The purpose of treating hypothyroidism is to maintain normal metabolism by correcting a deficient output of thyroid hormone. Once replacement therapy begins, the thyroid will stop producing hormones all together, and replacement must be continued for life. Most mainstream physicians prescribe the drug Synthroid, also known as levothyroxine, a synthetic analog of thyroxine (T-4) and monitor how much to give based on symptoms and levels of TSH. Physicians will generally check TSH levels after a couple of months of being on the medication and adjust it accordingly. They will often used a more cautious course in patients who have cardiovascular disease. This allows the heart time to adjust to an artificially increased metabolism. Side effects of taking too much thyroid hormone include shakiness, palpitations, insomnia and changes in appetite.

If you have subclinical hypothyroidism, discuss treatment with your doctor. For a relatively mild increase in TSH, you probably won't benefit from thyroid hormone therapy, and treatment could even be harmful. On the other hand, for a higher TSH level, thyroid hormones may improve your cholesterol level, the pumping ability of your heart and your energy level.
Iodine:  Iodine is critical for thyroid hormone production in the body.  A true iodine deficiency will cause hypothyroidism (43).  In western culture we often see subclinical iodine deficiencies which contribute to hypothyroidism (44). I typically don’t recommend high doses of iodine as it could be problematic with individuals with Hashimoto’s – especially with TPO anti-bodies.
60 patients with borderline hypothyroidism were given either 2 mg of soy isoflavones (the amount found in the typical omnivore’s diet) or 16 mg of soy isoflavones (the amount found in the typical vegetarian’s diet).  The “vegetarian” dose of soy isoflavones was 3 times more likely to cause patients to convert from borderline (“subclinical”) hypothyroidism to full-blown (“overt clinical”) hypothyroidism.
Thyroid hormone replacement has been used for more than a century to treat hypothyroidism. Natural thyroid preparations (thyroid extract, desiccated thyroid, or thyroglobulin), which contain both thyroxine (T4) and triiodothyronine (T3), were the first pharmacologic treatments available and dominated the market for the better part of the 20th century. Dosages were adjusted to resolve symptoms and to normalize the basal metabolic rate and/or serum protein-bound iodine level, but thyrotoxic adverse effects were not uncommon. Two major developments in the 1970s led to a transition in clinical practice: 1) The development of the serum thyroid-stimulating hormone (TSH) radioimmunoassay led to the discovery that many patients were overtreated, resulting in a dramatic reduction in thyroid hormone replacement dosage, and 2) the identification of peripheral deiodinase-mediated T4-to-T3 conversion provided a physiologic means to justify l-thyroxine monotherapy, obviating concerns about inconsistencies with desiccated thyroid. Thereafter, l-thyroxine mono-therapy at doses to normalize the serum TSH became the standard of care. Since then, a subgroup of thyroid hormone–treated patients with residual symptoms of hypothyroidism despite normalization of the serum TSH has been identified. This has brought into question the inability of l-thyroxine monotherapy to universally normalize serum T3 levels. New research suggests mechanisms for the inadequacies of l-thyroxine monotherapy and highlights the possible role for personalized medicine based on deiodinase polymorphisms. Understanding the historical events that affected clinical practice trends provides invaluable insight into formulation of an approach to help all patients achieve clinical and biochemical euthyroidism.
Less common causes of hypothyroidism include congenital (birth) defects (one of the reasons for newborn screening is to check for failure of the pituitary gland to produce enough thyroid stimulating hormone, usually due to a benign pituitary tumor), and pregnancy. Some women can develop hypothyroidism during or immediately following pregnancy, often as a result of developing antibodies against their own thyroid tissue. This is dangerous for both the developing fetus and mother, and can lead to miscarriage, developmental abnormalities, premature delivery and an increased risk of preeclampsia – a potentially dangerous complication in the later stages of pregnancy.
Making dietary changes is your first line of defense in treating hypothyroidism. Many people with hypothyroidism experience crippling fatigue and brain fog, which prompts reaching for non-nutritional forms of energy like sugar and caffeine. I’ve dubbed these rascals the terrible twosome, as they can burn out your thyroid (and destabilize blood sugar).
An unhealthy gut environment can contribute to nutrient deficiencies and raise autoimmune activity in the body. Gut inflammation can be triggered by food sensitivities or allergies, including those to gluten and dairy. Other causes of a damaged gut are high stress levels, toxin overload from diet and the environment, and bacterial imbalances. When leaky gut occurs, small particles that are normally trapped inside the gut start to leak out into the bloodstream through tiny openings in the gut lining, which creates an autoimmune cascade and a series of negative symptoms.
Rather than giving Synthroid (T-4) alone, Dr. Weil prefers combinations of the two natural hormones (T-3 and T-4), and often recommends the prescription drug Thyrolar. Under normal conditions, the body can convert T-4 into T-3; however, there is some question whether the body can do this optimally when under extreme physical or emotional stress. Giving a combination seems to elicit a more natural response for the body, and may also have a better effect on mood than T-4 alone.

Goitrogens are naturally occurring substances in certain foods that interfere with the production of thyroid hormones (the hormones that people with hypothyroidism lack). They include some of the most commonly consumed foods of the health-conscious community: broccoli, cauliflower, kale, spinach, radishes, soybeans, peanuts, pine nuts, peaches and millet. The good news is that many health professionals believe that cooking may inactivate goitrogens.


I don’t know all your symptoms or health challenges, but if you have thyroid issues and if you are losing hair (alopecia areata?), you may want to consider getting tested for celiac disease. It is quite common for people to have celiac disease and thyroid disease. It’s important not to eliminate gluten from your diet before being tested as it would cause a false-negative test result.

Similar to processed foods, fast food chains also aren't required to use iodized salt in their foods. And even when they do, it might not boost the iodine content all that much, according to one 2010 commentary in the journal Endocrine Practice, which tested products from two fast food restaurants in the Boston area. The study authors concluded that drive-thru fare might be pretty low in iodine.
People with celiac disease who can’t tolerate the gluten found in many baked goods, pasta and cereals often have Hashimoto’s thyroiditis, and vice versa. Hashimoto’s disease is an autoimmune condition in which your immune system attacks your thyroid. Once rare, Hashimoto’s is now the most common autoimmune disease, according to the May 2017 study in the journal Endocrine Connections.
Postpartum thyroiditis: Five percent to 10 percent of women develop mild to moderate hyperthyroidism within several months of giving birth. Hyperthyroidism in this condition usually lasts for approximately one to two months. It is often followed by several months of hypothyroidism, but most women will eventually recover normal thyroid function. In some cases, however, the thyroid gland does not heal, so the hypothyroidism becomes permanent and requires lifelong thyroid hormone replacement. This condition may occur again with subsequent pregnancies.
Because it helps balance hormone levels, selenium can lower the risk for experiencing thyroid disorder during pregnancy (postpartum thyroiditis) and afterward. (15) Other studies have shown that when selenium deficiency is resolved through supplementation, patients experience on average 40 percent reduction in thyroid antibodies compared to a 10 percent increase when given a placebo. (16)
Gluten is a protein found in wheat, rye, and barley. Unless you've been diagnosed with celiac disease, it probably won’t affect your thyroid. Gluten can damage the small intestines of people with celiac disease. They can have other autoimmune disorders like Hashimoto’s disease (which leads to an underactive thyroid) and Graves' disease (which leads to an overactive thyroid). If you have celiac disease, a gluten-free diet may help prevent these thyroid diseases.

Ashwagandha is an adaptogen herb that helps the body respond to stress, keeping hormone levels better in balance. Adaptogens helps lower cortisol and balance T4 levels. In fact, in clinical trials, supplementing with ashwagandha for eight weeks essentially worked as thyroxine treatment, helping hypothyroidism patients significantly increase thyroxine hormone levels and thus reduce the severity of the disorder. (13) Also, try other adaptogen herbs like rhodiola, licorice root, ginseng and holy basil, which have similar benefits.
Hypothyroidism is a condition in which the thyroid gland is underactive and doesn’t properly make or release thyroid hormones. The thyroid gland normally releases many crucial hormones that travel through the bloodstream to reach receptors found throughout the whole body. So a disturbance in thyroid function can cause widespread, noticeable health problems.
In humans, a factor associated with response to combination therapy in a large clinical trial is the Thr92Ala polymorphism in the type 2 deiodinase gene (DIO2), wherein the subpopulation of patients with this genetic alteration had improved well-being and preference for combination therapy (7). This has led investigators to consider whether this polymorphism could confer a defect in the D2 pathway, but normal Thr92AlaD2 enzyme kinetics have been demonstrated (73). Only recently has the Thr92AlaD2 protein been found to have a longer half-life, ectopically localize in the Golgi apparatus, and significantly alter the genetic fingerprint in cultured cells and in the temporal pole of the human brain without evidence of reduced thyroid hormone signaling (74). The significance of these studies transcends the thyroid field—this polymorphism has now been associated with a constellation of diseases, including mental retardation, bipolar disorder, and low IQ (75). If hypothyroid carriers of Thr92AlaD2 benefit from alternate therapeutic strategies in replicate studies, then personalized medicine—based on genotype— may have a role.
Central or pituitary hypothyroidism: TSH (Thyroid-stimulating hormone) is produced by the pituitary gland, which is located behind the nose at the base of the brain. Any destructive disease of the pituitary gland or hypothalamus, which sits just above the pituitary gland, may cause damage to the cells that secrete TSH, which stimulates the thyroid to produce normal amounts of thyroid hormone. This is a very rare cause of hypothyroidism.
Trisha Gilkerson is a homeschooling mom to four crazy boys. She blogs with her awesome hubby Luke at Intoxicated on Life where they talk about faith, homeschooling, and health. They’ve authored the Write Through the Bible curriculum and family Bible Studies and have recently released their first healthy living book – Weeding Out Wheat: A Simple Faith Based Guide. They love connecting with their readers, so be sure to follow them on their blog, Facebook, Twitter, Google+, and Pinterest.

In humans, a factor associated with response to combination therapy in a large clinical trial is the Thr92Ala polymorphism in the type 2 deiodinase gene (DIO2), wherein the subpopulation of patients with this genetic alteration had improved well-being and preference for combination therapy (7). This has led investigators to consider whether this polymorphism could confer a defect in the D2 pathway, but normal Thr92AlaD2 enzyme kinetics have been demonstrated (73). Only recently has the Thr92AlaD2 protein been found to have a longer half-life, ectopically localize in the Golgi apparatus, and significantly alter the genetic fingerprint in cultured cells and in the temporal pole of the human brain without evidence of reduced thyroid hormone signaling (74). The significance of these studies transcends the thyroid field—this polymorphism has now been associated with a constellation of diseases, including mental retardation, bipolar disorder, and low IQ (75). If hypothyroid carriers of Thr92AlaD2 benefit from alternate therapeutic strategies in replicate studies, then personalized medicine—based on genotype— may have a role.
Symptoms - Hypothyroidism doesn’t have any unique characteristic symptoms - all of its symptoms could potentially present as symptoms of a different illness. One way to differentiate whether your symptoms are a product of hypothyroidism is to consider whether you’ve always had the symptoms (in which case hypothyroidism in unlikely) or whether the symptom is a departure from the way you used to feel (which means hypothyroidism is more likely).

Clinicians noted several differences in the ability of l-thyroxine monotherapy to normalize markers of hypothyroidism at doses that normalized serum TSH (45). For instance, in many l-thyroxine-treated patients with a normal serum TSH, the BMR remained at about 10% less than that of normal controls even after 3 months of therapy (53). At the same time, doses of l-thyroxine that normalize the BMR can suppress serum TSH and cause iatrogenic thyrotoxicosis (28, 45, 46). The clinical significance of this was not fully understood because many patients appeared clinically euthyroid with a BMR between −20% and −10% (36, 37).
Dr. George Springer has practiced alternative medicine for 31 years with an emphasis on treating chronic disease conditions. He received his undergraduate BA from the University of Missouri in St. Louis and his Doctor of Chiropractic (D.C.) from Logan University where he graduated magna cum laude. He went on to receive his Doctor of Naturopathic Medicine (N.M.D.) from the American Naturopathic Medical Institute a division of Breyer State University in Los Angeles, California.
Choose foods that offer nutritional support for your thyroid.  The production of thyroid hormones requires iodine and omega-3 fatty acids; converting the inactive T4 to the active T3 requires selenium; and both the binding of T3 to the receptor on the nucleus and switching it on require vitamins A and D, as well as zinc. You will find these nutrients in a whole-food, clean, organic diet. To get therapeutic levels of these nutrients, please use the supplement protocol in strategy 4.

Everyone has bacteria in their digestive tract, or gut, that is essential to the function of the human body. A healthy adult has about 1.5 – 2 kg of bacteria in their gut, both good and bad.  Normal levels of bacteria, or flora, in the gut protect against invaders, undigested food, toxins, and parasites. When the good and bad bacteria in the gut get out of whack (i.e. more bad than good), a whole host of negative reactions can occur in the body.  Undigested foods can leak through into the bloodstream causing food allergies and intolerances, vitamins and minerals may not be absorbed, leading to deficiency, and the bad bacteria can produce a whole host of toxins, leading the immune system to not function properly. An effective thyroid diet includes probiotics that you can get from fermented foods.


Hypothyroidism is most commonly treated with thyroid hormone replacement therapy, and the most effective way to treat hypothyroidism is with synthetic T4 medication. (7, 5) While these hormones are identical to the natural T4 that the thyroid makes, several factors can affect the exact dosage you need. These include your age, the severity of symptoms, and your overall health profile.
High-fiber foods – People with hypothyroidism may have digestive difficulties, so aim for 30–40 grams of fiber daily. In addition to a high-fiber diet helping with digestive health, it improves heart health, balances blood sugar levels and supports a healthy weight by making you feel fuller. Some easy ways to increase fiber intake include eating more fresh vegetables, berries, beans, lentils and seeds.
If your sex hormones (estrogen, progesterone, testosterone) and adrenal hormones (cortisol, DHEA) are out of balance, this can make weight loss more difficult. Perimenopause and menopause, as well as estrogen dominance, can also cause a shift of weight to the belly, and make weight loss more difficult. Lack of testosterone in men and women can also make it harder to build fat-burning muscle. And adrenal imbalances can make you tired, less responsive to thyroid treatment, and less able to lose weight.

Affiliate Disclosure: There are links on this site that can be defined as affiliate links. This means that I may receive a small commission (at no cost to you) if you purchase something when clicking on the links that take you through to a different website. By clicking on the links, you are in no way obligated to buy.


Please Note: The material on this site is provided for informational purposes only and is not medical advice. Always consult your physician before beginning any diet or exercise program.

Copyright © livehopelupus.org

×