Feeling Sluggish? Check Your Thyroid
The thyroid gland hoards its hormones, whose sustained action in our bodies is vital for our health. Their main functions are to increase metabolic rate and to increase the rate and strength of the heartbeat. Ordinarily, the levels of these hormones are tightly regulated, ensuring an even metabolic keel as we navigate life’s turbulent waters. The levels can, however, go awry: overproduction leads to hyperthyroidism, and underproduction leads to hypothyroidism. The latter is more common; women are more susceptible than men, and in both sexes the incidence increases with age
Subclinical Hypothyroidism, a Subtle Disease . . .
The function of thyroid-stimulating hormone (TSH), also known as thyrotropin, is to stimulate the thyroid gland’s production of its principal hormone, thyroxine, which plays a central role in regulating our energy metabolism, among other things. But how can elevated TSH levels predict the likelihood (though never the date) of a heart attack? How, for that matter, can they even predict the likelihood of a heart attack’s common precursor, coronary artery disease, which is a less dramatic but nonetheless serious condition?
This is a subtle disease in which thyroid function is lower than it should be for optimal health, but not so low as to qualify as conventional (clinical) hypothyroidism, an overt disease in which thyroid function is measurably below the normal range.
Hypothyroidism, commonly known as “low thyroid,” entails a wide range of mostly common symptoms, including sluggishness, weakness, depression, low blood pressure, low heart rate, high cholesterol, weight gain, constipation, aching joints, poor memory, sensitivity to cold, declining libido, dry skin, and brittle nails and hair. In subclinical hypothyroidism, these symptoms are either totally absent or so subdued and gradual in onset that they can easily be overlooked, attributed to something else, or dismissed as elements of “normal aging.” Here is a more precise definition of subclinical hypothyroidism (SCH) than that given above: SCH is a disease in which TSH levels are elevated, but thyroxine levels are within the normal range (albeit usually near the low end of that range). Clearly, something is amiss with thyroid function when it takes an excessive amount of TSH to produce normal amounts of thyroxine.
The Thyroid Gland as a Clogged Air Filter
Consider a furnace of the kind you may very well have in your home. Natural gas is piped into the furnace, where it’s burned, producing carbon dioxide and water vapor. Some of the heat of combustion is transferred, via the heat exchanger, to air that’s drawn in through the inlet duct and expelled via the outlet duct to heat your house. Inside the furnace housing, between these ducts, is an air filter that traps dust from the inlet so that the heated outflow is clean.
With time, the air filter will gradually become clogged. This will retard the airflow and require the furnace to work longer and longer to force enough warm air into your house to maintain the desired temperature. You’ll probably still get all the heat you want (normal output), but it will take more and more gas to provide it (increased input), and you’ll see the evidence of that in your steadily mounting gas bills.
Thyroid function works similarly. Here the pituitary hormone TSH is the incoming “gas,” your thyroid gland is the “furnace,” and the thyroid hormone thyroxine is the outgoing “heat.” As long as your thyroid is functioning normally, your TSH and thyroxine levels will both fall within normal ranges, and you’ll be fine. If, however, some aspect of your thyroid’s inner functioning (the “air filter”) becomes degraded in some way, the biochemical pathway from TSH to thyroxine will become “clogged,” and it will take more and more TSH to stimulate the normal output of thyroxine.
When your TSH levels are elevated but your thyroxine output is normal, you have subclinical hypothyroidism (SCH). You may not know it, but your body knows it, because it has to pay the price (the “gas bill”) for the increasing amounts of TSH in your system.
And what is the price? It’s something far more precious than money: it’s your health, which will gradually be degraded by a poorly functioning thyroid gland. As the article shows, one consequence of SCH is a substantially increased risk for coronary artery disease (CAD), a serious, life-threatening condition.
You can spend a few dollars to replace the air filter in your furnace, but you can’t replace your thyroid gland, nor can you buy your health back. You can, however, maintain it in a better state by supplementing with whole natural thyroid, which might help reduce your risk for CAD.
SCH Should Be Treated
SCH is an age-related disease. Its incidence in the adult population of the United States is estimated to be 4.3%; its prevalence is about 10% in women over 60 years of age, and somewhat less than that in men.1 During the century or so since SCH became recognized as a disease, most physicians believed that it did not require treatment, especially since its symptoms-if any-are so mild. Their lack of concern is giving way, however, to a newfound appreciation for the fact that SCH is a “stealth” disease whose long-term consequences, especially on cardiovascular function, can be severe.
Thus, more and more physicians are embracing the idea that SCH should be treated. Treatment is exceptionally easy and effective: it usually consists of synthetic thyroxine, which is chemically identical to natural thyroxine. (Both are also called levothyroxine, the form in which thyroxine is found in our bodies.) Most physicians who practice alternative and complementary medicine, however, recommend using extracts of whole natural thyroid from livestock, which contains not just thyroxine but also the other hormones produced by the thyroid gland, in their biologically normal proportions. (As with synthetic thyroxine, the animal hormones are chemically identical to their human counterparts.)
A vexing problem for all physicians is that studies on the association between SCH and cardiovascular disease have been confusing and contradictory. Some studies have shown no association, whereas others have shown strong associations. Among the latter, there has been no universal agreement on which manifestations of cardiovascular disease are associated with SCH, but many of them have pointed to high total cholesterol and LDL-cholesterol (the “bad cholesterol”). Others have pointed to factors such as elevated levels of C-reactive protein (a marker of inflammation that’s implicated in cardiovascular disease) and a state of abnormally increased blood coagulability (a tendency to form clots).
Researchers Separate Wheat from Chaff
Recently a team of researchers from the United States and Switzerland tried to resolve some of the confusion by performing a meta-analysis-a systematic, rigorous analysis of the pooled data from a number of previously published studies; this allows a more nearly definitive conclusion to be reached than is possible from any individual study.1 Their objective was to determine the extent to which SCH is a risk factor for coronary artery disease (CAD), a category of cardiovascular disease that results from obstruction of the coronary arteries.* This life-threatening condition leads to myocardial ischemia, or insufficient blood flow to the heart muscle.
A search of the literature in English, French, and German between January 1966 and April 2005 turned up 753 reports of potential relevance. Of these, 719 were eliminated for any number of more or less obvious reasons, leaving 34 to be evaluated more closely. In that process, 20 more were eliminated owing to serious flaws in design or execution. That left 14 studies that met the eligibility criteria for inclusion in the meta-analysis. They encompassed a total of 13,011 men and women with SCH, the great majority of whom were 55 or older.
The total number of CAD outcomes recorded was 1362. These outcomes were: heart attack; angina pectoris (chest pain); acute coronary syndrome (an umbrella term used to cover any group of clinical symptoms compatible with acute myocardial ischemia); revascularization (surgical restoration of blood supply to the heart, as a result of CAD); significant coronary stenosis (a narrowing of the cross- sectional area of a coronary artery by 50% or more); and death caused by CAD in particular or cardiovascular disease in general.
SCH Leads to Increased Risk for CAD
Of the 14 studies included in the meta-analysis, most had shown a trend toward an increased risk for CAD in patients with SCH, but these findings reached statistical significance in only four studies.
In the meta-analysis, however, the result of pooling all the data (with much number crunching to make them comparable with each other) was that the overall risk for CAD was increased by a substantial 65%.
This appears to provide striking confirmation of what had long been suspected by some, and believed by others, despite the contradictory evidence. That SCH should be linked with CAD in this way is not surprising, considering that thyroid hormones interact strongly with the catecholamine hormones adrenaline and noradrenaline, which play profoundly important roles in cardiovascular function.
A Tale of Two Hormones
There are two thyroid hormones: tetraiodothyronine, commonly called thyroxine (T4), which contains four iodine atoms, and triiodothyronine (T3), which contains three iodine atoms. Two other compounds produced by the thyroid, diiodothyronine (T2) and monoiodothyronine (T1) are chemical precursors in the synthesis of T4 and T3. They are not secreted except in negligible amounts and are not believed to have any hormonal activity, although it’s possible that some hitherto undiscovered activity may exist.
The thyroid gland’s hormone output consists predominantly of T4, and some of that is slowly converted (mainly in the liver) to T3. Thus, the large, stable “pool” of T4 acts as a kind of reservoir for the steady production of T3. Both hormones are biologically active, but T3 is about 3-4 times more active than T4.
Thyroid hormones serve three important functions: (1) regulation of cellular energy metabolism; (2) control of cell differentiation and growth; and (3) modification of the actions of other hormones, especially adrenaline and noradrenaline, which play profoundly important roles in cardiovascular function. This third function of the thyroid hormones magnifies their already pervasive influence throughout the body.
Thyroid hormones are active from fetal life to the end of life, but their greatest activity occurs in cold weather, during childhood and adolescence, during pregnancy,* and during periods of emotional stress, which can wreak biochemical havoc on many bodily systems.
*The thyroid swells during pregnancy, a fact that some African tribes exploit as an early pregnancy test. The bride is fitted with a tight but delicate necklace. As the thyroid swells, the necklace will soon break, indicating pregnancy.
What determines thyroid activity at any given time is the pituitary, which secretes (among other things) thyroid-stimulating hormone (TSH).
True to its name, TSH causes the thyroid gland to produce and release thyroid hormones into the circulation. This system has an ingenious self- regulating mechanism: the thyroid hormones act on the pituitary gland, inhibiting the production of TSH.
Thus, if thyroid hormone levels become too high, TSH production drops, putting the brakes on further hormone production; conversely, if the hormone levels become too low, TSH production rises, causing a boost in thyroid output.
Because this feedback loop is such a sensitive regulator of thyroid hormone levels, TSH provides a simple and useful initial diagnostic test for thyroid function.
If TSH levels are normal, the thyroid hormone levels is likely but not necessarily be normal too, and no further testing is necessary.
If TSH levels are above normal and thyroid hormone levels are below normal, it indicates overt hypothyroidism (and vice versa for overt hyperthyroidism).
But If TSH levels are above normal and thyroid hormone levels are within normal limits, it indicates subclinical hypothyroidism (and vice versa for subclinical hyperthyroidism).
Panaxea’s Special T contains forskolin (an extract of Coleus forskohlii) which is shown to be effective with hypothyroidism – click here for further research. Forskolin stimulates the release of thyroid hormone. For more information about Special T, or any of the Panaxea range please call 1300 133 807 and speak to our chief practitioner consultant, Melanie Alexander. To shop online and to view the latest natural medicine research please visit www.panaxea.com with your username and password.
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1. Rodondi N, Aujesky D, Vittinghoff E, Cornuz J, Bauer DC. Subclinical hypothyroidism and the risk of coronary heart disease: a meta-analysis. Am J Med 2006;119:541-51.