The most common symptoms that come to mind when someone talks about hypothyroidism (low levels of thyroid hormones) are weight gain, fatigue, cold intolerance and depression  . However hypothyroidism is also associated with increased frequency of heart failure , coronary heart disease , dementia , insulin resistance , and dilated cardiomyopathy  , and increased risk of breast cancer . In addition it is quite common to also find hypothyroid disease in people that have other medical conditions including cancer , schizophrenia , chronic hepatitis C infection , bipolar disorders , other psychiatric illnesses , and adrenal insufficiency .
So hypothyroidism can occur by itself, or it can occur along with other diseases.
Traditionally, someone has been considered to be hypothyroid if they had lab tests that suggest they have low levels of thyroid hormones. However, there are other conditions in which there is low thyroid function, even when traditional lab tests are normal.
These conditions include subclinical hypothyroidism, thyroid hormone resistance, and reverse T3 elevation, each of which will be discussed briefly in this article.
When a condition, such as hypothyroidism, occurs with another disease it is called a comorbidity (co = with, together & morbidity = disease, sickness). Hypothyroidism has a very high comorbidity with other diseases – it often shows up with other diseases. This is an important point to grasp because if hypothyroidism must also be recognized when trying to treat other hormone imbalances. Menopause, andropause, PMS, and insulin resistance and even adrenal fatigue & adrenal dysfunction are all very difficult to treat if there is also a comorbidity of hypothyroid function. This is not to say that everyone with menopause, andropause, PMS, etc. also have hypothyroidism. But any healthcare professional who has worked with hormone health will tell you this: if a patient is having trouble improving with proper therapies, then suspect hypothyroid comorbidity. In truth, there are many other common comorbidities – some as simple as not getting enough sleep – but hypothyroidism is a common comorbidity. However, hypothyroidism can occur by itself as the primary cause of illness. When Unfortunately it is not always recognized, and may actually go undiagnosed for years.
When the cause of hypothyroidism is due to actual damage to the thyroid tissue it is called primary hypothyroidism. Most primary hypothyroidism is due to autoimmune hypothyroidism (Hashimoto’s disease), is the most common thyroid disease in the United States. It is an inherited condition that affects approximately 14 million Americans and is about 7 times more common in women than in men. While autoimmune hypothyroidism is a common condition, one study suggests that up to 10 percent of the population may have subclinical hypothyroidism , while others report that the prevalence of subclinical hypothyroidism is about 4 to 8.5 percent, but may be as high as 20 percent in women older than 60 years .
In primary hypothyroidism there is usually increased thyroid-stimulating hormone (TSH), which is secreted by the pituitary gland, as the body tries to stimulate the production of thyroid hormones. Recent review of research validates clinical observation that TSH resistance can be a cause of hypothyroidism . This is why Thyro-Mend™ was formulated with a specific coleus extract to increase thyroid function independent of TSH.
When the hypothyroidism is due to the pituitary gland not making enough thyroid-stimulating hormone (TSH). While that morphological form of this hypothyroidism (with actual damage to damage to the pituitary gland) is not as common, secondary hypothyroidism may also be due to a dysfunction of the hypothalamic-pituitary-thyroid (HPT) axis due to stress or disease . This is why Thyro-Mend™ was formulated with Withania and other adaptogens to improve HPT function.
One definition of subclinical hypothyroidism is defined as TSH above the upper reference limit with normal levels of free T4. Several investigations have shown that patients with subclinical hypothyroidism have subtle symptoms and signs of mild thyroid failure, that subclinical hypothyroidism can have significant effects on peripheral target organs, and there is a high rate of progression towards overt hypothyroidism   .
Unfortunately, some researchers downplay the significance of subclinical hypothyroidism and actually advise against the routine treatment of patients with TSH levels that indicated subclinical hypothyroidism. However, this may be for a number of reasons including too much attention is given on TSH, not enough attention being given to reverse T3 and the lack of understanding about thyroid hormone resistance.
Thyroid Hormone Resistance
The progressive worsening of thyroid function in subclinical hypothyroidism may be explained in part by the presence of T3 nuclear receptors (TR) in thyroid cells, which demonstrate autocrine actions of thyroid hormones, and suggests that decreased thyroid function propagates further decrease in thyroid function . In effect, a resistance to thyroid hormones can develop, just as we observe in insulin resistance. Even thyroid tissue requires proper function of thyroid hormones to perform the act of making those very hormones.
Although suboptimal thyroid function may be sub-classified into hypothyroidism and subclinical hypothyroidism, they both can present with subjective and objective data that indicate deterioration in quality of life and increased risks of diseases.
Reverse T3 Elevation
Reverse T3 is exactly what it sounds like; it is a backwards T3 molecule that has the reverse actions of T3. So, reverse T3 will slow down the metabolism. While it is normal to have some reverse T3, too much of it can cause a person to have hypothyroid signs and symptoms – even if other lab tests are normal. In fact, in a recent study or over 350 people who were considered “euthyroid” (normal thyroid function based on TSH), researchers found excessive reverse T3 in people who had insulin resistance – one of the signs of hypothyroidism. Reverse T3 becomes elevated due to starvations (or severe dieting), severe viral infections, some liver diseases, as well as extreme stress – such as surgery or medical conditions requiring intensive care. In addition, it can be elevated in some cases of heart failure. I have also seen it elevated in a number of less severe cases, such as some cases of chronic fatigue, and in hypothyroid cases that did not respond to thyroid replacement therapy.
Complete Thyroid Health
There are seven specific actions involved in the production and activity of thyroid hormones. Each of these actions is required to maintain optimal thyroid hormone health. These actions include consistent dietary intake of bioavialable iodine, uptake of iodine by thyroid cells, production and secretion of thyroid hormones (T3 & T4) by thyroid cells, conversion of T4 to T3 by liver cells, maintaining sufficient number of thyroid receptor proteins, pairing of two different receptors (heterodimerization), and expression in target genes. If any of those action is not performed, then optimal hormone health will not occur.
Supporting and restoring proper function each of these seven actions can result in a lower incidence of hypothyroid comorbidity, primary hypothyroidism, secondary hypothyroidism, subclinical hypothyroidism, thyroid hormone resistance, and reverse T3 elevation. The seven specific actions required for proper thyroid function can be achieved through phytotherapeutic support of thyroid function.
Complete thyroid health is dependent on the health of other body systems, and following the hormone health guidelines with attention being given to fundamental health needs such as a healthy diet and lifestyle, and regular intake of a high-grade multiple vitamin-mineral formulation, as well as essential fatty acids. Complete thyroid health requires both the support of healthy thyroid tissue, and support of optimal health in every tissue that is affected by thyroid hormones. This is best accomplished through the use of Thyro-Mend™, as discussed in the Thyroid Hypofunction Protocol.
© Dr Joseph J Collins, RN, ND, 2007 – 2011