Thyroid function

Changes with age…

Changes in thyroid structure and function occur with aging. Structurally, some glandular atrophy and fibrosis occur with nodularity and increasing inflammatory infiltrates. These infiltrative changes may reflect age-related auto-immune damage.
Changes relative to thyroid hormone and its function are more difficult to assess. One difficulty is finding older adults who are free of all systemic and thyroid-related illness, so that the resulting changes can be attributed to aging. Much of the available data is contradictory. Most evidence, however, supports the following age-related changes:

1. T4 secretion and turnover are decreased.
2. Plasma levels of T3 decline, especially in men.
3. Hypothyroidism is seen with increasing frequency as age advances.
4. Overall TSH secretion is diminished.
5. Responsiveness of plasma TSH concentration to TRH administration is reduced, especially in men.

In addition, the average dose for Thyroid Hormone (TH) replacement appears to be lower in elderly persons because the peripheral metabolism of TH decreases with age. TH must be replaced slowly and very carefully in elderly individuals with coronary artery disease to prevent angina and myocardial infarction. Clinical signs of thyroid disease are more difficult to detect in elderly persons.
Thyrovus® is designed for people with hypothyroidism. These persons may have a problem converting thyroxine (T4) into triiodothyronine (T3). The thyroid function and control system is a complex system of the human body with several feedback loops and controls. Not all of the details and functions of this system are known completely.
The thyroid hormones are iodothyronines, compounds formed by the coupling two iodinated tyrosine molecules in an ether linkage. The predominant hormones include the following: Thyroxine (T4), Triiodothyronine (T3) and Reverse T3 (rT3). The levels of these hormones are controlled by Thyroid Releasing Hormone (TRH) and Thyroid Stimulating Hormone (TSH). Although a very complex system, it is well accepted that the body produces more TSH if there is not sufficient T3 available for the body. TSH secretion is inhibited by high serum T4 and T3 levels. High TSH levels therefore can be seen as a marker for low T3 levels which is the most potent thyroid hormone. If the body lacks sufficient levels of T3, the hypothalamus will release more TRH, which stimulates the pituitary to produce and release more TSH. This will stimulate the thyroid gland to release more T4 (and some T3). T4 is the major secretory product of the thyroid gland. The predominant pathway for its metabolism is progressive deiodination. Because the thyroid secretes very little T3, 80% of the circulating T3 is produced by peripheral deiodination of T4 in the liver. If more T4 is produced, more T3 can be produced from T4. If the conversion of T4 into T3 is not efficient, more T4 is necessary.

Rejuvenal Thyrovus® is designed to improve the conversion rate from T4 into T3. The ingredients are well selected to stimulate this process, but may also improve T3 receptors. After using Thyrovus®, TSH levels should drop as an indicator of the resulting effect. Many people suffer from symptoms such as cold hands and feet, low body temperature, sensitivity to cold, a feeling of always being chilled, headaches, insomnia, dry skin, puffy eyes, hair loss, brittle nails, lethargy, somnolence, mental slowness, muscle aches, joint aches, constipation, mental dullness, fatigue, frequent infections, prolonged reflex times, hoarse voice, ringing in the ears, dizziness, loss of libido, and weight gain, which is sometimes uncontrollable. Approximately 65 percent of the U.S. population is overweight; 27 percent is clinically obese. Research is pointing to the fact that an underactive thyroid might be the number one cause of weight problems, especially among women.

Thyroid Hormones and Methylmercury Toxicity.

Soldin OP, O'Mara DM, Aschner M.
Departments of Medicine, Oncology and Physiology, Center for Sex Differences, Lombardi Comprehensive Cancer Center, LL, S-166, Georgetown University Medical Center, 3800 Reservoir Road, N.W., Washington, DC, 20057, USA, os35@georgetown.edu.

Thyroid hormones are essential for cellular metabolism, growth, and development. In particular, an adequate supply of thyroid hormones is critical for fetal neurodevelopment. Thyroid hormone tissue activation and inactivation in brain, liver, and other tissues is controlled by the deiodinases through the removal of iodine atoms. Selenium, an essential element critical for deiodinase activity, is sensitive to mercury and, therefore, when its availability is reduced, brain development might be altered. This review addresses the possibility that high exposures to the organometal, methylmercury (MeHg), may perturb neurodevelopmental processes by selectively affecting thyroid hormone homeostasis and function.

On the importance of selenium and iodine metabolism for thyroid hormone biosynthesis and human health.

Schomburg L, Köhrle J.
Institut für Experimentelle Endokrinologie und Endokrinologisches Forschungs-Centrum der Charité EnForCé, Charité Campus Virchow-Klinikum, Charité Universitätsmedizin, Berlin, Humboldt-Universität zu Berlin, Berlin, Germany. Fax: +49-30-450-524922.

The trace elements iodine and selenium (Se) are essential for thyroid gland functioning and thyroid hormone biosynthesis and metabolism. While iodine is needed as the eponymous constituent of the two major thyroid hormones triiodo-L-thyronine (T3), and tetraiodo-L-thyronine (T4), Se is essential for the biosynthesis and function of a small number of selenocysteine (Sec)-containing selenoproteins implicated in thyroid hormone metabolism and gland function. The Se-dependent iodothyronine deiodinases control thyroid hormone turnover, while both intracellular and secreted Se-dependent glutathione peroxidases are implicated in gland protection. Recently, a number of clinical supplementation trials have indicated positive effects of increasing the Se status of the participants in a variety of pathologies. These findings enforce the notion that many people might profit from improving their Se status, both as a means to reduce the individual health risk as well as to balance a Se deficiency which often develops during the course of illness. Even though the underlying mechanisms are still largely uncharacterised, the effects of Se appear to be exerted via multiple different mechanisms that impact most pronounced on the endocrine and the immune systems.