Editing Vitamin E (section)

== Deficiency ==
{{Main|Vitamin E deficiency}}

A worldwide summary of more than one hundred human studies reported a median of 22.1&nbsp;μmol/L for [[Serum (blood)|serum]] α-tocopherol and defined α-tocopherol deficiency as less than 12&nbsp;μmol/L. It cited a recommendation that serum α-tocopherol concentration be ≥30&nbsp;μmol/L to optimize health benefits.<ref name=Peter2016 /> In contrast, the U.S. Dietary Reference Intake text for vitamin E concluded that a [[blood plasma|plasma]] concentration of 12&nbsp;μmol/L was sufficient to achieve normal ex vivo hydrogen peroxide-induced [[hemolysis]].<ref name="DRItext" /> A 2014 review defined less than 9&nbsp;μmol/L as deficient, 9-12&nbsp;μmol/L as marginal, and greater than 12&nbsp;μmol/L as adequate.<ref name=Traber2014>{{cite journal | vauthors = Traber MG | title = Vitamin E inadequacy in humans: causes and consequences | journal = Advances in Nutrition | volume = 5 | issue = 5 | pages = 503–14 | date = September 2014 | pmid = 25469382 | pmc = 4188222 | doi = 10.3945/an.114.006254 }}</ref>

Regardless of which definition is used, vitamin E deficiency is rare in humans, occurring as a consequence of abnormalities in dietary fat absorption or metabolism rather than from a diet low in vitamin E.<ref name="DRItext" /> Cystic fibrosis and other fat malabsorption conditions can result in low serum vitamin E.<ref name=GOVe /> One example of a genetic abnormality in metabolism is mutations of genes coding for [[alpha-tocopherol transfer protein]] (α-TTP). Humans with this genetic defect exhibit a progressive neurodegenerative disorder known as [[ataxia]] with vitamin E deficiency (AVED) despite consuming normal amounts of vitamin E. Large amounts of alpha-tocopherol as a dietary supplement are needed to compensate for the lack of α-TTP.<ref name=Min2007>{{cite book |vauthors=Christopher Min K |title=Structure and function of alpha-tocopherol transfer protein: implications for vitamin E metabolism and AVED |volume=76 |pages=23–43 |date=2007 |pmid=17628170 |doi=10.1016/S0083-6729(07)76002-8 |series=Vitamins & Hormones |isbn=978-0-12-373592-8 |chapter=Structure and Function of α-Tocopherol Transfer Protein: Implications for Vitamin e Metabolism and AVED }}</ref><ref name=Niki2012>{{cite journal |vauthors = Niki E, Traber MG | title = A history of vitamin E |journal = Annals of Nutrition & Metabolism |volume = 61 |issue = 3 |pages = 207–12 |date = November 2012 |pmid = 23183290 |doi = 10.1159/000343106 | s2cid = 25667777 }}</ref>

[[Bariatric surgery]] as a treatment for obesity can lead to vitamin deficiencies. Long-term follow-up reported a 16.5% prevalence of vitamin E deficiency.<ref name=Chen2024>{{cite journal |vauthors=Chen L, Chen Y, Yu X, Liang S, Guan Y, Yang J, Guan B |title=Long-term prevalence of vitamin deficiencies after bariatric surgery: a meta-analysis |journal=Langenbecks Arch Surg |volume=409 |issue=1 |pages=226 |date=July 2024 |pmid=39030449 |doi=10.1007/s00423-024-03422-9 |url=}}</ref> There are guidelines for multivitamin supplementation, but adherence rates are reported to be less than 20%.<ref name=Ha2021>{{cite journal |vauthors=Ha J, Kwon Y, Kwon JW, Kim D, Park SH, Hwang J, Lee CM, Park S |title=Micronutrient status in bariatric surgery patients receiving postoperative supplementation per guidelines: Insights from a systematic review and meta-analysis of longitudinal studies |journal=Obes Rev |volume=22 |issue=7 |pages=e13249 |date=July 2021 |pmid=33938111 |doi=10.1111/obr.13249 |url=}}</ref>

Vitamin E deficiency due to either malabsorption or metabolic anomaly can cause [[Neurological disorder|nerve problems]] due to poor conduction of electrical impulses along [[nerve]]s due to changes in [[Myelin|nerve membrane]] structure and function. In addition to ataxia, vitamin E deficiency can cause [[peripheral neuropathy]], [[myopathy|myopathies]], [[retinopathy]], and impairment of immune responses.<ref name="DRItext" /><ref name=GOVe />