l-Thyroxine was the first synthetic molecule used to treat hypothyroidism (23) and was shown to be efficacious as monotherapy for myxedema (24). Around that time, serum protein-bound iodine (PBI) emerged as a diagnostic test and therapeutic marker; serum PBI quantitation was the only valid way to biochemically assess thyroid hormone status (25). This tool was limited in terms of treatment monitoring because the effect on serum PBI varied by agent (26). For example, l-triiodothyronine corrected BMR without much increase in serum PBI, l-thyroxine increased serum PBI sometimes to above normal, and combination l-thyroxine and l-triiodothyronine and desiccated thyroid had the advantage of normalizing serum PBI (27). In addition to BMR and serum PBI, other surrogates for treatment response included cholesterol levels, symptoms, and deep tendon reflexes, but their lack of sensitivity was always recognized (28).
The vast majority of individuals—one in seven are women—with hypothyroidism in the US have Hashimoto’s thyroiditis, an autoimmune disease in which your body doesn’t produce enough thyroid hormone, but this isn’t caused by iodine levels in the diet.2 Other less common causes of hypothyroidism include a deficiency of iodine in the diet, taking certain medications that interfere with thyroid absorption, surgical removal of the thyroid, and a genetic disorder.
From the early 1890s through the mid-1970s, desiccated thyroid was the preferred form of therapy for hypothyroidism (Appendix Table, available at www.annals.org). This preference was reinforced by the unique ability of desiccated thyroid to reproduce a normal serum PBI (33). The predominance of natural thyroid products was illustrated by prescribing patterns in the United States: In 1965, approximately 4 of every 5 prescriptions for thyroid hormone were for natural thyroid preparations (38). Concerns about inconsistencies in the potency of these tablets arose (26) after the discovery that some contained anywhere from double to no detectable metabolic activity (39). The shelf-life of desiccated tablets was limited, especially if the tablets were kept in humid conditions (36). There were reports of patients not responding to desiccated thyroid altogether because their tablets contained no active thyroid hormone. It was not until 1985 that the revision of the U.S. Pharmacopeia standard from iodine content to T3/thyroxine (T4) content resulted in stable potency (38), but by then the reputation of natural thyroid products was tarnished (40).
A discussion on thyroid disease and good health isn’t complete without stressing the importance of physical activity. Lisa Lilienfield, MD, a thyroid disease specialist at the Kaplan Center for Integrative Medicine in McLean, Virginia, and a certified yoga instructor, is a firm believer in the importance of exercise, particularly for clients with a thyroid disorder. “With hypothyroid patients, certainly exercise can help with weight gain, fatigue, and depression. With hyperthyroidism, anxiety and sleep disturbances are so common, and exercise can help regulate both.”
Also available on the market are combination medications that contain both synthetic T4 and T3 hormones, but such medications aren’t usually recommended. For one thing, most patients see their condition improve with synthetic T4 alone because of the ability of the thyroid to convert these hormones to T3 when needed. Also, synthetic T3-T4 combination drugs can cause anxiety — if you have a preexisting mental health disability, such side effects may be even greater. (3)
Giving appropriate doses of T3 is trickier than appropriately dosing T4. T4 is inactive, so if you give too much there is no immediate, direct tissue effect. T3 is a different story, though, as it is the active thyroid hormone. So if you give too much T3, you can produce hyperthyroid effects directly—a risk, for instance, to people with cardiac disease.
Another problem of conversion involves too much of the T4 converting into another thyroid hormone called Reverse T3. Reverse T3 is not metabolizing active and can contribute to symptoms of underactive thyroid. Again, proper testing of the thyroid will uncover this issue. Correct thyroid treatment requires the correct evaluation and that is what is performed at LifeWorks Wellness Center.
It has been hypothesized that these compounds activate a complex defense system that maintains normal thyroid function by protecting the gland from both hydrogen peroxide (H2O2), produced by thyrocytes and oxidative stress. This is the major cofactor for the key thyroid enzyme 5’deiodinase which is what converts T4 into T3. 5’deoidinase also degrades the inactive rT3.
Thank you so much… I am grateful for a response… I am doing most if not all of what you suggest with a DC over the past two years…so I believe almost there but still need to find that missing piece of the puzzle.. So still working on it..stopping the cause… Totally have changed my life habits .. So just need to find the next step.. I still have hair loss .. Not as bad …and am able to rejoin my life which has been great.. Also DC doing some genetic testing .. Getting that back soon along with a full panel thyroid blood work to see where I am now …. Taking many things in your thyroid pack ..maybe I need to look to see if yours includes something I am missing.. Thanks again for your reply..I truly consider it a blessing..truly grateful
In developing countries, insufficient amounts of iodine in the diet account for most cases of hypothyroidism. Iodine is necessary for the production of the two main thyroid hormones, thyroxine (T-4) and triiodothyronine (T-3). In the U.S. – where salt is iodized, and most Americans get plenty of iodine from table salt – an autoimmune condition known as Hashimoto’s thyroiditis is the most common cause. Hashimoto’s is more common in women and in those with a family history of autoimmune diseases. It involves immune-related inflammation and destruction of the thyroid gland, which reduces proper functioning and production of thyroid hormone. The exact cause and triggers of Hashimoto’s still remains unknown.
Despite these successes, authors have questioned the efficacy of l-thyroxine monotherapy because about 10% to 15% of patients are dissatisfied as a result of residual symptoms of hypothyroidism (1, 2), including neurocognitive impairment (3), and about 15% of patients do not achieve normal serum triiodothyronine (T3) levels (4). Studies of several animal models indicate that maintaining normal serum T3 levels is a biological priority (5). Although the clinical significance of relatively low serum T3 in humans is not well-defined (1), evidence shows that elevating serum T3 through the administration of both l-thyroxine and l-triiodothyronine has benefited some patients (6, 7). However, this has not been consistently demonstrated across trials (1). Novel findings highlight the molecular mechanisms underlying the inability of l-thyroxine monotherapy to universally normalize measures of thyroid hormone signaling (8, 9), and new evidence may lay the foundation for a role of personalized medicine (10). Understanding the historical rationale for the trend toward l-thyroxine monotherapy allows us to identify scientific and clinical targets for future trials.
Correcting these problems requires an integrative approach. It involves more than simply taking a thyroid pill. As you’ll see, it involves nutritional support, exercise, stress reduction, supplements, reducing inflammation, and sometimes eliminating certain foods and detoxification from heavy metals (such as mercury and lead) and petrochemical toxins (such as pesticides and PCBs).
Iodine intake often isn’t readily apparent on a dietary recall since the amount in foods is largely dependent on levels in the soil and added salt. However, Schneider says, “Clients taking iodine tablets are a red flag. Frequent intake of foods such as seaweed or an avoidance of all iodized salt may serve as signs that further exploration is needed.”
Autoimmune disease - Autoimmune disorders occur when the body’s immune system produces antibodies that attack its own tissues. Scientists aren’t sure why the body produces these antibodies and why it would attack itself. Some think that a virus or bacterium might trigger this, while others believe that genetic factors cause autoimmune disorders. It could also be a combination of the two factors. Regardless of the cause of autoimmune diseases they are thought to be a cause of hyperthyroidism. When the immune system attacks the body, it often targets the thyroid. This limits the thyroid’s ability to produce hormones and results in hyperthyroidism.
Other noticeable effects of hypothyroidism include moodiness and a sluggish metabolism. Essentially when your thyroid is underactive your metabolism will slow down, which might mean you always feel tired or struggle to keep off weight. Your mood is especially susceptible to changes in hormone levels, so some people with hypothyroidism wind up dealing with depression, anxiety, trouble getting good sleep, and low immunity. The thyroid gland helps regulate chemical messengers called neurotransmitters that control your emotions and nerve signaling, which is the reason an out-of-balance thyroid can mean drastic emotional changes at times.
Large predator fish—tuna, swordfish, shark, kingfish, mackerel—often have more mercury than smaller fish, as they’ve lived longer and had more time to accumulate harmful chemicals. Don’t eat more than two to three servings of these fish a week, Blum says. Also, farmed fish like salmon can have higher levels of mercury because they’re often fed the chum of other fish. All fish have a little mercury, so don’t freak out about it. Just don’t order in sushi every weeknight.
There is little mention of patients who did not respond symptomatically to treatment despite having normalization of their other measured variables, such as BMR or serum PBI, in the early clinical trials in the 1940s through 1960s. After the 1970s (38, 52), a new category of hypothyroid patient was recognized: the patient who received thyroid hormone replacement therapy, had normal serum TSH, and exhibited residual symptoms of hypothyroidism. Initially, such symptoms were largely dismissed as unrelated to the thyroid condition (62). Indeed, hypothyroidism is prevalent, and symptoms overlap with those of other common conditions, including menopause, depression, and chronic fatigue syndrome. Likewise, thyroid hormone had been administered for nonthyroid disorders, including obesity and psychiatric disease, for decades. Thus, it was difficult to assess whether patients with residual symptoms had been misdiagnosed. Residual symptoms were even attributed to nonadherence (63).
Cruciferous vegetables, such as broccoli and cabbage, are full of fiber and other nutrients, but they may interfere with the production of thyroid hormone if you have an iodine deficiency. So if you do, it’s a good idea to limit your intake of Brussels sprouts, cabbage, cauliflower, kale, turnips, and bok choy, because research suggests digesting these vegetables may block the thyroid's ability to utilize iodine, which is essential for normal thyroid function.
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