Brazil Nuts: Selenium Status and Antioxidant Enzymes

Table of Contents

1. From Nut to Selenocysteine
2. The Selenoproteins Behind the Numbers
3. How Selenium Status Is Measured
4. Why One Nut Is Not One Dose
5. The New Zealand Trial: Nuts Versus Selenomethionine
6. Trials in People With Health Conditions
7. Trials in Women With Obesity
8. Genetic Variation in the Response
9. What Very High Selenium Status Looks Like
10. A Rising Enzyme Is a Biomarker, Not a Health Outcome
11. The Large Selenium-Tablet Trials: More Is Not Better
12. What Is Not Known
13. Who the Research Raises Cautions For
14. Connections
15. Key Research Papers
16. Featured Videos

From Nut to Selenocysteine

Selenium is a trace mineral: the body needs only micrograms of it a day (a microgram, written mcg or µg, is a millionth of a gram). It does almost nothing on its own. Its job is to sit inside particular proteins, and to get there it has to become part of an amino acid.

The form in the nut. Brazil nut selenium is mainly in organic form, meaning it is bound into carbon-based compounds rather than present as a mineral salt (Lima 2019). Reviews of the nut’s chemistry identify selenomethionine as the main selenium compound studied in nuts (Alcântara 2022). Selenomethionine is simply the amino acid methionine with a selenium atom where the sulfur atom normally sits. A review of selenium speciation (the science of identifying exactly which selenium compounds are present) discusses Brazil nuts alongside garlic and selenium-enriched yeast as natural and enriched food sources, and how the forms in each are reflected in human tissues and body fluids (Dumont 2006).

Two fates for selenomethionine. Because the body cannot easily tell selenomethionine from methionine, some of it is built, unspecifically, into ordinary proteins wherever methionine would go (Alexander 2007). Selenium held that way still counts in a blood test, but it is not part of a selenium enzyme. Selenium’s specialised work depends on a different amino acid.

Selenocysteine, the twenty-first amino acid. Selenium’s biological role comes mainly from selenocysteine, the amino acid cysteine with selenium in place of sulfur. The genetic code has no ordinary “word” for it. Instead, cells reuse a three-letter code (UGA in the messenger RNA) that usually means “stop”, and a special decoding mechanism inserts selenocysteine there while the protein is being built. There is no free pool of selenocysteine floating around the cell waiting to be used; it is made on the spot for this purpose (Lu 2009). In the active site of the enzymes that carry it, selenocysteine is essential for the chemistry to work (Lu 2009).

This matters for interpreting the trials. A blood selenium number counts both kinds of selenium: the selenium doing work inside selenoproteins and the selenium parked in ordinary proteins as selenomethionine. That is one reason the studies below measure enzymes as well as total selenium.

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The Selenoproteins Behind the Numbers

Twenty-five genes for selenoproteins have been identified in the human genome (Lu 2009). The main groups are the glutathione peroxidases 1 to 5, the iodothyronine deiodinases 1 to 3, the thioredoxin reductases and selenoprotein P, plus others whose functions are mostly unknown (Alexander 2007). Selenoproteins are involved in oxidation-reduction (redox) reactions, redox signalling, antioxidant defence, thyroid hormone metabolism and immune responses (Lu 2009). Three of them carry most of the Brazil nut research.

• Glutathione peroxidases (GPx). These enzymes use glutathione, a small sulfur-containing molecule made by the body, to neutralise peroxides, the reactive molecules such as hydrogen peroxide that can damage fats, proteins and DNA. GPx1 works inside cells, including red blood cells, which is why trials measure “erythrocyte” (red-cell) or “whole-blood” GPx. GPx3 is the form that circulates in plasma, the liquid part of blood. Among Inuit adults, GPx3 carried about a quarter of all plasma selenium (Achouba 2016).
• Selenoprotein P (SELENOP, formerly SelP or SEPP1). Made in the liver, it is the body’s selenium delivery truck, carrying selenium to essential tissues such as the endocrine glands and the brain, which keep a privileged supply. Its gene predicts ten selenocysteine positions, although decoding is imperfect and not all are actually filled. It can break down peroxides and protect LDL particles from oxidation in the test tube, but whether it acts as an enzyme in the intact body is unclear (Schomburg 2022). In the Inuit study it carried about half of plasma selenium (Achouba 2016).
• Thioredoxin reductases. These recycle thioredoxin, a protein that keeps other proteins in their working, reduced state, and selenocysteine sits in their active site (Lu 2009). None of the Brazil nut trials reviewed for this page measured them, so what nuts do to thioredoxin reductase in people is not known from this evidence.

The deiodinases, which convert thyroid hormone into its active form, are covered in the sister article on selenium and the thyroid.

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How Selenium Status Is Measured

“Selenium status” is not one number. Each of the common measures captures a different slice of the body’s selenium, and they respond differently as intake rises. The Brazil nut trials used different ones, which makes them hard to compare directly.

• Plasma or serum selenium. The total selenium in the liquid part of blood. It includes selenium in selenoprotein P, in GPx3, and bound to albumin (the main blood protein). In 852 Inuit adults, these three carried about 52%, 25% and 23% of plasma selenium respectively. Plasma selenium appeared to level off at about 200 µg/L in that population even when whole-blood levels kept climbing (Achouba 2016).
• Whole-blood selenium. Plasma plus the cells, especially red blood cells. In the Inuit study it was higher and much more variable than plasma selenium (median 261 versus 139 µg/L). The authors noted that, in contrast to their own population, a linear relationship between whole-blood and plasma selenium had previously been reported in communities eating Brazil nuts, whose selenium is mainly selenomethionine (Achouba 2016). In other words, the form of selenium eaten changes how the two measures relate.
• GPx activity. A functional measure: how fast a blood sample’s glutathione peroxidase breaks down peroxide. Plasma GPx (GPx3) and red-cell or whole-blood GPx (mostly GPx1) are measured separately and do not always move together, as the New Zealand trial below shows. Studies of status markers describe them as rising with intake only until a saturated status is reached, after which they plateau (Schomburg 2022).
• Selenoprotein P concentration. Circulating SELENOP serves as a functional biomarker of selenium supply until a saturated status is reached and its level plateaus. With toxic intake a further rise in SELENOP is observed, so it can also give information about possible selenosis (selenium poisoning) (Schomburg 2022).
• Toenail selenium. A record of intake over months, used in population studies. In 230 pregnant women in the United Kingdom, toenail selenium was considerably lower than in U.S. women, and was the only selenium measure linked to the risk of pre-eclampsia or pregnancy-induced high blood pressure (Rayman 2015).

That same U.K. study gives a rare glimpse of Brazil nuts in ordinary diets. Its participants had whole-blood selenium below the mid-range of other populations, GPx3 activity considerably lower than U.S. and Australian pregnant women, and low selenoprotein P. After adjustment for other factors, whole-blood selenium was higher in women who reported eating Brazil nuts (Rayman 2015). This was an observational association within a trial of 60 mcg selenium tablets, not a nut feeding study.

A practical consequence: a trial that reports only total plasma or blood selenium can show a large rise even in people who were never short of selenium, because total selenium keeps climbing after the functional markers plateau. A rise in GPx activity or SELENOP is more informative about function, but only in people who started below the plateau. The site’s Selenium Test page describes the clinical blood test.

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Why One Nut Is Not One Dose

Every trial below describes its dose as a number of nuts, but the selenium those nuts delivered varied more than twenty-fold from study to study.

The plant explains the spread. How much selenium a plant can accumulate depends on the soil’s selenium profile, both how much selenium the soil holds and in which chemical forms (Alcântara 2022). Brazil nuts are harvested from wild trees across a huge area of the Amazon, so the soil under each tree differs. A study of two batches of shop-bought nuts found mean selenium levels of 28 to 49 mg per kg, with up to an eight-fold difference between individual seeds in the same batch. The selenium was concentrated in a ring 1 to 2 mm below the seed’s surface. The authors calculated that one 5 g seed from a high-selenium area meets the daily requirement and that a 30 g serving may exceed the 400 µg allowable daily intake, or even the 1,200 µg they cite as a toxicity threshold (Lima 2019).

For reading the trials, this means two studies that both gave “one nut a day” can be testing doses that differ by four times or more. It also means the dose in any one person’s kitchen is unknown without a laboratory analysis.

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The New Zealand Trial: Nuts Versus Selenomethionine

The cleanest comparison of nuts with a tablet comes from New Zealand, a country whose soils are low in selenium and whose population had relatively low selenium status. The authors noted that, before their study, no trial had investigated how well the selenium in Brazil nuts is absorbed and used in humans (Thomson 2008).

• Design. A randomized controlled trial in 59 adults. One group ate 2 Brazil nuts a day, thought to provide about 100 mcg selenium; one took 100 mcg selenium as selenomethionine; one took a placebo. It ran for 12 weeks, with blood tests at baseline and at 2, 4, 8 and 12 weeks.
• The dose surprise. When the study nuts were analysed, actual intake averaged only 53 mcg a day, with a possible range of 20 to 84 mcg.
• Plasma selenium rose 64.2% with nuts, 61.0% with selenomethionine and 7.6% with placebo. Both active groups differed significantly from placebo but not from each other.
• Plasma GPx rose 8.3% with nuts, 3.4% with selenomethionine and fell 1.2% with placebo. Both active groups differed from placebo but not from each other.
• Whole-blood GPx rose 13.2% with nuts, 5.3% with selenomethionine and 1.9% with placebo. Here the nut group did better than both placebo and the tablet.

The authors concluded that 2 Brazil nuts a day were as effective as 100 mcg of selenomethionine for raising selenium status and enhancing GPx activity (Thomson 2008). Two points are worth keeping in view. The nuts achieved this while delivering about half the selenium the tablet did, which suggests either very good use of nut selenium or a contribution from something else in the nut; the trial was not designed to say which. And the outcomes were blood measurements over three months. The trial did not measure any illness.

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Trials in People With Health Conditions

Most of the remaining trials come from Brazil and tested nuts in people with a particular disease. A systematic review counted 24 Brazil nut trials, of which 15 were non-randomized, and in all of them the nuts were eaten as part of a normal free-living diet (da Silva 2022). The design of each matters for how much weight it can bear.

High blood pressure and high cholesterol

In a randomized, double-blind, placebo-controlled crossover trial, 91 people with high blood pressure and abnormal blood fats (mean age 62, 51.6% men) received 13 g a day of partially defatted granulated Brazil nut (about 227.5 mcg selenium) or a placebo for 12 weeks each, with a four-week washout between. Plasma selenium rose from 87.0 to 180.6 µg/L. GPx3 activity rose 24.8%, from 112.66 to 128.32 nmol/min/mL. Oxidized LDL, a form of LDL cholesterol damaged by oxidation, fell 3.25%, from 66.31 to 60.68 U/L. Higher GPx3 was associated with lower oxidized LDL. The association between GPx3 and 8-epi-PGF2α, a marker of fat oxidation, did not reach significance (Huguenin 2015). A companion analysis from the same programme reported lower total and non-HDL cholesterol with the nut flour (Carvalho 2015); the lipid findings are in the sister article on cholesterol and inflammation.

Haemodialysis

People on long-term haemodialysis often have high oxidative stress and low selenium. The researchers noted that their earlier work had found one nut a day for 3 months raised selenium and GPx in these patients. In the follow-up study, 40 haemodialysis patients in Rio de Janeiro each ate one nut a day for 3 months. Plasma selenium and GPx activity rose. The inflammatory signalling molecules TNF-α and IL-6, the DNA-damage marker 8-OHdG and the fat-oxidation marker 8-isoprostane all fell. HDL cholesterol rose and LDL fell (Stockler-Pinto 2014). There was no control group: every patient got nuts, so the study cannot separate the nut’s effect from time, season or changes in dialysis care.

Older adults with mild cognitive impairment

In a randomized pilot trial in São Paulo, 31 older adults with mild cognitive impairment were assigned to one Brazil nut a day (estimated 288.75 mcg selenium) or no nuts for 6 months. Only 11 in the nut group and 9 controls completed it. Blood selenium rose in the nut group and did not change in controls. Of the antioxidant measures, only red-cell GPx activity changed significantly differently between the groups; oxygen radical absorbance capacity (a test-tube measure of overall antioxidant capacity) and malondialdehyde (a fat-oxidation marker) did not. The authors also reported greater improvements in verbal fluency and constructional praxis in the nut group (Cardoso 2016). Those cognitive results are covered in brain aging and cognition.

Coronary artery disease: a null result

In patients with coronary artery disease, 23 were randomized to one nut a day for 3 months and 14 to no supplement. Levels of TMAO (trimethylamine N-oxide, a compound produced from food by gut bacteria and linked to heart disease) and its precursors did not change in either group. GPx activity rose 41% in the nut group, but the change was not statistically significant, and the authors concluded that the nuts changed neither TMAO nor GPx activity (Coutinho-Wolino 2022). The systematic review also flagged controversial results for a fat-oxidation marker in coronary disease (da Silva 2022).

Type 2 diabetes: DNA damage down, fasting glucose up

In people with type 2 diabetes, blood was taken before and after six months of Brazil nut supplementation. Serum selenium rose significantly. When the blood cells were exposed to hydrogen peroxide in the laboratory (an ex vivo test, done on cells outside the body), cells taken after six months of nuts resisted DNA damage better, as measured by the comet assay. The same study also observed a significant increase in fasting blood glucose after six months, with no significant change in glycated haemoglobin (HbA1c, the longer-term glucose measure) (Macan 2022). The abstract does not describe a control group, so the glucose rise cannot be attributed to the nuts with confidence, but it was a measured result and it runs against the headline.

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Trials in Women With Obesity

Three trials in women with obesity show how much the result depends on dose and on the starting selenium level.

• A very high-selenium nut raised inflammatory gene activity. In a randomized trial of 55 women in São Paulo, one group ate one Brazil nut a day for 2 months, a nut supplying about 1,261 mcg of selenium; the control group had no intervention. Neither group was selenium-deficient at the start. In the nut group, all selenium biomarkers rose significantly, and so did the gene expression of several pro-inflammatory molecules: interleukin-6, tumour necrosis factor-α and the immune sensors Toll-like receptors 2 and 4. Plasma levels of the inflammatory biomarkers themselves did not change. The authors interpreted the gene-expression rise as possibly a pro-inflammatory stimulus from nuts with high selenium levels (Duarte 2019).
• MicroRNAs. In the same São Paulo programme (54 women, 29 given one nut of about 1,261 mcg a day and 25 controls, for 2 months), 2 of 25 circulating microRNAs measured (small RNA molecules that regulate genes), miR-454-3p and miR-584-5p, rose after nut intake (Reis 2019). What that change means for health is not established.
• A lower dose during weight loss. In an 8-week non-randomized controlled trial in Viçosa, 56 women with overweight or obesity followed an energy-restricted diet (500 kcal a day less), with or without 8 g of Brazil nut a day (347.2 mcg selenium); 46 completed it. The nut group ended with lower C-reactive protein, TNF, IL-1β, IL-8 and lower intestinal permeability on the lactulose/mannitol test than the control group. Changes in serum selenium predicted changes in IL-8. The authors wrote that the effects of Brazil nuts “seem to be Se status-dependent” (Silveira 2024).

Read together, these do not show that Brazil nuts are pro- or anti-inflammatory. They show that a nut delivering roughly three times the adult upper limit in a single kernel, given to women who were not deficient, produced a different signal from a smaller dose given during weight loss. The trials differed in dose, design, duration and measurements, so they cannot settle the question between them.

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Genetic Variation in the Response

Some people’s selenium biomarkers respond more than others to the same nut, and common variations in selenoprotein genes appear to be part of the reason. Such a variation is called a single nucleotide polymorphism (SNP): a one-letter difference in the DNA code that many people carry.

• Healthy adults. 130 healthy volunteers at the University of São Paulo ate one nut a day for 8 weeks, followed by 8 weeks without. They were genotyped for eight SNPs in selenoprotein genes. Total cholesterol and fasting glucose fell after the 8 weeks. Glucose levels were modulated by the SELENOP variant rs3877899, with significantly lower levels in people carrying the GA or AA genotype. The SELENOP variant rs7579 was associated with cholesterol, lower in people with the GG genotype, at a p-value of 0.053, which is at the edge of the usual threshold. The authors concluded that genetic variation “should be considered” in future trials (Donadio 2018). There was no control group.
• People taking statins. 32 patients using statins ate one nut a day for 3 months and were genotyped for a GPx1 variant (rs1050450) and two SELENOP variants (rs3877899 and rs7579). The variants were not associated with plasma or red-cell selenium. But the SELENOP variants did influence how red-cell GPx activity, creatine kinase (a marker of muscle stress, relevant because statins can affect muscle), triglycerides and LDL responded. The nuts raised GPx1 gene expression only in people with the rs1050450 CC genotype, and SELENOP gene expression was lower in people with the rs7579 GG genotype both before and after the nuts (Watanabe 2022).

These are small studies without placebo groups, and the variants have not been tested as a way to predict who benefits. What they show is that the same blood selenium level can be accompanied by different enzyme responses in different people.

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What Very High Selenium Status Looks Like

Two population studies show what happens at the top of the range, where diets supply far more selenium than any trial dose.

The Lower Tapajós River, Brazilian Amazon. The traditional diet there includes Brazil nuts, chicken, game and certain fish, all important selenium sources. In 448 people aged 15 to 87 from 12 communities, median whole-blood selenium was 228.4 µg/L (range 103.3–1,500.2) and median plasma selenium 134.8 µg/L (range 53.6–913.2). Some values exceeded the 1,000 µg/L whole-blood level the authors cite as toxic (U.S. EPA, 2002). A nurse examined hair, nails, skin and breath for signs of selenosis, and participants answered questions about symptoms. No dermal or breath signs or symptoms of selenium toxicity were associated with the selenium biomarkers. The authors called for re-assessing selenium toxicity in light of the chemical form, the route of exposure and co-exposures such as mercury, and for studying high selenium status and cardiometabolic health as diets in the region change (Lemire 2012).

Inuit adults, Nunavik. Here selenium comes from marine foods rather than nuts. Plasma selenium seemed to level off around 200 µg/L while 16% of people had whole-blood selenium above 500 µg/L and 3% above 1,000 µg/L. The authors suggested that a different selenium compound, possibly selenoneine, accumulates in their blood cells, in contrast with the selenomethionine of Brazil nuts (Achouba 2016).

Neither study shows that high intake is harmless for everyone. They show that blood levels alone do not predict toxicity well, and that the form of selenium matters. The cases of selenium overload, and the upper limit, are covered in selenium overload and safety.

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A Rising Enzyme Is a Biomarker, Not a Health Outcome

Almost every trial on this page reports the same type of outcome: a number in a blood sample went up or down. It is easy to read “antioxidant enzyme activity rose” as “people became healthier”. The research does not support that leap on its own.

• Plateaus. GPx activity and SELENOP rise with selenium intake only until they are saturated (Schomburg 2022). Selenomethionine can also be built unspecifically into ordinary proteins in place of methionine (Alexander 2007), so part of a rise in total blood selenium may not be in working selenoproteins at all.
• Short and small. The trials ran from 8 weeks to 6 months and enrolled between a few dozen and 130 people. None counted heart attacks, cancers, deaths or other clinical events.
• Mixed signals. The same nut that raises GPx can come with a rise in fasting glucose (Macan 2022) or in inflammatory gene expression at very high doses (Duarte 2019), and the GPx rise itself was not significant in one trial (Coutinho-Wolino 2022).
• Design. Several studies had no control group (Stockler-Pinto 2014; Donadio 2018; Watanabe 2022), and the systematic review found that 15 of its 24 included trials were non-randomized (da Silva 2022).

The most that can be said from this evidence is that Brazil nuts reliably raise selenium biomarkers, and that this matters most for people whose selenium status was low to begin with, as in the New Zealand and U.K. populations (Thomson 2008; Rayman 2015).

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The Large Selenium-Tablet Trials: More Is Not Better

None of the trials in this section gave Brazil nuts. They tested selenium tablets, at a fixed dose, in people who were not selected for deficiency. They are included because they are the strongest evidence on what happens to real health outcomes when selenium intake is raised, and because popular writing about Brazil nuts often borrows from them.

• SELECT (prostate cancer). 34,887 men in the United States, Canada and Puerto Rico were analysed after random assignment to 200 µg a day of selenium as L-selenomethionine, vitamin E, both, or placebo, for a planned 7 to 12 years. Compared with 529 prostate cancers on placebo, there were 575 on selenium alone (hazard ratio 1.09, not statistically significant) and 555 on selenium plus vitamin E (hazard ratio 1.05, not significant). Selenium did not reduce prostate cancer. Vitamin E alone significantly increased it (hazard ratio 1.17) (Klein 2011). See prostate cancer.
• Nutritional Prevention of Cancer Trial (skin cancer). 1,312 people in the eastern United States with a history of nonmelanoma skin cancer took 200 µg a day of selenium as selenized yeast or placebo. Over the whole blinded period, selenium did not significantly affect basal cell carcinoma (hazard ratio 1.09) and was associated with a significantly higher risk of squamous cell carcinoma (hazard ratio 1.25) and of total nonmelanoma skin cancer (hazard ratio 1.17) (Duffield-Lillico 2003).
• SELENIB (bladder cancer). 270 patients with newly diagnosed non-muscle-invasive bladder cancer in the U.K. were randomized to 200 µg a day of high-selenium yeast and/or vitamin E. Selenium did not change the time to recurrence (hazard ratio 0.92), progression or overall survival; vitamin E was associated with more recurrence. The trial was halted early because of slow recruitment (Bryan 2023).
• A combined supplement in Shandong, China. In a region at high risk of stomach cancer, a supplement of vitamin C, vitamin E and selenium taken for 7.3 years was associated with lower stomach-cancer incidence and mortality over 22 years of follow-up (Li 2019). Because selenium was given together with two vitamins, the trial cannot isolate selenium’s contribution.
• Gestational diabetes. In a small Turkish trial, pregnant women with gestational diabetes had lower blood selenium than healthy pregnant women; 200 µg a day of selenium plus diet for 4 weeks lowered fasting and post-load glucose more than diet alone (Yigit 2024). This was a short trial in women with low status, not a nut trial.

The pattern across these trials is the one an earlier review anticipated when it stated that supplementation studies should look for possible adverse effects as well as benefits, and that the apparent differences in biological activity between selenium compounds are not well understood (Alexander 2007). In well-nourished populations, raising selenium further with a tablet did not prevent the cancers studied, and in one trial was linked with more skin cancer. Whether any of this applies to Brazil nuts, which deliver a variable dose in a whole food, has not been tested in an outcome trial. The site’s page on selenium and cancer prevention covers the supplement trials in more detail.

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What Is Not Known

• Clinical outcomes. No trial reviewed here tested whether eating Brazil nuts, through their effect on selenium status, reduces any disease or death.
• Thioredoxin reductase and other selenoproteins. The nut trials measured GPx and occasionally SELENOP; none reviewed here measured thioredoxin reductases.
• Which part of the nut does the work. The New Zealand result, with nuts matching a tablet at half the selenium (Thomson 2008), has not been explained.
• The right dose. Because selenium per nut varies up to eight-fold within a batch (Lima 2019), and trials ranged from 53 to about 1,261 mcg a day, there is no trial-based answer to how many nuts produce a given status. Dose-response and single-meal studies of Brazil nut selenium were not among the records reviewed for this page; PubMed searches for them are listed below.
• Who benefits. Most trials enrolled people in Brazil, often with obesity, kidney failure, heart disease or diabetes. How their results apply to people with already-adequate selenium elsewhere is uncertain, and the genetic findings are preliminary (Donadio 2018; Watanabe 2022).

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Who the Research Raises Cautions For

• Anyone eating many nuts regularly. One 5 g nut from a high-selenium area can meet the daily requirement, and a 30 g serving may exceed the 400 µg allowable daily intake (Lima 2019). A review lists recommended selenium intakes of 40–55 µg a day and an upper tolerable level of 300 µg a day, the European figure, and notes that excess selenium can produce selenosis affecting the liver, skin, nails and hair (Alexander 2007).
• People already taking selenium supplements or multivitamins with selenium. Nut and tablet selenium add together. The tablet trials above found no cancer benefit from 200 µg a day in well-nourished people, and one found more skin cancer (Duffield-Lillico 2003; Klein 2011).
• People who are not deficient. In women with obesity who were not selenium-deficient, a nut supplying about 1,261 mcg raised pro-inflammatory gene expression (Duarte 2019).
• People with diabetes. One study found fasting glucose rose after six months of Brazil nuts in people with type 2 diabetes (Macan 2022), while another, in healthy adults, found it fell (Donadio 2018). Decisions about diet in diabetes, and about any supplement, belong with a clinician.
• People on haemodialysis or with kidney disease. This is the group in which trials reported the broadest biomarker changes (Stockler-Pinto 2014; da Silva 2022), and also a group whose mineral handling differs from that of healthy people; those trials were small and uncontrolled.

Allergy, aflatoxin and the selenium overload cases are covered on the main Brazil nuts page and in selenium overload and safety.

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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
• Brazil Nuts: Nutrient Profile — the full composition table
• Selenium and Thyroid — the deiodinases and the thyroid trials
• Cholesterol and Inflammation — the lipid and cytokine results
• Brain Aging and Cognition — the mild cognitive impairment trial
• Selenium Overload and Safety — the upper limit and selenosis
• Selenium — the mineral itself
• Selenium: Antioxidant Defense — the mineral-side view
• Selenium and Cancer Prevention — the supplement trials in depth
• Selenium Toxicity
• Selenium Test — the blood test
• Glutathione Peroxidase — the enzyme the trials measured
• Glutathione — the molecule GPx depends on
• Methionine — the amino acid selenomethionine imitates
• Oxidative Stress
• Dialysis and Transplant
• Type 2 Diabetes

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Key Research Papers

1. Thomson CD, Chisholm A, McLachlan SK, et al. Brazil nuts: an effective way to improve selenium status. The American journal of clinical nutrition. 2008;87(2):379-84. PubMed PMID: 18258628
2. da Silva A, Silveira BKS, de Freitas BVM, et al. Effects of Regular Brazil Nut (Bertholletia excelsa H.B.K.) Consumption on Health: A Systematic Review of Clinical Trials. Foods (Basel, Switzerland). 2022;11(18). PubMed PMID: 36141050
3. Huguenin GV, Oliveira GM, Moreira AS, et al. Improvement of antioxidant status after Brazil nut intake in hypertensive and dyslipidemic subjects. Nutrition journal. 2015;14:54. PubMed PMID: 26022214
4. Carvalho RF, Huguenin GV, Luiz RR, et al. Intake of partially defatted Brazil nut flour reduces serum cholesterol in hypercholesterolemic patients--a randomized controlled trial. Nutrition journal. 2015;14:59. PubMed PMID: 26077768
5. Stockler-Pinto MB, Mafra D, Moraes C, et al. Brazil nut (Bertholletia excelsa, H.B.K.) improves oxidative stress and inflammation biomarkers in hemodialysis patients. Biological trace element research. 2014;158(1):105-12. PubMed PMID: 24504745
6. Rita Cardoso B, Apolinário D, da Silva Bandeira V, et al. Effects of Brazil nut consumption on selenium status and cognitive performance in older adults with mild cognitive impairment: a randomized controlled pilot trial. European journal of nutrition. 2016;55(1):107-16. PubMed PMID: 25567069
7. Coutinho-Wolino KS, da Cruz BO, Cardozo LFMF, et al. Brazil nut supplementation does not affect trimethylamine-n-oxide plasma levels in patients with coronary artery disease. Journal of food biochemistry. 2022;46(8):e14201. PubMed PMID: 35467017
8. Macan TP, de Amorim TA, Damiani AP, et al. Brazil nut prevents oxidative DNA damage in type 2 diabetes patients. Drug and chemical toxicology. 2022;45(3):1066-1072. PubMed PMID: 32811197
9. Duarte GBS, Reis BZ, Rogero MM, et al. Consumption of Brazil nuts with high selenium levels increased inflammation biomarkers in obese women: A randomized controlled trial. Nutrition (Burbank, Los Angeles County, Calif.). 2019;63-64:162-168. PubMed PMID: 31026738
10. Reis BZ, Duarte GBS, Vargas-Mendez E, et al. Brazil nut intake increases circulating miR-454-3p and miR-584-5p in obese women. Nutrition research (New York, N.Y.). 2019;67:40-52. PubMed PMID: 31150916
11. Silveira BKS, Silva AD, Rocha DMUP, et al. Brazil Nut (Bertholletia excelsa H.B.K.) Consumption in Energy-Restricted Intervention Decreases Proinflammatory Markers and Intestinal Permeability of Women with Overweight/Obesity: A Controlled Trial (Brazilian Nuts Study). The Journal of nutrition. 2024;154(9):2670-2679. PubMed PMID: 39025334
12. Donadio JLS, Rogero MM, Guerra-Shinohara EM, et al. SEPP1 polymorphisms modulate serum glucose and lipid response to Brazil nut supplementation. European journal of nutrition. 2018;57(5):1873-1882. PubMed PMID: 28501922
13. Moriguchi Watanabe L, Bueno AC, de Lima LF, et al. Genetically determined variations of selenoprotein P are associated with antioxidant, muscular, and lipid biomarkers in response to Brazil nut consumption by patients using statins. The British journal of nutrition. 2022;127(5):679-686. PubMed PMID: 33947487
14. Lima LW, Stonehouse GC, Walters C, et al. Selenium Accumulation, Speciation and Localization in Brazil Nuts (Bertholletia excelsa H.B.K.). Plants (Basel, Switzerland). 2019;8(8). PubMed PMID: 31426292
15. Alcântara DB, Dionísio AP, Artur AG, et al. Selenium in Brazil nuts: An overview of agronomical aspects, recent trends in analytical chemistry, and health outcomes. Food chemistry. 2022;372:131207. PubMed PMID: 34634585
16. Dumont E, Vanhaecke F, Cornelis R. Selenium speciation from food source to metabolites: a critical review. Analytical and bioanalytical chemistry. 2006;385(7):1304-23. PubMed PMID: 16830114
17. Lu J, Holmgren A. Selenoproteins. The Journal of biological chemistry. 2009;284(2):723-7. PubMed PMID: 18757362
18. Alexander J. Selenium. Novartis Foundation symposium. 2007;282:143-9; discussion 149-53, 212-8. PubMed PMID: 17913229
19. Schomburg L. Selenoprotein P - Selenium transport protein, enzyme and biomarker of selenium status. Free radical biology & medicine. 2022;191:150-163. PubMed PMID: 36067902
20. Achouba A, Dumas P, Ouellet N, et al. Plasma levels of selenium-containing proteins in Inuit adults from Nunavik. Environment international. 2016;96:8-15. PubMed PMID: 27588697
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