Abstract
KEY POINTS
Many patients are interested in nutritional and lifestyle interventions for improving health, including for Hashimoto thyroiditis (HT), but high-quality data supporting treatments are absent or limited.
This double-blind, randomized, placebo-controlled clinical trial of curcumin versus placebo, combined with an antiinflammatory diet for 12 weeks, evaluated the effect on levels of thyroid peroxidase antibody (TPOAb), thyrotropin (TSH), triiodothyronine (T3), thyroxine (T4), lipids, and anthropomorphic parameters.
The results showed a significant reduction in TPOAb with curcumin compared to placebo, a decrease in TSH in the curcumin group, and a reduction in serum T3 in both groups.
The results suggest a potential immune-modifying effect that impacts TPOAb levels in patients with HT.
SUMMARY
Background
Hashimoto thyroiditis (HT) is prevalent in the population, and many patients diagnosed with HT based on positive thyroid peroxidase antibody (TPOAb) levels will be euthyroid. The association between symptoms and euthyroid HT remains controversial, and because thyroid hormone replacement is not indicated in general, numerous alternative therapeutic options have been investigated.1,2 Emerging evidence suggests that dietary strategies targeting inflammation may play an adjunctive role in disease management, and the effects of both specific diets and curcumin—the main active compound of turmeric—on inflammation have been previously suggested as potential interventions. 3 This study aimed to evaluate the combined effects of an anti-inflammatory diet and curcumin supplementation on thyroid function, thyroid autoimmunity, anthropometric indexes, and lipid profile in patients with HT. 4
Methods
In this 12-week double-blind, randomized, placebo-controlled clinical trial, 62 adults with confirmed HT were randomly assigned to receive a daily regimen of curcumin (347 mg of curcumin, 84 mg of desmethoxycurcumin, 9 mg of bis-desmethoxycurcumin, and 38 mg of turmeric oil) plus an anti-inflammatory diet (n = 31) or placebo plus the same anti-inflammatory diet (n = 31). After similar dropout rates and reasons for dropping out between groups, 57 participants completed the study. Adherence to diet, as well as physical activity were confirmed by interviews using a standardized recall instrument. Anthropometric measurements, serum thyrotropin (TSH), triiodothyronine (T3), thyroxine (T4), TPOAb, and lipid profile were assessed at baseline and at the conclusion of the study.
Results
The study population was 87.8% female, the mean age was between 40 and 50 years old, and approximately 72% were taking thyroid hormones. After 12 weeks, the mean serum TPOAb level significantly declined in the curcumin group as compared to the placebo group (p = 0.006). A lower mean serum T3 concentration was observed at the end of the 12-week intervention in both groups, with a mean (±SD) of −0.34 ± 0.49 ng/mL in the curcumin group (p = 0.001) and −0.18 ± 0.36 ng/mL in the placebo group (p = 0.011), with significant difference between groups. Although the mean TSH was significantly reduced in the curcumin group, from 4.39 ± 4.61 to 2.15 ± 1.68 mIU/L (p = 0.014) and was not in the placebo group, from 3.01 ± 3.13 to 2.51 ± 2.27 mIU/L (p = 0.221), the between-group difference only showed a trend toward significance (p = 0.056). No changes in T4 were observed.
Energy intake by kilocalories per day was similar between the curcumin and placebo groups both at baseline (1669.52 ± 751.04 and 1510.39 ± 457.41) and study conclusion (1431.98 ± 552.36 and 1283.68 ± 500.39). Waist circumference and waist-to-hip ratio declined significantly in both groups without no observed difference between groups. Nor were there any significant between-group findings with respect to individual lipoproteins measured in the lipid panel.
Conclusions
Curcumin supplementation combined with an anti-inflammatory diet reduced TPOAb, with limited and nonspecific changes in other thyroid hormone parameters, and no assessment of symptom or other health benefits.
COMMENTARY
HT is a predominant cause of hypothyroidism, and its presence, as evidenced by autoimmune antibodies directed against TPOAb, is prevalent in the population, with many patients being euthyroid.5,6 Endocrinologists are asked for consultation regarding the diagnosis of HT, often from patients who are highly motivated to find a solution. Whether or not treatment of HT is necessary, physicians face the challenge of having few reliable data upon which to make any therapeutic recommendation. The U.S. population spends billions of dollars annually on complementary and alternative approaches, of which a sizable portion is supplements. 7 It is generally recognized that patients are increasingly asking about such measures for a variety of conditions, including thyroid disease, 1 perhaps due to increased awareness, testing for TPOAb, and diverse sources of medical information.
With my own patients who are concerned about their diagnosis of HT, I make an effort to address their interest in nutritional and/or alternative treatment methods. For patients searching for answers for medically unexplained symptoms, validation along with consideration, and possibly exclusion, of nonthyroid etiologies can be valuable steps. 8 After having this discussion with the patient, I would be excited to provide effective, evidence-based nutritional strategies for HT if they were available. Discussing existing evidence is reasonable, but it is important to note what benefits can be expected. For example, selenium supplementation has been associated with reductions in TPOAb level, 9 but it has not been demonstrated to have benefit for thyroid hormone status and symptom burden.10,11
The results of the current study by Bourbour et al. show a significant decrease in TPOAb after 12 weeks of treatment with curcumin and an anti-inflammatory diet compared to an anti-inflammatory diet alone, suggesting a possible immunomodulatory effect in lowering the putative marker of HT. The ease of administration and relative safety of this intervention are characteristics that support its feasibility. In this study, serum TSH and T3 concentrations both seemed to be reduced. The relevance of this to thyroid autoimmunity or health is uncertain. Reduction in waist-to-hip ratio during the study may indicate that decreased adiposity could underlie these findings, as well as the possible influence of calorie restriction, despite the reduction in daily calorie consumption not reaching statistical significance.
Several limitations to recognize when interpreting this study and potentially incorporating it into our clinical considerations. Most importantly, other outcomes of thyroid and patient health were not assessed in this study. Change in levothyroxine dosing and any assessment of patient symptoms were not evaluated. Given the short intervention duration and limited sample size, these findings should be interpreted with caution. Additionally, I worry that results like this could increase nutraceutical purchases for curcumin products that may or may not recapitulate whatever benefits were observed with this very specific therapeutic intervention. Further robust trials would be needed to clarify the therapeutic role of curcumin as an adjunctive strategy in the management of autoimmune thyroid disorders. Nevertheless, I think being aware of these published data, and others like them, keep us as informed about HT as our patients who approach their diagnosis so passionately.