Thyroid Gland Challenges
The largest of the endocrine glands, the one-half to one-ounce thyroid gland is almost twice as large in women on average as in men. Its overt function seems to be to manufacture, store, and release, under strict controls, thyroid hormones, mostly thyroxin (T4) and triiodothyronine (T3), in about a 4:1 ration. The two main iodine-bearing thyroid gland hormones are T4 (65% iodine) and T3 (59% iodine). In very low iodine intake situations, the T4:T3 ratio is reversed to 1:4. The thyroid is a dynamic gland, as Robbins explains: “From the physiologic standpoint, the thyroid gland is one of the most sensitive organs in the body. It responds to many stimuli and is in a constant state of adaptation. … During puberty, pregnancy, and physiological stress from any source, the thyroid gland increases in size and becomes more active functionally. Changes in size and activity may be observed during a normal menstrual cycle. This extreme functional changeability is manifest as transient hyperplasia of thyroidal epithelium (follicular cells) changing (to tall, columnar). When stress abates, involution obtains and normal follicular cell shape (roughly spherical) and function resume.” Increasingly, in our environment, the thyroid is forced to adapt to new stimuli and stresses, sometimes successfully, other times not.
Situational iodine deficiency regularly occurs in modern Americans as a result of both dietary peculiarities and the chronic use of fluoridated, chlorinated, bromated water supplies, internally and externally. Fluorine, chlorine, and bromine are all more chemically reactive than iodine; when in the body, they all tend to disrupt stable iodine molecules, displacing the iodine and causing its excretion. When experimental rats are fed high-bromine diets, the bromine enters their respective thyroid glands and replaces the iodine already there; the proportion of bromine in the thyroid glands of those rats is directly proportional to the amount of bromine in their diet.
We can lose iodine from these aggressive halides; our bodies have no known mechanisms for dealing with relatively large amounts of fluorides, chlorine, and bromine, since these substances are normally too reactive to be available in the so-called natural environment; our exposure is totally modern. Gaseous chlorine is regularly released from shower and tub water freshly drawn from water supply taps. We are exposed to bromine in pesticides, dough conditioners, and disinfectants for water in hot tubs and commercial spas. I recommend showering with the window open; I recommend bathing in tubs filled with the hottest water and allowed to out- gas while they cool to bearable temperature. Reduce your exposure to iodine-robbing halides for optimal thyroid health.
In addition, aspirin and other related salicylates, as well as anticoagulants like Warfarin (di-Coumerol), increase iodine excretion and can induce mild hypothyroidism. Always inquire of mild hypothyroid patients about aspirin and anticoagulant use.
Compounding these environmental challenges to the thyroid gland is the impact of the atomic age. Since 1945 every human has been repeatedly dusted with radioactive fallout from both acknowledged and unacknowledged nuclear explosions, nuclear power plant disasters, and, most insidious of all, the steady release of radioactive Iodine-131 from all nuclear weapons facilities and all nuclear power plants. The government-sponsored nuclear industry has released experimental quantities of radioactive iodine, cesium, and strontium into the atmosphere. Continual exposure to this incidental I-131 may be the origin of most current thyroid disorders.
It takes about 18 minutes for all the blood in the body to pass through the thyroid gland; it is the most thoroughly vascularized of all the endocrine glands. Most of our respective bodies are iodine conservative: we can absorb it through our skin in minutes when painted on. I have had participants demonstrate transdermal movement of iodine absorbed from clothing through the skin. Iodine is easily absorbed from the intestines in efficiencies up to 98% in very low-iodine diets. The radioactive iodine we are all breathing and eating is released in bursts as a product of nuclear fission, usually within legally allowable amounts. These allowed amounts are calculated on a per day basis rather than as high-amount bursts or episodes. This helps perpetuate the myth that the allowable releases are no health hazard. The episodic rather than regular release of I-131 means we get big hits and then none at all, especially in milk and milk products.
The reason that I-131 is so dangerous is that it has a relatively short half-life of about 8 days; this means it has a radiogenic life of about 60 days, and then the amount remaining is probably biologically insignificant. Although this short half-life is touted as a great thing for patients and incidental accumulators of I-131, the short half-life means that most I-131 taken into the body will decay in the body rather than being excreted. Rather than occurring over a relatively long time, the short half-life means a lot of radioactive decay of I-131 within the thyroid gland, releasing unavoidably molecular-destructive gamma radiation to nearby cell molecules. There is no safe dosage of gamma radiation inside cells. Therapeutically, I-131 is fed to patients to fry their thyroids with gamma radiation, released by radioactive decay of I-131.
Our bodies tend to be iodine aggressive in absorption and iodine conservative in excretion. If we are at all iodine deficient, we will readily take in radioactive I-131 and deposit it in our thyroid glands just as we do with non-radioactive I-127. If we have a full, ongoing whole-body complement of I-127, our bodies tend to not take up any I-131.
The major health problems from the Chernobyl nuclear disaster on or about 26 April 1986 are related to the releases of radioactive I-131 into the atmosphere and onto the soils, surface waters, plants, animals, and cities within 1000 miles of the Chernobyl site. Within 5 years, large increases in thyroid disorders of all sorts began to occur, directly attributable to Chernobyl I-131 releases. The worst is still developing since we know that the cancer rates from short-term radiation exposure tend to peak 20 to 30 years after a particular release episode.
Women are particularly at risk due to environmental agents depleting iodine reserves and other agents exposing them to radioactive I-131. After the thyroid gland, the distal portions of the human mammary glands are the heaviest users/concentrators of iodine in tissue. Iodine is readily incorporated into the tissues surrounding the mammary nipples and is essential for the maintenance of healthy functioning breast tissue. The radioactive decay of I-131 in breast tissue may be a significant factor in the initiation and progression of both breast cancer and some types of breast nodules. Iodine also concentrates in the salivary glands and gonads. Salivary gland cancer and testicular cancer (especially in men over 25, a relatively recent phenomenon) and ovarian cancer are all increasing in actual numbers. Radioactive I- 131 decay may be a significant contributing factor.
Other tissues in the body, particularly the liver, can greatly influence the accessibility of T4 to body cells. For T4 to be physiologically active, it must first be converted to T3. This conversion is accomplished primarily by 5′ deiodinase in the liver. This enzyme requires selenium as its cationic enzymatic cofactor, which suggests that chronic selenium deficiency may present as hypothyroidism due to reduced T4 to T3 conversion. The thyroid test for TSH and T4 will not reveal this, and, as a result, unnecessary thyroid medication may be prescribed. In an associated consideration, mercury in the body tends to quell or cripple selenium in enzymes. This means that chronic or even possible acute mercury poisoning can present as hypothyroidism. We all have steadily increasing body burdens of mercury from both our foods and water. A test for selenium and mercury is indicated in cases of obvious hypothyroid signs and symptoms with normal range TSH and T4.
Isoflavones, such as genistein and equol, are inhibitors of thyroid peroxidase, the thyroid follicle enzyme that makes T4 and T3. This inhibition may generate goiters, hypothyroidism, and autoimmune thyroiditis. Since isoflavones are being touted as cancer preventatives, especially for breast and prostate cancers, their addition to non-soya foods may create further thyroid challenges. Isoflavones already available in soya foods may depress thyroid function through TPO inhibition.
Another challenge to thyroid function is the siutation with rT3 (reverse T3).
It is not reversed at all but instead is produced when the 5’iodine on the interior benzene ring is removed by 5-deiodinase, instead of the 5′ iodine on the exterior site. rT3 is nearly inert, and especially so as a thyroid hormone. It has an extremely short half-life in the body of a few hours; it is rapidly excreted via the liver. In our bodies normally, T4 converts to T3 at about 40% and to rT3 at about 45%. This is most curious in an otherwise innately metabolically conservative biological system. The rT3 mechanism is a way of regulating T3 and reducing the likelihood of incipient hyperthyroidism, while maintaining the capacity to boost T3 production as a situation may demand. The body can also decrease T3 production on demand: fasting, acute trauma, chronic illness, and grief all tend to increase rT3 production and decrease T3 production.
A decrease in T3 tends to mean a slower metabolism, less appetite, slower protein replacement, and much less energy on demand for spontaneous kinetics. A relatively high rT3 and low T3 is often accompanied by a relatively low body temperature (less than 97.5°F) as measured in the axillaries before rising in the morning; this low armpit temperature reading is often used as a simple test for hypothyroidism, since body temperature is tightly controlled by metabolic rate and that metabolic rate — the rate at which fuel is converted to heat and kinetics — is controlled by T3. A shortage of T3 means lower body temperature and possibly death if prolonged. The relatively high production of rT3 compared to T3 is sometimes referred to as Wilson’s Thyroid Syndrome, and is clinically treated with T3 until a normal body temperature is “captured” and maintained.
There is not yet a positive consensus about either the efficacy or desirability of T3 therapy. It is certainly indicated in life-threatening situations and maybe in other cases. The temporary low body resting temperature and accompanying low T3 may indicate physiological grieving and/or the need to slow down, get quiet, meditate, rest, regroup one’s life resources, and correct faulty attitudes or behaviors to more health-positive ones. In the trauma response, low T3 and high rT3 function to keep the body still calm to slow or prevent further trauma through activity. Up to a year of prolonged low T3 and or low T4 production might be a genetically programmed requirement for health renewal in a long-lived primate, such as ourselves (remember that chimpanzees have lived well past 65 years in captivity), so that we can remain healthy for up to 120 years.
A further challenge to healthy thyroid function is exposure to X-rays. Between 2 and 8 million North Americans (the exact numbers will never be known due to poor record-keeping) in the era from 1930 to 1980 were deliberately medically treated with X-rays to the head and chest, for a wide range of presenting conditions, includings calp ringworm, asthma, chronic bronchitis, tonsillitis, acne, and neonate respiratory problems. The thyroid glands of the respective patients received pathologically significant amounts of powerful ionizing radiation. These treatments have caused over 10,000 of cases of thyroid cancers, which develop 10 to 40 years after the medical exposures, with a peak incidence between 20 and 30 years after the episodes, and many as a million cases of other thyroid structural deformities, including nodular goiters (at least 27% of all children and adolescents irradiated). Treatment prognosis is mixed, with thyroidectomy usually recommended with subsequent lifelong obligatory thyroid replacement therapy.
