Selenium level
Serum selenium tracks intake. Selenoproteins stop rising at about 70 to 90 µg/L by a US report and near 125 for selenoprotein P by later trials. A European guideline calls 60 adequate and acts below 32. Trials that raised selenium did not lower cancer rates, and supplements raised type 2 diabetes risk about 11%. Inflammation lowers the result.
- Status
- A blood test ordered by a clinician. A US national survey laboratory measures it in serum by inductively coupled plasma mass spectrometry [1]. Reports print the result in µg/L or ng/mL, which give the same number.
- Measures
- The total concentration of selenium in serum or plasma, whose main components are selenoprotein P and extracellular glutathione peroxidase [2].
- Also called
- serum selenium, plasma selenium, selenium serum, selenium plasma, selenium blood test, Se
- Tested for
- selenium deficiency, thyroid health, immune function, hair loss, brittle nails, checking a selenium supplement, selenium excess, monitoring nutrition after surgery
Strong several reviews agree · Moderate one review or consistent trials · Limited one or a few small studies · Untested no study in people, listed with what it rests on
Linked in research3
- ModerateShown in trials to rise with selenoproteins only up to a plateau, near 70 to 90 µg/L for glutathione peroxidase and about 125 µg/L for selenoprotein P.
- ModerateShown in trials to raise type 2 diabetes risk about 11% when selenium supplements were taken, and linked to more diabetes at higher blood selenium.
- LimitedLimited evidence: one US cohort linked serum selenium to fewer deaths up to about 130 µg/L and more above 150, and one trial of 300 µg a day raised deaths.
Reported risks0
No risks sourced yet.
Reference ranges
Each range is the one its source published, in µg/L. Also reported in µmol/L. Where sources differ, each is shown.
Institute of Medicine Dietary Reference Intakes report, 2000
Adults, as the plasma level at which the report places the plateau of selenoprotein synthesis · [3]
| Range | What the source calls it |
|---|---|
| below 70 µg/L | No name given |
| 70 to 90 µg/L | "plateau concentration" |
| above 90 µg/L | No name given |
Printed as 7 µg/dL and 7 to 9 µg/dL, which are 70 and 70 to 90 µg/L. The report prints 0.8 and 0.8 to 1.1 µmol/L beside them, a rounded equivalent. It states that a plasma selenium below 7 µg/dL indicates that the synthesis of selenoproteins has not yet plateaued, and that concentrations above the plateau are associated with maximal plasma selenoproteins. Above the plateau, it states, plasma selenium depends heavily on the chemical form of selenium eaten. The report gives no plasma cut point for excess, so this block does not classify high results. It reports that in the US national survey of 1988 to 1994 the median serum selenium was 124 µg/L, and the 1st and 99th percentiles were 95 and 163 µg/L [3].
ESPEN micronutrient guideline, 2022
Adults under medical nutrition care without an inflammatory response, meaning a C-reactive protein below 20 mg/L · [2]
| Range | What the source calls it |
|---|---|
| below 32 µg/L | No name given |
| 32 to 59 µg/L | No name given |
| 60 or above µg/L | "adequate" |
Printed as below 0.4 µmol/L (below 32 µg/L) and 0.75 µmol/L (60 µg/L). Below 32 µg/L the guideline calls for selenium to be given in every case. Below 60 µg/L it calls for supplements in a patient without an inflammatory response. It describes 60 µg/L as adequate because plasma glutathione peroxidase begins to plateau there, and puts the level needed for full glutathione peroxidase function at around 90 µg/L. One recommendation in the same guideline prints the lower cut point as 30 µg/L. The guideline states that upper limits for plasma selenium before toxicity symptoms appear are not clear, ranging from about 6 to about 12 µmol/L in its sources, which is about 470 to 950 µg/L by its own factor. It also asks for reference intervals for selenium to be established locally, because blood selenium follows the local diet [2].
US national survey laboratory procedure manual, 2015 to 2016
People tested in the US national survey, as the reference range printed for the serum assay · [1], [3]
| Range | What the source calls it |
|---|---|
| below 95 µg/L | No name given |
| 95 to 165 µg/L | "reference range" |
| above 165 µg/L | No name given |
The manual lists 95 to 165 µg/L as the 95% reference range for serum selenium and attributes it to a clinical chemistry textbook and a handbook on metals, not to survey participants [1]. The range is close to the 1st and 99th percentiles of the 1988 to 1994 US survey, 95 and 163 µg/L [3]. It describes where results in the US fall. Its lower limit sits above the 60 to 90 µg/L at which the two sources above place the plateau of selenoproteins, so a result below 95 is not by itself below those thresholds. The manual's default boundary for reporting an elevated result is 330 µg/L [1].
Liu and colleagues, Chinese national survey, 2017, pregnancy
Pregnant women at any stage of pregnancy · [4]
| Range | What the source calls it |
|---|---|
| below 39.9 µg/L | No name given |
| 39.9 to 111.6 µg/L | "reference values" |
| above 111.6 µg/L | No name given |
The 2.5th to 97.5th percentiles in 1,400 pregnant women, mean age 27, in the China Nutrition and Health Survey of 2010 to 2012, measured by high-resolution inductively coupled plasma mass spectrometry. The median was 72.2 µg/L. By trimester the medians were 77.6, 76.0 and 65.0 µg/L, and the authors report that serum selenium decreased significantly as pregnancy advanced. The values describe where most women in one country's survey fell, and blood selenium differs between countries with the selenium content of the diet [4][2].
What has been shown to move it
Shown to lower it1
Selenium
Limited evidence: low selenium in 20% of children on the diet for epilepsy at one center, with one case of heart muscle disease.
The numbers and sources
- How common
- Very common: more than 1 in 10 people.
- Effect
- At one center, 9 children on the diet had low selenium, including one with cardiomyopathy and no detectable whole-blood selenium. Of 39 more children tested, 8 had levels below the normal range, 6 at first test and 2 on later testing. Supplementation raised levels in all [13]. In 91 children over 12 months, mean plasma selenium fell from 0.95 to 0.88 μmol/L [14].
- Population
- Children treated for drug-resistant epilepsy [13][14].
- Sources
- [13], [14]
- Caveats
- Children on a medical ketogenic diet with prescribed supplements. No adult data on selenium were located.
How it compares with the reference method
Mixed results1
Week to week variation in one person
One study found serum selenium varied 7.7% from week to week within the same person over 10 weeks.
The numbers and sources
- Compared with
- The same person's results on 10 weekly draws
- Effect
- Within-person variation was 7.7% (95% CI 7.2 to 8.2), similar in men and women. Mean selenium differed between men and women by 0.06 µmol/L (6.0%). The authors describe marked individuality for selenium and conclude that population reference limits are of limited use for following one person over time [14].
- Population
- 68 adults in Turkey whom the study classed as healthy, 36 women and 32 men, sampled weekly for 10 weeks and measured by inductively coupled plasma mass spectrometry [14].
- Sources
- [14]
- Caveats
- One laboratory and 68 people. The study states no threshold for agreement, so the result is given as numbers only [14].
Did not match the reference method2
Inflammation and infection
Limited evidence: plasma selenium falls as inflammation rises, by about half when C-reactive protein is above 80 mg/L, without a matching loss of body selenium.
The numbers and sources
- Compared with
- Plasma selenium in patients of the same laboratory with the lowest C-reactive protein
- Effect
- In blood samples from a hospital laboratory, plasma selenium fell with increasing severity of the acute inflammatory response, beginning at C-reactive protein of only 5 to 10 mg/L, and the median fell by more than 40% in the most inflamed group. The authors conclude that a plasma selenium can be interpreted reliably only when C-reactive protein is below 10 mg/L [13]. A European guideline gives expected falls of 15% to 25% at C-reactive protein of 10 to 40 mg/L, about 35% at 41 to 80 mg/L and about 50% above 80 mg/L. It attributes the fall to selenium moving out of the circulation, because plasma selenium returns to normal in many cases without supplementation [2].
- Population
- 2,217 samples from 1,303 patients screened for micronutrients in one UK laboratory between 2001 and 2011 [13].
- Sources
- [13], [2]
- Caveats
- The change varied markedly from patient to patient, so no single correction fits an individual result [13].
The form of selenium eaten
Shown in trials to keep rising with selenomethionine intake after selenoproteins have leveled off, so a high result reflects intake and its chemical form.
The numbers and sources
- Compared with
- Plasma selenoprotein P and glutathione peroxidase in the same trials
- Effect
- In a 40-week trial of selenomethionine in China, glutathione peroxidase and selenoprotein P reached a ceiling while plasma selenium showed no tendency to do so [5]. In a UK trial, 50, 100 and 200 µg a day of selenium-enriched yeast raised plasma selenium from a mean of 95.7 µg/L to 118.3, 152.0 and 177.4 µg/L [6]. A US report states that above the plateau of selenoprotein synthesis the plasma selenium concentration is highly dependent on the chemical form of the element ingested [3].
- Population
- 98 adults in China [5]. 119 adults aged 50 to 64 in the United Kingdom [6].
- Sources
- [5], [6], [3]
- Caveats
- Both trials used organic forms of selenium. The US report calls for studies of plasma selenium at intakes up to the tolerable upper intake level before it is used to assess high intakes [3].
What studies tie it to
Linked in research3
Selenoprotein levels and where they plateau
Shown in trials to rise with selenoproteins only up to a plateau, near 70 to 90 µg/L for glutathione peroxidase and about 125 µg/L for selenoprotein P.
The numbers and sources
- Effect
- A US report places the plateau of plasma selenoproteins at a serum or plasma selenium of 70 to 90 µg/L [3]. A European guideline states that plasma glutathione peroxidase begins to plateau at 60 µg/L and is saturated at about 1.20 µmol/L, about 95 µg/L [2]. In a 40-week trial in selenium-deficient adults in China, glutathione peroxidase activity reached its ceiling at a total intake of 35 µg a day and selenoprotein P at 49 µg a day, while plasma selenium itself showed no tendency to level off [5]. In a 12-week UK trial, adults started at a mean plasma selenium of 95.7 µg/L. Selenoprotein P rose in every selenium group, and the authors conclude that 50 µg a day on top of a habitual intake of about 55 µg a day was required to bring it to its ceiling. That dose took plasma selenium to 118.3 µg/L. Platelet glutathione peroxidase did not change [6]. Authors of a later trial put the plateau of selenoprotein P at a plasma selenium of about 125 µg/L [7].
- Population
- 98 adults in China with a dietary selenium intake of 14 µg a day [5]. 119 men and women aged 50 to 64 in the United Kingdom [6].
- Sources
- [3], [2], [5], [6], [7]
- Caveats
- These are laboratory endpoints. The trials did not count illness or deaths, and the sources place the plateau at different levels depending on which selenoprotein they measured. The authors of the 2018 trial write that whether sustained concentrations above the plateau are beneficial or detrimental is unknown [7].
Type 2 diabetes at higher levels
Shown in trials to raise type 2 diabetes risk about 11% when selenium supplements were taken, and linked to more diabetes at higher blood selenium.
The numbers and sources
- Effect
- In a meta-analysis, trials of 200 µg of selenium a day against placebo found more new type 2 diabetes with selenium (RR 1.11, 95% CI 1.01 to 1.22). In the observational studies the risk rose roughly in line with plasma or serum selenium, with a relative risk of 3.6 (1.4 to 9.4) at 140 µg/L against less than 45 µg/L [8]. In one of the trials, 200 µg a day for an average of 7.7 years produced a hazard ratio of 1.55 (1.03 to 2.33). Risk rose across thirds of plasma selenium at the start of the trial, and people in the top third had a hazard ratio of 2.70 (1.30 to 5.61) with supplementation [9]. Authors of a later trial give about 122 µg/L as the plasma selenium of that top third [10].
- Population
- 5 randomized trials and 50 potentially eligible nonexperimental studies [8]. 1,202 people seen in dermatology clinics in the eastern United States [9].
- Sources
- [8], [9], [10]
- Caveats
- Diabetes was a secondary outcome in the 2007 trial, and diagnoses were self-reported and then validated in most participants [9]. The meta-analysis authors describe the relative increase in risk as small [8]. The 122 µg/L figure is taken from a later paper's description of the trial, not from the trial report itself [10].
Death from any cause
Limited evidence: one US cohort linked serum selenium to fewer deaths up to about 130 µg/L and more above 150, and one trial of 300 µg a day raised deaths.
The numbers and sources
- Effect
- In US adults, the top third of serum selenium (130.39 µg/L or above) had fewer deaths from any cause than the bottom third (below 117.31 µg/L), with a hazard ratio of 0.83 (95% CI 0.72 to 0.96), and fewer cancer deaths (0.69, 0.53 to 0.90). The relation was not a straight line: deaths fell as selenium rose to 130 µg/L and rose modestly above 150 µg/L. Cardiovascular deaths showed no association [11]. In a Danish trial in older adults with relatively low selenium, 300 µg a day for 5 years was followed by more deaths from any cause over the full 15 years of follow-up than placebo (HR 1.59, 95% CI 1.02 to 2.46). Doses of 100 and 200 µg a day showed no significant difference [7].
- Population
- 13,887 adults in the US national survey of 1988 to 1994, followed for up to 12 years [11]. 491 volunteers aged 60 to 74 in Denmark, with 158 deaths [7].
- Sources
- [11], [7]
- Caveats
- The cohort is observational, and mean serum selenium in it was 125.6 µg/L [11]. The trial was not designed to study deaths, its sample was small, and the excess appeared only at the highest dose [7].
Mixed results1
Cancer
Mixed results: cohort studies linked higher selenium to less cancer, while trials that raised selenium found no change in cancer rates.
The numbers and sources
- Effect
- In a Cochrane review, cohort studies comparing the highest with the lowest category of selenium exposure found lower cancer incidence (OR 0.72, 95% CI 0.55 to 0.93) and lower cancer mortality (OR 0.76, 0.59 to 0.97). In randomized trials at low risk of bias, selenium supplements did not change the incidence of any cancer (RR 1.01, 0.93 to 1.10) or of prostate cancer (RR 1.01, 0.90 to 1.14). In the largest trial, supplementation raised the risk of high-grade prostate cancer in participants with the highest selenium status at the start. The review found no confirmation of the earlier hypothesis that people with low blood selenium could lower their cancer risk by taking more [12].
- Population
- 10 randomized trials with 27,232 participants and 70 observational cohort studies with more than 2,360,000 participants [12].
- Sources
- [12]
- Caveats
- The review rates the trial evidence as high certainty and the observational evidence as very low certainty, citing exposure misclassification and unmeasured confounding. Trial participants were 88% male [12].
Sources
- Centers for Disease Control and Prevention, National Center for Health Statistics. National Health and Nutrition Examination Survey 2015-2016 Laboratory Procedure Manual: Zinc, Copper and Selenium, serum, inductively coupled plasma dynamic reaction cell mass spectrometry. Performed by the Division of Laboratory Sciences, National Center for Environmental Health. https://wwwn.cdc.gov/nchs/data/nhanes/public/2015/labmethods/CUSEZN_I_MET.pdf
- Berger MM, Shenkin A, Schweinlin A, et al. ESPEN micronutrient guideline. Clinical Nutrition. 2022. https://doi.org/10.1016/j.clnu.2022.02.015
- Institute of Medicine, Panel on Dietary Antioxidants and Related Compounds. Dietary Reference Intakes for Vitamin C, Vitamin E, Selenium, and Carotenoids. National Academies Press. 2000. https://doi.org/10.17226/9810
- Liu X, Zhang Y, Piao J, et al. Reference Values of 14 Serum Trace Elements for Pregnant Chinese Women: A Cross-Sectional Study in the China Nutrition and Health Survey 2010-2012. Nutrients. 2017. https://doi.org/10.3390/nu9030309
- Xia Y, Hill KE, Li P, et al. Optimization of selenoprotein P and other plasma selenium biomarkers for the assessment of the selenium nutritional requirement: a placebo-controlled, double-blind study of selenomethionine supplementation in selenium-deficient Chinese subjects. The American Journal of Clinical Nutrition. 2010. https://doi.org/10.3945/ajcn.2010.29642
- Hurst R, Armah CN, Dainty JR, et al. Establishing optimal selenium status: results of a randomized, double-blind, placebo-controlled trial. The American Journal of Clinical Nutrition. 2010. https://doi.org/10.3945/ajcn.2009.28169
- Rayman MP, Winther KH, Pastor-Barriuso R, et al. Effect of long-term selenium supplementation on mortality: Results from a multiple-dose, randomised controlled trial. Free Radical Biology and Medicine. 2018. https://doi.org/10.1016/j.freeradbiomed.2018.02.015
- Vinceti M, Filippini T, Rothman KJ. Selenium exposure and the risk of type 2 diabetes: a systematic review and meta-analysis. European Journal of Epidemiology. 2018. https://doi.org/10.1007/s10654-018-0422-8
- Stranges S, Marshall JR, Natarajan R, et al. Effects of Long-Term Selenium Supplementation on the Incidence of Type 2 Diabetes: A Randomized Trial. Annals of Internal Medicine. 2007. https://doi.org/10.7326/0003-4819-147-4-200708210-00175
- Rayman MP, Blundell-Pound G, Pastor-Barriuso R, et al. A Randomized Trial of Selenium Supplementation and Risk of Type-2 Diabetes, as Assessed by Plasma Adiponectin. PLOS ONE. 2012. https://doi.org/10.1371/journal.pone.0045269
- Bleys J, Navas-Acien A, Guallar E. Serum Selenium Levels and All-Cause, Cancer, and Cardiovascular Mortality Among US Adults. Archives of Internal Medicine. 2008. https://doi.org/10.1001/archinternmed.2007.74
- Vinceti M, Filippini T, Del Giovane C, et al. Selenium for preventing cancer. Cochrane Database of Systematic Reviews. 2018. https://doi.org/10.1002/14651858.CD005195.pub4
- Duncan A, Talwar D, McMillan DC, et al. Quantitative data on the magnitude of the systemic inflammatory response and its effect on micronutrient status based on plasma measurements. The American Journal of Clinical Nutrition. 2012. https://doi.org/10.3945/ajcn.111.023812
- Coşkun A, Carobene A, Aarsand AK, et al. Within- and between-subject biological variation data for serum zinc, copper and selenium obtained from 68 apparently healthy Turkish subjects. Clinical Chemistry and Laboratory Medicine. 2022. https://doi.org/10.1515/cclm-2021-0886