Debunking the Myths of Hypothyroidism

Before reading this post, I need to give a little background:

I'm always asked my opinion about thyroid nutrition, so this post is a
little (itty) bit of what is known about thyroid nutrition. There's so much out there! 

I wrote this for an Integrative and Functional Nutrition
newsletter, so remember that my original audience was healthcare
providers.  I can get a lil science-y/jargon-y.

Oh, and if you want to learn more, check out the book Hashimoto's Thyroiditis: Lifestyle
Interventions for Finding and Treating the Root Cause by Dr. Izabella
Wentz PharmD (she also wrote an article about Subclinical
Hypothyroidism in the same newsletter where this will be published).
Her book is gold.

Ok, enjoy!(?)

Debunking Myths of Hypothyroidism

Leigh Wagner MS, RDN, LD

Hypothyroidism is a common and burdensome health condition. Symptoms of hypothyroidism include constipation, dry skin, muscle pain, brittle hair, hair loss, fatigue, and difficulty losing weight. Since one in 300 people (NHANES III)1 and nearly 10% of adult women have hypothyroidism,2 it is important to address some of the myths surrounding the disease. The following are some common myths and a brief summary of evidence to address the controversy or misconception.

Myth: Everyone with hypothyroidism needs iodine supplementation.

Iodine is required for healthy thyroid function, and iodine is most highly concentrated within the thyroid gland. Thus, adequate iodine levels are important for the thyroid to work properly. One situation where clinicians should be cautious with iodine supplementation is in the presence of anti-thyroid antibodies. Persons with elevated anti-thyroid antibodies are at increased risk of experiencing negative effects of iodine supplementation.3 In other words, when a person has elevated anti-thyroid antibodies, he or she should be wary of high, long-term iodine intake. Therefore, persons with hypothyroidism should be tested for the presence of anti-thyroid antibodies prior to iodine supplementation.

Myth: Anyone in the U.S. eating commercially prepared foods or consuming dairy products regularly gets enough iodine from salt or dairy foods.

Although iodized salt is widely available, salt iodization is not mandated in the U.S.4 Most food companies use non-iodized salt in their foods.5 As a result, Americans may not consume as much iodine through salty, processed foods as once thought.

Like salt, dairy foods are assumed to have high amounts of iodine because, historically, iodine has been supplemented in dairy cattle, and iodine-based disinfectants were used in tanks for dairy transportation. However, cattle are not as widely supplemented, and the iodine-based disinfectants are often replaced with chlorine-based antiseptics.6 As such, dairy cannot be considered a dependable source of iodine in the U.S. food supply.

Myth: Iodine deficiency is the main cause of hypothyroidism in the U.S.

Although worldwide iodine deficiency is a major factor for hypothyroidism, in the United States, Hashimoto’s thyroiditis is the primary cause of the disease.1 Keep in mind that one sign of iodine deficiency is low thyroxine (T4).6 When possible, doctors should check urinary iodine levels (preferably 24-hour urinary iodine) to determine iodine status. Knowing iodine status can help determine whether iodine supplementation is warranted.

Myth: People with hypothyroidism should avoid all goitrogenic foods.

Goitrogens are compounds in foods that inhibit thyroid function. When a person has hypothyroidism or is at risk for thyroid dysfunction, it may be recommended that they decrease goitrogenic foods. Goitrogenic foods primarily include soy, millet, and cruciferous vegetables (broccoli, cauliflower, cabbage, Brussels sprouts, mustard, kale, collard greens, kohlrabi, bok choy, rutabaga, and turnips).7 Although a person with hypothyroidism should be cautious of the amount of goitrogenic foods consumed, he or she can continue to eat cruciferous vegetables, as long as the vegetables are cooked. Cooking generally decreases cruciferous vegetables’ goitrogenic effects.2 Unfortunately, soy’s goitrogenic activity is not affected by heating or cooking,8 and cooking millet actually increases its goitrogenic activity.9

Myth: People with hypothyroidism should avoid soy completely.

Soy is commonly known to affect the thyroid gland.10 Its isoflavones (phytonutrients in soy) affect thyroid peroxidase (TPO),11 which is involved in the synthesis of thyroid hormones (T3 and T4). If there is a concern about the anti-thyroid effects of soy, clinicians should know that persons with deficient iodine levels are at higher risk for soy’s negative thyroid effect compared to iodine-replete individuals. Thus, iodine levels should be checked in individuals with hypothyroidism.

Myth: If thyroid stimulating hormone (TSH) is elevated but T4 is normal, then thyroid function is normal.

Subclinical hypothyroidism (SCH) is not a medical diagnosis but is defined biochemically as elevated thyroid stimulating hormone (TSH) with normal free thyroxine (fT4).12-14 Depending on the level of TSH elevation, SCH can be mild (4.5-9.0 mU/L) or severe (≥10 mU/L).13 Its prevalence varies widely, ranging between 4-10% in the general adult population and as high as 20% in older women.15-17

Despite the fact that SCH is not a medical diagnosis, SCH increases risk for cognitive impairment,18 cardiovascular disease,19 and for progression to overt hypothyroidism.1,13 Although screening and treatment recommendations vary,20-22 most experts recommend treatment with thyroid hormone (L-T4) at TSH >10 mU/L because higher TSH levels make progression to overt hypothyroidism more likely. When TSH is between 4.5 and 10 mU/L, treatment is typically left to clinicians’ judgment.17 Patients with both SCH and vitamin D deficiency also have increased cardiovascular risk.23

Myth: Measuring TSH is the only important test to screen for thyroid function.

Although TSH “with reflex T4” (i.e. when TSH is out of range, the laboratory will be triggered to test T4) is a commonly used lab test among clinicians, integrative medicine practitioners suggest to test, at a minimum, TSH, free T3, free T4, TPO antibodies, reverse T3, and possibly minerals like iron and zinc. Also, note that TSH is highest typically between 10 pm and 4 am, and it is lowest between 10 am and 6 pm.24

Take Home

The thyroid is a complex gland, and its activity influences more than metabolism and weight management. A healthy thyroid can influence cardiovascular health, cognitive function, bone health, and keep one feeling vibrant and energetic. Both the public and clinicians alike are easily overwhelmed and sometimes confused by conflicting information in the media. The information provided in this article is likely to change as we continue to learn more about the thyroid and the foods and nutrients that affect its function. Since nutritional science is evolving and growing, clinicians must stay up-to-date on thyroid-related clinical guidelines and existing science to help individualize patient care and to address the recurrent myths that circulate.

References

1. Gaitonde DY, Rowley KD, Sweeney LB. Hypothyroidism: an update. Am Fam Phys. 2012;86(3):244-251.

2. Escott-Stump S, Giroux I. Nutrition and Diagnosis-Related Care, 7th Ed. + Applications and Case Studies in Clinical Nutrition. Philadelphia, PA: Lippincott Williams & Wilkins; 2012.

3. Leung AM, Braverman LE. Iodine-induced thyroid dysfunction. Curr Opin Endocrinol Diabetes Obes. 2012;19(5):414-419.

4. Leung AM, Braverman LE, Pearce EN. History of U.S. iodine fortification and supplementation. Nutrients. 2012;4(11):1740-1746.

5. National Institutes of Health: Office of Dietary Supplements. Iodine:fact sheet for health professionals. https://ods.od.nih.gov/factsheets/Iodine-HealthProfessional/. Reviewed June 24, 2011. Accessed July 27, 2015.

6. Zimmermann MB, Boelaert K. Iodine deficiency and thyroid disorders. Lancet Diab Endocrinol. 2015;3(4):286-295. DOI: http://dx.doi.org/10.1016/S2213-8587(14)70225-6.

7. Higdon JV, Delage B, Williams DE, Dashwood RH. Cruciferous vegetables and human cancer risk: epidemiologic evidence and mechanistic basis. Pharmacological Res. 2007;55(3):224-236.

8. Divi RL, Chang HC, Doerge DR. Anti-thyroid isoflavones from soybeans. Biochem Pharma. 1997;54(10):1087-1096.

9. Gaitan E. Goitrogens in food and water. Ann Rev Nutr. 1990;10:21-39.

10. Messina M, Redmond G. Effects of soy protein and soybean isoflavones on thyroid function in healthy adults and hypothyroid patients: a review of the relevant literature. Thyroid. 2006;16(3):249-258.

11. Doerge DR, Chang HC. Inactivation of thyroid peroxidase by soy isoflavones, in vitro and in vivo. J Chromatogr B Analyt Technol Biomed Life Sci. 2002;777(1-2):269-279.

12. Surks, MI Ortiz E, Daniels GH, et al. Subclinical thyroid disease scientific review and guidelines for diagnosis and management. JAMA. 2004. 29;2:228-238.

13. Cooper DS, Biondi B. Subclinical thyroid disease. Lancet. 2012. 379:1142-1154.

14. Cooper DS. Subclinical hypothyroidism. NEJM. 2001;345:260-266.

15. Hollowell JG, Staehling NW, Flanders WD, et al. Serum TSH, T4, and Thyroid Antibodies in the United States Population (1988 to 1994): National Health and Nutrition Examination Survey (NHANES III). J Clin Endocrin. 2002;87(2):489-499.

16. Canaris GJ, Manowitz NR, Mayor G, Ridgway EC. The Colorado Thyroid Disease Prevalence Study. Arch Intern Med. 2000;160:526-534.

17. Gharib H, Tuttle RM, Baskin HJ. Subclinical thyroid dysfunction: a joint statement on management from the American Association of Clinical Endocrinologists, the American Thyroid Association, and the Endocrine Society. J Clin Endocrinol Metab. 2005;90(1):581-585.

18. Resta F, Triggiani V, Barile G, et al. Subclinical hypothyroidism and cognitive dysfunction in the elderly. Endocr Metab Immune Disord Drug Targets. 2012;12(3):260-267.

19. Rodondi N, den Elzen WP, Bauer DC, et al. Subclinical hypothyroidism and the risk of coronary heart disease and mortality. JAMA. 2010;304(12):1365-1374.

20. Ringel MD, Mazzaferri EL. Subclinical thyroid dysfunction--can there be a consensus about the consensus? J Clin Endocr Metab. 2005;90(1):588-590.

21. Cooper DS. Subclinical thyroid disease: consensus or conundrum? Clin Endocr (Oxf). 2004;60(4):410-412.

22. Chu JW, Crapo LM. The treatment of subclinical hypothyroidism is seldom necessary. J Clin Endocr Metab. 2001;86(10):4591-4599.

23. Yilmaz H, Cakmak M, Darcin T, et al. Subclinical hypothyroidism in combination with vitamin D deficiency increases the risk of impaired left ventricular diastolic function. Endocr Regul. 2015;49(2):84-90.

24. Rakel D. Integrative Medicine. 3rd ed. Philadelphia, PA: Saunders, Elsevier; 2012.