Common thyroid Issues overlooked by practitioners

Photo Cred: Freepik

By Carolina Brooks, BA, IFMCP

Recently, I’ve had several new patients come to clinic who have been given various supplements to support their thyroid, or had their medications adjusted only to feel worse.  I have also seen patients with other chronic illnesses who have not had any investigation around the thyroid, even though they are clearly presenting with a cluster of symptoms that point towards Hashimoto’s, which makes me wonder why the thyroid is not being investigated properly and whether clinicians are aware of some of these issues.

Below are some examples I have seen in my experience of common thyroid issues overlooked by clinicians.

Far-reaching consequences

Only 10 percent of patients display overt hypothyroid symptoms, such as cold intolerance, dry skin or hair, severe fatigue, chronic constipation, or depression, which often overlap with other health concerns. Thyroid dysfunction is also a contributing factor to many symptoms.

Optimizing thyroid function and addressing potential autoimmune activity are one of Dale Bredesen’s recommendations for his protocol to prevent and reverse cognitive decline. Hypothyroidism contributes to synaptic dysregulation, which contributes to an impaired blood brain barrier and neuroinflammatory processes.

Poor thyroid function negatively impacts intestinal motility, which can lead to impaired gall bladder function, stone and sludge formation, issues with digestive enzyme production and release, and small intestinal bacterial and fungal overgrowth.

A 2011 paper in The Open Cardiovascular Medicine Journal discusses the impact of thyroid dysfunction on lipid metabolism, endothelial dysfunction and pathogenesis of atherosclerosis. The thyroid sensitizes reproductive hormones to work more efficiently, and plays a role in the regulation of blood sugar metabolism.  

Antibody titers

Ninety percent of hypothyroid patients are experiencing autoimmune activity. A 2011 paper in the Journal of Clinical Endocrinology and Metabolism confirms that antibodies, which cause eventual destruction of the gland, are often present five to seven years prior to clinical diagnosis of disease. Thyroid dysregulation is often silent for some time before thyroid stimulating hormone (TSH) starts to rise. Silent autoimmunity is often ignored by conventional clinicians and patients alike, while side-effects of hypothyroidism and Hashimoto’s are often addressed with other medications.

Autoimmune diseases can go into remission, and they can be managed with dietary and lifestyle modifications, but the patient will often relapse again. Elevated antibodies do not correlate with severity of disease. If the thyroid is stable, antibodies can drop. When a patient relapses with an autoimmune flare, the antibodies can increase again.

Thyroid scans are often not recommended, and I refer patients to do these privately. A patient with a family history of Hashimoto’s disease pressed her doctor to have her antibodies tested as she was experiencing some fatigue, hair loss, and depression. When her antibody titers came back high and her TSH came back normal, she was old that they would monitor her thyroid until there was significant enough tissue destruction to warrant taking thyroid hormone replacement, and was offered anti-depressants to manage her mood dysregulation.

Reactions to ingredients in medication or supplement

A forty-one-year-old patient to see me after repeated miscarriages and failed in-vitro fertilization (IVF) attempts. She had recently been diagnosed with Hashimoto’s disease and put on synthetic levothyroxine by her primary care physician. Her TSH was not stable and her anti-thyroglobulin (TG) and anti-thyroid peroxidase (TPO)  antibodies had shot up since she had started her medication. Her primary care physician’s response was to increase her dose of medications so that her TSH was suppressed to attempt to stabilize the antibodies.

When I checked her medication’s ingredients, they contained gluten, which is known to cross-react with thyroid tissue, as well as corn-starch, which is a common autoimmune trigger, and other fillers. A 2019 review in Experimental & Clinical Endocrinology & Diabetes demonstrated the positive effects of a gluten-free diet on serum thyrotropin, 25-hydroxyvitamin D levels, and free thyroid hormone levels, as well as a reduction in antibody titers. I recommended the patient completely eliminate all sources of gluten from her diet and all personal care products and that the patient switch to a natural porcine thyroid glandular at a lower dose to her current synthetic thyroid hormone medication. When the patient repeated her bloodwork three months later, her antibody titers had dramatically reduced and her TSH had stabilized. 

It’s important to check ingredients of thyroid medications. Some patients will react to gluten, corn, lactose, acacia, dye, or filler in synthetic thyroid medication. Others will feel much better on a synthetic thyroid hormone replacement than a glandular simply because of their reactivity and loss of tolerance. Rarely, there are patients who may have antibodies to T4 and T3 hormone. If the patient requires support for poor thyroxine (T4) to triiodothyronine (T3) conversion, it may be preferable to switch to a bioidentical source, or supportive herbs such as ashwagandha are often used. I have seen clinicians prescribing ashwagandha supplements to patients who are sensitive to the nightshade (Solanaceae) plant family, who are unaware that ashwagandha is a nightshade plant. Another thing to consider is that nightshades

Medication or supplement impacting thyroid activity

Although it is in every interaction book and database available, I still see patients taking thyroid hormone replacement who have also been prescribed iron or calcium supplementation, yet have not been told that these supplements may interfere with absorption and be spaced three or four hours away from this medication.

A 2009 paper in Best Practice & Research – Clinical Endocrinology & Metabolism discusses medications such as glucocorticoids, dopamine agonists, somatostatin analogs, and rexinoids, which suppress TSH and affect thyroid function. Other examples include anti-nausea medications such as metoclopramide-blocking dopamine receptors and increasing TSH levels, cholestyramine and other cholesterol-lowering medications reducing absorption of T4, estrogen medications increasing production of thyroid-binding globulin and reducing the percentage of circulating free thyroid hormones. Beta-blockers and other arrythmia medications reduce conversion of T4 to the more active T3 hormone.

If a practitioner is working with a patient who is on numerous medications or supplements, they should always make sure that any interactions are properly addressed.

Given the thyroid’s role in governing metabolism, sub-optimal thyroid activity has many far-reaching consequences and will create an overall loss of function in all body systems, including cognitive function, bone health, detoxification, cardiovascular health, and pituitary feedback loop activity. Clinicians should familiarize themselves with these factors as thoroughly as possible.

References

Haugen BR (2009) Drugs that suppress TSH or cause Central Hypothyroidism. Best practice & research- Clinical Endocrinology & Metabolism, 23(6), 793–800. Retrieved from: https://doi.org/10.1016/j.beem.2009.08.003

Hutfless S, Matos P, Talor MV, Caturegli P, Rose NR (2011). Significance of Prediagnostic Thyroid Antibodies in Women with Autoimmune Thyroid Disease. The Journal of Clinical Endocrinology and Metabolism, 96(9), E1466–E1471. Retrieved from: https://doi.org/10.1210/jc.2011-0228

Krysiak R, Szkróbka W, Okopień B (2019) The Effect of Gluten-Free Diet on Thyroid Autoimmunity in Drug-Naïve Women with Hashimoto’s Thyroiditis: A Pilot Study. Experimental and Clinical Endocrinology & Diabetes. 127(7), 417–422. Retrieved from: https://doi.org/10.1055/a-0653-7108

Rizos CV, Elisaf MS, Liberopoulos EN.(2011). Effects of Thyroid Dysfunction on Lipid Profile. The Open Cardiovascular Medicine Journal, 5, 76–84. Retrieved from: https://doi.org/10.2174/1874192401105010076

Editor’s note: Photo courtesy of Freepik.