cells that attack the gland. Hashimoto's thyroiditis is more common in women than in men, and there is a genetic component to the disease.

Worldwide, a lack of dietary iodine is the leading cause of hypothyroidism. Iodine is necessary for the synthesis of thyroid hormones. Since table salt was iodized in the United States, lack of dietary iodine has not been a major problem, though cases of iodine deficiency are still reported.

Besides iodine, thyroid function can be affected by a number of nutrients, including zinc and selenium. Deficiencies in either of these have been shown to increase the risk of hypothyroidism.

Hypothyroidism is typically treated with supplemental thyroid hormones. There are a number of approaches to increasing thyroid hormone, including use of synthetic hormones (both T3 and T4) and natural desiccated thyroid hormone from animals. The choice of which form of thyroid hormone to use is an individual decision, to be made on the basis of blood tests and effectiveness of therapy. My personal favorite is desiccated, purified animal thyroid extract. It is a more biological and natural way of achieving the ideal balance of T3 to T4 ratios in the body.

"So, what are the consequences of low thyroid hormone levels?"

The vast majority of the thyroid hormone produced by the thyroid gland is T4. However, T4 has only a slight effect on the body's metabolic rate. The more active hormone is T3. To supply the necessary T3, the liver and other tissues convert T4 into T3.

T4 and T3 are essential for regulating metabolic processes throughout the body, including..

(1) maintaining the basal metabolic rate (burning calories!! YEAH...);

(2) making more glucose available to meet the elevated metabolic demands;

(3) stimulating new protein synthesis (making muscles!! YEAH...);

(4) increasing metabolism of lipids and conversion of cholesterol into bile acids, activating lipoprotein lipase, and increasing sensitivity of adipose tissue to hormones that stimulate the breakdown of fat (getting' rid of love handles!! YEAH...);

(5) increasing cardiac output and blood flow; and

(6) increasing neural transmission.

Untreated, chronic hypothyroidism can result in myxedema. This is a rare, life-threatening condition. Mental dysfunction, stupor, cardiovascular collapse, and coma can develop after the worsening of chronic hypothyroidism. In fact, the patient may even pass into a hypothermic coma and die. That is- the shutdown of your body's ability to burn calories to generate heat can actually shut down life-sustaining processes and put you in a coma resulting in death.

Additional possible complications of chronic hypothyroidism include:

• Depression and psychiatric disorders.
• Panic attacks,
• Anxiety,
• Depression,
• Phobias, and
• Obsessive compulsive disorders

All of these are commonly encountered in hypothyroidism and hyperthyroidism. In fact, subclinical hypothyroidism is the most commonly encountered organic cause of depression. And in as many cases seen of patients on cholesterol meds with untreated thyroid deficiencies I treat, I find and fix the depressed patients on multiple anti depressant cocktails with unaddressed thyroid deficiencies.

• Reduced cardiac output.

In overt hypothyroidism, the ability of the heart to contract and pump blood to the body are decreased, while vascular resistance is increased (blood vessels clamp down causing high blood pressure). These changes also affect people with subclinical hypothyroidism, but to a lesser degree

• High blood pressure.

Hypothyroidism is often accompanied by diastolic hypertension that together with elevated cholesterol may promote atherosclerosis (clogged arteries!). Hypertension is very common in patients with lab evidence of hypothyroidism.

• High cholesterol.

Hypothyroidism is characterized by hypercholesterolemia and a marked increase in low-density lipoproteins (LDL) and apolipoprotein A. The apolipoprotein A is a new marker we use that signals that a patient is at risk for very early atherosclerosis, or clogging of the arteries. Both of these changes accelerate atherosclerosis, which causes coronary artery disease.

Subclinical hypothyroidism has been associated with dysfunction of the walls of all blood vessels, including aortic atherosclerosis and with myocardial infarction. Thyroid hormone replacement therapy may slow the progression of coronary artery disease because of its beneficial effects on lipids. This is another thing that I look for when deciding to begin treatment for subclinical thyroid dysfunction in my patients.

• Elevated C-reactive protein.

This is a marker of inflammation that we use. In fact, clinical and subclinical hypothyroidism are associated with increased levels of low-grade inflammation as indicated by elevated C-reactive protein and may be a risk factor for development of cardiovascular disease in younger men.

• Musculoskeletal system.

Hypothyroid patients may exhibit joint aches, effusions & pseudo gout (arthritis that mimics a gout attack but is not gout).

• Reproductive system problems.

In women, hypothyroidism is associated with menstrual irregularities, absence of ovulation, and infertility. In men, hypothyroidism is associated with abnormalities of testicular function.

• Pregnancy complications.

Subclinical and postpartum hypothyroidism is gaining recognition as serious health problems among women. In pregnancy, the fetus depends on the mother for adequate thyroid hormone. Postpartum thyroiditis (chronic inflammation of the thyroid gland) can develop in as many as one out of 10 women after giving birth.

"What about using nutrients to enhance thyroid function as an alternative and early intervention for subclinical thyroid deficiency?"

Absolutely, in fact when the deficiency is mild and the patient shows little risks such as the above mentioned. Nutrition is the first thing that I reach for to help my patients back to recovering function.

• Iodine and minerals.

Iodine is required by the body to form thyroid hormone, and iodine deficiency can lead to goiter (abnormal enlargement of the thyroid gland) and hypothyroidism. Currently, most cases of iodine deficiency occur in developing nations. In industrialized countries where iodized salt is used, it has been presumed that iodine deficiency is rare. In my opinion, we are all very much iodine deplete and most good minerals are simply ‘farmed out' of the soil due to lack of crop rotation and proper handling of the earth's reserves.

Vegetarians, are at risk of developing iodine deficiency, especially if they live in areas where the soil is low in iodine. Vegans, who do not eat iodine-enriched dairy products, are at an even higher risk .

Other minerals, including iron & zinc, are essential for normal thyroid hormone metabolism. Coexisting deficiencies of these elements can impair thyroid function.

Iron deficiency impairs thyroid hormone synthesis by reducing activity of iron-dependent thyroid peroxidase. Iron supplementation improves the efficiency of iodine supplementation. A study found that TSH has a significant effect on the concentration of iodine, selenium, and zinc in normal and altered human thyroid. The roles of iron, zinc, and copper in the thyroid are less well defined, but reduced intake of all these elements can damage thyroid hormone metabolism.

Zinc In animal studies, single and multiple deficiencies of iodine, selenium, and zinc have distinct effects on thyroid metabolism and structure. In animal studies, zinc deficiency was associated with decreased concentrations of T3 and free thyroxine by 30 percent compared with controls. Zinc may play a role in thyroid hormone metabolism in patients with low T3 and may contribute to conversion of T4 to T3 in humans.

Selenium is required for appropriate thyroid hormone synthesis, activation, and metabolism. Adequate selenium supports efficient thyroid hormone synthesis and metabolism and protects the thyroid gland from damage caused by excessive exposure to iodide. Selenium deficiency may seriously influence the generation of free radicals, the conversion of thyroxineT4 to T3, and the autoimmune process.

One study also found that selenium deficiency decreased the inflammation that is associated with autoimmune thyroiditis. During this study, female patients with autoimmune thyroiditis and elevated antithyroid antibodies were given selenium. At the end of the study, researchers found that a significant percentage of the patients had normalized their antibody concentrations.

• Vitamins

Newer research has suggested that antioxidant vitamins, such as vitamin C and vitamin E, can reduce the oxidative stress caused by hypothyroidism. In one animal study, vitamin E was shown to protect animals from increased oxidation and thyroid cell damage. Another study found that vitamin E reduced proliferation of goiter cells and auto-antibodies.

"What about using diet to enhance thyroid function as an alternative and early intervention for subclinical thyroid deficiency?"

Certainly! It is true that some foods contain substances that induce goiter formation and prevent the utilization of iodine. These foods include canola oil, cruciferous vegetables (cabbage, Brussels sprouts, broccoli, and cauliflower), corn, cassava, sweet potatoes, lima beans, and pearl millet. The actual content of the goitrogens in these foods is quite low, however, and cooking destroys it. Hypothyroid patients should also consider avoiding soy supplements.

When I detect early signs of thyroid deficiency, I place my patients on certain food restrictions, advice healthy lifestyle choices, and recommend a very complete line of multi nutrient formulas as a first attempt to correct the problem. I follow them back in 3 months and retest to see if any corrections have been made along with changes in weight and fat distribution. If you are interested in the line of supplements that I use and recommend, visit us online and contact us today.

As always diet, exercise and a good relationship with your private family physician are the key to your overall health and success.

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About the Author: Dr. Ana Hernandez is the editor/publisher of The Youthful Aging Center's Medical Tid Bits Online. The Youthful Aging Center specializes in the treatment & prevention of age related disease and in preventative alternative medicine for achieving physical & mental wellness through applied nutritional therapies and natural hormone re balancing.

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