Definition and research guide
This page combines a MeSH definition, publication statistics and selected research abstracts. It is a starting point for reading the literature, not a medical textbook or a systematic evidence review.
Content available: 4 complete abstracts (747 words), 10 references. Full article text is not stored or reproduced here; follow the PMID, DOI or PMC links to read the original sources and their access terms.
Definition
A nutritional condition produced by a deficiency of vitamin E in the diet, characterized by posterior column and spinocerebellar tract abnormalities, areflexia, ophthalmoplegia, and disturbances of gait, proprioception, and vibration. In premature infants vitamin E deficiency is associated with hemolytic anemia, thrombocytosis, edema, intraventricular hemorrhage, and increasing risk of retrolental fibroplasia and bronchopulmonary dysplasia. An apparent inborn error of vitamin E metabolism, named familial isolated vitamin E deficiency, has recently been identified. (Cecil Textbook of Medicine, 19th ed, p1181)
Definition: NLM Medical Subject Headings (MeSH) scope note (Public domain (U.S. National Library of Medicine); attribution requested). View the MeSH record.
Also known as: Deficiency, Vitamin E; Deficiencies, Vitamin E; Vitamin E Deficiencies.
Where it fits in the MeSH classification
- Broader topics
- Avitaminosis
- Narrower topics
- Steatitis
Related concepts
Research landscape
PubMed indexes 3,630 records tagged with the MeSH heading “Vitamin E Deficiency” (counts retrieved 2026-10-31). 79 of them (2.2%) were published from 2020 onward, and the busiest period so far is through 1999 with 2,914 records.
Reviews account for 377 records (10.4%) and meta-analyses for 7. Randomized controlled trials number 24 (0.7%) as a share of all records on the topic. Randomized trials make up only a small share of this literature, so much of what is known comes from laboratory, observational or descriptive work.
Show the data
| Period | Records |
|---|---|
| through 1999 | 2,914 |
| 2000-2009 | 404 |
| 2010-2019 | 233 |
| 2020 onward | 79 |
Publication-type chart data
| Type | Records | Share |
|---|---|---|
| Reviews | 377 | 10.4% |
| Meta-analyses | 7 | 0.2% |
| Randomized controlled trials | 24 | 0.7% |
Method: PubMed query "Vitamin E Deficiency"[MeSH Terms] with publication-type and date filters, retrieved 2026-10-31.
Reading the evidence in metabolism and endocrine disease
Studies of diabetes, obesity and hormone disorders often follow blood tests such as glucose, HbA1c or hormone levels, which are stand-ins for outcomes that matter more, such as complications. Lifestyle and diet research is largely observational, and weight and diabetes trials can differ in how long people were followed. Nothing on this page is advice about medicines, insulin or diet; talk to a qualified clinician about your own situation. Check whether the outcome was a lab value or a clinical event, and the type and duration of the condition studied.
Evidence from open-access studies
These open-access studies come from PubMed’s best-match results for this heading (papers whose main topic it is), ranked here by citation count, with one recent addition. Each abstract is reproduced in full under its recorded open licence so that you can read the authors’ own words. They illustrate the literature; they are not a systematic summary of it. Citation counts measure attention, not reliability or clinical benefit.
| Study / authors | Year | Source label / design | Europe PMC citations | Licence / source |
|---|---|---|---|---|
| GPX4 and vitamin E cooperatively protect hematopoietic stem and progenitor cells from lipid peroxidation and ferroptosis | 2021 | Research article Design not recorded in structured metadata | 178 | cc by PMID 34267193 · DOI · PMC8282880 |
| Vitamin E deficiency and risk of equine motor neuron disease | 2007 | Research article Design not recorded in structured metadata | 28 | cc by PMID 17605810 · DOI · PMC1950518 |
| Complex Virome in a Mesenteric Lymph Node from a Californian Sea Lion (Zalophus Californianus) with Polyserositis and Steatitis | 2020 | Research article Design not recorded in structured metadata | 17 | cc by PMID 32718049 · DOI · PMC7472147 |
| Vitamin E Levels in Preterm and Full-Term Infants: A Systematic Review | 2022 | Systematic review Design not recorded in structured metadata | 10 | cc by PMID 35684057 · DOI · PMC9183035 |
GPX4 and vitamin E cooperatively protect hematopoietic stem and progenitor cells from lipid peroxidation and ferroptosis [1]
Abstract reading summary — source excerpts
- Opening excerpt
- Ferroptosis, a newly defined mode of regulated cell death caused by unbalanced lipid redox metabolism, is implicated in various tissue injuries and tumorigenesis.
- Closing excerpt
- Collectively, we demonstrate that GPX4 and vitamin E cooperatively maintain lipid redox balance and prevent ferroptosis in HSPCs.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (188 words)
Ferroptosis, a newly defined mode of regulated cell death caused by unbalanced lipid redox metabolism, is implicated in various tissue injuries and tumorigenesis. However, the role of ferroptosis in stem cells has not yet been investigated. Glutathione peroxidase 4 (GPX4) is a critical suppressor of lipid peroxidation and ferroptosis. Here, we study the function of GPX4 and ferroptosis in hematopoietic stem and progenitor cells (HSPCs) in mice with Gpx4 deficiency in the hematopoietic system. We find that Gpx4 deletion solely in the hematopoietic system has no significant effect on the number and function of HSPCs in mice. Notably, hematopoietic stem cells (HSCs) and hematopoietic progenitor cells lacking Gpx4 accumulated lipid peroxidation and underwent ferroptosis in vitro. α-Tocopherol, the main component of vitamin E, was shown to rescue the Gpx4-deficient HSPCs from ferroptosis in vitro. When Gpx4 knockout mice were fed a vitamin E-depleted diet, a reduced number of HSPCs and impaired function of HSCs were found. Furthermore, increased levels of lipid peroxidation and cell death indicated that HSPCs undergo ferroptosis. Collectively, we demonstrate that GPX4 and vitamin E cooperatively maintain lipid redox balance and prevent ferroptosis in HSPCs.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 34267193 · DOI · PMC8282880
Vitamin E deficiency and risk of equine motor neuron disease [2]
Abstract reading summary — source excerpts
- Opening excerpt
- BackgroundEquine motor neuron disease (EMND) is a spontaneous neurologic disorder of adult horses which results from the degeneration of motor neurons in the spinal cord and brain stem.
- Closing excerpt
- Reproducing this disease in a natural animal model for the first time will enable us to carry out studies to test specific hypotheses regarding the mechanism by which the disease occurs.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (233 words)
BackgroundEquine motor neuron disease (EMND) is a spontaneous neurologic disorder of adult horses which results from the degeneration of motor neurons in the spinal cord and brain stem. Clinical manifestations, pathological findings, and epidemiologic attributes resemble those of human motor neuron disease (MND). As in MND the etiology of the disease is not known. We evaluated the predisposition role of vitamin E deficiency on the risk of EMND.MethodsEleven horses at risk of EMND were identified and enrolled in a field trial at different times. The horses were maintained on a diet deficient in vitamin E and monitored periodically for levels of antioxidants--alpha-tocopherols, vitamins A, C, beta-carotene, glutathione peroxidase (GSH-Px), and erythrocytic superoxide dismutase (SOD1). In addition to the self-control another parallel control group was included. Survival analysis was used to assess the probability of developing EMND past a specific period of time.ResultsThere was large variability in the levels of vitamins A and C, beta-carotene, GSH-Px, and SOD1. Plasma vitamin E levels dropped significantly over time. Ten horses developed EMND within 44 months of enrollment. The median time to develop EMND was 38.5 months. None of the controls developed EMND.ConclusionThe study elucidated the role of vitamin E deficiency on the risk of EMND. Reproducing this disease in a natural animal model for the first time will enable us to carry out studies to test specific hypotheses regarding the mechanism by which the disease occurs.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 17605810 · DOI · PMC1950518
Complex Virome in a Mesenteric Lymph Node from a Californian Sea Lion (Zalophus Californianus) with Polyserositis and Steatitis [3]
Abstract reading summary — source excerpts
- Opening excerpt
- An emaciated subadult free-ranging California sea lion (Csl or Zalophus californianus) died following stranding with lesions similar to 11 other stranded animals characterized by chronic disseminated granulomatous inflammation with necrotizing steatitis and vasculitis, involving visceral adipose tissues in the thoracic and peritoneal cavities.
- Closing excerpt
- The causal or contributory role of these viruses to the gross and histologic lesions of this sea lion remains to be determined.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (111 words)
An emaciated subadult free-ranging California sea lion (Csl or Zalophus californianus) died following stranding with lesions similar to 11 other stranded animals characterized by chronic disseminated granulomatous inflammation with necrotizing steatitis and vasculitis, involving visceral adipose tissues in the thoracic and peritoneal cavities. Histologically, affected tissues had extensive accumulations of macrophages with perivascular lymphocytes, plasma cells, and fewer neutrophils. Using viral metagenomics on a mesenteric lymph node six mammalian viruses were identified consisting of novel parvovirus, polyomavirus, rotavirus, anellovirus, and previously described Csl adenovirus 1 and Csl bocavirus 4. The causal or contributory role of these viruses to the gross and histologic lesions of this sea lion remains to be determined.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 32718049 · DOI · PMC7472147
Vitamin E Levels in Preterm and Full-Term Infants: A Systematic Review [4]
Abstract reading summary — source excerpts
- Opening excerpt
- Vitamin E deficiency (VED) is associated with clinical repercussions in preterm newborns (PTN), but low levels are also found in full-term newborns (TN).
- Closing excerpt
- Our findings demonstrate that further investigations are needed to standardize this classification and to monitor vitamin E status in birth and postnatal with adequate bias control.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (215 words)
Vitamin E deficiency (VED) is associated with clinical repercussions in preterm newborns (PTN), but low levels are also found in full-term newborns (TN). As this inadequacy can compromise neurogenesis in childhood, studies are needed to assess whether there is a difference in vitamin E status among newborns according to gestational age to provide support for neonatal monitoring protocols. This systematic review presents a synthesis of the available information on the vitamin E status among PTN and TN. The review was performed according to Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA). Observational studies that evaluated alpha-tocopherol levels were searched in the databases reported in the protocol registered in PROSPERO (CRD42021165152). The Newcastle-Ottawa Scale was used to assess the methodological quality. Overall, 1809 articles were retrieved; 10 were included in the systematic review. In the PTN, the alpha-tocopherol levels ranged from 3.9 to 8.5 mmol/L, while in TN, they were 4.9 to 14.9 mmol/L, and VED ranged from 19% to 100% in newborns. Despite substantial heterogeneity in research methodology and VED classification, the results suggest that the alpha-tocopherol levels among preterm and full-term newborns is below the recommended levels. Our findings demonstrate that further investigations are needed to standardize this classification and to monitor vitamin E status in birth and postnatal with adequate bias control.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 35684057 · DOI · PMC9183035
Key reviews and meta-analyses
The most cited review-type papers among PubMed’s best-match results for this heading, listed with bibliographic details only. Follow the links for the full text and access terms.
- Research article Vitamin E regulatory mechanisms [5]
- Research article The ins and outs of mitochondrial dysfunction in NASH [6]
- Research article Vitamin E inadequacy in humans: causes and consequences [7]
- Research article Vitamin E: the shrew waiting to be tamed [8]
- Research article Vitamin E deficiency and neurologic disease [9]
- Research article Vitamin E deficiency in developing countries [10]
References
- Hu Q, Zhang Y, Lou H, Ou Z, Liu J, Duan W, et al.. GPX4 and vitamin E cooperatively protect hematopoietic stem and progenitor cells from lipid peroxidation and ferroptosis. . 2021. PMID 34267193 · DOI · PMC8282880
- Mohammed HO, Divers TJ, Summers BA, de Lahunta A. Vitamin E deficiency and risk of equine motor neuron disease. . 2007. PMID 17605810 · DOI · PMC1950518
- Altan E, Delaney MA, Colegrove KM, Spraker TR, Wheeler EA, Deng X, et al.. Complex Virome in a Mesenteric Lymph Node from a Californian Sea Lion (Zalophus Californianus) with Polyserositis and Steatitis. . 2020. PMID 32718049 · DOI · PMC7472147
- Assunção DGF, Silva LTPD, Camargo JDAS, Cobucci RN, Ribeiro KDDS. Vitamin E Levels in Preterm and Full-Term Infants: A Systematic Review. . 2022. PMID 35684057 · DOI · PMC9183035
- Traber MG. Vitamin E regulatory mechanisms. Annu Rev Nutr. 2007. PMID 17439363 · DOI
- Fromenty B, Robin MA, Igoudjil A, Mansouri A, Pessayre D. The ins and outs of mitochondrial dysfunction in NASH. Diabetes Metab. 2004. PMID 15223984 · DOI
- Traber MG. Vitamin E inadequacy in humans: causes and consequences. Adv Nutr. 2014. PMID 25469382 · DOI · PMC4188222
- Brigelius-Flohé R. Vitamin E: the shrew waiting to be tamed. Free Radic Biol Med. 2009. PMID 19133328 · DOI
- Sokol RJ. Vitamin E deficiency and neurologic disease. Annu Rev Nutr. 1988. PMID 3060170 · DOI
- Dror DK, Allen LH. Vitamin E deficiency in developing countries. Food Nutr Bull. 2011. PMID 22164974 · DOI
About this article
- Sources
- NLM Medical Subject Headings (definition, synonyms); NCBI PubMed (counts, identifiers); Europe PMC (open-access abstracts and citation counts).
- Verification
- Every reference was resolved against PubMed on 2026-11-04; title, year and DOI matched.
- Review state
- automated source verified; no human expert review has been recorded yet.
- Version
- 1, last updated 2026-11-04.
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Evidence strength
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