Hypothyroidism, nutrition and functional medicine

Posted on Wed, 20 Jul 16

Hypothyroidism is at epidemic proportions yet remains poorly diagnosed and treated. We need to consider better assessments as well as treatments beyond hormone replacement therapy. 

The prevalence of subclinical hypothyroidism is 3% to 18% in the adult population (up to 11 million people in the UK), with more women affected than men. Anyone working in a clinical setting knows that people with hypothyroidism may have a clear symptom picture despite normal blood tests, and that people frequently do not respond ideally to the most common treatment; thyroid hormone replacement.  

One of the core issues is that traditional assessments rely on thyroid stimulating hormone (TSH), but this can be inadequate for diagnosis and monitoring hypothyroidism. To improve assessment a non-traditional functional medicine-based approach has been suggested [1]. This would include routinely testing more detailed measures of thyroid function such as peroxidase (TPO) antibodies, thyroxine (T4) triiodothyronine (T3), and reverse T3 (rT3) to gain a better picture of thyroid hormone metabolism as well as to help direct more personalized treatments. Also considering functional imbalances that could affect thyroid function, such as gastrointestinal involvement and micronutrient deficiencies should form part of a comprehensive patient work up [1]. 

A number of other functional, environmental and nutritional factors may contribute to hypothyroidism, including celiac disease [2], oxidative stress [3], inflammation [4], environmental toxins [5], altered oestrogen metabolism [6], and psychological stress [7]. The notion that there are modifiable dietary, environmental and lifestyle factors that could contribute to hypothyroidism challenges the use of hormone replacement as the mainstay of treatment. And some of the most important non-drug treatments are nutritional. 

Nutritional deficiencies

Deficiencies in nutrients that support healthy thyroid function are alarmingly common and nutritional supplementation can improve thyroid function, yet nutritional supplements are not routinely considered in hypothyroid patients. There are a number of key nutritional deficiencies that have strong evidence to show they adversely affect thyroid hormone metabolism as well as influencing autoimmune related thyroid disease (AITD). The individual need for iron, selenium, zinc, vitamin A and, in particular, iodine supplementation should be considered.    

The United Kingdom ranks seventh amongst the ten most iodine deficient countries in the world, and is one of only two high-income countries on the list [8]. Iodine is an essential part of the thyroid hormones T4 and T3 and deficiency leads to increased TSH stimulation, increased iodine uptake, rapid iodine turnover and enhanced production of T3 in relation to T4. This initial compensatory increase in thyroid function, however, comes at a long-term cost and subclinical hypothyroidism, thyroid autoimmunity and goiter may ultimately result from inadequate iodine intake [9]. 

Iodine supplementation can help restore normal thyroid function with one study, for example, showing that people with iodine deficiency and goiter who were treated for 12 months with 200mcg/ day of potassium iodide had an increase in the levels of total T4, a reduction in thyroglobulin and a reduction in thyroid size [10]. And another showing that iodine-deficient, overweight or obese women who received 200mcg/ day potassium iodide for 6 month’s had improved iodine status, and improved thyroid function (increased T4 and a decreased TSH and thyroglobulin) [11].

In addition to iodine repletion, identification of vitamin A, iron, zinc, and selenium deficiencies and subsequent supplementation have all been shown to improve thyroid hormone metabolism, AITD and reduce symptoms such as goiter, alopecia and Graves’ orbitopathy [12-15]. Although the amino acid tyrosine is sometimes used in dietary supplements for thyroid function there is no convincing evidence to suggest it would be useful and amounts given are frequently well below the 12000mg (12g) or greater doses used in clinical research [16]. 

Dietary considerations  

There are a number of substances present in otherwise healthy diets that could interfere with normal thyroid function, and these are collectively known as goiterogens. Despite having been characterized decades ago much of the study on dietary goiterogens is experimental and there is surprisingly little research directed at the clinical relevance of goiterogens in humans. However, a few recent publications help shed some light on the matter. 

Two of the best known food sources of potential goiterogens are the brassica vegetables and soy foods. A recent review on the goiterogenic potential of brassicas concluded that unless an individual was to consume over 1 kg/day of species particularly high in the goiterogen progoitrin (e.g. Russian/Siberian kale of the species B. napus , some collards, and Brussels sprouts), raw, for several months, these foods would not impact thyroid function [17]. In contrast, usual dietary intakes of soy foods have been shown to exacerbate hypothyroidism in people with existing subclinical hypothyroid disease [18]. It is worth noting that a review of 14-clinical trials found that soy foods are unlikely problematic in those without thyroid illness, and thus soy does not need to be universally avoided [19].

Other important dietary goiterogens that could adversely affect thyroid function are fluoridated drinking water [20], excessive dietary calcium from hard-water [21], and common environmental pollutants such as plastics [22] and pesticides from non-organic food [23]. Kelp and seaweed-induced thyrotoxicosis has been widely reported with daily iodine doses equivalent to 580 to 990 mcg daily [24]. And a strict gluten-free diet can sometimes improve thyroid function in people with confirmed celiac disease [25].

A different view  

The thyroid does not exist in a vacuum, on the contrary it is exquisitely sensitive to our internal state of health (e.g. oxidative stress, inflammation, and hormonal imbalances) and environmental factors (e.g. nutritional deficiencies, environmental toxins, and dietary goiterogens). A different clinical lens that widens the view from assessment of TSH and subsequent hormone replacement therapy to a functional approach that aims to understand why the thyroid is dysfunctional in the first place could improve medical practice, move nutritional therapy to the forefront of patient care, and transform the lives of millions.  

*this article first appeared in CAM Magazine, July 2016 

References: 

1. Juby AG, Hanly MG, Lukaczer D. Clinical challenges in thyroid disease: Time for a new approach? Maturitas. 2016 May;87:72-8.

2. Sategna-Guidetti C, et al. Prevalence of thyroid disorders in untreated adult celiac disease patients and effect of gluten withdrawal: an Italian multicenter study. Am J Gastroenterol. 2001 Mar;96(3):751-7.

3. Karbownik-Lewińska M, Kokoszko-Bilska A. Oxidative damage to macromolecules in the thyroid - experimental evidence. Thyroid Res. 2012 Dec 27;5(1):25.

4. Mancini A, et al. Thyroid Hormones, Oxidative Stress, and Inflammation. Mediators Inflamm. 2016;2016:6757154.

5. Chen A, Kim SS, Chung E, Dietrich KN. Thyroid hormones in relation to lead, mercury, and cadmium exposure in the National Health and Nutrition Examination Survey, 2007-2008. Environ Health Perspect. 2013 Feb;121(2):181-6.

6. Fortunato RS, Ferreira AC, Hecht F, Dupuy C, Carvalho DP. Sexual dimorphism and thyroid dysfunction: a matter of oxidative stress? J Endocrinol. 2014 Apr 22;221(2):R31-40.

7. Vita R, Lapa D, Vita G, Trimarchi F, Benvenga S. A patient with stress-related onset and exacerbations of Graves disease. Nat Clin Pract Endocrinol Metab. 2009  Jan;5(1):55-61.

8. The Lancet Diabetes Endocrinology. Iodine deficiency in the UK: grabbing the low-hanging fruit. Lancet Diabetes Endocrinol. 2016 Jun;4(6):469.

9. Zimmermann MB, Boelaert K. Iodine deficiency and thyroid disorders.  Lancet Diabetes Endocrinol. 2015 Apr;3(4):286-95. 

10. Kahaly G, Dienes HP, Beyer J, Hommel G. Randomized, double blind, placebo-controlled trial of low dose iodide in endemic goiter. J Clin Endocrinol  Metab. 1997 Dec;82(12):4049-53.

11. Herter-Aeberli I, et al. Iodine Supplementation Decreases Hypercholesterolemia in Iodine-Deficient, Overweight Women: A Randomized Controlled Trial. J Nutr. 2015 Sep;145(9):2067-75.

12. Farhangi MA, Keshavarz SA, Eshraghian M, Ostadrahimi A, Saboor-Yaraghi AA. The effect of vitamin A supplementation on thyroid function in premenopausal women. J Am Coll Nutr. 2012 Aug;31(4):268-74.

13. Duntas LH, Papanastasiou L, Mantzou E, Koutras DA. Incidence of sideropenia and effects of iron repletion treatment in women with subclinical hypothyroidism. Exp Clin Endocrinol Diabetes. 1999;107(6):356-60.

14. Kandhro GA, Kazi TG, Afridi HI, Kazi N, Baig JA, Arain MB, Sirajuddin, Shah AQ, Sarfraz RA, Jamali MK, Syed N. Effect of zinc supplementation on the zinc level in serum and urine and their relation to thyroid hormone profile in male and female goitrous patients. Clin Nutr. 2009 Apr;28(2):162-8. 

15. Toulis KA, Anastasilakis AD, Tzellos TG, Goulis DG, Kouvelas D. Selenium supplementation in the treatment of Hashimoto's thyroiditis: a systematic review  and a meta-analysis. Thyroid. 2010 Oct;20(10):1163-73.

16. Palinkas LA, Reedy KR, Smith M, Anghel M, Steel GD, Reeves D, Shurtleff D, Case HS, Van Do N, Reed HL. Psychoneuroendocrine effects of combined thyroxine and triiodothyronine versus tyrosine during prolonged Antarctic residence. Int J  Circumpolar Health. 2007 Dec;66(5):401-17.

17. Felker P, Bunch R, Leung AM. Concentrations of thiocyanate and goitrin in human plasma, their precursor concentrations in brassica vegetables, and associated potential risk for hypothyroidism. Nutr Rev. 2016 Apr;74(4):248-58.

18. Sathyapalan T, Manuchehri AM, Thatcher NJ, Rigby AS, Chapman T, Kilpatrick ES, Atkin SL. The effect of soy phytoestrogen supplementation on thyroid status and cardiovascular risk markers in patients with subclinical hypothyroidism: a randomized, double-blind, crossover study. J Clin Endocrinol Metab. 2011 May;96(5):1442-9.

19. 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 Mar;16(3):249-58.

20. Peckham S, Lowery D, Spencer S. Are fluoride levels in drinking water associated with hypothyroidism prevalence in England? A large observational study of GP practice data and fluoride levels in drinking water. J Epidemiol Community  Health. 2015 Jul;69(7):619-24. 

21. Chandra AK, Goswami H, Sengupta P. Dietary calcium induced cytological and biochemical changes in thyroid. Environ Toxicol Pharmacol. 2012 Sep;34(2):454-65.

22. Wang N, Zhou Y, Fu C, Wang H, Huang P, Wang B, Su M, Jiang F, Fang H, Zhao Q,  Chen Y, Jiang Q. Influence of Bisphenol A on Thyroid Volume and Structure Independent of Iodine in School Children. PLoS One. 2015 Oct 23;10(10):e0141248.

23. Pelletier C, Doucet E, Imbeault P, Tremblay A. Associations between weight loss-induced changes in plasma organochlorine concentrations, serum T(3) concentration, and resting metabolic rate. Toxicol Sci. 2002 May;67(1):46-51.

24. Di Matola T, Zeppa P, Gasperi M, Vitale M. Thyroid dysfunction following a kelp-containing marketed diet. BMJ Case Rep. 2014 Oct 29;2014. 

25. Sategna-Guidetti C, et al. Prevalence of thyroid disorders in untreated adult celiac disease patients and effect of gluten withdrawal: an Italian multicenter study. Am J Gastroenterol. 2001 Mar;96(3):751-7.