Vitamin E

availability_state

machinery_impairment Imported condition classification; unverified.

evidence_span

{"source_cache": "artifacts/creatine-research/17407807.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "6174f6169ebf6ca7e61bc61642e38841a9089aecdd278ad8fb2f2221cf847c35", "start_char": 0, "end_char": 1929, "text_sha256": "6174f6169ebf6ca7e61bc61642e38841a9089aecdd278ad8fb2f2221cf847c35"}

experimental_model

Acute guanidinoacetate exposure with biochemical assays and antioxidant pretreatment

exposure

Intrastriatal guanidinoacetate and in-vitro assays; taurine or combined vitamins E plus C pretreatment

limitations

Acute experimental precursor toxicity is not a human supplement trial or proof that antioxidant treatment corrects GAMT deficiency. Vitamin E and C were combined.

nutrient_topic

Creatine research collection; topical membership is not evidence of a direct dietary effect. · Creatine

organism

Young rats and rat striatal preparations

plain_language

The study tested two antioxidant vitamins together; it did not establish either vitamin as an effective treatment on its own.

primary_references

[creatine-p17407807] Evidence that the inhibitory effects of guanidinoacetate on the activities of the respiratory chain, Na+,K+-ATPase and creatine kinase can be differentially prevented by taurine and vitamins E and C administration in rat striatum in vivo. (2007). https://pubmed.ncbi.nlm.nih.gov/17407807/ DOI: 10.1016/j.bbadis.2007.02.005

tissue_or_cell_type

Striatum

trigger_kind

machinery_impairment Imported condition classification; unverified.

Creatine: synthesis, transport, phosphocreatine energetics and nutrient interactions (2026-09-17) · lines 789–800

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Acute guanidinoacetate exposure with biochemical assays and antioxidant pretreatment · source_derived_draft · unverified_draft

### creatine-vitamins-gaa-ck Combined vitamin E plus C pretreatment prevented guanidinoacetate-associated inhibition of creatine kinase and sodium/potassium ATPase. Condition category: machinery_impairment nutrient_topic: Creatine research collection; topical membership is not evidence of a direct dietary effect. plain_language: The study tested two antioxidant vitamins together; it did not establish either vitamin as an effective treatment on its own. organism: Young rats and rat striatal preparations tissue_or_cell_type: Striatum experimental_model: Acute guanidinoacetate exposure with biochemical assays and antioxidant pretreatment limitations: Acute experimental precursor toxicity is not a human supplement trial or proof that antioxidant treatment corrects GAMT deficiency. Vitamin E and C were combined. exposure: Intrastriatal guanidinoacetate and in-vitro assays; taurine or combined vitamins E plus C pretreatment evidence_span: {"source_cache": "artifacts/creatine-research/17407807.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "6174f6169ebf6ca7e61bc61642e38841a9089aecdd278ad8fb2f2221cf847c35", "start_char": 0, "end_char": 1929, "text_sha256": "6174f6169ebf6ca7e61bc61642e38841a9089aecdd278ad8fb2f2221cf847c35"} [creatine-p17407807] Evidence that the inhibitory effects of guanidinoacetate on the activities of the respiratory chain, Na+,K+-ATPase and creatine kinase can be differentially prevented by taurine and vitamins E and C administration in rat striatum in vivo. (2007). https://pubmed.ncbi.nlm.nih.gov/17407807/ DOI: 10.1016/j.bbadis.2007.02.005

availability_state

machinery_impairment Imported condition classification; unverified.

evidence_span

{"source_cache": "artifacts/creatine-research/17407807.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "6174f6169ebf6ca7e61bc61642e38841a9089aecdd278ad8fb2f2221cf847c35", "start_char": 0, "end_char": 1929, "text_sha256": "6174f6169ebf6ca7e61bc61642e38841a9089aecdd278ad8fb2f2221cf847c35"}

experimental_model

Acute guanidinoacetate exposure with biochemical assays and antioxidant pretreatment

exposure

Intrastriatal guanidinoacetate and in-vitro assays; taurine or combined vitamins E plus C pretreatment

limitations

Acute experimental precursor toxicity is not a human supplement trial or proof that antioxidant treatment corrects GAMT deficiency. Vitamin E and C were combined.

nutrient_topic

Creatine research collection; topical membership is not evidence of a direct dietary effect. · Creatine

organism

Young rats and rat striatal preparations

plain_language

Oxidative damage markers were altered in this preparation, alongside the enzyme effects.

primary_references

[creatine-p17407807] Evidence that the inhibitory effects of guanidinoacetate on the activities of the respiratory chain, Na+,K+-ATPase and creatine kinase can be differentially prevented by taurine and vitamins E and C administration in rat striatum in vivo. (2007). https://pubmed.ncbi.nlm.nih.gov/17407807/ DOI: 10.1016/j.bbadis.2007.02.005

tissue_or_cell_type

Striatum

trigger_kind

machinery_impairment Imported condition classification; unverified.

Creatine: synthesis, transport, phosphocreatine energetics and nutrient interactions (2026-09-17) · lines 802–813

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Acute guanidinoacetate exposure with biochemical assays and antioxidant pretreatment · source_derived_draft · unverified_draft

### creatine-vitamins-gaa-oxidation Combined vitamin E plus C pretreatment prevented the rise in the lipid-peroxidation readout after guanidinoacetate exposure. Condition category: machinery_impairment nutrient_topic: Creatine research collection; topical membership is not evidence of a direct dietary effect. plain_language: Oxidative damage markers were altered in this preparation, alongside the enzyme effects. organism: Young rats and rat striatal preparations tissue_or_cell_type: Striatum experimental_model: Acute guanidinoacetate exposure with biochemical assays and antioxidant pretreatment limitations: Acute experimental precursor toxicity is not a human supplement trial or proof that antioxidant treatment corrects GAMT deficiency. Vitamin E and C were combined. exposure: Intrastriatal guanidinoacetate and in-vitro assays; taurine or combined vitamins E plus C pretreatment evidence_span: {"source_cache": "artifacts/creatine-research/17407807.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "6174f6169ebf6ca7e61bc61642e38841a9089aecdd278ad8fb2f2221cf847c35", "start_char": 0, "end_char": 1929, "text_sha256": "6174f6169ebf6ca7e61bc61642e38841a9089aecdd278ad8fb2f2221cf847c35"} [creatine-p17407807] Evidence that the inhibitory effects of guanidinoacetate on the activities of the respiratory chain, Na+,K+-ATPase and creatine kinase can be differentially prevented by taurine and vitamins E and C administration in rat striatum in vivo. (2007). https://pubmed.ncbi.nlm.nih.gov/17407807/ DOI: 10.1016/j.bbadis.2007.02.005

availability_state

machinery_impairment Imported condition classification; unverified.

cross_nutrient

true

experimental_model

Longitudinal treated cohort; 10 abetalipoproteinemia and 3 homozygous hypobetalipoproteinemia patients

exposure

Combined oral vitamins A and E; mean 11.7 years follow-up, range 4–20; exact doses unavailable in abstract.

limitations

No randomized A-only, E-only or untreated comparator. Residual retinal disease is compatible with partial benefit; it is not proof that supplementation has no effect.

nutrient_topic

Vitamin E research collection; topical membership is not evidence of a direct dietary effect. · Vitamin E

organism

Homo sapiens

plain_language

Combined treatment did not fully prevent retinal abnormalities in every patient.

primary_references

[e-clin-retina2001] Long-term assessment of combined vitamin A and E treatment for the prevention of retinal degeneration in abetalipoproteinaemia and hypobetalipoproteinaemia patients. (2001). https://pubmed.ncbi.nlm.nih.gov/11767031/ DOI: 10.1038/eye.2001.167

tissue_or_cell_type

Retina

trigger_kind

machinery_impairment Imported condition classification; unverified.

Vitamin E: transport, membrane protection and nutrient interactions (2026-09-17) · lines 1466–1477

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Longitudinal treated cohort; 10 abetalipoproteinemia and 3 homozygous hypobetalipoproteinemia patients · source_derived_draft · unverified_draft

### e-clin-abetalipo-residual-retinopathy Despite combined vitamin A and E treatment, 11 of 13 ABL/HBL patients had subnormal mixed cone-rod electroretinogram amplitudes at long-term follow-up. Condition category: machinery_impairment nutrient_topic: Vitamin E research collection; topical membership is not evidence of a direct dietary effect. plain_language: Combined treatment did not fully prevent retinal abnormalities in every patient. organism: Homo sapiens tissue_or_cell_type: Retina experimental_model: Longitudinal treated cohort; 10 abetalipoproteinemia and 3 homozygous hypobetalipoproteinemia patients limitations: No randomized A-only, E-only or untreated comparator. Residual retinal disease is compatible with partial benefit; it is not proof that supplementation has no effect. exposure: Combined oral vitamins A and E; mean 11.7 years follow-up, range 4–20; exact doses unavailable in abstract. cross_nutrient: true [e-clin-retina2001] Long-term assessment of combined vitamin A and E treatment for the prevention of retinal degeneration in abetalipoproteinaemia and hypobetalipoproteinaemia patients. (2001). https://pubmed.ncbi.nlm.nih.gov/11767031/ DOI: 10.1038/eye.2001.167

cross_nutrient

true

experimental_model

Ten-week double-blind feeding trial; 42 premature infants

exposure

Placebo, 5 or 15 mg/day extra vitamin E; all feeds had E:PUFA at least 0.6, and no supplemental iron was given.

limitations

These findings are bounded by the contemporary feeds and absence of supplemental iron; they do not refute hemolysis in actual vitamin E deficiency. The design does not isolate iron as a causal modifier or establish the reported ratio as a universal recommendation.

nutrient_topic

Vitamin E research collection; topical membership is not evidence of a direct dietary effect. · Vitamin E

organism

Homo sapiens

plain_language

Early anemia was not automatically a vitamin E-shortage syndrome under these feeding conditions.

primary_references

[e-clin-neonatal1987] The early anaemia of the premature infant: is there a place for vitamin E supplementation? (1986). https://pubmed.ncbi.nlm.nih.gov/3676185/ DOI: 10.1079/bjn19860090

tissue_or_cell_type

Blood and erythrocytes

Vitamin E: transport, membrane protection and nutrient interactions (2026-09-17) · lines 1219–1230

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Ten-week double-blind feeding trial; 42 premature infants · source_derived_draft · unverified_draft

### e-clin-adequate-infant-feeds No infant developed clinical or hematological vitamin E-deficiency signs during the ten-week trial when feeds maintained the reported E:PUFA balance and no supplemental iron was given. Condition category: normal nutrient_topic: Vitamin E research collection; topical membership is not evidence of a direct dietary effect. plain_language: Early anemia was not automatically a vitamin E-shortage syndrome under these feeding conditions. organism: Homo sapiens tissue_or_cell_type: Blood and erythrocytes experimental_model: Ten-week double-blind feeding trial; 42 premature infants limitations: These findings are bounded by the contemporary feeds and absence of supplemental iron; they do not refute hemolysis in actual vitamin E deficiency. The design does not isolate iron as a causal modifier or establish the reported ratio as a universal recommendation. exposure: Placebo, 5 or 15 mg/day extra vitamin E; all feeds had E:PUFA at least 0.6, and no supplemental iron was given. cross_nutrient: true [e-clin-neonatal1987] The early anaemia of the premature infant: is there a place for vitamin E supplementation? (1986). https://pubmed.ncbi.nlm.nih.gov/3676185/ DOI: 10.1079/bjn19860090

availability_state

machinery_impairment Imported condition classification; unverified.

cross_nutrient

false

experimental_model

Uncontrolled one-year supplementation study; 24 genetically investigated AVED patients

exposure

Vitamin E 800 mg/day for one year; formulation stereochemistry not specified in the retrieved abstract.

limitations

Small uncontrolled genetic-disease cohort; no inference of complete reversal, a general population dose or isolated dietary deficiency.

nutrient_topic

Vitamin E research collection; topical membership is not evidence of a direct dietary effect. · Vitamin E

organism

Homo sapiens

plain_language

Treating the inherited vitamin E shortage modestly improved coordination in this study.

primary_references

[e-clin-aved2001] Effect of vitamin E supplementation in patients with ataxia with vitamin E deficiency. (2001). https://pubmed.ncbi.nlm.nih.gov/11554913/ DOI: 10.1046/j.1468-1331.2001.00273.x

tissue_or_cell_type

Nervous system and serum

trigger_kind

machinery_impairment Imported condition classification; unverified.

Vitamin E: transport, membrane protection and nutrient interactions (2026-09-17) · lines 1167–1178

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Uncontrolled one-year supplementation study; 24 genetically investigated AVED patients · source_derived_draft · unverified_draft

### e-clin-aved-ataxia Ataxia Rating Scale scores improved modestly but significantly after one year of vitamin E in the AVED cohort; results were better with shorter disease duration. Condition category: machinery_impairment nutrient_topic: Vitamin E research collection; topical membership is not evidence of a direct dietary effect. plain_language: Treating the inherited vitamin E shortage modestly improved coordination in this study. organism: Homo sapiens tissue_or_cell_type: Nervous system and serum experimental_model: Uncontrolled one-year supplementation study; 24 genetically investigated AVED patients limitations: Small uncontrolled genetic-disease cohort; no inference of complete reversal, a general population dose or isolated dietary deficiency. exposure: Vitamin E 800 mg/day for one year; formulation stereochemistry not specified in the retrieved abstract. cross_nutrient: false [e-clin-aved2001] Effect of vitamin E supplementation in patients with ataxia with vitamin E deficiency. (2001). https://pubmed.ncbi.nlm.nih.gov/11554913/ DOI: 10.1046/j.1468-1331.2001.00273.x

availability_state

machinery_impairment Imported condition classification; unverified.

cross_nutrient

false

experimental_model

Uncontrolled one-year supplementation study; 24 genetically investigated AVED patients

exposure

Vitamin E 800 mg/day for one year; formulation stereochemistry not specified in the retrieved abstract.

limitations

Small uncontrolled genetic-disease cohort; no inference of complete reversal, a general population dose or isolated dietary deficiency.

nutrient_topic

Vitamin E research collection; topical membership is not evidence of a direct dietary effect. · Vitamin E

organism

Homo sapiens

plain_language

Correcting the blood level did not reverse every established nerve deficit.

primary_references

[e-clin-aved2001] Effect of vitamin E supplementation in patients with ataxia with vitamin E deficiency. (2001). https://pubmed.ncbi.nlm.nih.gov/11554913/ DOI: 10.1046/j.1468-1331.2001.00273.x

tissue_or_cell_type

Nervous system and serum

trigger_kind

machinery_impairment Imported condition classification; unverified.

Vitamin E: transport, membrane protection and nutrient interactions (2026-09-17) · lines 1180–1191

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Uncontrolled one-year supplementation study; 24 genetically investigated AVED patients · source_derived_draft · unverified_draft

### e-clin-aved-residual-deficits Absent reflexes and posterior-column disturbances persisted despite normalization of serum vitamin E during AVED supplementation. Condition category: machinery_impairment nutrient_topic: Vitamin E research collection; topical membership is not evidence of a direct dietary effect. plain_language: Correcting the blood level did not reverse every established nerve deficit. organism: Homo sapiens tissue_or_cell_type: Nervous system and serum experimental_model: Uncontrolled one-year supplementation study; 24 genetically investigated AVED patients limitations: Small uncontrolled genetic-disease cohort; no inference of complete reversal, a general population dose or isolated dietary deficiency. exposure: Vitamin E 800 mg/day for one year; formulation stereochemistry not specified in the retrieved abstract. cross_nutrient: false [e-clin-aved2001] Effect of vitamin E supplementation in patients with ataxia with vitamin E deficiency. (2001). https://pubmed.ncbi.nlm.nih.gov/11554913/ DOI: 10.1046/j.1468-1331.2001.00273.x

availability_state

machinery_impairment Imported condition classification; unverified.

cross_nutrient

false

experimental_model

Uncontrolled one-year supplementation study; 24 genetically investigated AVED patients

exposure

Vitamin E 800 mg/day for one year; formulation stereochemistry not specified in the retrieved abstract.

limitations

Small uncontrolled genetic-disease cohort; no inference of complete reversal, a general population dose or isolated dietary deficiency.

nutrient_topic

Vitamin E research collection; topical membership is not evidence of a direct dietary effect. · Vitamin E

organism

Homo sapiens

plain_language

Extra vitamin E restored the blood measurement despite the inherited transport disorder.

primary_references

[e-clin-aved2001] Effect of vitamin E supplementation in patients with ataxia with vitamin E deficiency. (2001). https://pubmed.ncbi.nlm.nih.gov/11554913/ DOI: 10.1046/j.1468-1331.2001.00273.x

tissue_or_cell_type

Nervous system and serum

trigger_kind

machinery_impairment Imported condition classification; unverified.

Vitamin E: transport, membrane protection and nutrient interactions (2026-09-17) · lines 1154–1165

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Uncontrolled one-year supplementation study; 24 genetically investigated AVED patients · source_derived_draft · unverified_draft

### e-clin-aved-serum Serum vitamin E normalized during one year of supplementation in the 24-patient AVED cohort. Condition category: machinery_impairment nutrient_topic: Vitamin E research collection; topical membership is not evidence of a direct dietary effect. plain_language: Extra vitamin E restored the blood measurement despite the inherited transport disorder. organism: Homo sapiens tissue_or_cell_type: Nervous system and serum experimental_model: Uncontrolled one-year supplementation study; 24 genetically investigated AVED patients limitations: Small uncontrolled genetic-disease cohort; no inference of complete reversal, a general population dose or isolated dietary deficiency. exposure: Vitamin E 800 mg/day for one year; formulation stereochemistry not specified in the retrieved abstract. cross_nutrient: false [e-clin-aved2001] Effect of vitamin E supplementation in patients with ataxia with vitamin E deficiency. (2001). https://pubmed.ncbi.nlm.nih.gov/11554913/ DOI: 10.1046/j.1468-1331.2001.00273.x

cross_nutrient

false

experimental_model

HOPE/HOPE-TOO randomized trial and extension in vascular disease or diabetes; initial n=9541

exposure

Natural-source vitamin E 400 IU/day; median follow-up 7 years; extension included ongoing treatment and passive follow-up.

limitations

High-risk population and extension participation limits. Heart failure was a secondary outcome; no specific molecular cause is established by the trial. Natural-source vitamin E is reported; an exact ester identity is not inferred from the abstract.

nutrient_topic

Vitamin E research collection; topical membership is not evidence of a direct dietary effect. · Vitamin E

organism

Homo sapiens

plain_language

Longer supplementation did not lower major cardiovascular events in the studied high-risk patients.

primary_references

[e-clin-hope2005] Effects of long-term vitamin E supplementation on cardiovascular events and cancer: a randomized controlled trial. (2005). https://pubmed.ncbi.nlm.nih.gov/15769967/ DOI: 10.1001/jama.293.11.1338

tissue_or_cell_type

Cardiovascular clinical events

Vitamin E: transport, membrane protection and nutrient interactions (2026-09-17) · lines 1375–1386

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · HOPE/HOPE-TOO randomized trial and extension in vascular disease or diabetes; initial n=9541 · source_derived_draft · unverified_draft

### e-clin-hope-cardiovascular In HOPE/HOPE-TOO, vitamin E did not reduce major cardiovascular events (RR 1.04, 95% CI 0.96–1.14). Condition category: normal nutrient_topic: Vitamin E research collection; topical membership is not evidence of a direct dietary effect. plain_language: Longer supplementation did not lower major cardiovascular events in the studied high-risk patients. organism: Homo sapiens tissue_or_cell_type: Cardiovascular clinical events experimental_model: HOPE/HOPE-TOO randomized trial and extension in vascular disease or diabetes; initial n=9541 limitations: High-risk population and extension participation limits. Heart failure was a secondary outcome; no specific molecular cause is established by the trial. Natural-source vitamin E is reported; an exact ester identity is not inferred from the abstract. exposure: Natural-source vitamin E 400 IU/day; median follow-up 7 years; extension included ongoing treatment and passive follow-up. cross_nutrient: false [e-clin-hope2005] Effects of long-term vitamin E supplementation on cardiovascular events and cancer: a randomized controlled trial. (2005). https://pubmed.ncbi.nlm.nih.gov/15769967/ DOI: 10.1001/jama.293.11.1338

cross_nutrient

false

experimental_model

HOPE/HOPE-TOO randomized trial and extension in vascular disease or diabetes; initial n=9541

exposure

Natural-source vitamin E 400 IU/day; median follow-up 7 years; extension included ongoing treatment and passive follow-up.

limitations

High-risk population and extension participation limits. Heart failure was a secondary outcome; no specific molecular cause is established by the trial. Natural-source vitamin E is reported; an exact ester identity is not inferred from the abstract.

nutrient_topic

Vitamin E research collection; topical membership is not evidence of a direct dietary effect. · Vitamin E

organism

Homo sapiens

plain_language

Heart failure was more frequent with the tested regimen in this high-risk trial.

primary_references

[e-clin-hope2005] Effects of long-term vitamin E supplementation on cardiovascular events and cancer: a randomized controlled trial. (2005). https://pubmed.ncbi.nlm.nih.gov/15769967/ DOI: 10.1001/jama.293.11.1338

tissue_or_cell_type

Cardiovascular clinical events

Vitamin E: transport, membrane protection and nutrient interactions (2026-09-17) · lines 1388–1399

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · HOPE/HOPE-TOO randomized trial and extension in vascular disease or diabetes; initial n=9541 · source_derived_draft · unverified_draft

### e-clin-hope-heart-failure Vitamin E assignment was associated with more heart failure in HOPE/HOPE-TOO (RR 1.13, 95% CI 1.01–1.26). Condition category: normal nutrient_topic: Vitamin E research collection; topical membership is not evidence of a direct dietary effect. plain_language: Heart failure was more frequent with the tested regimen in this high-risk trial. organism: Homo sapiens tissue_or_cell_type: Cardiovascular clinical events experimental_model: HOPE/HOPE-TOO randomized trial and extension in vascular disease or diabetes; initial n=9541 limitations: High-risk population and extension participation limits. Heart failure was a secondary outcome; no specific molecular cause is established by the trial. Natural-source vitamin E is reported; an exact ester identity is not inferred from the abstract. exposure: Natural-source vitamin E 400 IU/day; median follow-up 7 years; extension included ongoing treatment and passive follow-up. cross_nutrient: false [e-clin-hope2005] Effects of long-term vitamin E supplementation on cardiovascular events and cancer: a randomized controlled trial. (2005). https://pubmed.ncbi.nlm.nih.gov/15769967/ DOI: 10.1001/jama.293.11.1338

availability_state

nutrient_deficiency Imported condition classification; unverified.

cross_nutrient

false

experimental_model

Historical clinical series of 50 premature infants aged 6–8 weeks

exposure

Blood vitamin E and hydrogen-peroxide hemolysis were assessed; oral vitamin E 10 mg/day was administered.

limitations

Historical feeding conditions and infant ages; an ex vivo hemolysis assay is not a universal explanation for anemia of prematurity. Formulation not specified in the abstract.

nutrient_topic

Vitamin E research collection; topical membership is not evidence of a direct dietary effect. · Vitamin E

organism

Homo sapiens

plain_language

Restoring vitamin E reduced red-cell fragility in the tested infants.

primary_references

[e-clin-lo1973] Vitamin E and haemolytic anaemia in premature infants. (1973). https://pubmed.ncbi.nlm.nih.gov/4739911/ DOI: 10.1136/adc.48.5.360

tissue_or_cell_type

Blood and erythrocytes

trigger_kind

nutrient_deficiency Imported condition classification; unverified.

Vitamin E: transport, membrane protection and nutrient interactions (2026-09-17) · lines 1206–1217

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Historical clinical series of 50 premature infants aged 6–8 weeks · source_derived_draft · unverified_draft

### e-clin-infant-peroxide-repletion Peroxide hemolysis normalized within days of oral vitamin E administration and rising blood vitamin E in the premature-infant series. Condition category: nutrient_deficiency nutrient_topic: Vitamin E research collection; topical membership is not evidence of a direct dietary effect. plain_language: Restoring vitamin E reduced red-cell fragility in the tested infants. organism: Homo sapiens tissue_or_cell_type: Blood and erythrocytes experimental_model: Historical clinical series of 50 premature infants aged 6–8 weeks limitations: Historical feeding conditions and infant ages; an ex vivo hemolysis assay is not a universal explanation for anemia of prematurity. Formulation not specified in the abstract. exposure: Blood vitamin E and hydrogen-peroxide hemolysis were assessed; oral vitamin E 10 mg/day was administered. cross_nutrient: false [e-clin-lo1973] Vitamin E and haemolytic anaemia in premature infants. (1973). https://pubmed.ncbi.nlm.nih.gov/4739911/ DOI: 10.1136/adc.48.5.360

evidence_span

{"source_cache": "artifacts/coq10-research/24664227.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "b1f301e82d4650432dab586db0be51f96e131f3c6084af9aebde932e8072676b", "start_char": 0, "end_char": 3023, "text_sha256": "b1f301e82d4650432dab586db0be51f96e131f3c6084af9aebde932e8072676b"}

experimental_model

Randomized double-blind phase III trial

exposure

CoQ10 1200 or 2400 mg/day; all groups received 1200 IU/day vitamin E

limitations

Vitamin E was a common background intervention; this comparison cannot identify its independent effect.

nutrient_topic

Coenzyme Q10 research collection; topical membership is not evidence of a direct dietary effect. · Coenzyme Q10 / CoQ10 redox system

organism

600 early-Parkinson patients

plain_language

A plausible mitochondrial mechanism did not translate into slower Parkinson progression in this trial.

primary_references

[coq10-p24664227] A randomized clinical trial of high-dosage coenzyme Q10 in early Parkinson disease: no evidence of benefit. (2014). https://pubmed.ncbi.nlm.nih.gov/24664227/ DOI: 10.1001/jamaneurol.2014.131

tissue_or_cell_type

UPDRS progression

Coenzyme Q10: biosynthesis, electron transfer, antioxidant recycling and nutrient interactions (2026-09-17) · lines 1217–1228

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Randomized double-blind phase III trial · source_derived_draft · unverified_draft

### coq10-parkinson-null Neither CoQ dose slowed UPDRS worsening versus placebo; the trial stopped for futility. Condition category: normal nutrient_topic: Coenzyme Q10 research collection; topical membership is not evidence of a direct dietary effect. plain_language: A plausible mitochondrial mechanism did not translate into slower Parkinson progression in this trial. organism: 600 early-Parkinson patients tissue_or_cell_type: UPDRS progression experimental_model: Randomized double-blind phase III trial limitations: Vitamin E was a common background intervention; this comparison cannot identify its independent effect. exposure: CoQ10 1200 or 2400 mg/day; all groups received 1200 IU/day vitamin E evidence_span: {"source_cache": "artifacts/coq10-research/24664227.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "b1f301e82d4650432dab586db0be51f96e131f3c6084af9aebde932e8072676b", "start_char": 0, "end_char": 3023, "text_sha256": "b1f301e82d4650432dab586db0be51f96e131f3c6084af9aebde932e8072676b"} [coq10-p24664227] A randomized clinical trial of high-dosage coenzyme Q10 in early Parkinson disease: no evidence of benefit. (2014). https://pubmed.ncbi.nlm.nih.gov/24664227/ DOI: 10.1001/jamaneurol.2014.131

evidence_span

{"source_cache": "artifacts/lutein-research/23644932.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "1bd379926e56d7243222c2ef69d6367b74aede2b02faabfb77fadcbadf95008f", "start_char": 0, "end_char": 3037, "text_sha256": "1bd379926e56d7243222c2ef69d6367b74aede2b02faabfb77fadcbadf95008f"}

experimental_model

AREDS2 phase 3 factorial randomized trial

exposure

Lutein 10 mg + zeaxanthin 2 mg daily; background AREDS formula; median five years

limitations

Combination and background treatment prevent attribution to lutein alone; primary contrast differs from replacement and main-effects analyses. Published correction 10.1001/jama.2013.6403 changes the Table 3 lung-neoplasm row label and Table 4 lung-neoplasm entries. These records use the indexed abstract and do not reproduce the uncorrected Table 4. Correction: https://jamanetwork.com/journals/jama/fullarticle/1710434 .

nutrient_topic

Lutein research collection; topical membership is not evidence of a direct dietary effect. · Lutein

organism

4203 adults aged 50–85 at elevated AMD progression risk

plain_language

Adding the pair did not meet the primary statistical threshold.

primary_references

[lutein-p23644932] Lutein + zeaxanthin and omega-3 fatty acids for age-related macular degeneration: the Age-Related Eye Disease Study 2 (AREDS2) randomized clinical trial. (2013). https://pubmed.ncbi.nlm.nih.gov/23644932/ DOI: 10.1001/jama.2013.4997

tissue_or_cell_type

Eyes with large drusen and/or fellow-eye advanced AMD

Lutein: metabolism, signaling and nutrient connections (2026-09-17) · lines 723–734

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · AREDS2 phase 3 factorial randomized trial · source_derived_draft · unverified_draft

### lutein-areds-primary-null Primary L+Z versus placebo comparison gave HR 0.90 (98.7% CI 0.76–1.07; P=0.12). Condition category: normal nutrient_topic: Lutein research collection; topical membership is not evidence of a direct dietary effect. plain_language: Adding the pair did not meet the primary statistical threshold. organism: 4203 adults aged 50–85 at elevated AMD progression risk tissue_or_cell_type: Eyes with large drusen and/or fellow-eye advanced AMD experimental_model: AREDS2 phase 3 factorial randomized trial limitations: Combination and background treatment prevent attribution to lutein alone; primary contrast differs from replacement and main-effects analyses. Published correction 10.1001/jama.2013.6403 changes the Table 3 lung-neoplasm row label and Table 4 lung-neoplasm entries. These records use the indexed abstract and do not reproduce the uncorrected Table 4. Correction: https://jamanetwork.com/journals/jama/fullarticle/1710434 . exposure: Lutein 10 mg + zeaxanthin 2 mg daily; background AREDS formula; median five years evidence_span: {"source_cache": "artifacts/lutein-research/23644932.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "1bd379926e56d7243222c2ef69d6367b74aede2b02faabfb77fadcbadf95008f", "start_char": 0, "end_char": 3037, "text_sha256": "1bd379926e56d7243222c2ef69d6367b74aede2b02faabfb77fadcbadf95008f"} [lutein-p23644932] Lutein + zeaxanthin and omega-3 fatty acids for age-related macular degeneration: the Age-Related Eye Disease Study 2 (AREDS2) randomized clinical trial. (2013). https://pubmed.ncbi.nlm.nih.gov/23644932/ DOI: 10.1001/jama.2013.4997

availability_state

machinery_impairment Imported condition classification; unverified.

cross_nutrient

true

experimental_model

Six-patient long-term abetalipoproteinemia case series

exposure

Large oral vitamin E doses for 12–18 years alongside low-fat diet and other fat-soluble vitamins; exact dose absent from the abstract.

limitations

Uncontrolled co-treatment series; cannot isolate vitamin E effect or demonstrate nutrient synergy. Genetic lipid transport disease differs from simple low intake.

nutrient_topic

Vitamin E research collection; topical membership is not evidence of a direct dietary effect. · Vitamin E

organism

Homo sapiens

plain_language

In this transport disease, vitamin A alone did not substitute for the broader treatment that included vitamin E.

primary_references

[e-clin-retina1986] Oral vitamin E supplements can prevent the retinopathy of abetalipoproteinaemia. (1986). https://pubmed.ncbi.nlm.nih.gov/3954973/ DOI: 10.1136/bjo.70.3.166

tissue_or_cell_type

Retina

trigger_kind

machinery_impairment Imported condition classification; unverified.

Vitamin E: transport, membrane protection and nutrient interactions (2026-09-17) · lines 1453–1464

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Six-patient long-term abetalipoproteinemia case series · source_derived_draft · unverified_draft

### e-clin-abetalipo-a-alone The six-patient abetalipoproteinemia report noted that vitamin A alone had not prevented or arrested the retinal lesion, whereas long-term regimens including vitamin E modified its course. Condition category: machinery_impairment nutrient_topic: Vitamin E research collection; topical membership is not evidence of a direct dietary effect. plain_language: In this transport disease, vitamin A alone did not substitute for the broader treatment that included vitamin E. organism: Homo sapiens tissue_or_cell_type: Retina experimental_model: Six-patient long-term abetalipoproteinemia case series limitations: Uncontrolled co-treatment series; cannot isolate vitamin E effect or demonstrate nutrient synergy. Genetic lipid transport disease differs from simple low intake. exposure: Large oral vitamin E doses for 12–18 years alongside low-fat diet and other fat-soluble vitamins; exact dose absent from the abstract. cross_nutrient: true [e-clin-retina1986] Oral vitamin E supplements can prevent the retinopathy of abetalipoproteinaemia. (1986). https://pubmed.ncbi.nlm.nih.gov/3954973/ DOI: 10.1136/bjo.70.3.166