Brazil Nuts: Selenium and Thyroid Health

Table of Contents

1. The Most Selenium-Rich Organ
2. The Selenoproteins at Work
3. Selenium and Iodine Together
4. Selenium Status and Thyroid Disease in Populations
5. Hashimoto's: The Individual Trials
6. Hashimoto's: What the Meta-Analyses Found
7. Pregnancy and Postpartum Thyroiditis
8. Graves' Disease and Graves' Orbitopathy
9. What the Brazil-Nut Studies Measured
10. Tablet Versus Nut: Why the Distinction Matters
11. What Is Not Known
12. The Upper Limit and the Cautions
13. Connections
14. Key Research Papers
15. Featured Videos

The Most Selenium-Rich Organ

A 2023 review of selenium and thyroid disease states that in adults the thyroid contains the highest amount of selenium per gram of tissue of any organ, and that most of the known selenoproteins are made in the thyroid, where they take part in thyroid hormone metabolism, in controlling the balance between oxidation and protection, and in keeping thyroid cells working normally (Wang F 2023). An Italian trial team writing about selenium in thyroid disease likewise describes the thyroid as an organ with one of the highest selenium concentrations, containing many selenoproteins involved in thyroid hormone metabolism (Pirola 2016).

The body does not leave this to chance. Selenium arriving from food is taken up by the liver, which builds a carrier protein called selenoprotein P (SELENOP). A 2022 review explains that SELENOP carries selenium out to tissues with a high demand, naming the endocrine glands and the brain, so that these organs keep a privileged selenium supply even when intake is limited (Schomburg 2022). The thyroid, in other words, is near the front of the queue.

Why would a small gland in the neck need so much of a trace mineral? The answer comes in two parts, described in the next section: the thyroid makes hormones with the help of selenium-containing enzymes, and it does this using hydrogen peroxide, a reactive chemical that would damage the gland without selenium-based protection.

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The Selenoproteins at Work

Selenium does its work as part of proteins. A review in the Journal of Biological Chemistry explains that selenium is built into proteins as the "21st amino acid," selenocysteine, and that 25 genes for selenoproteins have been identified in the human genome. These include the glutathione peroxidases, the thioredoxin reductases and the iodothyronine deiodinases, and in each the selenocysteine sits at the active site where the chemistry happens (Lu 2009). The same review lists their roles as oxidation-reduction reactions, antioxidant defence, thyroid hormone metabolism and immune responses.

The deiodinases: turning T4 into T3

The thyroid releases mostly thyroxine (T4), a hormone with four iodine atoms. T4 is largely a storage and transport form. To act on the body's cells it has to lose one iodine atom and become triiodothyronine (T3), the active hormone. The enzymes that remove that iodine are the iodothyronine deiodinases, and they are selenoproteins (Lu 2009). A 2023 review by Köhrle describes deiodinase-mediated activation and inactivation of thyroid hormones as critical for the way thyroid hormone acts through its receptors in cells (Köhrle 2023). Without selenium, the body's ability to switch thyroid hormone on and off in the tissues depends on enzymes that cannot be built properly.

The glutathione peroxidases: protecting the gland from its own chemistry

To make thyroid hormone, the gland has to attach iodine to a large protein called thyroglobulin. The enzyme that does this, thyroid peroxidase (TPO), needs hydrogen peroxide as a co-factor. Köhrle describes how this hydrogen peroxide is generated by a "dual oxidase" system at the inner surface of the thyroid follicles, and how various selenoproteins in thyroid cells defend the follicles against a lifetime of exposure to hydrogen peroxide and the reactive oxygen species that come from it (Köhrle 2023). Reviews by Hu and Rayman make the same point more simply: the glutathione peroxidases protect the thyroid by removing the excess hydrogen peroxide made for thyroglobulin iodination (Hu 2017; Rayman 2019).

TPO matters for another reason. Antibodies against TPO are the hallmark blood test of Hashimoto's thyroiditis, and most of the trials below use the TPO-antibody level (often written TPOAb) as their main measure. The site's Anti-TPO Antibodies page explains the test.

Other selenoproteins in the picture

Hu and Rayman's review notes that genetic data link the anti-inflammatory selenoprotein S to the risk of Hashimoto's thyroiditis (Hu 2017). An early trial report proposed that in areas of severe selenium deficiency the higher rate of thyroiditis reflects reduced glutathione peroxidase activity inside thyroid cells, and that selenium-dependent enzymes also have several effects on the immune system (Gärtner 2002). These are explanations researchers offer for why selenium might matter; they are not, on their own, proof that adding selenium changes the course of disease. That question belongs to the trials.

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Selenium and Iodine Together

Iodine is the raw material of thyroid hormone; selenium runs the enzymes that activate the hormone and protect the gland while it is made. Köhrle's 2023 review treats iodine, selenium and iron as the three essential trace elements of the thyroid system, and states that imbalances between them challenge the feedback loop between the brain, the pituitary gland and the thyroid, causing or facilitating common disorders such as autoimmune thyroid disease (Köhrle 2023). Iron enters because TPO itself is an iron-containing (heme) enzyme (Hu 2017).

Iodine and selenium interact in both directions. Hu and Rayman report that chronic exposure to excess iodine induces autoimmune thyroiditis, partly because heavily iodinated thyroglobulin is more likely to provoke the immune system, and that the introduction of universal salt iodisation can have a similar, though transient, effect (Hu 2017). More iodine means more hydrogen-peroxide-driven iodination in the gland, which is the very chemistry the glutathione peroxidases are there to mop up. The authors conclude that adequate selenium intake is "vital in areas of iodine deficiency/excess" (Hu 2017).

The one trial in this page's sources that tested selenium in an iodine-deficient population did not find an antibody effect. In the UK SPRINT trial, 230 pregnant women from a population with mild-to-moderate iodine deficiency took 60 mcg of selenium a day or placebo from 12 weeks of pregnancy until delivery. Selenium had no more effect than placebo on TPO-antibody levels or on the share of women who were TPO-antibody positive (Mao 2016). The site's Selenium, Zinc, Iron and Iodine in Hashimoto's page looks at the four minerals side by side.

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Selenium Status and Thyroid Disease in Populations

Observational studies measure selenium in the blood of groups of people and compare it with thyroid findings. They can show associations; they cannot show that low selenium caused a thyroid problem, or that a person with thyroid disease has low selenium for that reason. The results in this page's sources point in different directions.

• Berlin, Germany. A cross-sectional study of 323 thyroid patients found lower average serum selenium than in 200 healthy people (76.9 vs 85.1 mcg/L). 37.5% of the patients were classed as selenium-deficient (below 70 mcg/L), and 59% of those with thyroid cancer were. Yet the analysis found no relation between circulating selenium, iodine, copper or zinc and thyroid hormone levels (Mehl 2020).
• Chengdu, China. In 1,205 adults living in an iodine-sufficient area, median serum selenium was 52.63 mcg/L. Selenium was not associated with thyroid volume, with goitre or with thyroid-stimulating hormone (TSH), and was not a risk factor for goitre (Liu 2013).
• Nodular goitre, Turkey. In 98 people with euthyroid multinodular goitre and 83 healthy controls, serum selenium and zinc were lower in the goitre group, but the trace elements were not correlated with thyroid hormone levels or thyroid volume (Turan 2021). The authors' interpretation, that deficiency "may be associated" with nodular goitre, is a hypothesis from a cross-sectional comparison.
• Colombia. In 412 urban and rural residents, 96.6% had normal selenium levels, and no significant associations were found between selenium and goitre or thyroid antibody positivity (Vargas-Uricoechea 2023).

Read together, these studies suggest that low selenium is common among thyroid patients in some low-selenium regions, while in populations with adequate selenium the link with goitre, gland size and antibodies is weak or absent. Hu and Rayman's review states that evidence from both observational studies and randomised trials indicates selenium or selenoproteins can reduce TPO-antibody levels, hypothyroidism and postpartum thyroiditis (Hu 2017; Rayman 2019). Where a person lives, and how much selenium their soil and food already supply, keeps returning as a factor in how these findings are read. The site's Selenium Deficiency and Thyroid Problems page covers the deficiency side.

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Hashimoto's: The Individual Trials

Hashimoto's thyroiditis is an autoimmune disease in which the immune system attacks the thyroid; over time it is the most common cause of hypothyroidism in iodine-sufficient areas (Huwiler 2024). Many patients take levothyroxine (LT4), a synthetic T4 tablet. The trials below gave selenium as a supplement. None gave Brazil nuts.

• Gärtner 2002, Germany (sodium selenite, 200 mcg, 3 months). 70 women with autoimmune thyroiditis and high antibody levels, all on levothyroxine, were randomised to selenium or placebo. Mean TPO-antibody levels fell to 63.6% of baseline in the selenium group versus 88% in the placebo group. Nine selenium-treated women had completely normalised antibodies compared with two on placebo. TSH, free T4 and free T3 did not change in either group (Gärtner 2002).
• Gärtner 2003, follow-up (sodium selenite, 200 mcg, 6 more months). 47 of the original 70 continued. Antibodies kept falling in those who stayed on selenium and rose significantly in those who stopped it; people who switched from placebo to selenium saw their antibodies fall (Gärtner 2003).
• Turker 2006, Turkey (L-selenomethionine, 200 or 100 mcg, up to 9 months). 88 women on levothyroxine. 200 mcg a day for 3 months lowered TPO antibodies by 26.2%; placebo did not change them. When some participants were stepped down to 100 mcg a day, their TPO antibodies rose by 38.1%. The authors concluded that suppression of antibodies required more than 100 mcg a day, a dose they described as already sufficient to maximise glutathione peroxidase activity, and that the effect weakened with time (Turker 2006).
• Esposito 2017, Italy (L-selenomethionine, 166 mcg, 6 months). 76 untreated people with Hashimoto's and normal thyroid function were randomised to selenium or placebo. TSH, free T4, free T3, TPO antibodies, ultrasound appearance and an inflammatory marker (CXCL10) did not differ between groups at 3 or 6 months. The authors judged that their results "tip the balance toward the ineffectiveness" of short-term selenomethionine in this group (Esposito 2017). This is a null trial.
• Pirola 2016, Italy (selenomethionine, 83 mcg, 4 months). 196 people with autoimmune thyroiditis and mild subclinical hypothyroidism (TSH below 10 mU/L) were assigned to receive or not receive selenium; the abstract describes no placebo. Normal thyroid function returned in 31.3% of the selenium group versus 3.1% of controls (Pirola 2016). The site's Subclinical Hypothyroidism page explains the condition.
• Kyrgios 2019, Greece (L-selenomethionine, 200 mcg, 6 months). 71 children and adolescents (ages 4.5 to 17.8) with autoimmune thyroiditis were randomised, double-blind, to selenium or placebo. Thyroglobulin antibodies fell more on selenium. TPO antibodies also fell, but the difference from placebo was not statistically significant, and thyroid volume did not differ (Kyrgios 2019).
• Hu 2021, China (selenium-yeast tablets, 6 months). 90 people with Hashimoto's were assigned to selenium or no treatment. TPO antibodies, thyroglobulin antibodies and TSH fell in the selenium group, alongside rises in blood selenium, glutathione peroxidase 3 and selenoprotein P. The researchers also measured more "activated" regulatory T cells, immune cells that restrain autoimmunity (Hu 2021).
• Hajyasini 2025, Iran (selenium 200 mcg, 60 days). 40 people with Hashimoto's in a double-blind trial. Malondialdehyde, a marker of fat oxidation, fell; the decreases in TSH and anti-TPO antibodies were not statistically significant (Hajyasini 2025).
• Nordio 2017, Italy. 168 people with Hashimoto's and TSH between 3 and 6 were randomised to myo-inositol plus selenium or to selenium alone. TSH and both antibodies fell in the combined group after six months (Nordio 2017). Because both arms received selenium, this trial does not test selenium against no selenium.

A larger trial designed to settle the question of how patients feel, the Danish CATALYST trial, was set up to randomise 472 levothyroxine-treated patients to 200 mcg of selenium-enriched yeast or placebo for 12 months, with thyroid-related quality of life as its main outcome (Winther 2014). The protocol is in this page's sources; its results are not, so they are not reported here.

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Hashimoto's: What the Meta-Analyses Found

A meta-analysis pools the results of several trials. Over fifteen years the pooled picture has been consistent on one point (antibody levels tend to fall) and unsettled on the points patients care about most (thyroid function, symptoms and quality of life).

• Toulis 2010. Pooling four trials in people on levothyroxine, selenium for 3 months was linked with lower TPO antibodies and with a higher chance of reporting better well-being or mood (three studies). Effects on levothyroxine dose and on ultrasound appearance were "either unaltered or underreported." The authors wrote that improvement in thyroid function and structure should be demonstrated before routine selenium could be recommended in Hashimoto's (Toulis 2010).
• Cochrane review, van Zuuren 2013. Four trials, 463 participants, judged at unclear to high risk of bias. Two found that 200 mcg of selenomethionine lowered TPO antibodies; one trial of sodium selenite did not. Quality of life, levothyroxine dose and cost were not assessed by any study. The reviewers concluded that the evidence "to support or refute the efficacy" of selenium in Hashimoto's was incomplete and did not allow confident decisions (van Zuuren 2013).
• Wichman 2016. Sixteen controlled trials. In people on levothyroxine, TPO antibodies were lower with selenium at 3, 6 and 12 months. In newly diagnosed, untreated people, they were lower at 3 months but not at 6 or 12. Quality of evidence was generally low, and participants on selenium had a significantly higher risk of reporting adverse effects than controls. The authors noted that whether antibody changes translate into clinically meaningful benefits remained to be shown (Wichman 2016).
• Winther 2017. The same Danish group then looked at clinical outcomes. In people not taking levothyroxine, selenium did not change TSH, health-related quality of life or ultrasound appearance compared with placebo. Three trials reported some improvement in well-being in levothyroxine-treated patients but could not be pooled. The title states the conclusion: "insufficient documentation for clinical efficacy" (Winther 2017). This is a null result on the outcomes it tested.
• Kong 2023. Seven trials, 342 patients. No significant change in TPO antibodies at 3 months; significant falls in TPO and thyroglobulin antibodies at 6 months (Kong 2023).
• Wang YS 2023, an overview of six systematic reviews (75 trials). Only one review was rated high quality. TPO antibodies fell at 3 and 6 months, but the certainty of evidence was graded very low to low, and adverse effects did not differ significantly from controls (Wang YS 2023).
• Huwiler 2024, the largest pooled analysis in this set. 35 studies. In people not on levothyroxine, selenium lowered TSH slightly (a standardised mean difference of -0.21; 7 groups, 869 participants). TPO antibodies fell in people with and without levothyroxine (29 groups, 2,358 participants), though the trials varied widely. Malondialdehyde fell. There were no significant changes in free or total T4 or T3, thyroglobulin antibodies, thyroid volume or two immune signalling molecules, and adverse effects were similar to control. Overall certainty was rated moderate (Huwiler 2024).
• Zhang 2025. 21 trials, 1,610 people. TPO antibodies fell at 3 and 6 months, thyroglobulin antibodies at 3 months only, and TSH at 6 months. The authors report selenomethionine as more effective than sodium selenite or selenium yeast (Zhang 2025).
• Peng 2024, a network meta-analysis comparing supplements in Hashimoto's with normal thyroid function. Selenium lowered TPO and thyroglobulin antibodies compared with placebo; over 6 months, myo-inositol, vitamin D alone and selenium plus myo-inositol did not significantly lower either. The authors themselves recommend selenium as an add-on to standard care (Peng 2024); that is their stated view, based on antibody outcomes.
• Zuo 2021. 17 trials, 1,911 subjects with autoimmune thyroid disease. Selenium was associated with lower free T3 and TPO antibodies; TSH and thyroglobulin antibodies did not differ from control (Zuo 2021).

The common thread: antibody levels are a laboratory marker of the autoimmune process, not a symptom. Several reviews state directly that it is not yet shown whether lowering them changes how the disease progresses or how people feel (Wichman 2016; Winther 2017; Kong 2023). A 2025 narrative review summarises the field the same way: consistent antibody reductions, inconsistent evidence on hypothyroidism itself, and a need for better trials on form, dose and duration (Linn 2025).

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Pregnancy and Postpartum Thyroiditis

Women who carry TPO antibodies in pregnancy are prone to thyroid trouble in the year after birth, called postpartum thyroid dysfunction or postpartum thyroiditis, and some go on to permanent hypothyroidism (Negro 2007). Three trials in this page's sources tested selenium supplements in pregnancy; none used Brazil nuts.

• Negro 2007, Italy (selenomethionine, 200 mcg, during pregnancy and after). Of 2,143 pregnant women with normal thyroid function, 7.9% were TPO-antibody positive. 77 antibody-positive women took selenium and 74 took placebo. Postpartum thyroid dysfunction occurred in 28.6% on selenium versus 48.6% on placebo, and permanent hypothyroidism in 11.7% versus 20.3% (Negro 2007).
• SERENA, Mantovani 2019, Italy (L-selenomethionine, 83 mcg). 45 pregnant women with thyroiditis in a double-blind trial. Six months after delivery, antibody levels were lower in the selenium group, while the placebo group showed an antibody rebound. There were no differences in thyroid volume, ultrasound appearance, quality of life, or complications for mother or baby (Mantovani 2019).
• SPRINT, Mao 2016, UK (selenium, 60 mcg). 230 pregnant women in a mildly-to-moderately iodine-deficient population. Selenium did not reduce TPO antibodies. In women who were antibody-positive at the start, free T4 fell more on selenium than on placebo and was significantly lower at 35 weeks (Mao 2016). The meaning of that finding is unclear, but it is one reason the authors describe the effect on thyroid function as a change, not a benefit.

The results differ by dose, by the women studied and by local iodine status. The site's Pregnancy and Hashimoto's page covers the wider topic. Questions about any supplement during pregnancy belong with the clinician looking after the pregnancy.

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Graves' Disease and Graves' Orbitopathy

Graves' disease is the autoimmune opposite of Hashimoto's: antibodies switch the thyroid on and cause an overactive gland. In some patients the same process inflames the tissues behind the eyes, a condition called Graves' orbitopathy or thyroid eye disease. A 2023 review states that selenium treatment in Graves' orbitopathy has been shown to delay disease progression and improve quality of life (Wang F 2023). The trials in this page's sources give a more mixed picture.

• Kahaly 2017, Germany (sodium selenite, 300 mcg, 24 weeks), the overactive gland itself. 70 untreated people with Graves' hyperthyroidism took the anti-thyroid drug methimazole plus selenium or placebo. Response at 24 weeks was 80% with selenium and 82% with placebo; relapse in the following 12 weeks was 48% and 44%. Blood selenium and selenoprotein P levels were unrelated to response. The authors concluded that supplemental selenium did not affect response or recurrence rates (Kahaly 2017). A null trial.
• Wang C 2024, China (selenium yeast, 6 months, 5-year follow-up). 74 people with mild-to-moderate orbitopathy took selenium or placebo. Over 3 to 6 months the selenium group improved in tearing, grittiness and redness and had a higher improvement rate than placebo. At 5 years, both groups had improved and selenium made no difference to long-term outcomes (Wang C 2024).
• Potita 2024, Thailand (selenium 200 mcg, 6 months). 25 people with inactive moderate-to-severe orbitopathy who already had adequate blood selenium. The eyelid opening narrowed more on selenium, but eye bulging, eye movement, soft-tissue signs, activity score and quality of life did not differ from placebo (Potita 2024).
• Le Moli 2025, Italy (a food-based approach). The only orbitopathy trial in this set to use food rather than tablets. 40 people with Graves' disease and mild active orbitopathy were randomised to a Mediterranean diet with its selenium content raised about 30% (to roughly 178 mcg a day) or a free diet for 24 weeks. The activity score improved at the first visit, soft-tissue involvement improved, and eyelid opening was smaller in the Mediterranean-diet group; antibody levels and thyroid function did not differ (Le Moli 2025). The abstract does not say which foods supplied the selenium, and because the whole diet changed, the effect cannot be put down to selenium alone.

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What the Brazil-Nut Studies Measured

The Brazil-nut trials in this page's sources were not thyroid trials. They measured whether the nut raises selenium in the blood and switches on the selenium enzymes, which is the first step any thyroid effect would depend on.

• Thomson 2008, New Zealand. 59 adults ate 2 Brazil nuts a day, took 100 mcg of selenomethionine, or took placebo for 12 weeks. The nuts were expected to supply about 100 mcg a day, but when analysed they averaged 53 mcg (range 20 to 84). Plasma selenium rose 64.2% on nuts and 61.0% on the tablet, versus 7.6% on placebo; plasma glutathione peroxidase rose 8.3% and 3.4%. Whole-blood glutathione peroxidase rose more on nuts than on either placebo or the tablet. The authors concluded that 2 nuts a day were as effective as the tablet at raising selenium status (Thomson 2008).
• Huguenin 2015, Brazil. 91 people with high blood pressure and abnormal blood fats took 13 g a day of partially defatted granulated Brazil nut (about 227.5 mcg of selenium) or placebo for 12 weeks in a crossover trial. Plasma selenium rose from 87.0 to 180.6 mcg/L, glutathione peroxidase 3 activity rose 24.8%, and oxidised LDL fell 3.25% (Huguenin 2015).
• Cardoso 2016, São Paulo. Older adults with mild cognitive impairment ate one Brazil nut a day (estimated 288.75 mcg) for 6 months; 20 completed. Selenium levels rose and red-cell glutathione peroxidase activity changed significantly compared with controls (Cardoso 2016).
• Stockler-Pinto 2014, Rio de Janeiro. 40 people on hemodialysis ate one nut a day for 3 months, with no control group. Plasma selenium and glutathione peroxidase rose, and markers of inflammation and oxidative damage fell (Stockler-Pinto 2014).
• Duarte 2019, São Paulo. 55 women with obesity, none selenium-deficient at the start, ate one nut a day (about 1,261 mcg of selenium, roughly three times the US adult upper limit) or nothing for 2 months. All selenium markers rose, and so did the gene activity of several pro-inflammatory signals, although blood levels of inflammatory markers did not change (Duarte 2019).

A 2022 systematic review of 24 Brazil-nut trials, 15 of them non-randomised, found that every study measuring antioxidant status saw selenium and/or glutathione peroxidase rise. It lists thyroid function among the outcomes that improved in people on hemodialysis (da Silva 2022); the individual trial behind that statement is not among this page's sources. Observationally, in the UK SPRINT pregnancy cohort, whole-blood selenium was higher in women who reported eating Brazil nuts (Rayman 2015).

No randomised trial in this page's sources gave Brazil nuts to people with Hashimoto's, Graves' disease or postpartum thyroiditis and measured thyroid antibodies, thyroid hormones or symptoms. A 2018 commentary notes that Brazil nuts are "often suggested as therapeutic" for autoimmune thyroid disease and goes on to discuss the health concerns of eating them, including selenium toxicity, a possible link between high selenium and type 2 diabetes, weight gain, radioactivity, aflatoxins and allergy (Mazokopakis 2018).

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Tablet Versus Nut: Why the Distinction Matters

A thyroid trial supplement has a stated dose, usually 83, 100, 166 or 200 mcg a day, and the same dose every day. The Brazil-nut studies above show what a nut can supply: an estimated 288.75 mcg in one nut in one trial (Cardoso 2016), about 1,261 mcg in one nut in another (Duarte 2019), and about 26 mcg per nut on average in a third, where two nuts expected to give 100 mcg gave 53 (Thomson 2008). The NIH Office of Dietary Supplements gives an average of 544 mcg per ounce of Brazil nuts and notes that values from other analyses vary widely (NIH ODS, Selenium Fact Sheet for Health Professionals). A food-chemistry review explains that the amount depends on how much selenium the soil holds and in what forms (Alcântara 2022).

The chemical form differs as well. Several trials used sodium selenite, an inorganic salt; others used selenomethionine or selenium-enriched yeast. One meta-analysis found selenomethionine more effective than the other forms for Hashimoto's antibodies (Zhang 2025), and a food-chemistry review notes that selenomethionine is the selenium form researchers have investigated in most nuts (Alcântara 2022). Even so, a shared chemical form does not make the tablet trial results transferable to a nut whose dose is unknown.

The Turker trial adds a dose-specific detail: 100 mcg a day was not enough to keep antibodies down, though the authors described it as already enough to maximise glutathione peroxidase (Turker 2006). If that finding holds, a lower-selenium batch of nuts and a higher-selenium batch would sit on different sides of the line the trial drew.

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What Is Not Known

• Whether Brazil nuts do anything measurable for thyroid disease. No trial in this page's sources tested them on thyroid outcomes.
• Whether lower antibodies mean better health. The best-replicated finding is a fall in TPO antibodies. Whether that slows progression to hypothyroidism, reduces levothyroxine needs or improves symptoms is, in the reviewers' words, still to be demonstrated (Wichman 2016; Winther 2017).
• Quality of life. The Cochrane review found no trial that measured it as a primary outcome (van Zuuren 2013), and the later pooled analysis of untreated patients found no improvement (Winther 2017). The results of the large trial designed for this question are not in this page's sources (Winther 2014).
• Who might respond. Results may depend on baseline antibody level (Toulis 2010; Gärtner 2002), on whether a person takes levothyroxine (Wichman 2016), and on regional selenium and iodine status (Linn 2025).
• How long any effect lasts. Antibodies rose again when selenium was stopped (Gärtner 2003), the suppression weakened with time (Turker 2006), and the orbitopathy benefit had vanished by five years (Wang C 2024).
• Trial quality. Many trials were small, several were not placebo-controlled, and the reviews repeatedly grade the evidence low or very low (Wang YS 2023; Wichman 2016).

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The Upper Limit and the Cautions

The NIH Office of Dietary Supplements lists the adult Recommended Dietary Allowance for selenium as 55 mcg a day and the adult Tolerable Upper Intake Level as 400 mcg a day, figures that come from the U.S. Institute of Medicine's 2000 Dietary Reference Intakes (Institute of Medicine 2000; NIH ODS). By the ODS average of 544 mcg per ounce, a single ounce of Brazil nuts is above that upper limit, and one trial measured a single nut at about three times it (Duarte 2019). In that trial, one high-selenium nut a day for two months increased the gene activity of pro-inflammatory signals in women who were not deficient to begin with (Duarte 2019).

Several findings bear on people who combine sources. The thyroid trials commonly gave 200 mcg a day as a tablet; the Wichman meta-analysis found that participants on selenium had a significantly higher risk of reporting adverse effects than controls (Wichman 2016), while other pooled analyses found adverse effects similar to control (Huwiler 2024; Wang YS 2023). A narrative review notes that excessive intake carries a risk of selenium toxicity, called selenosis, and describes the topic as one to approach with caution (Linn 2025). The commentary on Brazil nuts lists selenium toxicity and a possible type 2 diabetes link among the concerns (Mazokopakis 2018). On the other side, a study of 448 people in Amazon communities whose traditional diet includes Brazil nuts found no signs or symptoms of selenosis even at blood levels above toxicity thresholds (Lemire 2012), which the authors suggest shows that the chemical form and diet context matter.

The full safety picture, including selenosis symptoms, contaminants and allergy, is on the sibling page Brazil Nuts: Selenium Overload and Safety. A selenium blood test is the measurement the trials used to track status. Decisions about selenium supplements alongside thyroid medicines belong with a clinician.

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Connections

• Nuts — the nuts landing page
• Brazil Nuts — the main topic page
• Brazil Nuts — Benefits Deep Dive — the hub for these articles
• Selenium Status and Antioxidant Enzymes — the blood-selenium trials in depth
• Selenium Overload and Safety — the upper limit and selenosis
• Selenium — the mineral itself
• Selenium and Thyroid Function — the mineral-side view
• Selenium Deficiency: Thyroid Problems
• Hashimoto's Thyroiditis
• Selenium, Zinc, Iron and Iodine in Hashimoto's
• Hypothyroidism
• Graves' Disease
• Thyroid Eye Disease
• Iodine — selenium's partner in the thyroid
• Glutathione Peroxidase — the enzyme the nut trials measured
• Anti-TPO Antibodies — the main trial outcome
• TSH

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Key Research Papers

1. Wang F, Li C, Li S, et al. Selenium and thyroid diseases. Frontiers in endocrinology. 2023;14:1133000. PubMed PMID: 37033262
2. Köhrle J. Selenium, Iodine and Iron-Essential Trace Elements for Thyroid Hormone Synthesis and Metabolism. International journal of molecular sciences. 2023;24(4). PubMed PMID: 36834802
3. Lu J, Holmgren A. Selenoproteins. The Journal of biological chemistry. 2009;284(2):723-7. PubMed PMID: 18757362
4. Schomburg L. Selenoprotein P - Selenium transport protein, enzyme and biomarker of selenium status. Free radical biology & medicine. 2022;191:150-163. PubMed PMID: 36067902
5. Hu S, Rayman MP. Multiple Nutritional Factors and the Risk of Hashimoto's Thyroiditis. Thyroid. 2017;27(5):597-610. PubMed PMID: 28290237
6. Rayman MP. Multiple nutritional factors and thyroid disease, with particular reference to autoimmune thyroid disease. The Proceedings of the Nutrition Society. 2019;78(1):34-44. PubMed PMID: 30208979
7. Mehl S, Sun Q, Görlich CL, et al. Cross-sectional analysis of trace element status in thyroid disease. Journal of trace elements in medicine and biology. 2020;58:126430. PubMed PMID: 31835129
8. Liu Y, Huang H, Zeng J, et al. Thyroid volume, goiter prevalence, and selenium levels in an iodine-sufficient area: a cross-sectional study. BMC public health. 2013;13:1153. PubMed PMID: 24321191
9. Turan E, Turksoy VA. Selenium, Zinc, and Copper Status in Euthyroid Nodular Goiter: A Cross-Sectional Study. International journal of preventive medicine. 2021;12:46. PubMed PMID: 34211677
10. Vargas-Uricoechea H, Bastidas B, Pinzón MV. Population status of selenium in Colombia and associated factors: a cross-sectional study. Hormone molecular biology and clinical investigation. 2023;44(2):153-158. PubMed PMID: 36573323
11. Gärtner R, Gasnier BC, Dietrich JW, et al. Selenium supplementation in patients with autoimmune thyroiditis decreases thyroid peroxidase antibodies concentrations. The Journal of clinical endocrinology and metabolism. 2002;87(4):1687-91. PubMed PMID: 11932302
12. Gärtner R, Gasnier BC. Selenium in the treatment of autoimmune thyroiditis. BioFactors (Oxford, England). 2003;19(3-4):165-70. PubMed PMID: 14757967
13. Turker O, Kumanlioglu K, Karapolat I, et al. Selenium treatment in autoimmune thyroiditis: 9-month follow-up with variable doses. The Journal of endocrinology. 2006;190(1):151-6. PubMed PMID: 16837619
14. Esposito D, Rotondi M, Accardo G, et al. Influence of short-term selenium supplementation on the natural course of Hashimoto's thyroiditis: clinical results of a blinded placebo-controlled randomized prospective trial. Journal of endocrinological investigation. 2017;40(1):83-89. PubMed PMID: 27572248
15. Pirola I, Gandossi E, Agosti B, et al. Selenium supplementation could restore euthyroidism in subclinical hypothyroid patients with autoimmune thyroiditis. Endokrynologia Polska. 2016;67(6):567-571. PubMed PMID: 28042649
16. Kyrgios I, Giza S, Kotanidou EP, et al. l-selenomethionine supplementation in children and adolescents with autoimmune thyroiditis: A randomized double-blind placebo-controlled clinical trial. Journal of clinical pharmacy and therapeutics. 2019;44(1):102-108. PubMed PMID: 30306604
17. Hu Y, Feng W, Chen H, et al. Effect of selenium on thyroid autoimmunity and regulatory T cells in patients with Hashimoto's thyroiditis: A prospective randomized-controlled trial. Clinical and translational science. 2021;14(4):1390-1402. PubMed PMID: 33650299
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