Nutrient chapter

Lutein

Lutein. Species, exposure and limitations are retained in each linked claim.

75 recorded mechanisms · 5 availability situations · 6 preserved sources. Draft and verified records are labeled separately.

Read recorded mechanisms Open recursive mind map

The mechanisms

What the sources say this nutrient does, one relationship at a time. Plain wording comes first; the technical statement follows.

Recombinant human StARD3 bound lutein selectively, with dissociation constant 0.45 micromolar.
Human StARD3 / MLN64 lutein-binding protein → Lutein source_derived_draftungraded
Experimental context and source evidence
evidence_span
{"source_cache": "artifacts/lutein-research/21322544.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "e0362dd86389ecba7d75e2628ffcd785ea404e40a709084dd5a0749a4cfb89fa", "start_char": 0, "end_char": 1825, "text_sha256": "e0362dd86389ecba7d75e2628ffcd785ea404e40a709084dd5a0749a4cfb89fa"}
experimental_model
Recombinant binding assays and primate retinal localization
exposure
Surface plasmon resonance and immunohistochemistry
limitations
Binding does not prove net retinal delivery or clinical benefit; localization is from monkey tissue.
nutrient_topic
Lutein research collection; topical membership is not evidence of a direct dietary effect. · Lutein
organism
Human protein and monkey retinal tissue
plain_language
A retinal protein selectively holds lutein.
primary_references
[lutein-p21322544] Identification of StARD3 as a lutein-binding protein in the macula of the primate retina. (2011). https://pubmed.ncbi.nlm.nih.gov/21322544/ DOI: 10.1021/bi101906y
tissue_or_cell_type
Retina and purified protein
Lutein: metabolism, signaling and nutrient connections (2026-09-17) · lines 125–136
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Recombinant binding assays and primate retinal localization · source_derived_draft · unverified_draft
### lutein-stard3-binding Recombinant human StARD3 bound lutein selectively, with dissociation constant 0.45 micromolar. Condition category: normal nutrient_topic: Lutein research collection; topical membership is not evidence of a direct dietary effect. plain_language: A retinal protein selectively holds lutein. organism: Human protein and monkey retinal tissue tissue_or_cell_type: Retina and purified protein experimental_model: Recombinant binding assays and primate retinal localization limitations: Binding does not prove net retinal delivery or clinical benefit; localization is from monkey tissue. exposure: Surface plasmon resonance and immunohistochemistry evidence_span: {"source_cache": "artifacts/lutein-research/21322544.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "e0362dd86389ecba7d75e2628ffcd785ea404e40a709084dd5a0749a4cfb89fa", "start_char": 0, "end_char": 1825, "text_sha256": "e0362dd86389ecba7d75e2628ffcd785ea404e40a709084dd5a0749a4cfb89fa"} [lutein-p21322544] Identification of StARD3 as a lutein-binding protein in the macula of the primate retina. (2011). https://pubmed.ncbi.nlm.nih.gov/21322544/ DOI: 10.1021/bi101906y
Complete structured claim and evidence
SR-BI antibody and BLT1 reduced lutein transport by approximately 30% and 57%, respectively.
Scavenger receptor class B type 1 / SCARB1 → Intestinal epithelial lutein uptake source_derived_draftungraded
Experimental context and source evidence
evidence_span
{"source_cache": "artifacts/lutein-research/15554873.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "3dfbef37e3c73db4732f66083063e548a1654cb759ff46392c981c50f338d8a0", "start_char": 0, "end_char": 2014, "text_sha256": "3dfbef37e3c73db4732f66083063e548a1654cb759ff46392c981c50f338d8a0"}
experimental_model
Mixed-micelle transport across Caco-2 TC-7 monolayers
exposure
Micellar lutein 1.5–15 micromolar; antibodies and BLT1
limitations
Partial inhibition supports a contribution, not an exclusive route; cell experiments do not set clinical supplement spacing.
nutrient_topic
Lutein research collection; topical membership is not evidence of a direct dietary effect. · Lutein
organism
Human intestinal cell model
plain_language
Part of intestinal uptake used the SR-BI pathway.
primary_references
[lutein-p15554873] Lutein transport by Caco-2 TC-7 cells occurs partly by a facilitated process involving the scavenger receptor class B type I (SR-BI). (2005). https://pubmed.ncbi.nlm.nih.gov/15554873/ DOI: 10.1042/bj20040554
tissue_or_cell_type
Apical intestinal epithelial transport
Lutein: metabolism, signaling and nutrient connections (2026-09-17) · lines 476–487
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Mixed-micelle transport across Caco-2 TC-7 monolayers · source_derived_draft · unverified_draft
### lutein-srbi-intestine SR-BI antibody and BLT1 reduced lutein transport by approximately 30% and 57%, respectively. Condition category: normal nutrient_topic: Lutein research collection; topical membership is not evidence of a direct dietary effect. plain_language: Part of intestinal uptake used the SR-BI pathway. organism: Human intestinal cell model tissue_or_cell_type: Apical intestinal epithelial transport experimental_model: Mixed-micelle transport across Caco-2 TC-7 monolayers limitations: Partial inhibition supports a contribution, not an exclusive route; cell experiments do not set clinical supplement spacing. exposure: Micellar lutein 1.5–15 micromolar; antibodies and BLT1 evidence_span: {"source_cache": "artifacts/lutein-research/15554873.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "3dfbef37e3c73db4732f66083063e548a1654cb759ff46392c981c50f338d8a0", "start_char": 0, "end_char": 2014, "text_sha256": "3dfbef37e3c73db4732f66083063e548a1654cb759ff46392c981c50f338d8a0"} [lutein-p15554873] Lutein transport by Caco-2 TC-7 cells occurs partly by a facilitated process involving the scavenger receptor class B type I (SR-BI). (2005). https://pubmed.ncbi.nlm.nih.gov/15554873/ DOI: 10.1042/bj20040554
Complete structured claim and evidence
Overexpressed human RPE65 supported conversion of lutein into meso-zeaxanthin in cultured cells.
RPE65 retinoid isomerohydrolase → meso-Zeaxanthin / (3R,3-prime-S)-zeaxanthin source_derived_draftungraded
Experimental context and source evidence
evidence_span
{"source_cache": "artifacts/lutein-research/28874556.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "240bde60bb175fdfd5f556b9f2f7aab97f5d5b03e9640160418c34c74194d8c9", "start_char": 0, "end_char": 1679, "text_sha256": "240bde60bb175fdfd5f556b9f2f7aab97f5d5b03e9640160418c34c74194d8c9"}
experimental_model
Overexpression, developmental expression and pharmacological inhibition
exposure
RPE65 expression with lutein; inhibitor experiments in developing chicken eye
limitations
Cell and animal evidence; docking near iron is not a human iron-supplementation experiment.
nutrient_topic
Lutein research collection; topical membership is not evidence of a direct dietary effect. · Lutein
organism
Human/chicken proteins in cells and chicken embryos
plain_language
The visual-cycle enzyme can also rearrange lutein.
primary_references
[lutein-p28874556] RPE65 has an additional function as the lutein to meso-zeaxanthin isomerase in the vertebrate eye. (2017). https://pubmed.ncbi.nlm.nih.gov/28874556/ DOI: 10.1073/pnas.1706332114
tissue_or_cell_type
Cultured cells and embryonic RPE/choroid
Lutein: metabolism, signaling and nutrient connections (2026-09-17) · lines 151–162
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Overexpression, developmental expression and pharmacological inhibition · source_derived_draft · unverified_draft
### lutein-human-rpe65-isomerase Overexpressed human RPE65 supported conversion of lutein into meso-zeaxanthin in cultured cells. Condition category: normal nutrient_topic: Lutein research collection; topical membership is not evidence of a direct dietary effect. plain_language: The visual-cycle enzyme can also rearrange lutein. organism: Human/chicken proteins in cells and chicken embryos tissue_or_cell_type: Cultured cells and embryonic RPE/choroid experimental_model: Overexpression, developmental expression and pharmacological inhibition limitations: Cell and animal evidence; docking near iron is not a human iron-supplementation experiment. exposure: RPE65 expression with lutein; inhibitor experiments in developing chicken eye evidence_span: {"source_cache": "artifacts/lutein-research/28874556.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "240bde60bb175fdfd5f556b9f2f7aab97f5d5b03e9640160418c34c74194d8c9", "start_char": 0, "end_char": 1679, "text_sha256": "240bde60bb175fdfd5f556b9f2f7aab97f5d5b03e9640160418c34c74194d8c9"} [lutein-p28874556] RPE65 has an additional function as the lutein to meso-zeaxanthin isomerase in the vertebrate eye. (2017). https://pubmed.ncbi.nlm.nih.gov/28874556/ DOI: 10.1073/pnas.1706332114
Complete structured claim and evidence
High-lutein feeding left WHAM retinal lutein near 6% of controls despite increases in plasma, liver and heart.
Lutein → Chicken retinal lutein content source_derived_draftungraded
Experimental context and source evidence
availability_state
machinery_impairment Imported condition classification; unverified.
evidence_span
{"source_cache": "artifacts/lutein-research/17724211.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "7d7044cc9e41a7d859e5d5d75fc3fb7381d11fa635fa7232bf9dc97b83bd4cf4", "start_char": 0, "end_char": 1727, "text_sha256": "7d7044cc9e41a7d859e5d5d75fc3fb7381d11fa635fa7232bf9dc97b83bd4cf4"}
experimental_model
High-lutein feeding in WHAM versus control chicks
exposure
High-lutein or control diet from hatching for 28 days
limitations
Animal transport failure; raising human HDL cholesterol is not established as a way to improve retinal lutein.
nutrient_topic
Lutein research collection; topical membership is not evidence of a direct dietary effect. · Lutein
organism
Chicken
plain_language
More intake did not repair retinal delivery in this model.
primary_references
[lutein-p17724211] The prime role of HDL to transport lutein into the retina: evidence from HDL-deficient WHAM chicks having a mutant ABCA1 transporter. (2007). https://pubmed.ncbi.nlm.nih.gov/17724211/ DOI: 10.1167/iovs.06-1275
tissue_or_cell_type
Plasma, retina, liver and heart
trigger_kind
machinery_impairment Imported condition classification; unverified.
Lutein: metabolism, signaling and nutrient connections (2026-09-17) · lines 411–422
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · High-lutein feeding in WHAM versus control chicks · source_derived_draft · unverified_draft
### lutein-wham-retinal-repletion-failure High-lutein feeding left WHAM retinal lutein near 6% of controls despite increases in plasma, liver and heart. Condition category: machinery_impairment nutrient_topic: Lutein research collection; topical membership is not evidence of a direct dietary effect. plain_language: More intake did not repair retinal delivery in this model. organism: Chicken tissue_or_cell_type: Plasma, retina, liver and heart experimental_model: High-lutein feeding in WHAM versus control chicks limitations: Animal transport failure; raising human HDL cholesterol is not established as a way to improve retinal lutein. exposure: High-lutein or control diet from hatching for 28 days evidence_span: {"source_cache": "artifacts/lutein-research/17724211.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "7d7044cc9e41a7d859e5d5d75fc3fb7381d11fa635fa7232bf9dc97b83bd4cf4", "start_char": 0, "end_char": 1727, "text_sha256": "7d7044cc9e41a7d859e5d5d75fc3fb7381d11fa635fa7232bf9dc97b83bd4cf4"} [lutein-p17724211] The prime role of HDL to transport lutein into the retina: evidence from HDL-deficient WHAM chicks having a mutant ABCA1 transporter. (2007). https://pubmed.ncbi.nlm.nih.gov/17724211/ DOI: 10.1167/iovs.06-1275
Complete structured claim and evidence
Co-incubated lutein reduced alpha-tocopherol uptake in Caco-2 TC-7 cells.
Lutein → Intestinal alpha-tocopherol uptake source_derived_draftungraded
Experimental context and source evidence
evidence_span
{"source_cache": "artifacts/lutein-research/16380385.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "410a6cc6c3325e6d2f459b06ddaf9c7b7806f9b82a918f1df02b1626f5f84074", "start_char": 0, "end_char": 1960, "text_sha256": "410a6cc6c3325e6d2f459b06ddaf9c7b7806f9b82a918f1df02b1626f5f84074"}
experimental_model
Mixed-micelle uptake in Caco-2 TC-7 cells
exposure
Alpha-tocopherol with co-incubated lutein
limitations
In vitro competition is not demonstrated vitamin E deficiency or a clinical dose-spacing rule.
nutrient_topic
Lutein research collection; topical membership is not evidence of a direct dietary effect. · Lutein
organism
Human cell model
plain_language
Lutein and vitamin E can interact during intestinal uptake.
primary_references
[lutein-p16380385] Scavenger receptor class B type I (SR-BI) is involved in vitamin E transport across the enterocyte. (2006). https://pubmed.ncbi.nlm.nih.gov/16380385/ DOI: 10.1074/jbc.m509042200
tissue_or_cell_type
Intestinal epithelium
Lutein: metabolism, signaling and nutrient connections (2026-09-17) · lines 541–552
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Mixed-micelle uptake in Caco-2 TC-7 cells · source_derived_draft · unverified_draft
### lutein-vitamin-e-competition Co-incubated lutein reduced alpha-tocopherol uptake in Caco-2 TC-7 cells. Condition category: normal nutrient_topic: Lutein research collection; topical membership is not evidence of a direct dietary effect. plain_language: Lutein and vitamin E can interact during intestinal uptake. organism: Human cell model tissue_or_cell_type: Intestinal epithelium experimental_model: Mixed-micelle uptake in Caco-2 TC-7 cells limitations: In vitro competition is not demonstrated vitamin E deficiency or a clinical dose-spacing rule. exposure: Alpha-tocopherol with co-incubated lutein evidence_span: {"source_cache": "artifacts/lutein-research/16380385.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "410a6cc6c3325e6d2f459b06ddaf9c7b7806f9b82a918f1df02b1626f5f84074", "start_char": 0, "end_char": 1960, "text_sha256": "410a6cc6c3325e6d2f459b06ddaf9c7b7806f9b82a918f1df02b1626f5f84074"} [lutein-p16380385] Scavenger receptor class B type I (SR-BI) is involved in vitamin E transport across the enterocyte. (2006). https://pubmed.ncbi.nlm.nih.gov/16380385/ DOI: 10.1074/jbc.m509042200
Complete structured claim and evidence
Removing the mitochondrial targeting sequence improved human BCO2a solubility and enabled carotenoid-cleavage activity.
Human BCO2a with mitochondrial targeting sequence removed → Human BCO2 carotenoid cleavage activity source_derived_draftungraded
Experimental context and source evidence
evidence_span
{"source_cache": "artifacts/lutein-research/32873706.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "1555914c4a5090c968595f2aba72ce276054594a66423916be600a600a28349f", "start_char": 0, "end_char": 1517, "text_sha256": "1555914c4a5090c968595f2aba72ce276054594a66423916be600a600a28349f"}
experimental_model
Isoform targeting, recombinant expression and enzyme assays
exposure
Removal of N-terminal mitochondrial targeting sequence; expression optimization
limitations
Activity of processed recombinant protein does not quantify retinal flux; mouse chimeric substrate results remain mouse-specific.
nutrient_topic
Lutein research collection; topical membership is not evidence of a direct dietary effect. · Lutein
organism
Human BCO2 isoforms and engineered mouse protein
plain_language
Processing and expression conditions revealed active human enzyme.
primary_references
[lutein-p32873706] The human mitochondrial enzyme BCO2 exhibits catalytic activity toward carotenoids and apocarotenoids. (2020). https://pubmed.ncbi.nlm.nih.gov/32873706/ DOI: 10.1074/jbc.ra120.015515
tissue_or_cell_type
ARPE-19 cells and bacterial expression
Lutein: metabolism, signaling and nutrient connections (2026-09-17) · lines 281–292
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Isoform targeting, recombinant expression and enzyme assays · source_derived_draft · unverified_draft
### lutein-bco2-mature-active Removing the mitochondrial targeting sequence improved human BCO2a solubility and enabled carotenoid-cleavage activity. Condition category: normal nutrient_topic: Lutein research collection; topical membership is not evidence of a direct dietary effect. plain_language: Processing and expression conditions revealed active human enzyme. organism: Human BCO2 isoforms and engineered mouse protein tissue_or_cell_type: ARPE-19 cells and bacterial expression experimental_model: Isoform targeting, recombinant expression and enzyme assays limitations: Activity of processed recombinant protein does not quantify retinal flux; mouse chimeric substrate results remain mouse-specific. exposure: Removal of N-terminal mitochondrial targeting sequence; expression optimization evidence_span: {"source_cache": "artifacts/lutein-research/32873706.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "1555914c4a5090c968595f2aba72ce276054594a66423916be600a600a28349f", "start_char": 0, "end_char": 1517, "text_sha256": "1555914c4a5090c968595f2aba72ce276054594a66423916be600a600a28349f"} [lutein-p32873706] The human mitochondrial enzyme BCO2 exhibits catalytic activity toward carotenoids and apocarotenoids. (2020). https://pubmed.ncbi.nlm.nih.gov/32873706/ DOI: 10.1074/jbc.ra120.015515
Complete structured claim and evidence
Primary L+Z versus placebo comparison gave HR 0.90 (98.7% CI 0.76–1.07; P=0.12).
AREDS2 lutein/zeaxanthin addition to background AREDS formulation → Progression to late age-related macular degeneration source_derived_draftungraded
Experimental context and source evidence
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
Complete structured claim and evidence
Exploratory L+Z versus beta-carotene comparison gave late-AMD HR 0.82 (95% CI 0.69–0.96).
AREDS2 lutein/zeaxanthin versus beta-carotene comparison → Progression to late age-related macular degeneration source_derived_draftungraded
Experimental context and source evidence
evidence_span
{"source_cache": "artifacts/lutein-research/24310343.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "617cbda47a00c8fc552395a255003b013afa72aca6640c5c2e49d2b4caf09a72", "start_char": 0, "end_char": 2419, "text_sha256": "617cbda47a00c8fc552395a255003b013afa72aca6640c5c2e49d2b4caf09a72"}
experimental_model
Exploratory secondary analyses of AREDS2
exposure
L+Z 10/2 mg; direct comparison with beta-carotene on AREDS background
limitations
Exploratory contrasts and different confidence thresholds do not contradict the prespecified primary analysis.
nutrient_topic
Lutein research collection; topical membership is not evidence of a direct dietary effect. · Lutein
organism
Same AREDS2 cohort, not an independent replication
plain_language
Replacement comparison favored the xanthophyll pair.
primary_references
[lutein-p24310343] Secondary analyses of the effects of lutein/zeaxanthin on age-related macular degeneration progression: AREDS2 report No. 3. (2014). https://pubmed.ncbi.nlm.nih.gov/24310343/ DOI: 10.1001/jamaophthalmol.2013.7376
tissue_or_cell_type
Late AMD subtypes
Lutein: metabolism, signaling and nutrient connections (2026-09-17) · lines 749–760
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Exploratory secondary analyses of AREDS2 · source_derived_draft · unverified_draft
### lutein-areds-replacement-late Exploratory L+Z versus beta-carotene comparison gave late-AMD HR 0.82 (95% CI 0.69–0.96). Condition category: normal nutrient_topic: Lutein research collection; topical membership is not evidence of a direct dietary effect. plain_language: Replacement comparison favored the xanthophyll pair. organism: Same AREDS2 cohort, not an independent replication tissue_or_cell_type: Late AMD subtypes experimental_model: Exploratory secondary analyses of AREDS2 limitations: Exploratory contrasts and different confidence thresholds do not contradict the prespecified primary analysis. exposure: L+Z 10/2 mg; direct comparison with beta-carotene on AREDS background evidence_span: {"source_cache": "artifacts/lutein-research/24310343.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "617cbda47a00c8fc552395a255003b013afa72aca6640c5c2e49d2b4caf09a72", "start_char": 0, "end_char": 2419, "text_sha256": "617cbda47a00c8fc552395a255003b013afa72aca6640c5c2e49d2b4caf09a72"} [lutein-p24310343] Secondary analyses of the effects of lutein/zeaxanthin on age-related macular degeneration progression: AREDS2 report No. 3. (2014). https://pubmed.ncbi.nlm.nih.gov/24310343/ DOI: 10.1001/jamaophthalmol.2013.7376
Complete structured claim and evidence
L+Z improved photostress recovery time versus placebo.
Lutein 10 mg plus zeaxanthin 2 mg daily combination → Human photostress recovery time source_derived_draftungraded
Experimental context and source evidence
evidence_span
{"source_cache": "artifacts/lutein-research/25468896.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "01231d6577e7c30e79a74525772191092df003b42344095a53faf0279f138ac3", "start_char": 0, "end_char": 2007, "text_sha256": "01231d6577e7c30e79a74525772191092df003b42344095a53faf0279f138ac3"}
experimental_model
Randomized double-blind placebo-controlled visual-performance study
exposure
Lutein 10 mg + zeaxanthin 2 mg daily for one year
limitations
Combined intervention; improved task performance is not evidence of AMD prevention or treatment.
nutrient_topic
Lutein research collection; topical membership is not evidence of a direct dietary effect. · Lutein
organism
115 young healthy adults
plain_language
Vision recovered faster after the experimental bright flash.
primary_references
[lutein-p25468896] A double-blind, placebo-controlled study on the effects of lutein and zeaxanthin on photostress recovery, glare disability, and chromatic contrast. (2014). https://pubmed.ncbi.nlm.nih.gov/25468896/ DOI: 10.1167/iovs.14-15573
tissue_or_cell_type
Serum, macular pigment and visual tasks
Lutein: metabolism, signaling and nutrient connections (2026-09-17) · lines 853–864
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Randomized double-blind placebo-controlled visual-performance study · source_derived_draft · unverified_draft
### lutein-photostress-improvement L+Z improved photostress recovery time versus placebo. Condition category: normal nutrient_topic: Lutein research collection; topical membership is not evidence of a direct dietary effect. plain_language: Vision recovered faster after the experimental bright flash. organism: 115 young healthy adults tissue_or_cell_type: Serum, macular pigment and visual tasks experimental_model: Randomized double-blind placebo-controlled visual-performance study limitations: Combined intervention; improved task performance is not evidence of AMD prevention or treatment. exposure: Lutein 10 mg + zeaxanthin 2 mg daily for one year evidence_span: {"source_cache": "artifacts/lutein-research/25468896.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "01231d6577e7c30e79a74525772191092df003b42344095a53faf0279f138ac3", "start_char": 0, "end_char": 2007, "text_sha256": "01231d6577e7c30e79a74525772191092df003b42344095a53faf0279f138ac3"} [lutein-p25468896] A double-blind, placebo-controlled study on the effects of lutein and zeaxanthin on photostress recovery, glare disability, and chromatic contrast. (2014). https://pubmed.ncbi.nlm.nih.gov/25468896/ DOI: 10.1167/iovs.14-15573
Complete structured claim and evidence
L+Z produced no significant difference in yearly cognitive composite change: 0.03 (99% CI −0.14 to 0.19; P=0.66).
Lutein 10 mg plus zeaxanthin 2 mg daily combination → AREDS2 composite cognitive function score source_derived_draftungraded
Experimental context and source evidence
evidence_span
{"source_cache": "artifacts/lutein-research/26305649.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "6b4498bace6ac4564fae52aef2f95e564154631bdfa1e19b02fa6878043dbe72", "start_char": 0, "end_char": 2936, "text_sha256": "6b4498bace6ac4564fae52aef2f95e564154631bdfa1e19b02fa6878043dbe72"}
experimental_model
AREDS2 ancillary randomized cognitive study
exposure
L+Z 10/2 mg daily; five-year study on background nutrient formulas
limitations
Cognitive outcome, not a direct brain-lutein assay; no attribution to isolated lutein.
nutrient_topic
Lutein research collection; topical membership is not evidence of a direct dietary effect. · Lutein
organism
3501 tested older participants at AMD risk
plain_language
The large older-adult study did not show cognitive benefit.
primary_references
[lutein-p26305649] Effect of Omega-3 Fatty Acids, Lutein/Zeaxanthin, or Other Nutrient Supplementation on Cognitive Function: The AREDS2 Randomized Clinical Trial. (2015). https://pubmed.ncbi.nlm.nih.gov/26305649/ DOI: 10.1001/jama.2015.9677
tissue_or_cell_type
Telephone cognitive test battery
Lutein: metabolism, signaling and nutrient connections (2026-09-17) · lines 892–903
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · AREDS2 ancillary randomized cognitive study · source_derived_draft · unverified_draft
### lutein-cognition-areds-null L+Z produced no significant difference in yearly cognitive composite change: 0.03 (99% CI −0.14 to 0.19; P=0.66). Condition category: normal nutrient_topic: Lutein research collection; topical membership is not evidence of a direct dietary effect. plain_language: The large older-adult study did not show cognitive benefit. organism: 3501 tested older participants at AMD risk tissue_or_cell_type: Telephone cognitive test battery experimental_model: AREDS2 ancillary randomized cognitive study limitations: Cognitive outcome, not a direct brain-lutein assay; no attribution to isolated lutein. exposure: L+Z 10/2 mg daily; five-year study on background nutrient formulas evidence_span: {"source_cache": "artifacts/lutein-research/26305649.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "6b4498bace6ac4564fae52aef2f95e564154631bdfa1e19b02fa6878043dbe72", "start_char": 0, "end_char": 2936, "text_sha256": "6b4498bace6ac4564fae52aef2f95e564154631bdfa1e19b02fa6878043dbe72"} [lutein-p26305649] Effect of Omega-3 Fatty Acids, Lutein/Zeaxanthin, or Other Nutrient Supplementation on Cognitive Function: The AREDS2 Randomized Clinical Trial. (2015). https://pubmed.ncbi.nlm.nih.gov/26305649/ DOI: 10.1001/jama.2015.9677
Complete structured claim and evidence
The study distinguishes GSTP1-associated zeaxanthin binding from StARD3-associated lutein binding.
Human glutathione S-transferase P1 / GSTP1 → Dietary (3R,3-prime-R)-zeaxanthin source_derived_draftungraded
Experimental context and source evidence
evidence_span
{"source_cache": "artifacts/lutein-research/21322544.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "e0362dd86389ecba7d75e2628ffcd785ea404e40a709084dd5a0749a4cfb89fa", "start_char": 0, "end_char": 1825, "text_sha256": "e0362dd86389ecba7d75e2628ffcd785ea404e40a709084dd5a0749a4cfb89fa"}
experimental_model
Recombinant binding assays and primate retinal localization
exposure
Surface plasmon resonance and immunohistochemistry
limitations
Binding does not prove net retinal delivery or clinical benefit; localization is from monkey tissue.
nutrient_topic
Lutein research collection; topical membership is not evidence of a direct dietary effect. · Lutein
organism
Human protein and monkey retinal tissue
plain_language
The two pigments have different identified binding proteins.
primary_references
[lutein-p21322544] Identification of StARD3 as a lutein-binding protein in the macula of the primate retina. (2011). https://pubmed.ncbi.nlm.nih.gov/21322544/ DOI: 10.1021/bi101906y
tissue_or_cell_type
Retina and purified protein
Lutein: metabolism, signaling and nutrient connections (2026-09-17) · lines 138–149
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Recombinant binding assays and primate retinal localization · source_derived_draft · unverified_draft
### lutein-gstp1-distinction The study distinguishes GSTP1-associated zeaxanthin binding from StARD3-associated lutein binding. Condition category: normal nutrient_topic: Lutein research collection; topical membership is not evidence of a direct dietary effect. plain_language: The two pigments have different identified binding proteins. organism: Human protein and monkey retinal tissue tissue_or_cell_type: Retina and purified protein experimental_model: Recombinant binding assays and primate retinal localization limitations: Binding does not prove net retinal delivery or clinical benefit; localization is from monkey tissue. exposure: Surface plasmon resonance and immunohistochemistry evidence_span: {"source_cache": "artifacts/lutein-research/21322544.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "e0362dd86389ecba7d75e2628ffcd785ea404e40a709084dd5a0749a4cfb89fa", "start_char": 0, "end_char": 1825, "text_sha256": "e0362dd86389ecba7d75e2628ffcd785ea404e40a709084dd5a0749a4cfb89fa"} [lutein-p21322544] Identification of StARD3 as a lutein-binding protein in the macula of the primate retina. (2011). https://pubmed.ncbi.nlm.nih.gov/21322544/ DOI: 10.1021/bi101906y
Complete structured claim and evidence
Chicken RPE65 overexpression supported meso-zeaxanthin production from lutein.
Chicken RPE65 → meso-Zeaxanthin / (3R,3-prime-S)-zeaxanthin source_derived_draftungraded
Experimental context and source evidence
evidence_span
{"source_cache": "artifacts/lutein-research/28874556.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "240bde60bb175fdfd5f556b9f2f7aab97f5d5b03e9640160418c34c74194d8c9", "start_char": 0, "end_char": 1679, "text_sha256": "240bde60bb175fdfd5f556b9f2f7aab97f5d5b03e9640160418c34c74194d8c9"}
experimental_model
Overexpression, developmental expression and pharmacological inhibition
exposure
RPE65 expression with lutein; inhibitor experiments in developing chicken eye
limitations
Cell and animal evidence; docking near iron is not a human iron-supplementation experiment.
nutrient_topic
Lutein research collection; topical membership is not evidence of a direct dietary effect. · Lutein
organism
Human/chicken proteins in cells and chicken embryos
plain_language
The conversion was also observed with the chicken enzyme.
primary_references
[lutein-p28874556] RPE65 has an additional function as the lutein to meso-zeaxanthin isomerase in the vertebrate eye. (2017). https://pubmed.ncbi.nlm.nih.gov/28874556/ DOI: 10.1073/pnas.1706332114
tissue_or_cell_type
Cultured cells and embryonic RPE/choroid
Lutein: metabolism, signaling and nutrient connections (2026-09-17) · lines 164–175
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Overexpression, developmental expression and pharmacological inhibition · source_derived_draft · unverified_draft
### lutein-chicken-rpe65-isomerase Chicken RPE65 overexpression supported meso-zeaxanthin production from lutein. Condition category: normal nutrient_topic: Lutein research collection; topical membership is not evidence of a direct dietary effect. plain_language: The conversion was also observed with the chicken enzyme. organism: Human/chicken proteins in cells and chicken embryos tissue_or_cell_type: Cultured cells and embryonic RPE/choroid experimental_model: Overexpression, developmental expression and pharmacological inhibition limitations: Cell and animal evidence; docking near iron is not a human iron-supplementation experiment. exposure: RPE65 expression with lutein; inhibitor experiments in developing chicken eye evidence_span: {"source_cache": "artifacts/lutein-research/28874556.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "240bde60bb175fdfd5f556b9f2f7aab97f5d5b03e9640160418c34c74194d8c9", "start_char": 0, "end_char": 1679, "text_sha256": "240bde60bb175fdfd5f556b9f2f7aab97f5d5b03e9640160418c34c74194d8c9"} [lutein-p28874556] RPE65 has an additional function as the lutein to meso-zeaxanthin isomerase in the vertebrate eye. (2017). https://pubmed.ncbi.nlm.nih.gov/28874556/ DOI: 10.1073/pnas.1706332114
Complete structured claim and evidence
RPE65 inhibition reduced meso-zeaxanthin biosynthesis during chicken eye development.
RPE65 pharmacological inhibition during chicken eye development → Lutein to meso-zeaxanthin isomerization source_derived_draftungraded
Experimental context and source evidence
availability_state
machinery_impairment Imported condition classification; unverified.
evidence_span
{"source_cache": "artifacts/lutein-research/28874556.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "240bde60bb175fdfd5f556b9f2f7aab97f5d5b03e9640160418c34c74194d8c9", "start_char": 0, "end_char": 1679, "text_sha256": "240bde60bb175fdfd5f556b9f2f7aab97f5d5b03e9640160418c34c74194d8c9"}
experimental_model
Overexpression, developmental expression and pharmacological inhibition
exposure
RPE65 expression with lutein; inhibitor experiments in developing chicken eye
limitations
Cell and animal evidence; docking near iron is not a human iron-supplementation experiment.
nutrient_topic
Lutein research collection; topical membership is not evidence of a direct dietary effect. · Lutein
organism
Human/chicken proteins in cells and chicken embryos
plain_language
An enzyme block reduced pigment production despite the distinct dietary precursor.
primary_references
[lutein-p28874556] RPE65 has an additional function as the lutein to meso-zeaxanthin isomerase in the vertebrate eye. (2017). https://pubmed.ncbi.nlm.nih.gov/28874556/ DOI: 10.1073/pnas.1706332114
tissue_or_cell_type
Cultured cells and embryonic RPE/choroid
trigger_kind
machinery_impairment Imported condition classification; unverified.
Lutein: metabolism, signaling and nutrient connections (2026-09-17) · lines 177–188
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Overexpression, developmental expression and pharmacological inhibition · source_derived_draft · unverified_draft
### lutein-rpe65-inhibition RPE65 inhibition reduced meso-zeaxanthin biosynthesis during chicken eye development. Condition category: machinery_impairment nutrient_topic: Lutein research collection; topical membership is not evidence of a direct dietary effect. plain_language: An enzyme block reduced pigment production despite the distinct dietary precursor. organism: Human/chicken proteins in cells and chicken embryos tissue_or_cell_type: Cultured cells and embryonic RPE/choroid experimental_model: Overexpression, developmental expression and pharmacological inhibition limitations: Cell and animal evidence; docking near iron is not a human iron-supplementation experiment. exposure: RPE65 expression with lutein; inhibitor experiments in developing chicken eye evidence_span: {"source_cache": "artifacts/lutein-research/28874556.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "240bde60bb175fdfd5f556b9f2f7aab97f5d5b03e9640160418c34c74194d8c9", "start_char": 0, "end_char": 1679, "text_sha256": "240bde60bb175fdfd5f556b9f2f7aab97f5d5b03e9640160418c34c74194d8c9"} [lutein-p28874556] RPE65 has an additional function as the lutein to meso-zeaxanthin isomerase in the vertebrate eye. (2017). https://pubmed.ncbi.nlm.nih.gov/28874556/ DOI: 10.1073/pnas.1706332114
Complete structured claim and evidence
Mouse RPE65 supported lutein isomerization in cultured cells despite mice not normally concentrating meso-zeaxanthin in the eye.
Mouse RPE65 → meso-Zeaxanthin / (3R,3-prime-S)-zeaxanthin source_derived_draftungraded
Experimental context and source evidence
evidence_span
{"source_cache": "artifacts/lutein-research/41415389.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "b4eb5b9290310947be962df7dae42190e5afa6ffd726e869cb842d7f7ed15a41", "start_char": 0, "end_char": 1304, "text_sha256": "b4eb5b9290310947be962df7dae42190e5afa6ffd726e869cb842d7f7ed15a41"}
experimental_model
Cultured-cell enzyme expression, mutagenesis and structural modeling
exposure
Lutein substrate; E148Q substitution; binding-protein coexpression
limitations
Proposed radical transition state remains a mechanistic interpretation, not directly observed chemistry.
nutrient_topic
Lutein research collection; topical membership is not evidence of a direct dietary effect. · Lutein
organism
Human, chicken and mouse RPE65
plain_language
Enzyme capacity and whole-tissue pigment accumulation are different.
primary_references
[lutein-p41415389] Mechanism of Lutein to meso-Zeaxanthin Isomerization by RPE65 Catalysis. (2025). https://pubmed.ncbi.nlm.nih.gov/41415389/ DOI: 10.64898/2025.12.10.693550
tissue_or_cell_type
Cultured cells and molecular models
Lutein: metabolism, signaling and nutrient connections (2026-09-17) · lines 190–201
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Cultured-cell enzyme expression, mutagenesis and structural modeling · source_derived_draft · unverified_draft
### lutein-mouse-rpe65-isomerase Mouse RPE65 supported lutein isomerization in cultured cells despite mice not normally concentrating meso-zeaxanthin in the eye. Condition category: normal nutrient_topic: Lutein research collection; topical membership is not evidence of a direct dietary effect. plain_language: Enzyme capacity and whole-tissue pigment accumulation are different. organism: Human, chicken and mouse RPE65 tissue_or_cell_type: Cultured cells and molecular models experimental_model: Cultured-cell enzyme expression, mutagenesis and structural modeling limitations: Proposed radical transition state remains a mechanistic interpretation, not directly observed chemistry. exposure: Lutein substrate; E148Q substitution; binding-protein coexpression evidence_span: {"source_cache": "artifacts/lutein-research/41415389.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "b4eb5b9290310947be962df7dae42190e5afa6ffd726e869cb842d7f7ed15a41", "start_char": 0, "end_char": 1304, "text_sha256": "b4eb5b9290310947be962df7dae42190e5afa6ffd726e869cb842d7f7ed15a41"} [lutein-p41415389] Mechanism of Lutein to meso-Zeaxanthin Isomerization by RPE65 Catalysis. (2025). https://pubmed.ncbi.nlm.nih.gov/41415389/ DOI: 10.64898/2025.12.10.693550
Complete structured claim and evidence
RPE65 E148Q substitution did not reduce meso-zeaxanthin yield in the reported cultured-cell experiments.
Human RPE65 E148Q experimental substitution → Lutein to meso-zeaxanthin isomerization source_derived_draftungraded
Experimental context and source evidence
evidence_span
{"source_cache": "artifacts/lutein-research/41415389.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "b4eb5b9290310947be962df7dae42190e5afa6ffd726e869cb842d7f7ed15a41", "start_char": 0, "end_char": 1304, "text_sha256": "b4eb5b9290310947be962df7dae42190e5afa6ffd726e869cb842d7f7ed15a41"}
experimental_model
Cultured-cell enzyme expression, mutagenesis and structural modeling
exposure
Lutein substrate; E148Q substitution; binding-protein coexpression
limitations
Proposed radical transition state remains a mechanistic interpretation, not directly observed chemistry.
nutrient_topic
Lutein research collection; topical membership is not evidence of a direct dietary effect. · Lutein
organism
Human, chicken and mouse RPE65
plain_language
A change important to other RPE65 chemistry spared this measured reaction.
primary_references
[lutein-p41415389] Mechanism of Lutein to meso-Zeaxanthin Isomerization by RPE65 Catalysis. (2025). https://pubmed.ncbi.nlm.nih.gov/41415389/ DOI: 10.64898/2025.12.10.693550
tissue_or_cell_type
Cultured cells and molecular models
Lutein: metabolism, signaling and nutrient connections (2026-09-17) · lines 203–214
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Cultured-cell enzyme expression, mutagenesis and structural modeling · source_derived_draft · unverified_draft
### lutein-e148q-maintained RPE65 E148Q substitution did not reduce meso-zeaxanthin yield in the reported cultured-cell experiments. Condition category: normal nutrient_topic: Lutein research collection; topical membership is not evidence of a direct dietary effect. plain_language: A change important to other RPE65 chemistry spared this measured reaction. organism: Human, chicken and mouse RPE65 tissue_or_cell_type: Cultured cells and molecular models experimental_model: Cultured-cell enzyme expression, mutagenesis and structural modeling limitations: Proposed radical transition state remains a mechanistic interpretation, not directly observed chemistry. exposure: Lutein substrate; E148Q substitution; binding-protein coexpression evidence_span: {"source_cache": "artifacts/lutein-research/41415389.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "b4eb5b9290310947be962df7dae42190e5afa6ffd726e869cb842d7f7ed15a41", "start_char": 0, "end_char": 1304, "text_sha256": "b4eb5b9290310947be962df7dae42190e5afa6ffd726e869cb842d7f7ed15a41"} [lutein-p41415389] Mechanism of Lutein to meso-Zeaxanthin Isomerization by RPE65 Catalysis. (2025). https://pubmed.ncbi.nlm.nih.gov/41415389/ DOI: 10.64898/2025.12.10.693550
Complete structured claim and evidence
Lutein quenched singlet oxygen in the solution assay comparing individual macular carotenoids and mixtures.
Lutein → Singlet molecular oxygen source_derived_draftungraded
Experimental context and source evidence
evidence_span
{"source_cache": "artifacts/lutein-research/20678467.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "aaf88f567941ed16adb101981a218960bbd8ae3cfe0919868de63462e7c7be01", "start_char": 0, "end_char": 989, "text_sha256": "aaf88f567941ed16adb101981a218960bbd8ae3cfe0919868de63462e7c7be01"}
experimental_model
EPR of donor eye tissue and solution quenching assays
exposure
White-light challenge and equal-total-concentration carotenoid comparisons
limitations
Solution mixture effects do not establish an optimal oral ratio or clinical benefit; exogenous pigment addition differs from delivery in a living eye.
nutrient_topic
Lutein research collection; topical membership is not evidence of a direct dietary effect. · Lutein
organism
Postmortem human tissue and cell-free systems
plain_language
Lutein can reduce excited oxygen in a chemical experiment.
primary_references
[lutein-p20678467] Studies on the singlet oxygen scavenging mechanism of human macular pigment. (2010). https://pubmed.ncbi.nlm.nih.gov/20678467/ DOI: 10.1016/j.abb.2010.07.024
tissue_or_cell_type
Macula, RPE/choroid and carotenoid solutions
Lutein: metabolism, signaling and nutrient connections (2026-09-17) · lines 216–227
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · EPR of donor eye tissue and solution quenching assays · source_derived_draft · unverified_draft
### lutein-singlet-quenching Lutein quenched singlet oxygen in the solution assay comparing individual macular carotenoids and mixtures. Condition category: normal nutrient_topic: Lutein research collection; topical membership is not evidence of a direct dietary effect. plain_language: Lutein can reduce excited oxygen in a chemical experiment. organism: Postmortem human tissue and cell-free systems tissue_or_cell_type: Macula, RPE/choroid and carotenoid solutions experimental_model: EPR of donor eye tissue and solution quenching assays limitations: Solution mixture effects do not establish an optimal oral ratio or clinical benefit; exogenous pigment addition differs from delivery in a living eye. exposure: White-light challenge and equal-total-concentration carotenoid comparisons evidence_span: {"source_cache": "artifacts/lutein-research/20678467.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "aaf88f567941ed16adb101981a218960bbd8ae3cfe0919868de63462e7c7be01", "start_char": 0, "end_char": 989, "text_sha256": "aaf88f567941ed16adb101981a218960bbd8ae3cfe0919868de63462e7c7be01"} [lutein-p20678467] Studies on the singlet oxygen scavenging mechanism of human macular pigment. (2010). https://pubmed.ncbi.nlm.nih.gov/20678467/ DOI: 10.1016/j.abb.2010.07.024
Complete structured claim and evidence
The equal-ratio meso-zeaxanthin, zeaxanthin and lutein mixture quenched more singlet oxygen than each individual pigment at the same total concentration.
Meso-zeaxanthin, zeaxanthin and lutein 1:1:1 assay mixture → Singlet molecular oxygen source_derived_draftungraded
Experimental context and source evidence
evidence_span
{"source_cache": "artifacts/lutein-research/20678467.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "aaf88f567941ed16adb101981a218960bbd8ae3cfe0919868de63462e7c7be01", "start_char": 0, "end_char": 989, "text_sha256": "aaf88f567941ed16adb101981a218960bbd8ae3cfe0919868de63462e7c7be01"}
experimental_model
EPR of donor eye tissue and solution quenching assays
exposure
White-light challenge and equal-total-concentration carotenoid comparisons
limitations
Solution mixture effects do not establish an optimal oral ratio or clinical benefit; exogenous pigment addition differs from delivery in a living eye.
nutrient_topic
Lutein research collection; topical membership is not evidence of a direct dietary effect. · Lutein
organism
Postmortem human tissue and cell-free systems
plain_language
The three pigments worked better together in this solution experiment.
primary_references
[lutein-p20678467] Studies on the singlet oxygen scavenging mechanism of human macular pigment. (2010). https://pubmed.ncbi.nlm.nih.gov/20678467/ DOI: 10.1016/j.abb.2010.07.024
tissue_or_cell_type
Macula, RPE/choroid and carotenoid solutions
Lutein: metabolism, signaling and nutrient connections (2026-09-17) · lines 229–240
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · EPR of donor eye tissue and solution quenching assays · source_derived_draft · unverified_draft
### lutein-mixture-quenching The equal-ratio meso-zeaxanthin, zeaxanthin and lutein mixture quenched more singlet oxygen than each individual pigment at the same total concentration. Condition category: normal nutrient_topic: Lutein research collection; topical membership is not evidence of a direct dietary effect. plain_language: The three pigments worked better together in this solution experiment. organism: Postmortem human tissue and cell-free systems tissue_or_cell_type: Macula, RPE/choroid and carotenoid solutions experimental_model: EPR of donor eye tissue and solution quenching assays limitations: Solution mixture effects do not establish an optimal oral ratio or clinical benefit; exogenous pigment addition differs from delivery in a living eye. exposure: White-light challenge and equal-total-concentration carotenoid comparisons evidence_span: {"source_cache": "artifacts/lutein-research/20678467.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "aaf88f567941ed16adb101981a218960bbd8ae3cfe0919868de63462e7c7be01", "start_char": 0, "end_char": 989, "text_sha256": "aaf88f567941ed16adb101981a218960bbd8ae3cfe0919868de63462e7c7be01"} [lutein-p20678467] Studies on the singlet oxygen scavenging mechanism of human macular pigment. (2010). https://pubmed.ncbi.nlm.nih.gov/20678467/ DOI: 10.1016/j.abb.2010.07.024
Complete structured claim and evidence
Lutein protected cells against hydroxyl-radical challenge across the oxygen concentrations tested.
Lutein → Lutein-associated cellular protection against hydroxyl-radical challenge source_derived_draftungraded
Experimental context and source evidence
evidence_span
{"source_cache": "artifacts/lutein-research/32589182.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "3f863a2aea3b3d98ffd13bc0a4cf8783ab05ef2cb196f8706ba0b9af08ed859c", "start_char": 0, "end_char": 851, "text_sha256": "3f863a2aea3b3d98ffd13bc0a4cf8783ab05ef2cb196f8706ba0b9af08ed859c"}
experimental_model
Pulsed-laser, radiation chemistry and cellular protection experiments
exposure
Hydroxyl radicals across tested oxygen conditions
limitations
Radical species and oxygen conditions matter; no general claim that every carotenoid always acts as an antioxidant.
nutrient_topic
Lutein research collection; topical membership is not evidence of a direct dietary effect. · Lutein
organism
In vitro/ex vivo systems; cell identity not specified in indexed abstract
plain_language
Protection was demonstrated for a defined oxidative challenge.
primary_references
[lutein-p32589182] Anti- and pro-oxidative mechanisms comparing the macular carotenoids zeaxanthin and lutein with other dietary carotenoids - a singlet oxygen, free-radical in vitro and ex vivo study. (2020). https://pubmed.ncbi.nlm.nih.gov/32589182/ DOI: 10.1039/d0pp00120a
tissue_or_cell_type
Radical challenge assays
Lutein: metabolism, signaling and nutrient connections (2026-09-17) · lines 242–253
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Pulsed-laser, radiation chemistry and cellular protection experiments · source_derived_draft · unverified_draft
### lutein-hydroxyl-protection Lutein protected cells against hydroxyl-radical challenge across the oxygen concentrations tested. Condition category: normal nutrient_topic: Lutein research collection; topical membership is not evidence of a direct dietary effect. plain_language: Protection was demonstrated for a defined oxidative challenge. organism: In vitro/ex vivo systems; cell identity not specified in indexed abstract tissue_or_cell_type: Radical challenge assays experimental_model: Pulsed-laser, radiation chemistry and cellular protection experiments limitations: Radical species and oxygen conditions matter; no general claim that every carotenoid always acts as an antioxidant. exposure: Hydroxyl radicals across tested oxygen conditions evidence_span: {"source_cache": "artifacts/lutein-research/32589182.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "3f863a2aea3b3d98ffd13bc0a4cf8783ab05ef2cb196f8706ba0b9af08ed859c", "start_char": 0, "end_char": 851, "text_sha256": "3f863a2aea3b3d98ffd13bc0a4cf8783ab05ef2cb196f8706ba0b9af08ed859c"} [lutein-p32589182] Anti- and pro-oxidative mechanisms comparing the macular carotenoids zeaxanthin and lutein with other dietary carotenoids - a singlet oxygen, free-radical in vitro and ex vivo study. (2020). https://pubmed.ncbi.nlm.nih.gov/32589182/ DOI: 10.1039/d0pp00120a
Complete structured claim and evidence
The 2014 expression assay detected zeaxanthin cleavage by mouse BCO2 but not human BCO2.
Human beta-carotene oxygenase 2 / BCO2 → Human BCO2 carotenoid cleavage activity source_derived_draftungraded
Experimental context and source evidence
evidence_span
{"source_cache": "artifacts/lutein-research/24982131.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "975bef59c81c57ad6e18b45581b23174165732965e8d7e017275fe98ca3ab4a0", "start_char": 0, "end_char": 1743, "text_sha256": "975bef59c81c57ad6e18b45581b23174165732965e8d7e017275fe98ca3ab4a0"}
experimental_model
Recombinant enzyme expression and comparative binding
exposure
Zeaxanthin-producing bacteria; surface plasmon resonance
limitations
Historical assay result; later work demonstrates human catalytic competence with altered protein processing and expression conditions.
nutrient_topic
Lutein research collection; topical membership is not evidence of a direct dietary effect. · Lutein
organism
Human and mouse proteins; bacterial expression
plain_language
One early assay found no detectable human enzyme activity.
primary_references
[lutein-p24982131] Inactivity of human β,β-carotene-9',10'-dioxygenase (BCO2) underlies retinal accumulation of the human macular carotenoid pigment. (2014). https://pubmed.ncbi.nlm.nih.gov/24982131/ DOI: 10.1073/pnas.1402526111
tissue_or_cell_type
Recombinant BCO2 and retina
Lutein: metabolism, signaling and nutrient connections (2026-09-17) · lines 255–266
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Recombinant enzyme expression and comparative binding · source_derived_draft · unverified_draft
### lutein-bco2-2014-inactive The 2014 expression assay detected zeaxanthin cleavage by mouse BCO2 but not human BCO2. Condition category: normal nutrient_topic: Lutein research collection; topical membership is not evidence of a direct dietary effect. plain_language: One early assay found no detectable human enzyme activity. organism: Human and mouse proteins; bacterial expression tissue_or_cell_type: Recombinant BCO2 and retina experimental_model: Recombinant enzyme expression and comparative binding limitations: Historical assay result; later work demonstrates human catalytic competence with altered protein processing and expression conditions. exposure: Zeaxanthin-producing bacteria; surface plasmon resonance evidence_span: {"source_cache": "artifacts/lutein-research/24982131.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "975bef59c81c57ad6e18b45581b23174165732965e8d7e017275fe98ca3ab4a0", "start_char": 0, "end_char": 1743, "text_sha256": "975bef59c81c57ad6e18b45581b23174165732965e8d7e017275fe98ca3ab4a0"} [lutein-p24982131] Inactivity of human β,β-carotene-9',10'-dioxygenase (BCO2) underlies retinal accumulation of the human macular carotenoid pigment. (2014). https://pubmed.ncbi.nlm.nih.gov/24982131/ DOI: 10.1073/pnas.1402526111
Complete structured claim and evidence
Human BCO2 binding to tested macular carotenoids was 10–40-fold weaker than mouse BCO2 in the 2014 comparison.
Human beta-carotene oxygenase 2 / BCO2 → Lutein source_derived_draftungraded
Experimental context and source evidence
evidence_span
{"source_cache": "artifacts/lutein-research/24982131.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "975bef59c81c57ad6e18b45581b23174165732965e8d7e017275fe98ca3ab4a0", "start_char": 0, "end_char": 1743, "text_sha256": "975bef59c81c57ad6e18b45581b23174165732965e8d7e017275fe98ca3ab4a0"}
experimental_model
Recombinant enzyme expression and comparative binding
exposure
Zeaxanthin-producing bacteria; surface plasmon resonance
limitations
Historical assay result; later work demonstrates human catalytic competence with altered protein processing and expression conditions.
nutrient_topic
Lutein research collection; topical membership is not evidence of a direct dietary effect. · Lutein
organism
Human and mouse proteins; bacterial expression
plain_language
The early protein preparations differed in pigment binding.
primary_references
[lutein-p24982131] Inactivity of human β,β-carotene-9',10'-dioxygenase (BCO2) underlies retinal accumulation of the human macular carotenoid pigment. (2014). https://pubmed.ncbi.nlm.nih.gov/24982131/ DOI: 10.1073/pnas.1402526111
tissue_or_cell_type
Recombinant BCO2 and retina
Lutein: metabolism, signaling and nutrient connections (2026-09-17) · lines 268–279
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Recombinant enzyme expression and comparative binding · source_derived_draft · unverified_draft
### lutein-bco2-2014-binding Human BCO2 binding to tested macular carotenoids was 10–40-fold weaker than mouse BCO2 in the 2014 comparison. Condition category: normal nutrient_topic: Lutein research collection; topical membership is not evidence of a direct dietary effect. plain_language: The early protein preparations differed in pigment binding. organism: Human and mouse proteins; bacterial expression tissue_or_cell_type: Recombinant BCO2 and retina experimental_model: Recombinant enzyme expression and comparative binding limitations: Historical assay result; later work demonstrates human catalytic competence with altered protein processing and expression conditions. exposure: Zeaxanthin-producing bacteria; surface plasmon resonance evidence_span: {"source_cache": "artifacts/lutein-research/24982131.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "975bef59c81c57ad6e18b45581b23174165732965e8d7e017275fe98ca3ab4a0", "start_char": 0, "end_char": 1743, "text_sha256": "975bef59c81c57ad6e18b45581b23174165732965e8d7e017275fe98ca3ab4a0"} [lutein-p24982131] Inactivity of human β,β-carotene-9',10'-dioxygenase (BCO2) underlies retinal accumulation of the human macular carotenoid pigment. (2014). https://pubmed.ncbi.nlm.nih.gov/24982131/ DOI: 10.1073/pnas.1402526111
Complete structured claim and evidence
The BCO2a targeting sequence directed a reporter to mitochondria in ARPE-19 cells; this experiment establishes mitochondrial import, not precise membrane topology.
Human BCO2a precursor isoform → Mitochondria source_derived_draftungraded
Experimental context and source evidence
evidence_span
{"source_cache": "artifacts/lutein-research/32873706.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "1555914c4a5090c968595f2aba72ce276054594a66423916be600a600a28349f", "start_char": 0, "end_char": 1517, "text_sha256": "1555914c4a5090c968595f2aba72ce276054594a66423916be600a600a28349f"}
experimental_model
Isoform targeting, recombinant expression and enzyme assays
exposure
Removal of N-terminal mitochondrial targeting sequence; expression optimization
limitations
Activity of processed recombinant protein does not quantify retinal flux; mouse chimeric substrate results remain mouse-specific.
nutrient_topic
Lutein research collection; topical membership is not evidence of a direct dietary effect. · Lutein
organism
Human BCO2 isoforms and engineered mouse protein
plain_language
An amino-terminal address directs the protein into mitochondria.
primary_references
[lutein-p32873706] The human mitochondrial enzyme BCO2 exhibits catalytic activity toward carotenoids and apocarotenoids. (2020). https://pubmed.ncbi.nlm.nih.gov/32873706/ DOI: 10.1074/jbc.ra120.015515
tissue_or_cell_type
ARPE-19 cells and bacterial expression
Lutein: metabolism, signaling and nutrient connections (2026-09-17) · lines 294–305
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Isoform targeting, recombinant expression and enzyme assays · source_derived_draft · unverified_draft
### lutein-bco2-targeting The BCO2a targeting sequence directed a reporter to mitochondria in ARPE-19 cells; this experiment establishes mitochondrial import, not precise membrane topology. Condition category: normal nutrient_topic: Lutein research collection; topical membership is not evidence of a direct dietary effect. plain_language: An amino-terminal address directs the protein into mitochondria. organism: Human BCO2 isoforms and engineered mouse protein tissue_or_cell_type: ARPE-19 cells and bacterial expression experimental_model: Isoform targeting, recombinant expression and enzyme assays limitations: Activity of processed recombinant protein does not quantify retinal flux; mouse chimeric substrate results remain mouse-specific. exposure: Removal of N-terminal mitochondrial targeting sequence; expression optimization evidence_span: {"source_cache": "artifacts/lutein-research/32873706.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "1555914c4a5090c968595f2aba72ce276054594a66423916be600a600a28349f", "start_char": 0, "end_char": 1517, "text_sha256": "1555914c4a5090c968595f2aba72ce276054594a66423916be600a600a28349f"} [lutein-p32873706] The human mitochondrial enzyme BCO2 exhibits catalytic activity toward carotenoids and apocarotenoids. (2020). https://pubmed.ncbi.nlm.nih.gov/32873706/ DOI: 10.1074/jbc.ra120.015515
Complete structured claim and evidence
Human BCO2 associated with the inner mitochondrial membrane in cell-line experiments.
Human beta-carotene oxygenase 2 / BCO2 → Inner mitochondrial membrane source_derived_draftungraded
Experimental context and source evidence
evidence_span
{"source_cache": "artifacts/lutein-research/25002123.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "13eecc413b623871f99140525333718bec180923ca6673fab15a9dee19a0551b", "start_char": 0, "end_char": 1308, "text_sha256": "13eecc413b623871f99140525333718bec180923ca6673fab15a9dee19a0551b"}
experimental_model
Subcellular localization and mitochondrial fractionation
exposure
Cleavable N-terminal leaders and compartment analyses
limitations
Human cell localization and mouse organelle fractionation are separate evidence components.
nutrient_topic
Lutein research collection; topical membership is not evidence of a direct dietary effect. · Lutein
organism
Human isoforms in cell lines and mouse liver
plain_language
Carotenoid breakdown is organized within a particular compartment.
primary_references
[lutein-p25002123] Evidence for compartmentalization of mammalian carotenoid metabolism. (2014). https://pubmed.ncbi.nlm.nih.gov/25002123/ DOI: 10.1096/fj.14-252411
tissue_or_cell_type
Inner mitochondrial membrane
Lutein: metabolism, signaling and nutrient connections (2026-09-17) · lines 307–318
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Subcellular localization and mitochondrial fractionation · source_derived_draft · unverified_draft
### lutein-bco2-inner-membrane Human BCO2 associated with the inner mitochondrial membrane in cell-line experiments. Condition category: normal nutrient_topic: Lutein research collection; topical membership is not evidence of a direct dietary effect. plain_language: Carotenoid breakdown is organized within a particular compartment. organism: Human isoforms in cell lines and mouse liver tissue_or_cell_type: Inner mitochondrial membrane experimental_model: Subcellular localization and mitochondrial fractionation limitations: Human cell localization and mouse organelle fractionation are separate evidence components. exposure: Cleavable N-terminal leaders and compartment analyses evidence_span: {"source_cache": "artifacts/lutein-research/25002123.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "13eecc413b623871f99140525333718bec180923ca6673fab15a9dee19a0551b", "start_char": 0, "end_char": 1308, "text_sha256": "13eecc413b623871f99140525333718bec180923ca6673fab15a9dee19a0551b"} [lutein-p25002123] Evidence for compartmentalization of mammalian carotenoid metabolism. (2014). https://pubmed.ncbi.nlm.nih.gov/25002123/ DOI: 10.1096/fj.14-252411
Complete structured claim and evidence
Expression temperature and detergent choice affected recombinant BCO2 binding and xanthophyll turnover, including meso-zeaxanthin.
Primate BCO2 preparations in the 2015 enzyme comparison → meso-Zeaxanthin / (3R,3-prime-S)-zeaxanthin source_derived_draftungraded
Experimental context and source evidence
evidence_span
{"source_cache": "artifacts/lutein-research/26307071.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "6b225e90d2edb66a12583bcdaefb8247cf57c26dffd4f02a1a189907c6f97916", "start_char": 0, "end_char": 1495, "text_sha256": "6b225e90d2edb66a12583bcdaefb8247cf57c26dffd4f02a1a189907c6f97916"}
experimental_model
Comparative recombinant enzyme and cell experiments
exposure
Low-temperature expression and detergent variation
limitations
Conserved activity does not demonstrate identical rates across species or diets.
nutrient_topic
Lutein research collection; topical membership is not evidence of a direct dietary effect. · Lutein
organism
Primate and murine BCO2
plain_language
How the protein was prepared changed the measured activity.
primary_references
[lutein-p26307071] Characterization of the Role of β-Carotene 9,10-Dioxygenase in Macular Pigment Metabolism. (2015). https://pubmed.ncbi.nlm.nih.gov/26307071/ DOI: 10.1074/jbc.m115.668822
tissue_or_cell_type
Protein preparations and human hepatic cell line
Lutein: metabolism, signaling and nutrient connections (2026-09-17) · lines 320–331
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Comparative recombinant enzyme and cell experiments · source_derived_draft · unverified_draft
### lutein-bco2-method-dependence Expression temperature and detergent choice affected recombinant BCO2 binding and xanthophyll turnover, including meso-zeaxanthin. Condition category: normal nutrient_topic: Lutein research collection; topical membership is not evidence of a direct dietary effect. plain_language: How the protein was prepared changed the measured activity. organism: Primate and murine BCO2 tissue_or_cell_type: Protein preparations and human hepatic cell line experimental_model: Comparative recombinant enzyme and cell experiments limitations: Conserved activity does not demonstrate identical rates across species or diets. exposure: Low-temperature expression and detergent variation evidence_span: {"source_cache": "artifacts/lutein-research/26307071.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "6b225e90d2edb66a12583bcdaefb8247cf57c26dffd4f02a1a189907c6f97916", "start_char": 0, "end_char": 1495, "text_sha256": "6b225e90d2edb66a12583bcdaefb8247cf57c26dffd4f02a1a189907c6f97916"} [lutein-p26307071] Characterization of the Role of β-Carotene 9,10-Dioxygenase in Macular Pigment Metabolism. (2015). https://pubmed.ncbi.nlm.nih.gov/26307071/ DOI: 10.1074/jbc.m115.668822
Complete structured claim and evidence
Human donor retina had higher BCO2 protein expression peripherally than centrally.
Human beta-carotene oxygenase 2 / BCO2 → Human retinal BCO2 regional protein abundance source_derived_draftungraded
Experimental context and source evidence
evidence_span
{"source_cache": "artifacts/lutein-research/39978586.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "3546acef9586e54733ec1f03797741c67643606de59f80a7762815b32c3c03fe", "start_char": 0, "end_char": 1561, "text_sha256": "3546acef9586e54733ec1f03797741c67643606de59f80a7762815b32c3c03fe"}
experimental_model
Validated antibodies, localization, donor-retina analysis and activity assays
exposure
BCO2 precursor/processed protein comparison; Aster interactions
limitations
Protein expression and interaction evidence does not by itself quantify lutein cleavage in living human retina.
nutrient_topic
Lutein research collection; topical membership is not evidence of a direct dietary effect. · Lutein
organism
Human cells/donor retina and macaque retina
plain_language
The breakdown enzyme was unevenly distributed across the retina.
primary_references
[lutein-p39978586] Unveiling BCO2 function in macular pigment metabolism: Mitochondrial processing and expression in the primate retina. (2025). https://pubmed.ncbi.nlm.nih.gov/39978586/ DOI: 10.1016/j.bbalip.2025.159600
tissue_or_cell_type
Retinal regions and mitochondria
Lutein: metabolism, signaling and nutrient connections (2026-09-17) · lines 333–344
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Validated antibodies, localization, donor-retina analysis and activity assays · source_derived_draft · unverified_draft
### lutein-bco2-regional Human donor retina had higher BCO2 protein expression peripherally than centrally. Condition category: normal nutrient_topic: Lutein research collection; topical membership is not evidence of a direct dietary effect. plain_language: The breakdown enzyme was unevenly distributed across the retina. organism: Human cells/donor retina and macaque retina tissue_or_cell_type: Retinal regions and mitochondria experimental_model: Validated antibodies, localization, donor-retina analysis and activity assays limitations: Protein expression and interaction evidence does not by itself quantify lutein cleavage in living human retina. exposure: BCO2 precursor/processed protein comparison; Aster interactions evidence_span: {"source_cache": "artifacts/lutein-research/39978586.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "3546acef9586e54733ec1f03797741c67643606de59f80a7762815b32c3c03fe", "start_char": 0, "end_char": 1561, "text_sha256": "3546acef9586e54733ec1f03797741c67643606de59f80a7762815b32c3c03fe"} [lutein-p39978586] Unveiling BCO2 function in macular pigment metabolism: Mitochondrial processing and expression in the primate retina. (2025). https://pubmed.ncbi.nlm.nih.gov/39978586/ DOI: 10.1016/j.bbalip.2025.159600
Complete structured claim and evidence
Activity assays indicated interaction between BCO2 and intracellular carotenoid-transporting Aster proteins.
Human beta-carotene oxygenase 2 / BCO2 → Aster intracellular carotenoid-transfer proteins; members unresolved in indexed abstract source_derived_draftungraded
Experimental context and source evidence
evidence_span
{"source_cache": "artifacts/lutein-research/39978586.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "3546acef9586e54733ec1f03797741c67643606de59f80a7762815b32c3c03fe", "start_char": 0, "end_char": 1561, "text_sha256": "3546acef9586e54733ec1f03797741c67643606de59f80a7762815b32c3c03fe"}
experimental_model
Validated antibodies, localization, donor-retina analysis and activity assays
exposure
BCO2 precursor/processed protein comparison; Aster interactions
limitations
Protein expression and interaction evidence does not by itself quantify lutein cleavage in living human retina.
nutrient_topic
Lutein research collection; topical membership is not evidence of a direct dietary effect. · Lutein
organism
Human cells/donor retina and macaque retina
plain_language
Transport and breakdown machinery can work together in the assay.
primary_references
[lutein-p39978586] Unveiling BCO2 function in macular pigment metabolism: Mitochondrial processing and expression in the primate retina. (2025). https://pubmed.ncbi.nlm.nih.gov/39978586/ DOI: 10.1016/j.bbalip.2025.159600
tissue_or_cell_type
Retinal regions and mitochondria
Lutein: metabolism, signaling and nutrient connections (2026-09-17) · lines 346–357
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Validated antibodies, localization, donor-retina analysis and activity assays · source_derived_draft · unverified_draft
### lutein-bco2-aster Activity assays indicated interaction between BCO2 and intracellular carotenoid-transporting Aster proteins. Condition category: normal nutrient_topic: Lutein research collection; topical membership is not evidence of a direct dietary effect. plain_language: Transport and breakdown machinery can work together in the assay. organism: Human cells/donor retina and macaque retina tissue_or_cell_type: Retinal regions and mitochondria experimental_model: Validated antibodies, localization, donor-retina analysis and activity assays limitations: Protein expression and interaction evidence does not by itself quantify lutein cleavage in living human retina. exposure: BCO2 precursor/processed protein comparison; Aster interactions evidence_span: {"source_cache": "artifacts/lutein-research/39978586.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "3546acef9586e54733ec1f03797741c67643606de59f80a7762815b32c3c03fe", "start_char": 0, "end_char": 1561, "text_sha256": "3546acef9586e54733ec1f03797741c67643606de59f80a7762815b32c3c03fe"} [lutein-p39978586] Unveiling BCO2 function in macular pigment metabolism: Mitochondrial processing and expression in the primate retina. (2025). https://pubmed.ncbi.nlm.nih.gov/39978586/ DOI: 10.1016/j.bbalip.2025.159600
Complete structured claim and evidence
WHAM chickens with ABCA1 E89K had over 90% lower plasma HDL.
Chicken ABCA1 E89K / WHAM genotype → WHAM chicken circulating HDL abundance source_derived_draftungraded
Experimental context and source evidence
availability_state
machinery_impairment Imported condition classification; unverified.
evidence_span
{"source_cache": "artifacts/lutein-research/12364545.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "e3deaf99143042e2667f6be249df15574ba1f975f3b537f5b779fbe69bd20c4c", "start_char": 0, "end_char": 913, "text_sha256": "e3deaf99143042e2667f6be249df15574ba1f975f3b537f5b779fbe69bd20c4c"}
experimental_model
WHAM sequencing and functional expression of corresponding mutation
exposure
Naturally occurring chicken E89K; analogous mouse protein substitution
limitations
Trafficking experiment used mouse protein; do not silently relabel it as human or chicken protein.
nutrient_topic
Lutein research collection; topical membership is not evidence of a direct dietary effect. · Lutein
organism
Chicken genotype and engineered mouse ABCA1
plain_language
A transporter mutation severely reduced a circulating carrier.
primary_references
[lutein-p12364545] Identification and functional analysis of a naturally occurring E89K mutation in the ABCA1 gene of the WHAM chicken. (2002). https://pubmed.ncbi.nlm.nih.gov/12364545/ DOI: 10.1194/jlr.m200223-jlr200
tissue_or_cell_type
Lipoprotein phenotype and cellular membrane trafficking
trigger_kind
machinery_impairment Imported condition classification; unverified.
Lutein: metabolism, signaling and nutrient connections (2026-09-17) · lines 359–370
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · WHAM sequencing and functional expression of corresponding mutation · source_derived_draft · unverified_draft
### lutein-wham-hdl WHAM chickens with ABCA1 E89K had over 90% lower plasma HDL. Condition category: machinery_impairment nutrient_topic: Lutein research collection; topical membership is not evidence of a direct dietary effect. plain_language: A transporter mutation severely reduced a circulating carrier. organism: Chicken genotype and engineered mouse ABCA1 tissue_or_cell_type: Lipoprotein phenotype and cellular membrane trafficking experimental_model: WHAM sequencing and functional expression of corresponding mutation limitations: Trafficking experiment used mouse protein; do not silently relabel it as human or chicken protein. exposure: Naturally occurring chicken E89K; analogous mouse protein substitution evidence_span: {"source_cache": "artifacts/lutein-research/12364545.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "e3deaf99143042e2667f6be249df15574ba1f975f3b537f5b779fbe69bd20c4c", "start_char": 0, "end_char": 913, "text_sha256": "e3deaf99143042e2667f6be249df15574ba1f975f3b537f5b779fbe69bd20c4c"} [lutein-p12364545] Identification and functional analysis of a naturally occurring E89K mutation in the ABCA1 gene of the WHAM chicken. (2002). https://pubmed.ncbi.nlm.nih.gov/12364545/ DOI: 10.1194/jlr.m200223-jlr200
Complete structured claim and evidence
The analogous mouse ABCA1 E89K substitution impaired intracellular trafficking, leaving little transporter at the cell surface.
Mouse ABCA1 E89K experimental variant → Mouse ABCA1 cell-surface localization source_derived_draftungraded
Experimental context and source evidence
availability_state
machinery_impairment Imported condition classification; unverified.
evidence_span
{"source_cache": "artifacts/lutein-research/12364545.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "e3deaf99143042e2667f6be249df15574ba1f975f3b537f5b779fbe69bd20c4c", "start_char": 0, "end_char": 913, "text_sha256": "e3deaf99143042e2667f6be249df15574ba1f975f3b537f5b779fbe69bd20c4c"}
experimental_model
WHAM sequencing and functional expression of corresponding mutation
exposure
Naturally occurring chicken E89K; analogous mouse protein substitution
limitations
Trafficking experiment used mouse protein; do not silently relabel it as human or chicken protein.
nutrient_topic
Lutein research collection; topical membership is not evidence of a direct dietary effect. · Lutein
organism
Chicken genotype and engineered mouse ABCA1
plain_language
The protein failed to reach its working location.
primary_references
[lutein-p12364545] Identification and functional analysis of a naturally occurring E89K mutation in the ABCA1 gene of the WHAM chicken. (2002). https://pubmed.ncbi.nlm.nih.gov/12364545/ DOI: 10.1194/jlr.m200223-jlr200
tissue_or_cell_type
Lipoprotein phenotype and cellular membrane trafficking
trigger_kind
machinery_impairment Imported condition classification; unverified.
Lutein: metabolism, signaling and nutrient connections (2026-09-17) · lines 372–383
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · WHAM sequencing and functional expression of corresponding mutation · source_derived_draft · unverified_draft
### lutein-abca1-trafficking The analogous mouse ABCA1 E89K substitution impaired intracellular trafficking, leaving little transporter at the cell surface. Condition category: machinery_impairment nutrient_topic: Lutein research collection; topical membership is not evidence of a direct dietary effect. plain_language: The protein failed to reach its working location. organism: Chicken genotype and engineered mouse ABCA1 tissue_or_cell_type: Lipoprotein phenotype and cellular membrane trafficking experimental_model: WHAM sequencing and functional expression of corresponding mutation limitations: Trafficking experiment used mouse protein; do not silently relabel it as human or chicken protein. exposure: Naturally occurring chicken E89K; analogous mouse protein substitution evidence_span: {"source_cache": "artifacts/lutein-research/12364545.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "e3deaf99143042e2667f6be249df15574ba1f975f3b537f5b779fbe69bd20c4c", "start_char": 0, "end_char": 913, "text_sha256": "e3deaf99143042e2667f6be249df15574ba1f975f3b537f5b779fbe69bd20c4c"} [lutein-p12364545] Identification and functional analysis of a naturally occurring E89K mutation in the ABCA1 gene of the WHAM chicken. (2002). https://pubmed.ncbi.nlm.nih.gov/12364545/ DOI: 10.1194/jlr.m200223-jlr200
Complete structured claim and evidence
WHAM chicks had retinal lutein around 6% of control levels.
Chicken ABCA1 E89K / WHAM genotype → Chicken retinal lutein content source_derived_draftungraded
Experimental context and source evidence
availability_state
machinery_impairment Imported condition classification; unverified.
evidence_span
{"source_cache": "artifacts/lutein-research/17724211.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "7d7044cc9e41a7d859e5d5d75fc3fb7381d11fa635fa7232bf9dc97b83bd4cf4", "start_char": 0, "end_char": 1727, "text_sha256": "7d7044cc9e41a7d859e5d5d75fc3fb7381d11fa635fa7232bf9dc97b83bd4cf4"}
experimental_model
High-lutein feeding in WHAM versus control chicks
exposure
High-lutein or control diet from hatching for 28 days
limitations
Animal transport failure; raising human HDL cholesterol is not established as a way to improve retinal lutein.
nutrient_topic
Lutein research collection; topical membership is not evidence of a direct dietary effect. · Lutein
organism
Chicken
plain_language
Very little lutein reached or remained in the retina.
primary_references
[lutein-p17724211] The prime role of HDL to transport lutein into the retina: evidence from HDL-deficient WHAM chicks having a mutant ABCA1 transporter. (2007). https://pubmed.ncbi.nlm.nih.gov/17724211/ DOI: 10.1167/iovs.06-1275
tissue_or_cell_type
Plasma, retina, liver and heart
trigger_kind
machinery_impairment Imported condition classification; unverified.
Lutein: metabolism, signaling and nutrient connections (2026-09-17) · lines 385–396
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · High-lutein feeding in WHAM versus control chicks · source_derived_draft · unverified_draft
### lutein-wham-retina WHAM chicks had retinal lutein around 6% of control levels. Condition category: machinery_impairment nutrient_topic: Lutein research collection; topical membership is not evidence of a direct dietary effect. plain_language: Very little lutein reached or remained in the retina. organism: Chicken tissue_or_cell_type: Plasma, retina, liver and heart experimental_model: High-lutein feeding in WHAM versus control chicks limitations: Animal transport failure; raising human HDL cholesterol is not established as a way to improve retinal lutein. exposure: High-lutein or control diet from hatching for 28 days evidence_span: {"source_cache": "artifacts/lutein-research/17724211.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "7d7044cc9e41a7d859e5d5d75fc3fb7381d11fa635fa7232bf9dc97b83bd4cf4", "start_char": 0, "end_char": 1727, "text_sha256": "7d7044cc9e41a7d859e5d5d75fc3fb7381d11fa635fa7232bf9dc97b83bd4cf4"} [lutein-p17724211] The prime role of HDL to transport lutein into the retina: evidence from HDL-deficient WHAM chicks having a mutant ABCA1 transporter. (2007). https://pubmed.ncbi.nlm.nih.gov/17724211/ DOI: 10.1167/iovs.06-1275
Complete structured claim and evidence
High-lutein feeding increased plasma lutein greatly in WHAM chicks.
Lutein → Chicken circulating lutein content source_derived_draftungraded
Experimental context and source evidence
availability_state
machinery_impairment Imported condition classification; unverified.
evidence_span
{"source_cache": "artifacts/lutein-research/17724211.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "7d7044cc9e41a7d859e5d5d75fc3fb7381d11fa635fa7232bf9dc97b83bd4cf4", "start_char": 0, "end_char": 1727, "text_sha256": "7d7044cc9e41a7d859e5d5d75fc3fb7381d11fa635fa7232bf9dc97b83bd4cf4"}
experimental_model
High-lutein feeding in WHAM versus control chicks
exposure
High-lutein or control diet from hatching for 28 days
limitations
Animal transport failure; raising human HDL cholesterol is not established as a way to improve retinal lutein.
nutrient_topic
Lutein research collection; topical membership is not evidence of a direct dietary effect. · Lutein
organism
Chicken
plain_language
Blood levels rose when more was supplied.
primary_references
[lutein-p17724211] The prime role of HDL to transport lutein into the retina: evidence from HDL-deficient WHAM chicks having a mutant ABCA1 transporter. (2007). https://pubmed.ncbi.nlm.nih.gov/17724211/ DOI: 10.1167/iovs.06-1275
tissue_or_cell_type
Plasma, retina, liver and heart
trigger_kind
machinery_impairment Imported condition classification; unverified.
Lutein: metabolism, signaling and nutrient connections (2026-09-17) · lines 398–409
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · High-lutein feeding in WHAM versus control chicks · source_derived_draft · unverified_draft
### lutein-wham-plasma-repletion High-lutein feeding increased plasma lutein greatly in WHAM chicks. Condition category: machinery_impairment nutrient_topic: Lutein research collection; topical membership is not evidence of a direct dietary effect. plain_language: Blood levels rose when more was supplied. organism: Chicken tissue_or_cell_type: Plasma, retina, liver and heart experimental_model: High-lutein feeding in WHAM versus control chicks limitations: Animal transport failure; raising human HDL cholesterol is not established as a way to improve retinal lutein. exposure: High-lutein or control diet from hatching for 28 days evidence_span: {"source_cache": "artifacts/lutein-research/17724211.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "7d7044cc9e41a7d859e5d5d75fc3fb7381d11fa635fa7232bf9dc97b83bd4cf4", "start_char": 0, "end_char": 1727, "text_sha256": "7d7044cc9e41a7d859e5d5d75fc3fb7381d11fa635fa7232bf9dc97b83bd4cf4"} [lutein-p17724211] The prime role of HDL to transport lutein into the retina: evidence from HDL-deficient WHAM chicks having a mutant ABCA1 transporter. (2007). https://pubmed.ncbi.nlm.nih.gov/17724211/ DOI: 10.1167/iovs.06-1275
Complete structured claim and evidence
Lifelong xanthophyll-free animals had no detectable macular pigment.
Lifelong xanthophyll-free diet in rhesus monkeys → Rhesus macular pigment content source_derived_draftungraded
Experimental context and source evidence
availability_state
nutrient_deficiency Imported condition classification; unverified.
evidence_span
{"source_cache": "artifacts/lutein-research/21245404.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "74fa1a576a92084789e1a2d4afcd7c657e9ef2acaf9b0a6eaca46d543447ee2b", "start_char": 0, "end_char": 1712, "text_sha256": "74fa1a576a92084789e1a2d4afcd7c657e9ef2acaf9b0a6eaca46d543447ee2b"}
experimental_model
Dietary deprivation/repletion and controlled laser challenge
exposure
Eight lifelong xanthophyll-deprived animals, n-3 intake strata; 22–28 weeks L or Z; 476-nm exposures
limitations
Extreme animal depletion and laser injury are not a defined human deficiency syndrome or ordinary screen exposure.
nutrient_topic
Lutein research collection; topical membership is not evidence of a direct dietary effect. · Lutein
organism
Rhesus macaque
plain_language
The pigment pool disappeared under extreme dietary deprivation.
primary_references
[lutein-p21245404] Nutritional manipulation of primate retinas, V: effects of lutein, zeaxanthin, and n-3 fatty acids on retinal sensitivity to blue-light-induced damage. (2011). https://pubmed.ncbi.nlm.nih.gov/21245404/ DOI: 10.1167/iovs.10-5898
tissue_or_cell_type
Foveal and parafoveal retina
trigger_kind
nutrient_deficiency Imported condition classification; unverified.
Lutein: metabolism, signaling and nutrient connections (2026-09-17) · lines 424–435
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Dietary deprivation/repletion and controlled laser challenge · source_derived_draft · unverified_draft
### lutein-deprivation-pigment Lifelong xanthophyll-free animals had no detectable macular pigment. Condition category: nutrient_deficiency nutrient_topic: Lutein research collection; topical membership is not evidence of a direct dietary effect. plain_language: The pigment pool disappeared under extreme dietary deprivation. organism: Rhesus macaque tissue_or_cell_type: Foveal and parafoveal retina experimental_model: Dietary deprivation/repletion and controlled laser challenge limitations: Extreme animal depletion and laser injury are not a defined human deficiency syndrome or ordinary screen exposure. exposure: Eight lifelong xanthophyll-deprived animals, n-3 intake strata; 22–28 weeks L or Z; 476-nm exposures evidence_span: {"source_cache": "artifacts/lutein-research/21245404.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "74fa1a576a92084789e1a2d4afcd7c657e9ef2acaf9b0a6eaca46d543447ee2b", "start_char": 0, "end_char": 1712, "text_sha256": "74fa1a576a92084789e1a2d4afcd7c657e9ef2acaf9b0a6eaca46d543447ee2b"} [lutein-p21245404] Nutritional manipulation of primate retinas, V: effects of lutein, zeaxanthin, and n-3 fatty acids on retinal sensitivity to blue-light-induced damage. (2011). https://pubmed.ncbi.nlm.nih.gov/21245404/ DOI: 10.1167/iovs.10-5898
Complete structured claim and evidence
The foveal protection observed in controls was absent in xanthophyll-free animals.
Lifelong xanthophyll-free diet in rhesus monkeys → Rhesus foveal laser-induced blue-light damage susceptibility source_derived_draftungraded
Experimental context and source evidence
availability_state
nutrient_deficiency Imported condition classification; unverified.
evidence_span
{"source_cache": "artifacts/lutein-research/21245404.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "74fa1a576a92084789e1a2d4afcd7c657e9ef2acaf9b0a6eaca46d543447ee2b", "start_char": 0, "end_char": 1712, "text_sha256": "74fa1a576a92084789e1a2d4afcd7c657e9ef2acaf9b0a6eaca46d543447ee2b"}
experimental_model
Dietary deprivation/repletion and controlled laser challenge
exposure
Eight lifelong xanthophyll-deprived animals, n-3 intake strata; 22–28 weeks L or Z; 476-nm exposures
limitations
Extreme animal depletion and laser injury are not a defined human deficiency syndrome or ordinary screen exposure.
nutrient_topic
Lutein research collection; topical membership is not evidence of a direct dietary effect. · Lutein
organism
Rhesus macaque
plain_language
The central retina lost its relative protection in the challenge.
primary_references
[lutein-p21245404] Nutritional manipulation of primate retinas, V: effects of lutein, zeaxanthin, and n-3 fatty acids on retinal sensitivity to blue-light-induced damage. (2011). https://pubmed.ncbi.nlm.nih.gov/21245404/ DOI: 10.1167/iovs.10-5898
tissue_or_cell_type
Foveal and parafoveal retina
trigger_kind
nutrient_deficiency Imported condition classification; unverified.
Lutein: metabolism, signaling and nutrient connections (2026-09-17) · lines 437–448
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Dietary deprivation/repletion and controlled laser challenge · source_derived_draft · unverified_draft
### lutein-deprivation-protection The foveal protection observed in controls was absent in xanthophyll-free animals. Condition category: nutrient_deficiency nutrient_topic: Lutein research collection; topical membership is not evidence of a direct dietary effect. plain_language: The central retina lost its relative protection in the challenge. organism: Rhesus macaque tissue_or_cell_type: Foveal and parafoveal retina experimental_model: Dietary deprivation/repletion and controlled laser challenge limitations: Extreme animal depletion and laser injury are not a defined human deficiency syndrome or ordinary screen exposure. exposure: Eight lifelong xanthophyll-deprived animals, n-3 intake strata; 22–28 weeks L or Z; 476-nm exposures evidence_span: {"source_cache": "artifacts/lutein-research/21245404.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "74fa1a576a92084789e1a2d4afcd7c657e9ef2acaf9b0a6eaca46d543447ee2b", "start_char": 0, "end_char": 1712, "text_sha256": "74fa1a576a92084789e1a2d4afcd7c657e9ef2acaf9b0a6eaca46d543447ee2b"} [lutein-p21245404] Nutritional manipulation of primate retinas, V: effects of lutein, zeaxanthin, and n-3 fatty acids on retinal sensitivity to blue-light-induced damage. (2011). https://pubmed.ncbi.nlm.nih.gov/21245404/ DOI: 10.1167/iovs.10-5898
Complete structured claim and evidence
Lutein or zeaxanthin supplementation restored foveal protection after deprivation.
Lutein → Rhesus foveal laser-induced blue-light damage susceptibility source_derived_draftungraded
Experimental context and source evidence
availability_state
nutrient_deficiency Imported condition classification; unverified.
evidence_span
{"source_cache": "artifacts/lutein-research/21245404.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "74fa1a576a92084789e1a2d4afcd7c657e9ef2acaf9b0a6eaca46d543447ee2b", "start_char": 0, "end_char": 1712, "text_sha256": "74fa1a576a92084789e1a2d4afcd7c657e9ef2acaf9b0a6eaca46d543447ee2b"}
experimental_model
Dietary deprivation/repletion and controlled laser challenge
exposure
Eight lifelong xanthophyll-deprived animals, n-3 intake strata; 22–28 weeks L or Z; 476-nm exposures
limitations
Extreme animal depletion and laser injury are not a defined human deficiency syndrome or ordinary screen exposure.
nutrient_topic
Lutein research collection; topical membership is not evidence of a direct dietary effect. · Lutein
organism
Rhesus macaque
plain_language
Supplying a missing pigment improved this animal endpoint.
primary_references
[lutein-p21245404] Nutritional manipulation of primate retinas, V: effects of lutein, zeaxanthin, and n-3 fatty acids on retinal sensitivity to blue-light-induced damage. (2011). https://pubmed.ncbi.nlm.nih.gov/21245404/ DOI: 10.1167/iovs.10-5898
tissue_or_cell_type
Foveal and parafoveal retina
trigger_kind
nutrient_deficiency Imported condition classification; unverified.
Lutein: metabolism, signaling and nutrient connections (2026-09-17) · lines 450–461
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Dietary deprivation/repletion and controlled laser challenge · source_derived_draft · unverified_draft
### lutein-deprivation-lutein-repletion Lutein or zeaxanthin supplementation restored foveal protection after deprivation. Condition category: nutrient_deficiency nutrient_topic: Lutein research collection; topical membership is not evidence of a direct dietary effect. plain_language: Supplying a missing pigment improved this animal endpoint. organism: Rhesus macaque tissue_or_cell_type: Foveal and parafoveal retina experimental_model: Dietary deprivation/repletion and controlled laser challenge limitations: Extreme animal depletion and laser injury are not a defined human deficiency syndrome or ordinary screen exposure. exposure: Eight lifelong xanthophyll-deprived animals, n-3 intake strata; 22–28 weeks L or Z; 476-nm exposures evidence_span: {"source_cache": "artifacts/lutein-research/21245404.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "74fa1a576a92084789e1a2d4afcd7c657e9ef2acaf9b0a6eaca46d543447ee2b", "start_char": 0, "end_char": 1712, "text_sha256": "74fa1a576a92084789e1a2d4afcd7c657e9ef2acaf9b0a6eaca46d543447ee2b"} [lutein-p21245404] Nutritional manipulation of primate retinas, V: effects of lutein, zeaxanthin, and n-3 fatty acids on retinal sensitivity to blue-light-induced damage. (2011). https://pubmed.ncbi.nlm.nih.gov/21245404/ DOI: 10.1167/iovs.10-5898
Complete structured claim and evidence
Low n-3 intake increased parafoveal damage sensitivity relative to adequate n-3 intake.
Low n-3 fatty-acid intake in the rhesus photodamage study → Rhesus parafoveal laser-induced photodamage susceptibility source_derived_draftungraded
Experimental context and source evidence
availability_state
nutrient_deficiency Imported condition classification; unverified.
evidence_span
{"source_cache": "artifacts/lutein-research/21245404.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "74fa1a576a92084789e1a2d4afcd7c657e9ef2acaf9b0a6eaca46d543447ee2b", "start_char": 0, "end_char": 1712, "text_sha256": "74fa1a576a92084789e1a2d4afcd7c657e9ef2acaf9b0a6eaca46d543447ee2b"}
experimental_model
Dietary deprivation/repletion and controlled laser challenge
exposure
Eight lifelong xanthophyll-deprived animals, n-3 intake strata; 22–28 weeks L or Z; 476-nm exposures
limitations
Extreme animal depletion and laser injury are not a defined human deficiency syndrome or ordinary screen exposure.
nutrient_topic
Lutein research collection; topical membership is not evidence of a direct dietary effect. · Lutein
organism
Rhesus macaque
plain_language
The fatty-acid effect occurred in a different retinal region.
primary_references
[lutein-p21245404] Nutritional manipulation of primate retinas, V: effects of lutein, zeaxanthin, and n-3 fatty acids on retinal sensitivity to blue-light-induced damage. (2011). https://pubmed.ncbi.nlm.nih.gov/21245404/ DOI: 10.1167/iovs.10-5898
tissue_or_cell_type
Foveal and parafoveal retina
trigger_kind
nutrient_deficiency Imported condition classification; unverified.
Lutein: metabolism, signaling and nutrient connections (2026-09-17) · lines 463–474
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Dietary deprivation/repletion and controlled laser challenge · source_derived_draft · unverified_draft
### lutein-n3-region Low n-3 intake increased parafoveal damage sensitivity relative to adequate n-3 intake. Condition category: nutrient_deficiency nutrient_topic: Lutein research collection; topical membership is not evidence of a direct dietary effect. plain_language: The fatty-acid effect occurred in a different retinal region. organism: Rhesus macaque tissue_or_cell_type: Foveal and parafoveal retina experimental_model: Dietary deprivation/repletion and controlled laser challenge limitations: Extreme animal depletion and laser injury are not a defined human deficiency syndrome or ordinary screen exposure. exposure: Eight lifelong xanthophyll-deprived animals, n-3 intake strata; 22–28 weeks L or Z; 476-nm exposures evidence_span: {"source_cache": "artifacts/lutein-research/21245404.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "74fa1a576a92084789e1a2d4afcd7c657e9ef2acaf9b0a6eaca46d543447ee2b", "start_char": 0, "end_char": 1712, "text_sha256": "74fa1a576a92084789e1a2d4afcd7c657e9ef2acaf9b0a6eaca46d543447ee2b"} [lutein-p21245404] Nutritional manipulation of primate retinas, V: effects of lutein, zeaxanthin, and n-3 fatty acids on retinal sensitivity to blue-light-induced damage. (2011). https://pubmed.ncbi.nlm.nih.gov/21245404/ DOI: 10.1167/iovs.10-5898
Complete structured claim and evidence
Co-incubated beta-carotene reduced lutein absorption by approximately 20% in this cell model.
All-trans-beta-carotene → Intestinal epithelial lutein uptake source_derived_draftungraded
Experimental context and source evidence
evidence_span
{"source_cache": "artifacts/lutein-research/15554873.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "3dfbef37e3c73db4732f66083063e548a1654cb759ff46392c981c50f338d8a0", "start_char": 0, "end_char": 2014, "text_sha256": "3dfbef37e3c73db4732f66083063e548a1654cb759ff46392c981c50f338d8a0"}
experimental_model
Mixed-micelle transport across Caco-2 TC-7 monolayers
exposure
Micellar lutein 1.5–15 micromolar; antibodies and BLT1
limitations
Partial inhibition supports a contribution, not an exclusive route; cell experiments do not set clinical supplement spacing.
nutrient_topic
Lutein research collection; topical membership is not evidence of a direct dietary effect. · Lutein
organism
Human intestinal cell model
plain_language
Another carotenoid competed under these conditions.
primary_references
[lutein-p15554873] Lutein transport by Caco-2 TC-7 cells occurs partly by a facilitated process involving the scavenger receptor class B type I (SR-BI). (2005). https://pubmed.ncbi.nlm.nih.gov/15554873/ DOI: 10.1042/bj20040554
tissue_or_cell_type
Apical intestinal epithelial transport
Lutein: metabolism, signaling and nutrient connections (2026-09-17) · lines 489–500
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Mixed-micelle transport across Caco-2 TC-7 monolayers · source_derived_draft · unverified_draft
### lutein-beta-competition Co-incubated beta-carotene reduced lutein absorption by approximately 20% in this cell model. Condition category: normal nutrient_topic: Lutein research collection; topical membership is not evidence of a direct dietary effect. plain_language: Another carotenoid competed under these conditions. organism: Human intestinal cell model tissue_or_cell_type: Apical intestinal epithelial transport experimental_model: Mixed-micelle transport across Caco-2 TC-7 monolayers limitations: Partial inhibition supports a contribution, not an exclusive route; cell experiments do not set clinical supplement spacing. exposure: Micellar lutein 1.5–15 micromolar; antibodies and BLT1 evidence_span: {"source_cache": "artifacts/lutein-research/15554873.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "3dfbef37e3c73db4732f66083063e548a1654cb759ff46392c981c50f338d8a0", "start_char": 0, "end_char": 2014, "text_sha256": "3dfbef37e3c73db4732f66083063e548a1654cb759ff46392c981c50f338d8a0"} [lutein-p15554873] Lutein transport by Caco-2 TC-7 cells occurs partly by a facilitated process involving the scavenger receptor class B type I (SR-BI). (2005). https://pubmed.ncbi.nlm.nih.gov/15554873/ DOI: 10.1042/bj20040554
Complete structured claim and evidence
Lycopene did not significantly reduce lutein uptake in the same mixed-micelle assay.
Lycopene → Intestinal epithelial lutein uptake source_derived_draftungraded
Experimental context and source evidence
evidence_span
{"source_cache": "artifacts/lutein-research/15554873.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "3dfbef37e3c73db4732f66083063e548a1654cb759ff46392c981c50f338d8a0", "start_char": 0, "end_char": 2014, "text_sha256": "3dfbef37e3c73db4732f66083063e548a1654cb759ff46392c981c50f338d8a0"}
experimental_model
Mixed-micelle transport across Caco-2 TC-7 monolayers
exposure
Micellar lutein 1.5–15 micromolar; antibodies and BLT1
limitations
Partial inhibition supports a contribution, not an exclusive route; cell experiments do not set clinical supplement spacing.
nutrient_topic
Lutein research collection; topical membership is not evidence of a direct dietary effect. · Lutein
organism
Human intestinal cell model
plain_language
Shared transport does not mean every pair competes equally.
primary_references
[lutein-p15554873] Lutein transport by Caco-2 TC-7 cells occurs partly by a facilitated process involving the scavenger receptor class B type I (SR-BI). (2005). https://pubmed.ncbi.nlm.nih.gov/15554873/ DOI: 10.1042/bj20040554
tissue_or_cell_type
Apical intestinal epithelial transport
Lutein: metabolism, signaling and nutrient connections (2026-09-17) · lines 502–513
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Mixed-micelle transport across Caco-2 TC-7 monolayers · source_derived_draft · unverified_draft
### lutein-lycopene-null Lycopene did not significantly reduce lutein uptake in the same mixed-micelle assay. Condition category: normal nutrient_topic: Lutein research collection; topical membership is not evidence of a direct dietary effect. plain_language: Shared transport does not mean every pair competes equally. organism: Human intestinal cell model tissue_or_cell_type: Apical intestinal epithelial transport experimental_model: Mixed-micelle transport across Caco-2 TC-7 monolayers limitations: Partial inhibition supports a contribution, not an exclusive route; cell experiments do not set clinical supplement spacing. exposure: Micellar lutein 1.5–15 micromolar; antibodies and BLT1 evidence_span: {"source_cache": "artifacts/lutein-research/15554873.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "3dfbef37e3c73db4732f66083063e548a1654cb759ff46392c981c50f338d8a0", "start_char": 0, "end_char": 2014, "text_sha256": "3dfbef37e3c73db4732f66083063e548a1654cb759ff46392c981c50f338d8a0"} [lutein-p15554873] Lutein transport by Caco-2 TC-7 cells occurs partly by a facilitated process involving the scavenger receptor class B type I (SR-BI). (2005). https://pubmed.ncbi.nlm.nih.gov/15554873/ DOI: 10.1042/bj20040554
Complete structured claim and evidence
Ezetimibe-sensitive lutein uptake supported a contribution from NPC1L1 in Caco-2 cells.
Human Niemann-Pick C1-like protein 1 / NPC1L1 → Intestinal epithelial lutein uptake source_derived_draftungraded
Experimental context and source evidence
evidence_span
{"source_cache": "artifacts/lutein-research/22579005.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "1dd51af5fd10e865810b3fa2fdab5ed4f6613212a3cd418a009554ae601c076b", "start_char": 0, "end_char": 1895, "text_sha256": "1dd51af5fd10e865810b3fa2fdab5ed4f6613212a3cd418a009554ae601c076b"}
experimental_model
Transporter-inhibitor uptake/permeability experiment
exposure
Ezetimibe, BLT1 and ATP-depletion reagents
limitations
Pharmacological evidence supports involvement, not an exclusive transporter or proven human clinical interaction.
nutrient_topic
Lutein research collection; topical membership is not evidence of a direct dietary effect. · Lutein
organism
Human Caco-2 cells
plain_language
A cholesterol-uptake pathway also contributed to lutein entry.
primary_references
[lutein-p22579005] Involvement of cholesterol membrane transporter Niemann-Pick C1-like 1 in the intestinal absorption of lutein. (2012). https://pubmed.ncbi.nlm.nih.gov/22579005/ DOI: 10.18433/j38k56
tissue_or_cell_type
Intestinal epithelial model
Lutein: metabolism, signaling and nutrient connections (2026-09-17) · lines 515–526
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Transporter-inhibitor uptake/permeability experiment · source_derived_draft · unverified_draft
### lutein-npc1l1-intestine Ezetimibe-sensitive lutein uptake supported a contribution from NPC1L1 in Caco-2 cells. Condition category: normal nutrient_topic: Lutein research collection; topical membership is not evidence of a direct dietary effect. plain_language: A cholesterol-uptake pathway also contributed to lutein entry. organism: Human Caco-2 cells tissue_or_cell_type: Intestinal epithelial model experimental_model: Transporter-inhibitor uptake/permeability experiment limitations: Pharmacological evidence supports involvement, not an exclusive transporter or proven human clinical interaction. exposure: Ezetimibe, BLT1 and ATP-depletion reagents evidence_span: {"source_cache": "artifacts/lutein-research/22579005.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "1dd51af5fd10e865810b3fa2fdab5ed4f6613212a3cd418a009554ae601c076b", "start_char": 0, "end_char": 1895, "text_sha256": "1dd51af5fd10e865810b3fa2fdab5ed4f6613212a3cd418a009554ae601c076b"} [lutein-p22579005] Involvement of cholesterol membrane transporter Niemann-Pick C1-like 1 in the intestinal absorption of lutein. (2012). https://pubmed.ncbi.nlm.nih.gov/22579005/ DOI: 10.18433/j38k56
Complete structured claim and evidence
Ezetimibe reduced lutein accumulation by up to 40% in Caco-2 monolayers.
Ezetimibe → Intestinal epithelial lutein uptake source_derived_draftungraded
Experimental context and source evidence
evidence_span
{"source_cache": "artifacts/lutein-research/22579005.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "1dd51af5fd10e865810b3fa2fdab5ed4f6613212a3cd418a009554ae601c076b", "start_char": 0, "end_char": 1895, "text_sha256": "1dd51af5fd10e865810b3fa2fdab5ed4f6613212a3cd418a009554ae601c076b"}
experimental_model
Transporter-inhibitor uptake/permeability experiment
exposure
Ezetimibe, BLT1 and ATP-depletion reagents
limitations
Pharmacological evidence supports involvement, not an exclusive transporter or proven human clinical interaction.
nutrient_topic
Lutein research collection; topical membership is not evidence of a direct dietary effect. · Lutein
organism
Human Caco-2 cells
plain_language
The medicine reduced cellular uptake in this experiment.
primary_references
[lutein-p22579005] Involvement of cholesterol membrane transporter Niemann-Pick C1-like 1 in the intestinal absorption of lutein. (2012). https://pubmed.ncbi.nlm.nih.gov/22579005/ DOI: 10.18433/j38k56
tissue_or_cell_type
Intestinal epithelial model
Lutein: metabolism, signaling and nutrient connections (2026-09-17) · lines 528–539
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Transporter-inhibitor uptake/permeability experiment · source_derived_draft · unverified_draft
### lutein-ezetimibe-intestine Ezetimibe reduced lutein accumulation by up to 40% in Caco-2 monolayers. Condition category: normal nutrient_topic: Lutein research collection; topical membership is not evidence of a direct dietary effect. plain_language: The medicine reduced cellular uptake in this experiment. organism: Human Caco-2 cells tissue_or_cell_type: Intestinal epithelial model experimental_model: Transporter-inhibitor uptake/permeability experiment limitations: Pharmacological evidence supports involvement, not an exclusive transporter or proven human clinical interaction. exposure: Ezetimibe, BLT1 and ATP-depletion reagents evidence_span: {"source_cache": "artifacts/lutein-research/22579005.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "1dd51af5fd10e865810b3fa2fdab5ed4f6613212a3cd418a009554ae601c076b", "start_char": 0, "end_char": 1895, "text_sha256": "1dd51af5fd10e865810b3fa2fdab5ed4f6613212a3cd418a009554ae601c076b"} [lutein-p22579005] Involvement of cholesterol membrane transporter Niemann-Pick C1-like 1 in the intestinal absorption of lutein. (2012). https://pubmed.ncbi.nlm.nih.gov/22579005/ DOI: 10.18433/j38k56
Complete structured claim and evidence
Adding lutein reduced the postprandial beta-carotene response, more strongly when lutein predominated.
Lutein → Human post-meal plasma beta-carotene response source_derived_draftungraded
Experimental context and source evidence
evidence_span
{"source_cache": "artifacts/lutein-research/9857262.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "22d6d633851b14b6c170fecfb2b3ef493c263f1640d690a2ee3a1d3bf9ccc77f", "start_char": 0, "end_char": 892, "text_sha256": "22d6d633851b14b6c170fecfb2b3ef493c263f1640d690a2ee3a1d3bf9ccc77f"}
experimental_model
Original single-meal volunteer data reported alongside a literature discussion
exposure
Beta-carotene alone or combined with lutein; beta-carotene:lutein ratios 2:1 and 1:2
limitations
Record uses the original experiment, not the review portion; reduced uptake did not imply impaired cleavage of absorbed beta-carotene.
nutrient_topic
Lutein research collection; topical membership is not evidence of a direct dietary effect. · Lutein
organism
Human volunteers
plain_language
The ratio of carotenoids mattered in the test meal.
primary_references
[lutein-p9857262] Effect of lutein on beta-carotene absorption and cleavage. (1998). https://pubmed.ncbi.nlm.nih.gov/9857262/
tissue_or_cell_type
Postprandial triglyceride-rich lipoproteins
Lutein: metabolism, signaling and nutrient connections (2026-09-17) · lines 554–565
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Original single-meal volunteer data reported alongside a literature discussion · source_derived_draft · unverified_draft
### lutein-human-beta-absorption Adding lutein reduced the postprandial beta-carotene response, more strongly when lutein predominated. Condition category: normal nutrient_topic: Lutein research collection; topical membership is not evidence of a direct dietary effect. plain_language: The ratio of carotenoids mattered in the test meal. organism: Human volunteers tissue_or_cell_type: Postprandial triglyceride-rich lipoproteins experimental_model: Original single-meal volunteer data reported alongside a literature discussion limitations: Record uses the original experiment, not the review portion; reduced uptake did not imply impaired cleavage of absorbed beta-carotene. exposure: Beta-carotene alone or combined with lutein; beta-carotene:lutein ratios 2:1 and 1:2 evidence_span: {"source_cache": "artifacts/lutein-research/9857262.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "22d6d633851b14b6c170fecfb2b3ef493c263f1640d690a2ee3a1d3bf9ccc77f", "start_char": 0, "end_char": 892, "text_sha256": "22d6d633851b14b6c170fecfb2b3ef493c263f1640d690a2ee3a1d3bf9ccc77f"} [lutein-p9857262] Effect of lutein on beta-carotene absorption and cleavage. (1998). https://pubmed.ncbi.nlm.nih.gov/9857262/
Complete structured claim and evidence
The retinyl-ester response suggested no apparent inhibition of beta-carotene cleavage despite reduced absorption.
Lutein → Beta-carotene central cleavage source_derived_draftungraded
Experimental context and source evidence
evidence_span
{"source_cache": "artifacts/lutein-research/9857262.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "22d6d633851b14b6c170fecfb2b3ef493c263f1640d690a2ee3a1d3bf9ccc77f", "start_char": 0, "end_char": 892, "text_sha256": "22d6d633851b14b6c170fecfb2b3ef493c263f1640d690a2ee3a1d3bf9ccc77f"}
experimental_model
Original single-meal volunteer data reported alongside a literature discussion
exposure
Beta-carotene alone or combined with lutein; beta-carotene:lutein ratios 2:1 and 1:2
limitations
Record uses the original experiment, not the review portion; reduced uptake did not imply impaired cleavage of absorbed beta-carotene.
nutrient_topic
Lutein research collection; topical membership is not evidence of a direct dietary effect. · Lutein
organism
Human volunteers
plain_language
Less absorption and blocked vitamin A conversion are different claims.
primary_references
[lutein-p9857262] Effect of lutein on beta-carotene absorption and cleavage. (1998). https://pubmed.ncbi.nlm.nih.gov/9857262/
tissue_or_cell_type
Postprandial triglyceride-rich lipoproteins
Lutein: metabolism, signaling and nutrient connections (2026-09-17) · lines 567–578
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Original single-meal volunteer data reported alongside a literature discussion · source_derived_draft · unverified_draft
### lutein-human-beta-cleavage-null The retinyl-ester response suggested no apparent inhibition of beta-carotene cleavage despite reduced absorption. Condition category: normal nutrient_topic: Lutein research collection; topical membership is not evidence of a direct dietary effect. plain_language: Less absorption and blocked vitamin A conversion are different claims. organism: Human volunteers tissue_or_cell_type: Postprandial triglyceride-rich lipoproteins experimental_model: Original single-meal volunteer data reported alongside a literature discussion limitations: Record uses the original experiment, not the review portion; reduced uptake did not imply impaired cleavage of absorbed beta-carotene. exposure: Beta-carotene alone or combined with lutein; beta-carotene:lutein ratios 2:1 and 1:2 evidence_span: {"source_cache": "artifacts/lutein-research/9857262.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "22d6d633851b14b6c170fecfb2b3ef493c263f1640d690a2ee3a1d3bf9ccc77f", "start_char": 0, "end_char": 892, "text_sha256": "22d6d633851b14b6c170fecfb2b3ef493c263f1640d690a2ee3a1d3bf9ccc77f"} [lutein-p9857262] Effect of lutein on beta-carotene absorption and cleavage. (1998). https://pubmed.ncbi.nlm.nih.gov/9857262/
Complete structured claim and evidence
Lutein rose 207% with the high-fat spread versus 88% with the low-fat spread during lutein-ester supplementation.
High-fat meal with lutein esters in the 2000 crossover study → Human plasma lutein concentration source_derived_draftungraded
Experimental context and source evidence
evidence_span
{"source_cache": "artifacts/lutein-research/10799382.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "68c85cb7c391b6bffddcdc9ca0620c8db353400604353ce62873fe74501a0868", "start_char": 0, "end_char": 1602, "text_sha256": "68c85cb7c391b6bffddcdc9ca0620c8db353400604353ce62873fe74501a0868"}
experimental_model
Random-sequence crossover supplementation
exposure
Lutein esters providing 8 mg lutein; 3 versus 36 g meal fat; seven-day periods
limitations
Formulation-specific short-term response; not a universal minimum fat requirement.
nutrient_topic
Lutein research collection; topical membership is not evidence of a direct dietary effect. · Lutein
organism
Human volunteers in four groups of 14–15
plain_language
Meal fat changed uptake from this ester formulation.
primary_references
[lutein-p10799382] Amount of fat in the diet affects bioavailability of lutein esters but not of alpha-carotene, beta-carotene, and vitamin E in humans. (2000). https://pubmed.ncbi.nlm.nih.gov/10799382/ DOI: 10.1093/ajcn/71.5.1187
tissue_or_cell_type
Plasma carotenoid response
Lutein: metabolism, signaling and nutrient connections (2026-09-17) · lines 580–591
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Random-sequence crossover supplementation · source_derived_draft · unverified_draft
### lutein-dietary-fat Lutein rose 207% with the high-fat spread versus 88% with the low-fat spread during lutein-ester supplementation. Condition category: normal nutrient_topic: Lutein research collection; topical membership is not evidence of a direct dietary effect. plain_language: Meal fat changed uptake from this ester formulation. organism: Human volunteers in four groups of 14–15 tissue_or_cell_type: Plasma carotenoid response experimental_model: Random-sequence crossover supplementation limitations: Formulation-specific short-term response; not a universal minimum fat requirement. exposure: Lutein esters providing 8 mg lutein; 3 versus 36 g meal fat; seven-day periods evidence_span: {"source_cache": "artifacts/lutein-research/10799382.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "68c85cb7c391b6bffddcdc9ca0620c8db353400604353ce62873fe74501a0868", "start_char": 0, "end_char": 1602, "text_sha256": "68c85cb7c391b6bffddcdc9ca0620c8db353400604353ce62873fe74501a0868"} [lutein-p10799382] Amount of fat in the diet affects bioavailability of lutein esters but not of alpha-carotene, beta-carotene, and vitamin E in humans. (2000). https://pubmed.ncbi.nlm.nih.gov/10799382/ DOI: 10.1093/ajcn/71.5.1187
Complete structured claim and evidence
The high-egg salad meal increased lutein/zeaxanthin lipoprotein AUC about four- to fivefold versus salad without egg.
Salad plus 150 g scrambled whole eggs in the 2015 crossover study → Human post-meal plasma lutein response source_derived_draftungraded
Experimental context and source evidence
evidence_span
{"source_cache": "artifacts/lutein-research/26016861.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "c275d8263df6d127f722fc47b45e9bc513c6d871653afbc878bc50a911b1df55", "start_char": 0, "end_char": 2045, "text_sha256": "c275d8263df6d127f722fc47b45e9bc513c6d871653afbc878bc50a911b1df55"}
experimental_model
Randomized three-meal crossover trial
exposure
Salad plus 0, 75 or 150 g scrambled whole eggs; ten-hour sampling
limitations
Eggs supplied both fat and carotenoids; the experiment does not isolate a choline effect. Published erratum 10.3945/ajcn.115.120956 corrects an author affiliation to Department of Nutrition Science; it does not change the trial outcomes. Correction: https://doi.org/10.3945/ajcn.115.120956 .
nutrient_topic
Lutein research collection; topical membership is not evidence of a direct dietary effect. · Lutein
organism
16 healthy young men
plain_language
The whole-food meal increased carotenoid appearance in blood.
primary_references
[lutein-p26016861] Effects of egg consumption on carotenoid absorption from co-consumed, raw vegetables. (2015). https://pubmed.ncbi.nlm.nih.gov/26016861/ DOI: 10.3945/ajcn.115.111062
tissue_or_cell_type
Post-meal triglyceride-rich lipoproteins
Lutein: metabolism, signaling and nutrient connections (2026-09-17) · lines 593–604
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Randomized three-meal crossover trial · source_derived_draft · unverified_draft
### lutein-egg-matrix The high-egg salad meal increased lutein/zeaxanthin lipoprotein AUC about four- to fivefold versus salad without egg. Condition category: normal nutrient_topic: Lutein research collection; topical membership is not evidence of a direct dietary effect. plain_language: The whole-food meal increased carotenoid appearance in blood. organism: 16 healthy young men tissue_or_cell_type: Post-meal triglyceride-rich lipoproteins experimental_model: Randomized three-meal crossover trial limitations: Eggs supplied both fat and carotenoids; the experiment does not isolate a choline effect. Published erratum 10.3945/ajcn.115.120956 corrects an author affiliation to Department of Nutrition Science; it does not change the trial outcomes. Correction: https://doi.org/10.3945/ajcn.115.120956 . exposure: Salad plus 0, 75 or 150 g scrambled whole eggs; ten-hour sampling evidence_span: {"source_cache": "artifacts/lutein-research/26016861.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "c275d8263df6d127f722fc47b45e9bc513c6d871653afbc878bc50a911b1df55", "start_char": 0, "end_char": 2045, "text_sha256": "c275d8263df6d127f722fc47b45e9bc513c6d871653afbc878bc50a911b1df55"} [lutein-p26016861] Effects of egg consumption on carotenoid absorption from co-consumed, raw vegetables. (2015). https://pubmed.ncbi.nlm.nih.gov/26016861/ DOI: 10.3945/ajcn.115.111062
Complete structured claim and evidence
The high-lutein/zeaxanthin diet increased circulating xanthophylls approximately two- to threefold in both groups.
Lutein → Human plasma lutein concentration source_derived_draftungraded
Experimental context and source evidence
evidence_span
{"source_cache": "artifacts/lutein-research/17344498.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "582744e7beef9ad8341bf862c9d344c1f188e6087676bcaa4c32679547fffe79", "start_char": 0, "end_char": 1666, "text_sha256": "582744e7beef9ad8341bf862c9d344c1f188e6087676bcaa4c32679547fffe79"}
experimental_model
Controlled low- then high-xanthophyll diet
exposure
About 1.1 mg/day L+Z for two weeks then 11 mg/day for four weeks
limitations
Small dietary study; circulating distribution is not retinal delivery or an intervention to raise HDL cholesterol.
nutrient_topic
Lutein research collection; topical membership is not evidence of a direct dietary effect. · Lutein
organism
Seven AMD patients and five controls
plain_language
Both groups absorbed the higher dietary supply.
primary_references
[lutein-p17344498] Effect of dietary lutein and zeaxanthin on plasma carotenoids and their transport in lipoproteins in age-related macular degeneration. (2007). https://pubmed.ncbi.nlm.nih.gov/17344498/ DOI: 10.1093/ajcn/85.3.762
tissue_or_cell_type
Plasma and separated lipoprotein fractions
Lutein: metabolism, signaling and nutrient connections (2026-09-17) · lines 606–617
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Controlled low- then high-xanthophyll diet · source_derived_draft · unverified_draft
### lutein-human-diet-plasma The high-lutein/zeaxanthin diet increased circulating xanthophylls approximately two- to threefold in both groups. Condition category: normal nutrient_topic: Lutein research collection; topical membership is not evidence of a direct dietary effect. plain_language: Both groups absorbed the higher dietary supply. organism: Seven AMD patients and five controls tissue_or_cell_type: Plasma and separated lipoprotein fractions experimental_model: Controlled low- then high-xanthophyll diet limitations: Small dietary study; circulating distribution is not retinal delivery or an intervention to raise HDL cholesterol. exposure: About 1.1 mg/day L+Z for two weeks then 11 mg/day for four weeks evidence_span: {"source_cache": "artifacts/lutein-research/17344498.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "582744e7beef9ad8341bf862c9d344c1f188e6087676bcaa4c32679547fffe79", "start_char": 0, "end_char": 1666, "text_sha256": "582744e7beef9ad8341bf862c9d344c1f188e6087676bcaa4c32679547fffe79"} [lutein-p17344498] Effect of dietary lutein and zeaxanthin on plasma carotenoids and their transport in lipoproteins in age-related macular degeneration. (2007). https://pubmed.ncbi.nlm.nih.gov/17344498/ DOI: 10.1093/ajcn/85.3.762
Complete structured claim and evidence
After the high-xanthophyll diet, HDL carried 52% of measured plasma lutein; LDL carried approximately 22%.
High-density lipoprotein particles; preparation specified → Lutein source_derived_draftungraded
Experimental context and source evidence
evidence_span
{"source_cache": "artifacts/lutein-research/17344498.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "582744e7beef9ad8341bf862c9d344c1f188e6087676bcaa4c32679547fffe79", "start_char": 0, "end_char": 1666, "text_sha256": "582744e7beef9ad8341bf862c9d344c1f188e6087676bcaa4c32679547fffe79"}
experimental_model
Controlled low- then high-xanthophyll diet
exposure
About 1.1 mg/day L+Z for two weeks then 11 mg/day for four weeks
limitations
Small dietary study; circulating distribution is not retinal delivery or an intervention to raise HDL cholesterol.
nutrient_topic
Lutein research collection; topical membership is not evidence of a direct dietary effect. · Lutein
organism
Seven AMD patients and five controls
plain_language
Lutein traveled in more than one lipoprotein class.
primary_references
[lutein-p17344498] Effect of dietary lutein and zeaxanthin on plasma carotenoids and their transport in lipoproteins in age-related macular degeneration. (2007). https://pubmed.ncbi.nlm.nih.gov/17344498/ DOI: 10.1093/ajcn/85.3.762
tissue_or_cell_type
Plasma and separated lipoprotein fractions
Lutein: metabolism, signaling and nutrient connections (2026-09-17) · lines 619–630
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Controlled low- then high-xanthophyll diet · source_derived_draft · unverified_draft
### lutein-human-hdl-carriage After the high-xanthophyll diet, HDL carried 52% of measured plasma lutein; LDL carried approximately 22%. Condition category: normal nutrient_topic: Lutein research collection; topical membership is not evidence of a direct dietary effect. plain_language: Lutein traveled in more than one lipoprotein class. organism: Seven AMD patients and five controls tissue_or_cell_type: Plasma and separated lipoprotein fractions experimental_model: Controlled low- then high-xanthophyll diet limitations: Small dietary study; circulating distribution is not retinal delivery or an intervention to raise HDL cholesterol. exposure: About 1.1 mg/day L+Z for two weeks then 11 mg/day for four weeks evidence_span: {"source_cache": "artifacts/lutein-research/17344498.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "582744e7beef9ad8341bf862c9d344c1f188e6087676bcaa4c32679547fffe79", "start_char": 0, "end_char": 1666, "text_sha256": "582744e7beef9ad8341bf862c9d344c1f188e6087676bcaa4c32679547fffe79"} [lutein-p17344498] Effect of dietary lutein and zeaxanthin on plasma carotenoids and their transport in lipoproteins in age-related macular degeneration. (2007). https://pubmed.ncbi.nlm.nih.gov/17344498/ DOI: 10.1093/ajcn/85.3.762
Complete structured claim and evidence
LDL delivery produced the greatest lutein uptake in the tested ARPE-19 system.
Low-density lipoprotein particles; preparation specified → Lutein source_derived_draftungraded
Experimental context and source evidence
evidence_span
{"source_cache": "artifacts/lutein-research/27538825.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "1db014221931676349f15dc3c5138fba122417fb49fec5de481594c72b0596f3", "start_char": 0, "end_char": 1346, "text_sha256": "1db014221931676349f15dc3c5138fba122417fb49fec5de481594c72b0596f3"}
experimental_model
Carotenoid delivery using isolated human lipoproteins
exposure
Carotenoid-loaded LDL versus HDL
limitations
Cell delivery ranking is not identical to circulating carriage fractions or the WHAM-chicken phenotype.
nutrient_topic
Lutein research collection; topical membership is not evidence of a direct dietary effect. · Lutein
organism
Human ARPE-19 cells
plain_language
The best carrier in this cell assay was LDL.
primary_references
[lutein-p27538825] Mechanisms of selective delivery of xanthophylls to retinal pigment epithelial cells by human lipoproteins. (2016). https://pubmed.ncbi.nlm.nih.gov/27538825/ DOI: 10.1194/jlr.m070193
tissue_or_cell_type
Retinal pigment epithelial model
Lutein: metabolism, signaling and nutrient connections (2026-09-17) · lines 632–643
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Carotenoid delivery using isolated human lipoproteins · source_derived_draft · unverified_draft
### lutein-ldl-rpe-delivery LDL delivery produced the greatest lutein uptake in the tested ARPE-19 system. Condition category: normal nutrient_topic: Lutein research collection; topical membership is not evidence of a direct dietary effect. plain_language: The best carrier in this cell assay was LDL. organism: Human ARPE-19 cells tissue_or_cell_type: Retinal pigment epithelial model experimental_model: Carotenoid delivery using isolated human lipoproteins limitations: Cell delivery ranking is not identical to circulating carriage fractions or the WHAM-chicken phenotype. exposure: Carotenoid-loaded LDL versus HDL evidence_span: {"source_cache": "artifacts/lutein-research/27538825.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "1db014221931676349f15dc3c5138fba122417fb49fec5de481594c72b0596f3", "start_char": 0, "end_char": 1346, "text_sha256": "1db014221931676349f15dc3c5138fba122417fb49fec5de481594c72b0596f3"} [lutein-p27538825] Mechanisms of selective delivery of xanthophylls to retinal pigment epithelial cells by human lipoproteins. (2016). https://pubmed.ncbi.nlm.nih.gov/27538825/ DOI: 10.1194/jlr.m070193
Complete structured claim and evidence
HDL most effectively delivered zeaxanthin and meso-zeaxanthin; SR-BI inhibition suppressed zeaxanthin delivery.
High-density lipoprotein particles; preparation specified → Dietary (3R,3-prime-R)-zeaxanthin source_derived_draftungraded
Experimental context and source evidence
evidence_span
{"source_cache": "artifacts/lutein-research/27538825.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "1db014221931676349f15dc3c5138fba122417fb49fec5de481594c72b0596f3", "start_char": 0, "end_char": 1346, "text_sha256": "1db014221931676349f15dc3c5138fba122417fb49fec5de481594c72b0596f3"}
experimental_model
Carotenoid delivery using isolated human lipoproteins
exposure
Carotenoid-loaded LDL versus HDL
limitations
Cell delivery ranking is not identical to circulating carriage fractions or the WHAM-chicken phenotype.
nutrient_topic
Lutein research collection; topical membership is not evidence of a direct dietary effect. · Lutein
organism
Human ARPE-19 cells
plain_language
The preferred delivery route differed between pigments.
primary_references
[lutein-p27538825] Mechanisms of selective delivery of xanthophylls to retinal pigment epithelial cells by human lipoproteins. (2016). https://pubmed.ncbi.nlm.nih.gov/27538825/ DOI: 10.1194/jlr.m070193
tissue_or_cell_type
Retinal pigment epithelial model
Lutein: metabolism, signaling and nutrient connections (2026-09-17) · lines 645–656
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Carotenoid delivery using isolated human lipoproteins · source_derived_draft · unverified_draft
### lutein-hdl-z-delivery HDL most effectively delivered zeaxanthin and meso-zeaxanthin; SR-BI inhibition suppressed zeaxanthin delivery. Condition category: normal nutrient_topic: Lutein research collection; topical membership is not evidence of a direct dietary effect. plain_language: The preferred delivery route differed between pigments. organism: Human ARPE-19 cells tissue_or_cell_type: Retinal pigment epithelial model experimental_model: Carotenoid delivery using isolated human lipoproteins limitations: Cell delivery ranking is not identical to circulating carriage fractions or the WHAM-chicken phenotype. exposure: Carotenoid-loaded LDL versus HDL evidence_span: {"source_cache": "artifacts/lutein-research/27538825.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "1db014221931676349f15dc3c5138fba122417fb49fec5de481594c72b0596f3", "start_char": 0, "end_char": 1346, "text_sha256": "1db014221931676349f15dc3c5138fba122417fb49fec5de481594c72b0596f3"} [lutein-p27538825] Mechanisms of selective delivery of xanthophylls to retinal pigment epithelial cells by human lipoproteins. (2016). https://pubmed.ncbi.nlm.nih.gov/27538825/ DOI: 10.1194/jlr.m070193
Complete structured claim and evidence
This ARPE-19 delivery experiment detected no lutein conversion to meso-zeaxanthin.
Lutein → meso-Zeaxanthin / (3R,3-prime-S)-zeaxanthin source_derived_draftungraded
Experimental context and source evidence
evidence_span
{"source_cache": "artifacts/lutein-research/27538825.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "1db014221931676349f15dc3c5138fba122417fb49fec5de481594c72b0596f3", "start_char": 0, "end_char": 1346, "text_sha256": "1db014221931676349f15dc3c5138fba122417fb49fec5de481594c72b0596f3"}
experimental_model
Carotenoid delivery using isolated human lipoproteins
exposure
Carotenoid-loaded LDL versus HDL
limitations
Cell delivery ranking is not identical to circulating carriage fractions or the WHAM-chicken phenotype.
nutrient_topic
Lutein research collection; topical membership is not evidence of a direct dietary effect. · Lutein
organism
Human ARPE-19 cells
plain_language
Uptake alone did not reproduce the separate RPE65 overexpression result.
primary_references
[lutein-p27538825] Mechanisms of selective delivery of xanthophylls to retinal pigment epithelial cells by human lipoproteins. (2016). https://pubmed.ncbi.nlm.nih.gov/27538825/ DOI: 10.1194/jlr.m070193
tissue_or_cell_type
Retinal pigment epithelial model
Lutein: metabolism, signaling and nutrient connections (2026-09-17) · lines 658–669
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Carotenoid delivery using isolated human lipoproteins · source_derived_draft · unverified_draft
### lutein-rpe-isomerization-null This ARPE-19 delivery experiment detected no lutein conversion to meso-zeaxanthin. Condition category: normal nutrient_topic: Lutein research collection; topical membership is not evidence of a direct dietary effect. plain_language: Uptake alone did not reproduce the separate RPE65 overexpression result. organism: Human ARPE-19 cells tissue_or_cell_type: Retinal pigment epithelial model experimental_model: Carotenoid delivery using isolated human lipoproteins limitations: Cell delivery ranking is not identical to circulating carriage fractions or the WHAM-chicken phenotype. exposure: Carotenoid-loaded LDL versus HDL evidence_span: {"source_cache": "artifacts/lutein-research/27538825.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "1db014221931676349f15dc3c5138fba122417fb49fec5de481594c72b0596f3", "start_char": 0, "end_char": 1346, "text_sha256": "1db014221931676349f15dc3c5138fba122417fb49fec5de481594c72b0596f3"} [lutein-p27538825] Mechanisms of selective delivery of xanthophylls to retinal pigment epithelial cells by human lipoproteins. (2016). https://pubmed.ncbi.nlm.nih.gov/27538825/ DOI: 10.1194/jlr.m070193
Complete structured claim and evidence
SR-BI expression increased lutein and zeaxanthin uptake preferentially over beta-carotene.
Scavenger receptor class B type 1 / SCARB1 → Lutein uptake by engineered human HEK293 cells source_derived_draftungraded
Experimental context and source evidence
evidence_span
{"source_cache": "artifacts/lutein-research/36863431.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "530dd42d442890be2e5cd11c18bf95c0bd850d8f67ad6682d12360dfc7f8aec0", "start_char": 0, "end_char": 1551, "text_sha256": "530dd42d442890be2e5cd11c18bf95c0bd850d8f67ad6682d12360dfc7f8aec0"}
experimental_model
SR-BI expression, tunnel mutation, binding and lipoprotein-partner assays
exposure
Wild-type or C384Y SR-BI; HDL and hepatic lipase additions
limitations
Engineered-cell mechanisms, not a clinical HDL-raising recommendation; no selective direct binding to lutein demonstrated.
nutrient_topic
Lutein research collection; topical membership is not evidence of a direct dietary effect. · Lutein
organism
Human HEK293 cell system
plain_language
The receptor changed which pigments entered these cells.
primary_references
[lutein-p36863431] Mechanism for the selective uptake of macular carotenoids mediated by the HDL cholesterol receptor SR-BI. (2023). https://pubmed.ncbi.nlm.nih.gov/36863431/ DOI: 10.1016/j.exer.2023.109429
tissue_or_cell_type
Engineered cells without endogenous SR-BI
Lutein: metabolism, signaling and nutrient connections (2026-09-17) · lines 671–682
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · SR-BI expression, tunnel mutation, binding and lipoprotein-partner assays · source_derived_draft · unverified_draft
### lutein-srbi-cell-uptake SR-BI expression increased lutein and zeaxanthin uptake preferentially over beta-carotene. Condition category: normal nutrient_topic: Lutein research collection; topical membership is not evidence of a direct dietary effect. plain_language: The receptor changed which pigments entered these cells. organism: Human HEK293 cell system tissue_or_cell_type: Engineered cells without endogenous SR-BI experimental_model: SR-BI expression, tunnel mutation, binding and lipoprotein-partner assays limitations: Engineered-cell mechanisms, not a clinical HDL-raising recommendation; no selective direct binding to lutein demonstrated. exposure: Wild-type or C384Y SR-BI; HDL and hepatic lipase additions evidence_span: {"source_cache": "artifacts/lutein-research/36863431.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "530dd42d442890be2e5cd11c18bf95c0bd850d8f67ad6682d12360dfc7f8aec0", "start_char": 0, "end_char": 1551, "text_sha256": "530dd42d442890be2e5cd11c18bf95c0bd850d8f67ad6682d12360dfc7f8aec0"} [lutein-p36863431] Mechanism for the selective uptake of macular carotenoids mediated by the HDL cholesterol receptor SR-BI. (2023). https://pubmed.ncbi.nlm.nih.gov/36863431/ DOI: 10.1016/j.exer.2023.109429
Complete structured claim and evidence
Hepatic lipase increased carotenoid uptake in HDL-treated SR-BI-expressing cells, favoring lutein/zeaxanthin over beta-carotene.
Human hepatic lipase / LIPC → Lutein uptake by engineered human HEK293 cells source_derived_draftungraded
Experimental context and source evidence
evidence_span
{"source_cache": "artifacts/lutein-research/36863431.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "530dd42d442890be2e5cd11c18bf95c0bd850d8f67ad6682d12360dfc7f8aec0", "start_char": 0, "end_char": 1551, "text_sha256": "530dd42d442890be2e5cd11c18bf95c0bd850d8f67ad6682d12360dfc7f8aec0"}
experimental_model
SR-BI expression, tunnel mutation, binding and lipoprotein-partner assays
exposure
Wild-type or C384Y SR-BI; HDL and hepatic lipase additions
limitations
Engineered-cell mechanisms, not a clinical HDL-raising recommendation; no selective direct binding to lutein demonstrated.
nutrient_topic
Lutein research collection; topical membership is not evidence of a direct dietary effect. · Lutein
organism
Human HEK293 cell system
plain_language
A lipoprotein-processing partner changed pigment delivery.
primary_references
[lutein-p36863431] Mechanism for the selective uptake of macular carotenoids mediated by the HDL cholesterol receptor SR-BI. (2023). https://pubmed.ncbi.nlm.nih.gov/36863431/ DOI: 10.1016/j.exer.2023.109429
tissue_or_cell_type
Engineered cells without endogenous SR-BI
Lutein: metabolism, signaling and nutrient connections (2026-09-17) · lines 684–695
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · SR-BI expression, tunnel mutation, binding and lipoprotein-partner assays · source_derived_draft · unverified_draft
### lutein-lipc-cell-uptake Hepatic lipase increased carotenoid uptake in HDL-treated SR-BI-expressing cells, favoring lutein/zeaxanthin over beta-carotene. Condition category: normal nutrient_topic: Lutein research collection; topical membership is not evidence of a direct dietary effect. plain_language: A lipoprotein-processing partner changed pigment delivery. organism: Human HEK293 cell system tissue_or_cell_type: Engineered cells without endogenous SR-BI experimental_model: SR-BI expression, tunnel mutation, binding and lipoprotein-partner assays limitations: Engineered-cell mechanisms, not a clinical HDL-raising recommendation; no selective direct binding to lutein demonstrated. exposure: Wild-type or C384Y SR-BI; HDL and hepatic lipase additions evidence_span: {"source_cache": "artifacts/lutein-research/36863431.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "530dd42d442890be2e5cd11c18bf95c0bd850d8f67ad6682d12360dfc7f8aec0", "start_char": 0, "end_char": 1551, "text_sha256": "530dd42d442890be2e5cd11c18bf95c0bd850d8f67ad6682d12360dfc7f8aec0"} [lutein-p36863431] Mechanism for the selective uptake of macular carotenoids mediated by the HDL cholesterol receptor SR-BI. (2023). https://pubmed.ncbi.nlm.nih.gov/36863431/ DOI: 10.1016/j.exer.2023.109429
Complete structured claim and evidence
Adding HDL reduced cellular lutein in the HEK293 assay despite preferential retention relative to beta-carotene.
High-density lipoprotein particles; preparation specified → Lutein uptake by engineered human HEK293 cells source_derived_draftungraded
Experimental context and source evidence
evidence_span
{"source_cache": "artifacts/lutein-research/36863431.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "530dd42d442890be2e5cd11c18bf95c0bd850d8f67ad6682d12360dfc7f8aec0", "start_char": 0, "end_char": 1551, "text_sha256": "530dd42d442890be2e5cd11c18bf95c0bd850d8f67ad6682d12360dfc7f8aec0"}
experimental_model
SR-BI expression, tunnel mutation, binding and lipoprotein-partner assays
exposure
Wild-type or C384Y SR-BI; HDL and hepatic lipase additions
limitations
Engineered-cell mechanisms, not a clinical HDL-raising recommendation; no selective direct binding to lutein demonstrated.
nutrient_topic
Lutein research collection; topical membership is not evidence of a direct dietary effect. · Lutein
organism
Human HEK293 cell system
plain_language
More carrier did not simply mean more uptake in this assay.
primary_references
[lutein-p36863431] Mechanism for the selective uptake of macular carotenoids mediated by the HDL cholesterol receptor SR-BI. (2023). https://pubmed.ncbi.nlm.nih.gov/36863431/ DOI: 10.1016/j.exer.2023.109429
tissue_or_cell_type
Engineered cells without endogenous SR-BI
Lutein: metabolism, signaling and nutrient connections (2026-09-17) · lines 697–708
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · SR-BI expression, tunnel mutation, binding and lipoprotein-partner assays · source_derived_draft · unverified_draft
### lutein-hdl-cell-context Adding HDL reduced cellular lutein in the HEK293 assay despite preferential retention relative to beta-carotene. Condition category: normal nutrient_topic: Lutein research collection; topical membership is not evidence of a direct dietary effect. plain_language: More carrier did not simply mean more uptake in this assay. organism: Human HEK293 cell system tissue_or_cell_type: Engineered cells without endogenous SR-BI experimental_model: SR-BI expression, tunnel mutation, binding and lipoprotein-partner assays limitations: Engineered-cell mechanisms, not a clinical HDL-raising recommendation; no selective direct binding to lutein demonstrated. exposure: Wild-type or C384Y SR-BI; HDL and hepatic lipase additions evidence_span: {"source_cache": "artifacts/lutein-research/36863431.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "530dd42d442890be2e5cd11c18bf95c0bd850d8f67ad6682d12360dfc7f8aec0", "start_char": 0, "end_char": 1551, "text_sha256": "530dd42d442890be2e5cd11c18bf95c0bd850d8f67ad6682d12360dfc7f8aec0"} [lutein-p36863431] Mechanism for the selective uptake of macular carotenoids mediated by the HDL cholesterol receptor SR-BI. (2023). https://pubmed.ncbi.nlm.nih.gov/36863431/ DOI: 10.1016/j.exer.2023.109429
Complete structured claim and evidence
SR-BI C384Y abolished the preferential lutein/zeaxanthin uptake effect observed with wild-type receptor.
Human SR-BI C384Y tunnel-blocking variant → Lutein uptake by engineered human HEK293 cells source_derived_draftungraded
Experimental context and source evidence
availability_state
machinery_impairment Imported condition classification; unverified.
evidence_span
{"source_cache": "artifacts/lutein-research/36863431.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "530dd42d442890be2e5cd11c18bf95c0bd850d8f67ad6682d12360dfc7f8aec0", "start_char": 0, "end_char": 1551, "text_sha256": "530dd42d442890be2e5cd11c18bf95c0bd850d8f67ad6682d12360dfc7f8aec0"}
experimental_model
SR-BI expression, tunnel mutation, binding and lipoprotein-partner assays
exposure
Wild-type or C384Y SR-BI; HDL and hepatic lipase additions
limitations
Engineered-cell mechanisms, not a clinical HDL-raising recommendation; no selective direct binding to lutein demonstrated.
nutrient_topic
Lutein research collection; topical membership is not evidence of a direct dietary effect. · Lutein
organism
Human HEK293 cell system
plain_language
An altered transport tunnel disrupted the effect.
primary_references
[lutein-p36863431] Mechanism for the selective uptake of macular carotenoids mediated by the HDL cholesterol receptor SR-BI. (2023). https://pubmed.ncbi.nlm.nih.gov/36863431/ DOI: 10.1016/j.exer.2023.109429
tissue_or_cell_type
Engineered cells without endogenous SR-BI
trigger_kind
machinery_impairment Imported condition classification; unverified.
Lutein: metabolism, signaling and nutrient connections (2026-09-17) · lines 710–721
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · SR-BI expression, tunnel mutation, binding and lipoprotein-partner assays · source_derived_draft · unverified_draft
### lutein-srbi-mutant SR-BI C384Y abolished the preferential lutein/zeaxanthin uptake effect observed with wild-type receptor. Condition category: machinery_impairment nutrient_topic: Lutein research collection; topical membership is not evidence of a direct dietary effect. plain_language: An altered transport tunnel disrupted the effect. organism: Human HEK293 cell system tissue_or_cell_type: Engineered cells without endogenous SR-BI experimental_model: SR-BI expression, tunnel mutation, binding and lipoprotein-partner assays limitations: Engineered-cell mechanisms, not a clinical HDL-raising recommendation; no selective direct binding to lutein demonstrated. exposure: Wild-type or C384Y SR-BI; HDL and hepatic lipase additions evidence_span: {"source_cache": "artifacts/lutein-research/36863431.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "530dd42d442890be2e5cd11c18bf95c0bd850d8f67ad6682d12360dfc7f8aec0", "start_char": 0, "end_char": 1551, "text_sha256": "530dd42d442890be2e5cd11c18bf95c0bd850d8f67ad6682d12360dfc7f8aec0"} [lutein-p36863431] Mechanism for the selective uptake of macular carotenoids mediated by the HDL cholesterol receptor SR-BI. (2023). https://pubmed.ncbi.nlm.nih.gov/36863431/ DOI: 10.1016/j.exer.2023.109429
Complete structured claim and evidence
Lung cancers occurred in 2.0% with beta-carotene versus 0.9% without, predominantly among former smokers.
AREDS2 randomized beta-carotene assignment → Human lung cancer incidence source_derived_draftungraded
Experimental context and source evidence
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
The comparator carotenoid had a separate safety signal.
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 736–747
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-beta-lung Lung cancers occurred in 2.0% with beta-carotene versus 0.9% without, predominantly among former smokers. Condition category: normal nutrient_topic: Lutein research collection; topical membership is not evidence of a direct dietary effect. plain_language: The comparator carotenoid had a separate safety signal. 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
Complete structured claim and evidence
The corresponding neovascular-AMD HR was 0.78 (95% CI 0.64–0.94).
AREDS2 lutein/zeaxanthin versus beta-carotene comparison → Progression to neovascular age-related macular degeneration source_derived_draftungraded
Experimental context and source evidence
evidence_span
{"source_cache": "artifacts/lutein-research/24310343.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "617cbda47a00c8fc552395a255003b013afa72aca6640c5c2e49d2b4caf09a72", "start_char": 0, "end_char": 2419, "text_sha256": "617cbda47a00c8fc552395a255003b013afa72aca6640c5c2e49d2b4caf09a72"}
experimental_model
Exploratory secondary analyses of AREDS2
exposure
L+Z 10/2 mg; direct comparison with beta-carotene on AREDS background
limitations
Exploratory contrasts and different confidence thresholds do not contradict the prespecified primary analysis.
nutrient_topic
Lutein research collection; topical membership is not evidence of a direct dietary effect. · Lutein
organism
Same AREDS2 cohort, not an independent replication
plain_language
The subtype result favored the pair for neovascular AMD.
primary_references
[lutein-p24310343] Secondary analyses of the effects of lutein/zeaxanthin on age-related macular degeneration progression: AREDS2 report No. 3. (2014). https://pubmed.ncbi.nlm.nih.gov/24310343/ DOI: 10.1001/jamaophthalmol.2013.7376
tissue_or_cell_type
Late AMD subtypes
Lutein: metabolism, signaling and nutrient connections (2026-09-17) · lines 762–773
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Exploratory secondary analyses of AREDS2 · source_derived_draft · unverified_draft
### lutein-areds-replacement-neovascular The corresponding neovascular-AMD HR was 0.78 (95% CI 0.64–0.94). Condition category: normal nutrient_topic: Lutein research collection; topical membership is not evidence of a direct dietary effect. plain_language: The subtype result favored the pair for neovascular AMD. organism: Same AREDS2 cohort, not an independent replication tissue_or_cell_type: Late AMD subtypes experimental_model: Exploratory secondary analyses of AREDS2 limitations: Exploratory contrasts and different confidence thresholds do not contradict the prespecified primary analysis. exposure: L+Z 10/2 mg; direct comparison with beta-carotene on AREDS background evidence_span: {"source_cache": "artifacts/lutein-research/24310343.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "617cbda47a00c8fc552395a255003b013afa72aca6640c5c2e49d2b4caf09a72", "start_char": 0, "end_char": 2419, "text_sha256": "617cbda47a00c8fc552395a255003b013afa72aca6640c5c2e49d2b4caf09a72"} [lutein-p24310343] Secondary analyses of the effects of lutein/zeaxanthin on age-related macular degeneration progression: AREDS2 report No. 3. (2014). https://pubmed.ncbi.nlm.nih.gov/24310343/ DOI: 10.1001/jamaophthalmol.2013.7376
Complete structured claim and evidence
Central geographic atrophy HR was 0.94 (95% CI 0.70–1.26), without a significant difference.
AREDS2 lutein/zeaxanthin versus beta-carotene comparison → Progression to central geographic atrophy source_derived_draftungraded
Experimental context and source evidence
evidence_span
{"source_cache": "artifacts/lutein-research/24310343.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "617cbda47a00c8fc552395a255003b013afa72aca6640c5c2e49d2b4caf09a72", "start_char": 0, "end_char": 2419, "text_sha256": "617cbda47a00c8fc552395a255003b013afa72aca6640c5c2e49d2b4caf09a72"}
experimental_model
Exploratory secondary analyses of AREDS2
exposure
L+Z 10/2 mg; direct comparison with beta-carotene on AREDS background
limitations
Exploratory contrasts and different confidence thresholds do not contradict the prespecified primary analysis.
nutrient_topic
Lutein research collection; topical membership is not evidence of a direct dietary effect. · Lutein
organism
Same AREDS2 cohort, not an independent replication
plain_language
The same comparison did not show benefit for every subtype.
primary_references
[lutein-p24310343] Secondary analyses of the effects of lutein/zeaxanthin on age-related macular degeneration progression: AREDS2 report No. 3. (2014). https://pubmed.ncbi.nlm.nih.gov/24310343/ DOI: 10.1001/jamaophthalmol.2013.7376
tissue_or_cell_type
Late AMD subtypes
Lutein: metabolism, signaling and nutrient connections (2026-09-17) · lines 775–786
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Exploratory secondary analyses of AREDS2 · source_derived_draft · unverified_draft
### lutein-areds-replacement-atrophy-null Central geographic atrophy HR was 0.94 (95% CI 0.70–1.26), without a significant difference. Condition category: normal nutrient_topic: Lutein research collection; topical membership is not evidence of a direct dietary effect. plain_language: The same comparison did not show benefit for every subtype. organism: Same AREDS2 cohort, not an independent replication tissue_or_cell_type: Late AMD subtypes experimental_model: Exploratory secondary analyses of AREDS2 limitations: Exploratory contrasts and different confidence thresholds do not contradict the prespecified primary analysis. exposure: L+Z 10/2 mg; direct comparison with beta-carotene on AREDS background evidence_span: {"source_cache": "artifacts/lutein-research/24310343.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "617cbda47a00c8fc552395a255003b013afa72aca6640c5c2e49d2b4caf09a72", "start_char": 0, "end_char": 2419, "text_sha256": "617cbda47a00c8fc552395a255003b013afa72aca6640c5c2e49d2b4caf09a72"} [lutein-p24310343] Secondary analyses of the effects of lutein/zeaxanthin on age-related macular degeneration progression: AREDS2 report No. 3. (2014). https://pubmed.ncbi.nlm.nih.gov/24310343/ DOI: 10.1001/jamaophthalmol.2013.7376
Complete structured claim and evidence
Ten-year analysis by original L+Z assignment gave late-AMD HR 0.91 (95% CI 0.84–0.99).
AREDS2 lutein/zeaxanthin addition to background AREDS formulation → Progression to late age-related macular degeneration source_derived_draftungraded
Experimental context and source evidence
evidence_span
{"source_cache": "artifacts/lutein-research/35653117.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "66ae960c242e18fe246c623e055e94d52a638b6ac6330f8a85208a58d52c13cb", "start_char": 0, "end_char": 3155, "text_sha256": "66ae960c242e18fe246c623e055e94d52a638b6ac6330f8a85208a58d52c13cb"}
experimental_model
Ten-year epidemiologic follow-up of randomized AREDS2 assignments
exposure
Original randomization followed by common AREDS2 supplementation for everyone
limitations
Not ten years of continuously separated randomized treatment; same cohort, additional follow-up.
nutrient_topic
Lutein research collection; topical membership is not evidence of a direct dietary effect. · Lutein
organism
3882 original participants
plain_language
A modest long-term association favored original assignment.
primary_references
[lutein-p35653117] Long-term Outcomes of Adding Lutein/Zeaxanthin and ω-3 Fatty Acids to the AREDS Supplements on Age-Related Macular Degeneration Progression: AREDS2 Report 28. (2022). https://pubmed.ncbi.nlm.nih.gov/35653117/ DOI: 10.1001/jamaophthalmol.2022.1640
tissue_or_cell_type
Late AMD and lung cancer
Lutein: metabolism, signaling and nutrient connections (2026-09-17) · lines 788–799
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Ten-year epidemiologic follow-up of randomized AREDS2 assignments · source_derived_draft · unverified_draft
### lutein-areds-longterm Ten-year analysis by original L+Z assignment gave late-AMD HR 0.91 (95% CI 0.84–0.99). Condition category: normal nutrient_topic: Lutein research collection; topical membership is not evidence of a direct dietary effect. plain_language: A modest long-term association favored original assignment. organism: 3882 original participants tissue_or_cell_type: Late AMD and lung cancer experimental_model: Ten-year epidemiologic follow-up of randomized AREDS2 assignments limitations: Not ten years of continuously separated randomized treatment; same cohort, additional follow-up. exposure: Original randomization followed by common AREDS2 supplementation for everyone evidence_span: {"source_cache": "artifacts/lutein-research/35653117.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "66ae960c242e18fe246c623e055e94d52a638b6ac6330f8a85208a58d52c13cb", "start_char": 0, "end_char": 3155, "text_sha256": "66ae960c242e18fe246c623e055e94d52a638b6ac6330f8a85208a58d52c13cb"} [lutein-p35653117] Long-term Outcomes of Adding Lutein/Zeaxanthin and ω-3 Fatty Acids to the AREDS Supplements on Age-Related Macular Degeneration Progression: AREDS2 Report 28. (2022). https://pubmed.ncbi.nlm.nih.gov/35653117/ DOI: 10.1001/jamaophthalmol.2022.1640
Complete structured claim and evidence
L+Z assignment had lung-cancer OR 1.15 (95% CI 0.79–1.66), without a significant increase.
AREDS2 lutein/zeaxanthin addition to background AREDS formulation → Human lung cancer incidence source_derived_draftungraded
Experimental context and source evidence
evidence_span
{"source_cache": "artifacts/lutein-research/35653117.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "66ae960c242e18fe246c623e055e94d52a638b6ac6330f8a85208a58d52c13cb", "start_char": 0, "end_char": 3155, "text_sha256": "66ae960c242e18fe246c623e055e94d52a638b6ac6330f8a85208a58d52c13cb"}
experimental_model
Ten-year epidemiologic follow-up of randomized AREDS2 assignments
exposure
Original randomization followed by common AREDS2 supplementation for everyone
limitations
Not ten years of continuously separated randomized treatment; same cohort, additional follow-up.
nutrient_topic
Lutein research collection; topical membership is not evidence of a direct dietary effect. · Lutein
organism
3882 original participants
plain_language
The beta-carotene signal was not demonstrated for the pair.
primary_references
[lutein-p35653117] Long-term Outcomes of Adding Lutein/Zeaxanthin and ω-3 Fatty Acids to the AREDS Supplements on Age-Related Macular Degeneration Progression: AREDS2 Report 28. (2022). https://pubmed.ncbi.nlm.nih.gov/35653117/ DOI: 10.1001/jamaophthalmol.2022.1640
tissue_or_cell_type
Late AMD and lung cancer
Lutein: metabolism, signaling and nutrient connections (2026-09-17) · lines 801–812
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Ten-year epidemiologic follow-up of randomized AREDS2 assignments · source_derived_draft · unverified_draft
### lutein-areds-longterm-lung-null L+Z assignment had lung-cancer OR 1.15 (95% CI 0.79–1.66), without a significant increase. Condition category: normal nutrient_topic: Lutein research collection; topical membership is not evidence of a direct dietary effect. plain_language: The beta-carotene signal was not demonstrated for the pair. organism: 3882 original participants tissue_or_cell_type: Late AMD and lung cancer experimental_model: Ten-year epidemiologic follow-up of randomized AREDS2 assignments limitations: Not ten years of continuously separated randomized treatment; same cohort, additional follow-up. exposure: Original randomization followed by common AREDS2 supplementation for everyone evidence_span: {"source_cache": "artifacts/lutein-research/35653117.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "66ae960c242e18fe246c623e055e94d52a638b6ac6330f8a85208a58d52c13cb", "start_char": 0, "end_char": 3155, "text_sha256": "66ae960c242e18fe246c623e055e94d52a638b6ac6330f8a85208a58d52c13cb"} [lutein-p35653117] Long-term Outcomes of Adding Lutein/Zeaxanthin and ω-3 Fatty Acids to the AREDS Supplements on Age-Related Macular Degeneration Progression: AREDS2 Report 28. (2022). https://pubmed.ncbi.nlm.nih.gov/35653117/ DOI: 10.1001/jamaophthalmol.2022.1640
Complete structured claim and evidence
Overall cataract-surgery HR was 0.96 (95% CI 0.84–1.10; P=0.54).
Lutein 10 mg plus zeaxanthin 2 mg daily combination → Cataract surgery occurrence source_derived_draftungraded
Experimental context and source evidence
evidence_span
{"source_cache": "artifacts/lutein-research/23645227.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "3e75988c75dde9e6525246ae68335c49c03c31f02c7419dcf74110966b7dce32", "start_char": 0, "end_char": 2245, "text_sha256": "3e75988c75dde9e6525246ae68335c49c03c31f02c7419dcf74110966b7dce32"}
experimental_model
AREDS2 cataract secondary outcome and dietary subgroup analysis
exposure
L+Z 10/2 mg daily; median 4.7 years
limitations
Lowest-intake subgroup is not a clinical deficiency diagnosis; overall and subgroup results must stay separate.
nutrient_topic
Lutein research collection; topical membership is not evidence of a direct dietary effect. · Lutein
organism
3159 participants phakic in at least one eye
plain_language
The trial did not show an overall cataract-surgery benefit.
primary_references
[lutein-p23645227] Lutein/zeaxanthin for the treatment of age-related cataract: AREDS2 randomized trial report no. 4. (2013). https://pubmed.ncbi.nlm.nih.gov/23645227/ DOI: 10.1001/jamaophthalmol.2013.4412
tissue_or_cell_type
6027 study eyes
Lutein: metabolism, signaling and nutrient connections (2026-09-17) · lines 814–825
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · AREDS2 cataract secondary outcome and dietary subgroup analysis · source_derived_draft · unverified_draft
### lutein-cataract-overall-null Overall cataract-surgery HR was 0.96 (95% CI 0.84–1.10; P=0.54). Condition category: normal nutrient_topic: Lutein research collection; topical membership is not evidence of a direct dietary effect. plain_language: The trial did not show an overall cataract-surgery benefit. organism: 3159 participants phakic in at least one eye tissue_or_cell_type: 6027 study eyes experimental_model: AREDS2 cataract secondary outcome and dietary subgroup analysis limitations: Lowest-intake subgroup is not a clinical deficiency diagnosis; overall and subgroup results must stay separate. exposure: L+Z 10/2 mg daily; median 4.7 years evidence_span: {"source_cache": "artifacts/lutein-research/23645227.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "3e75988c75dde9e6525246ae68335c49c03c31f02c7419dcf74110966b7dce32", "start_char": 0, "end_char": 2245, "text_sha256": "3e75988c75dde9e6525246ae68335c49c03c31f02c7419dcf74110966b7dce32"} [lutein-p23645227] Lutein/zeaxanthin for the treatment of age-related cataract: AREDS2 randomized trial report no. 4. (2013). https://pubmed.ncbi.nlm.nih.gov/23645227/ DOI: 10.1001/jamaophthalmol.2013.4412
Complete structured claim and evidence
In the lowest dietary L+Z quintile, cataract-surgery HR was 0.68 (95% CI 0.48–0.96; P=0.03).
Lutein 10 mg plus zeaxanthin 2 mg daily combination → Cataract surgery occurrence source_derived_draftungraded
Experimental context and source evidence
availability_state
biomarker_context Imported condition classification; unverified.
evidence_span
{"source_cache": "artifacts/lutein-research/23645227.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "3e75988c75dde9e6525246ae68335c49c03c31f02c7419dcf74110966b7dce32", "start_char": 0, "end_char": 2245, "text_sha256": "3e75988c75dde9e6525246ae68335c49c03c31f02c7419dcf74110966b7dce32"}
experimental_model
AREDS2 cataract secondary outcome and dietary subgroup analysis
exposure
L+Z 10/2 mg daily; median 4.7 years
limitations
Lowest-intake subgroup is not a clinical deficiency diagnosis; overall and subgroup results must stay separate.
nutrient_topic
Lutein research collection; topical membership is not evidence of a direct dietary effect. · Lutein
organism
3159 participants phakic in at least one eye
plain_language
A subgroup with lower intake had a favorable estimate.
primary_references
[lutein-p23645227] Lutein/zeaxanthin for the treatment of age-related cataract: AREDS2 randomized trial report no. 4. (2013). https://pubmed.ncbi.nlm.nih.gov/23645227/ DOI: 10.1001/jamaophthalmol.2013.4412
tissue_or_cell_type
6027 study eyes
trigger_kind
biomarker_context Imported condition classification; unverified.
Lutein: metabolism, signaling and nutrient connections (2026-09-17) · lines 827–838
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · AREDS2 cataract secondary outcome and dietary subgroup analysis · source_derived_draft · unverified_draft
### lutein-cataract-low-intake In the lowest dietary L+Z quintile, cataract-surgery HR was 0.68 (95% CI 0.48–0.96; P=0.03). Condition category: biomarker_context nutrient_topic: Lutein research collection; topical membership is not evidence of a direct dietary effect. plain_language: A subgroup with lower intake had a favorable estimate. organism: 3159 participants phakic in at least one eye tissue_or_cell_type: 6027 study eyes experimental_model: AREDS2 cataract secondary outcome and dietary subgroup analysis limitations: Lowest-intake subgroup is not a clinical deficiency diagnosis; overall and subgroup results must stay separate. exposure: L+Z 10/2 mg daily; median 4.7 years evidence_span: {"source_cache": "artifacts/lutein-research/23645227.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "3e75988c75dde9e6525246ae68335c49c03c31f02c7419dcf74110966b7dce32", "start_char": 0, "end_char": 2245, "text_sha256": "3e75988c75dde9e6525246ae68335c49c03c31f02c7419dcf74110966b7dce32"} [lutein-p23645227] Lutein/zeaxanthin for the treatment of age-related cataract: AREDS2 randomized trial report no. 4. (2013). https://pubmed.ncbi.nlm.nih.gov/23645227/ DOI: 10.1001/jamaophthalmol.2013.4412
Complete structured claim and evidence
L+Z increased macular pigment optical density versus placebo at all measured eccentricities.
Lutein 10 mg plus zeaxanthin 2 mg daily combination → Human macular pigment optical density source_derived_draftungraded
Experimental context and source evidence
evidence_span
{"source_cache": "artifacts/lutein-research/25468896.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "01231d6577e7c30e79a74525772191092df003b42344095a53faf0279f138ac3", "start_char": 0, "end_char": 2007, "text_sha256": "01231d6577e7c30e79a74525772191092df003b42344095a53faf0279f138ac3"}
experimental_model
Randomized double-blind placebo-controlled visual-performance study
exposure
Lutein 10 mg + zeaxanthin 2 mg daily for one year
limitations
Combined intervention; improved task performance is not evidence of AMD prevention or treatment.
nutrient_topic
Lutein research collection; topical membership is not evidence of a direct dietary effect. · Lutein
organism
115 young healthy adults
plain_language
More pigment was measured in the macula.
primary_references
[lutein-p25468896] A double-blind, placebo-controlled study on the effects of lutein and zeaxanthin on photostress recovery, glare disability, and chromatic contrast. (2014). https://pubmed.ncbi.nlm.nih.gov/25468896/ DOI: 10.1167/iovs.14-15573
tissue_or_cell_type
Serum, macular pigment and visual tasks
Lutein: metabolism, signaling and nutrient connections (2026-09-17) · lines 840–851
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Randomized double-blind placebo-controlled visual-performance study · source_derived_draft · unverified_draft
### lutein-mpod-increase L+Z increased macular pigment optical density versus placebo at all measured eccentricities. Condition category: normal nutrient_topic: Lutein research collection; topical membership is not evidence of a direct dietary effect. plain_language: More pigment was measured in the macula. organism: 115 young healthy adults tissue_or_cell_type: Serum, macular pigment and visual tasks experimental_model: Randomized double-blind placebo-controlled visual-performance study limitations: Combined intervention; improved task performance is not evidence of AMD prevention or treatment. exposure: Lutein 10 mg + zeaxanthin 2 mg daily for one year evidence_span: {"source_cache": "artifacts/lutein-research/25468896.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "01231d6577e7c30e79a74525772191092df003b42344095a53faf0279f138ac3", "start_char": 0, "end_char": 2007, "text_sha256": "01231d6577e7c30e79a74525772191092df003b42344095a53faf0279f138ac3"} [lutein-p25468896] A double-blind, placebo-controlled study on the effects of lutein and zeaxanthin on photostress recovery, glare disability, and chromatic contrast. (2014). https://pubmed.ncbi.nlm.nih.gov/25468896/ DOI: 10.1167/iovs.14-15573
Complete structured claim and evidence
L+Z improved the tested chromatic-contrast threshold versus placebo.
Lutein 10 mg plus zeaxanthin 2 mg daily combination → Human chromatic contrast performance source_derived_draftungraded
Experimental context and source evidence
evidence_span
{"source_cache": "artifacts/lutein-research/25468896.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "01231d6577e7c30e79a74525772191092df003b42344095a53faf0279f138ac3", "start_char": 0, "end_char": 2007, "text_sha256": "01231d6577e7c30e79a74525772191092df003b42344095a53faf0279f138ac3"}
experimental_model
Randomized double-blind placebo-controlled visual-performance study
exposure
Lutein 10 mg + zeaxanthin 2 mg daily for one year
limitations
Combined intervention; improved task performance is not evidence of AMD prevention or treatment.
nutrient_topic
Lutein research collection; topical membership is not evidence of a direct dietary effect. · Lutein
organism
115 young healthy adults
plain_language
Participants detected the test contrast better.
primary_references
[lutein-p25468896] A double-blind, placebo-controlled study on the effects of lutein and zeaxanthin on photostress recovery, glare disability, and chromatic contrast. (2014). https://pubmed.ncbi.nlm.nih.gov/25468896/ DOI: 10.1167/iovs.14-15573
tissue_or_cell_type
Serum, macular pigment and visual tasks
Lutein: metabolism, signaling and nutrient connections (2026-09-17) · lines 866–877
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Randomized double-blind placebo-controlled visual-performance study · source_derived_draft · unverified_draft
### lutein-contrast-improvement L+Z improved the tested chromatic-contrast threshold versus placebo. Condition category: normal nutrient_topic: Lutein research collection; topical membership is not evidence of a direct dietary effect. plain_language: Participants detected the test contrast better. organism: 115 young healthy adults tissue_or_cell_type: Serum, macular pigment and visual tasks experimental_model: Randomized double-blind placebo-controlled visual-performance study limitations: Combined intervention; improved task performance is not evidence of AMD prevention or treatment. exposure: Lutein 10 mg + zeaxanthin 2 mg daily for one year evidence_span: {"source_cache": "artifacts/lutein-research/25468896.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "01231d6577e7c30e79a74525772191092df003b42344095a53faf0279f138ac3", "start_char": 0, "end_char": 2007, "text_sha256": "01231d6577e7c30e79a74525772191092df003b42344095a53faf0279f138ac3"} [lutein-p25468896] A double-blind, placebo-controlled study on the effects of lutein and zeaxanthin on photostress recovery, glare disability, and chromatic contrast. (2014). https://pubmed.ncbi.nlm.nih.gov/25468896/ DOI: 10.1167/iovs.14-15573
Complete structured claim and evidence
Glare disability did not improve significantly in the treated group despite correlation with pigment density.
Lutein 10 mg plus zeaxanthin 2 mg daily combination → Human disability-glare performance source_derived_draftungraded
Experimental context and source evidence
evidence_span
{"source_cache": "artifacts/lutein-research/25468896.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "01231d6577e7c30e79a74525772191092df003b42344095a53faf0279f138ac3", "start_char": 0, "end_char": 2007, "text_sha256": "01231d6577e7c30e79a74525772191092df003b42344095a53faf0279f138ac3"}
experimental_model
Randomized double-blind placebo-controlled visual-performance study
exposure
Lutein 10 mg + zeaxanthin 2 mg daily for one year
limitations
Combined intervention; improved task performance is not evidence of AMD prevention or treatment.
nutrient_topic
Lutein research collection; topical membership is not evidence of a direct dietary effect. · Lutein
organism
115 young healthy adults
plain_language
A biomarker correlation did not guarantee a treatment effect.
primary_references
[lutein-p25468896] A double-blind, placebo-controlled study on the effects of lutein and zeaxanthin on photostress recovery, glare disability, and chromatic contrast. (2014). https://pubmed.ncbi.nlm.nih.gov/25468896/ DOI: 10.1167/iovs.14-15573
tissue_or_cell_type
Serum, macular pigment and visual tasks
Lutein: metabolism, signaling and nutrient connections (2026-09-17) · lines 879–890
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Randomized double-blind placebo-controlled visual-performance study · source_derived_draft · unverified_draft
### lutein-glare-null Glare disability did not improve significantly in the treated group despite correlation with pigment density. Condition category: normal nutrient_topic: Lutein research collection; topical membership is not evidence of a direct dietary effect. plain_language: A biomarker correlation did not guarantee a treatment effect. organism: 115 young healthy adults tissue_or_cell_type: Serum, macular pigment and visual tasks experimental_model: Randomized double-blind placebo-controlled visual-performance study limitations: Combined intervention; improved task performance is not evidence of AMD prevention or treatment. exposure: Lutein 10 mg + zeaxanthin 2 mg daily for one year evidence_span: {"source_cache": "artifacts/lutein-research/25468896.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "01231d6577e7c30e79a74525772191092df003b42344095a53faf0279f138ac3", "start_char": 0, "end_char": 2007, "text_sha256": "01231d6577e7c30e79a74525772191092df003b42344095a53faf0279f138ac3"} [lutein-p25468896] A double-blind, placebo-controlled study on the effects of lutein and zeaxanthin on photostress recovery, glare disability, and chromatic contrast. (2014). https://pubmed.ncbi.nlm.nih.gov/25468896/ DOI: 10.1167/iovs.14-15573
Complete structured claim and evidence
The young-adult trial reported improved visual memory associated with supplementation.
Lutein 10 mg plus zeaxanthin 2 mg daily combination → Visual memory score in young adults source_derived_draftungraded
Experimental context and source evidence
evidence_span
{"source_cache": "artifacts/lutein-research/29135938.fulltext.txt", "locator": "Primary full-text span; zero-based, end-exclusive Unicode character offsets", "file_sha256": "f60146e188d1a3093c572c3f637ebd659184f72727a75b35afd265b5ef0be71b", "start_char": 21132, "end_char": 25480, "text_sha256": "02d9398a25880c0ead3b3ef0ed91d12a98f837a8c8f89c141986dd926e1010a8"}
experimental_model
Small randomized double-masked placebo-controlled trial with biomarker-response analyses
exposure
Lutein 10 mg + zeaxanthin 2 mg daily for one year
limitations
Small unequal groups and multiple outcomes; attention/reasoning findings depended on pigment-response analysis. MPOD does not directly measure brain tissue.
nutrient_topic
Lutein research collection; topical membership is not evidence of a direct dietary effect. · Lutein
organism
51 analyzable healthy adults aged 18–30; 37 active and 14 placebo
plain_language
A small study found a benefit on a specific memory task.
primary_references
[lutein-p29135938] Effects of a Lutein and Zeaxanthin Intervention on Cognitive Function: A Randomized, Double-Masked, Placebo-Controlled Trial of Younger Healthy Adults. (2017). https://pubmed.ncbi.nlm.nih.gov/29135938/ DOI: 10.3390/nu9111246
tissue_or_cell_type
Cognitive testing and retinal pigment measurement
Lutein: metabolism, signaling and nutrient connections (2026-09-17) · lines 905–916
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Small randomized double-masked placebo-controlled trial with biomarker-response analyses · source_derived_draft · unverified_draft
### lutein-young-memory The young-adult trial reported improved visual memory associated with supplementation. Condition category: normal nutrient_topic: Lutein research collection; topical membership is not evidence of a direct dietary effect. plain_language: A small study found a benefit on a specific memory task. organism: 51 analyzable healthy adults aged 18–30; 37 active and 14 placebo tissue_or_cell_type: Cognitive testing and retinal pigment measurement experimental_model: Small randomized double-masked placebo-controlled trial with biomarker-response analyses limitations: Small unequal groups and multiple outcomes; attention/reasoning findings depended on pigment-response analysis. MPOD does not directly measure brain tissue. exposure: Lutein 10 mg + zeaxanthin 2 mg daily for one year evidence_span: {"source_cache": "artifacts/lutein-research/29135938.fulltext.txt", "locator": "Primary full-text span; zero-based, end-exclusive Unicode character offsets", "file_sha256": "f60146e188d1a3093c572c3f637ebd659184f72727a75b35afd265b5ef0be71b", "start_char": 21132, "end_char": 25480, "text_sha256": "02d9398a25880c0ead3b3ef0ed91d12a98f837a8c8f89c141986dd926e1010a8"} [lutein-p29135938] Effects of a Lutein and Zeaxanthin Intervention on Cognitive Function: A Randomized, Double-Masked, Placebo-Controlled Trial of Younger Healthy Adults. (2017). https://pubmed.ncbi.nlm.nih.gov/29135938/ DOI: 10.3390/nu9111246
Complete structured claim and evidence
Attention and reasoning improvements were observed in analyses requiring significant macular-pigment increases.
Human macular pigment optical density → Complex attention and reasoning scores in young adults source_derived_draftungraded
Experimental context and source evidence
evidence_span
{"source_cache": "artifacts/lutein-research/29135938.fulltext.txt", "locator": "Primary full-text span; zero-based, end-exclusive Unicode character offsets", "file_sha256": "f60146e188d1a3093c572c3f637ebd659184f72727a75b35afd265b5ef0be71b", "start_char": 21132, "end_char": 25480, "text_sha256": "02d9398a25880c0ead3b3ef0ed91d12a98f837a8c8f89c141986dd926e1010a8"}
experimental_model
Small randomized double-masked placebo-controlled trial with biomarker-response analyses
exposure
Lutein 10 mg + zeaxanthin 2 mg daily for one year
limitations
Small unequal groups and multiple outcomes; attention/reasoning findings depended on pigment-response analysis. MPOD does not directly measure brain tissue.
nutrient_topic
Lutein research collection; topical membership is not evidence of a direct dietary effect. · Lutein
organism
51 analyzable healthy adults aged 18–30; 37 active and 14 placebo
plain_language
These findings depended on a biomarker-response subgroup.
primary_references
[lutein-p29135938] Effects of a Lutein and Zeaxanthin Intervention on Cognitive Function: A Randomized, Double-Masked, Placebo-Controlled Trial of Younger Healthy Adults. (2017). https://pubmed.ncbi.nlm.nih.gov/29135938/ DOI: 10.3390/nu9111246
tissue_or_cell_type
Cognitive testing and retinal pigment measurement
Lutein: metabolism, signaling and nutrient connections (2026-09-17) · lines 918–929
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Small randomized double-masked placebo-controlled trial with biomarker-response analyses · source_derived_draft · unverified_draft
### lutein-young-response-dependent Attention and reasoning improvements were observed in analyses requiring significant macular-pigment increases. Condition category: normal nutrient_topic: Lutein research collection; topical membership is not evidence of a direct dietary effect. plain_language: These findings depended on a biomarker-response subgroup. organism: 51 analyzable healthy adults aged 18–30; 37 active and 14 placebo tissue_or_cell_type: Cognitive testing and retinal pigment measurement experimental_model: Small randomized double-masked placebo-controlled trial with biomarker-response analyses limitations: Small unequal groups and multiple outcomes; attention/reasoning findings depended on pigment-response analysis. MPOD does not directly measure brain tissue. exposure: Lutein 10 mg + zeaxanthin 2 mg daily for one year evidence_span: {"source_cache": "artifacts/lutein-research/29135938.fulltext.txt", "locator": "Primary full-text span; zero-based, end-exclusive Unicode character offsets", "file_sha256": "f60146e188d1a3093c572c3f637ebd659184f72727a75b35afd265b5ef0be71b", "start_char": 21132, "end_char": 25480, "text_sha256": "02d9398a25880c0ead3b3ef0ed91d12a98f837a8c8f89c141986dd926e1010a8"} [lutein-p29135938] Effects of a Lutein and Zeaxanthin Intervention on Cognitive Function: A Randomized, Double-Masked, Placebo-Controlled Trial of Younger Healthy Adults. (2017). https://pubmed.ncbi.nlm.nih.gov/29135938/ DOI: 10.3390/nu9111246
Complete structured claim and evidence
Lutein AUC was reduced with the tested fibers, including pectin.
Pectin, structurally heterogeneous plant polysaccharides → Human post-meal plasma lutein response source_derived_draftungraded
Experimental context and source evidence
evidence_span
{"source_cache": "artifacts/pectin-research/10573545.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "f0828162b0e41d10d79784cea5cc96e55409b4ee80be3afc399132a7ad087332", "start_char": 0, "end_char": 1340, "text_sha256": "f0828162b0e41d10d79784cea5cc96e55409b4ee80be3afc399132a7ad087332"}
experimental_model
Crossover mixed-carotenoid meal study in six healthy women
exposure
Pectin or other fibers at 0.15 g/kg with a carotenoid and alpha-tocopherol mixture
limitations
Reported effect-size ranges cover multiple fibers, not one pectin-specific estimate. Plasma exposure does not establish long-term deficiency.
nutrient_topic
Pectin research collection; topical membership is not evidence of a direct dietary effect. · Pectin, structurally heterogeneous plant polysaccharides
organism
Homo sapiens
plain_language
The finding also involved lutein.
primary_references
[pectin-p10573545] Some dietary fibers reduce the absorption of carotenoids in women. (1999). https://pubmed.ncbi.nlm.nih.gov/10573545/ DOI: 10.1093/jn/129.12.2170
tissue_or_cell_type
Plasma 24-hour area under the curve
Pectin: metabolism, signaling and nutrient connections (2026-09-17) · lines 698–709
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Crossover mixed-carotenoid meal study in six healthy women · source_derived_draft · unverified_draft
### pectin-lutein-auc Lutein AUC was reduced with the tested fibers, including pectin. Condition category: normal nutrient_topic: Pectin research collection; topical membership is not evidence of a direct dietary effect. plain_language: The finding also involved lutein. organism: Homo sapiens tissue_or_cell_type: Plasma 24-hour area under the curve experimental_model: Crossover mixed-carotenoid meal study in six healthy women limitations: Reported effect-size ranges cover multiple fibers, not one pectin-specific estimate. Plasma exposure does not establish long-term deficiency. exposure: Pectin or other fibers at 0.15 g/kg with a carotenoid and alpha-tocopherol mixture evidence_span: {"source_cache": "artifacts/pectin-research/10573545.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "f0828162b0e41d10d79784cea5cc96e55409b4ee80be3afc399132a7ad087332", "start_char": 0, "end_char": 1340, "text_sha256": "f0828162b0e41d10d79784cea5cc96e55409b4ee80be3afc399132a7ad087332"} [pectin-p10573545] Some dietary fibers reduce the absorption of carotenoids in women. (1999). https://pubmed.ncbi.nlm.nih.gov/10573545/ DOI: 10.1093/jn/129.12.2170
Complete structured claim and evidence
FeSO4 restored chelator-inhibited RPE65 isomerohydrolase activity in bovine microsomes and recombinant assays; ferric salts did not.
Ferrous iron → RPE65 retinoid isomerohydrolase source_derived_draftungraded
Experimental context and source evidence
cross_nutrient
Iron availability at RPE65 enables formation of the cis-retinoid visual-cycle intermediate.
experimental_model
Chelation and metal rescue
limitations
This is enzyme-cofactor evidence, not a human iron-deficiency threshold.
nutrient_topic
Vitamin A research collection; topical membership is not evidence of a direct dietary effect. · Vitamin A
organism
Bos taurus; recombinant RPE65 in human 293A cells
plain_language
Ferrous iron is required for this vitamin A recycling enzyme.
primary_references
[moiseyev-2006] RPE65 is an iron(II)-dependent isomerohydrolase in the retinoid visual cycle (2006). https://pubmed.ncbi.nlm.nih.gov/16319067/ DOI: 10.1074/jbc.M508903200
tissue_or_cell_type
RPE microsomes and cultured-cell preparations
Vitamin A: forms, mechanisms, deficiency and excess (2026-09-17) · lines 677–687
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Chelation and metal rescue · source_derived_draft · unverified_draft
### a-vision-rpe65-iron FeSO4 restored chelator-inhibited RPE65 isomerohydrolase activity in bovine microsomes and recombinant assays; ferric salts did not. Condition category: normal nutrient_topic: Vitamin A research collection; topical membership is not evidence of a direct dietary effect. plain_language: Ferrous iron is required for this vitamin A recycling enzyme. organism: Bos taurus; recombinant RPE65 in human 293A cells tissue_or_cell_type: RPE microsomes and cultured-cell preparations experimental_model: Chelation and metal rescue limitations: This is enzyme-cofactor evidence, not a human iron-deficiency threshold. cross_nutrient: Iron availability at RPE65 enables formation of the cis-retinoid visual-cycle intermediate. [moiseyev-2006] RPE65 is an iron(II)-dependent isomerohydrolase in the retinoid visual cycle (2006). https://pubmed.ncbi.nlm.nih.gov/16319067/ DOI: 10.1074/jbc.M508903200
Complete structured claim and evidence
Recombinant RPE65 catalyzed conversion of all-trans-retinyl esters to 11-cis-retinol in visual-cycle reconstitution.
RPE65 retinoid isomerohydrolase → 11-cis-retinol source_derived_draftungraded
Experimental context and source evidence
experimental_model
Recombinant enzyme reconstitution
limitations
Production of the aldehyde requires a subsequent oxidation step.
nutrient_topic
Vitamin A research collection; topical membership is not evidence of a direct dietary effect. · Vitamin A
organism
QBI-293A human cells and COS-1 monkey cells
plain_language
RPE65 converts the ester pool into the cis alcohol needed for chromophore renewal.
primary_references
[moiseyev-2005] RPE65 is the isomerohydrolase in the retinoid visual cycle (2005). https://pubmed.ncbi.nlm.nih.gov/16116091/ DOI: 10.1073/pnas.0503460102
tissue_or_cell_type
RPE visual-cycle biochemical model
Vitamin A: forms, mechanisms, deficiency and excess (2026-09-17) · lines 666–675
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Recombinant enzyme reconstitution · source_derived_draft · unverified_draft
### a-vision-rpe65-isomerization Recombinant RPE65 catalyzed conversion of all-trans-retinyl esters to 11-cis-retinol in visual-cycle reconstitution. Condition category: normal nutrient_topic: Vitamin A research collection; topical membership is not evidence of a direct dietary effect. plain_language: RPE65 converts the ester pool into the cis alcohol needed for chromophore renewal. organism: QBI-293A human cells and COS-1 monkey cells tissue_or_cell_type: RPE visual-cycle biochemical model experimental_model: Recombinant enzyme reconstitution limitations: Production of the aldehyde requires a subsequent oxidation step. [moiseyev-2005] RPE65 is the isomerohydrolase in the retinoid visual cycle (2005). https://pubmed.ncbi.nlm.nih.gov/16116091/ DOI: 10.1073/pnas.0503460102
Complete structured claim and evidence
ZnCl2 did not restore isomerohydrolase activity after metal chelation in the bovine RPE assay, whereas FeSO4 did.
Zinc(II) ion → RPE65 retinoid isomerohydrolase source_derived_draftungraded
Experimental context and source evidence
cross_nutrient
Iron and zinc are not interchangeable RPE65 cofactors in the tested preparation.
experimental_model
Metal-rescue comparison
limitations
Does not test systemic zinc status or other zinc-dependent visual functions.
nutrient_topic
Vitamin A research collection; topical membership is not evidence of a direct dietary effect. · Vitamin A
organism
Bos taurus
plain_language
Zinc could not replace iron in this enzyme assay.
primary_references
[moiseyev-2006] RPE65 is an iron(II)-dependent isomerohydrolase in the retinoid visual cycle (2006). https://pubmed.ncbi.nlm.nih.gov/16319067/ DOI: 10.1074/jbc.M508903200
tissue_or_cell_type
RPE microsomes
Vitamin A: forms, mechanisms, deficiency and excess (2026-09-17) · lines 689–699
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Metal-rescue comparison · source_derived_draft · unverified_draft
### a-vision-rpe65-zinc-not-substitute ZnCl2 did not restore isomerohydrolase activity after metal chelation in the bovine RPE assay, whereas FeSO4 did. Condition category: normal nutrient_topic: Vitamin A research collection; topical membership is not evidence of a direct dietary effect. plain_language: Zinc could not replace iron in this enzyme assay. organism: Bos taurus tissue_or_cell_type: RPE microsomes experimental_model: Metal-rescue comparison limitations: Does not test systemic zinc status or other zinc-dependent visual functions. cross_nutrient: Iron and zinc are not interchangeable RPE65 cofactors in the tested preparation. [moiseyev-2006] RPE65 is an iron(II)-dependent isomerohydrolase in the retinoid visual cycle (2006). https://pubmed.ncbi.nlm.nih.gov/16319067/ DOI: 10.1074/jbc.M508903200
Complete structured claim and evidence
Retinoic-acid receptor signaling increased intestinal ISX expression.
All-trans-retinoic acid → Intestine-specific homeobox protein / ISX source_derived_draftungraded
Experimental context and source evidence
evidence_location
Abstract
experimental_model
Mouse diet/retinoic-acid interventions and human cell lines.
exposure
Retinoic-acid treatment with receptor-dependent tests.
limitations
Pharmacological treatment supports feedback circuitry, not a universal dietary threshold.
nutrient_topic
Vitamin A research collection; topical membership is not evidence of a direct dietary effect. · Vitamin A
organism
Mus musculus and Homo sapiens cell lines
outcome
Retinoic-acid receptor signaling increased intestinal ISX expression.
plain_language
The active retinoid metabolite induces a brake on further precursor uptake.
primary_references
[va-lobo-2010] ISX is a retinoic acid-sensitive gatekeeper that controls intestinal beta,beta-carotene absorption and vitamin A production (2010). https://pubmed.ncbi.nlm.nih.gov/20061533/ DOI: 10.1096/fj.09-150995
tissue_or_cell_type
Intestine and cultured cells
Vitamin A: forms, mechanisms, deficiency and excess (2026-09-17) · lines 260–272
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Mouse diet/retinoic-acid interventions and human cell lines. · source_derived_draft · unverified_draft
### va-retinoic-acid-isx-feedback Retinoic-acid receptor signaling increased intestinal ISX expression. Condition category: normal nutrient_topic: Vitamin A research collection; topical membership is not evidence of a direct dietary effect. plain_language: The active retinoid metabolite induces a brake on further precursor uptake. organism: Mus musculus and Homo sapiens cell lines tissue_or_cell_type: Intestine and cultured cells experimental_model: Mouse diet/retinoic-acid interventions and human cell lines. limitations: Pharmacological treatment supports feedback circuitry, not a universal dietary threshold. exposure: Retinoic-acid treatment with receptor-dependent tests. outcome: Retinoic-acid receptor signaling increased intestinal ISX expression. evidence_location: Abstract [va-lobo-2010] ISX is a retinoic acid-sensitive gatekeeper that controls intestinal beta,beta-carotene absorption and vitamin A production (2010). https://pubmed.ncbi.nlm.nih.gov/20061533/ DOI: 10.1096/fj.09-150995
Complete structured claim and evidence
ISX bound upstream SCARB1 regulatory motifs and repressed intestinal SCARB1 expression.
Intestine-specific homeobox protein / ISX → Scavenger receptor class B type 1 / SCARB1 source_derived_draftungraded
Experimental context and source evidence
evidence_location
Abstract
experimental_model
Isx, Bco1, Bco2 and Scarb1 mouse mutants; promoter binding and controlled diets.
exposure
Isx genotypes and promoter-binding experiments.
limitations
Tissue-specific regulation, not suppression in every organ.
nutrient_topic
Vitamin A research collection; topical membership is not evidence of a direct dietary effect. · Vitamin A
organism
Mus musculus and promoter-binding preparations
outcome
ISX bound upstream SCARB1 regulatory motifs and repressed intestinal SCARB1 expression.
plain_language
The feedback factor lowers the uptake receptor.
primary_references
[va-widjajaadhi-2015] A genetic dissection of intestinal fat-soluble vitamin and carotenoid absorption (2015). https://pmc.ncbi.nlm.nih.gov/articles/PMC4424956/ DOI: 10.1093/hmg/ddv072
tissue_or_cell_type
Jejunum and DNA-binding assays
Vitamin A: forms, mechanisms, deficiency and excess (2026-09-17) · lines 274–286
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Isx, Bco1, Bco2 and Scarb1 mouse mutants; promoter binding and controlled diets. · source_derived_draft · unverified_draft
### va-isx-scarb1-repression ISX bound upstream SCARB1 regulatory motifs and repressed intestinal SCARB1 expression. Condition category: normal nutrient_topic: Vitamin A research collection; topical membership is not evidence of a direct dietary effect. plain_language: The feedback factor lowers the uptake receptor. organism: Mus musculus and promoter-binding preparations tissue_or_cell_type: Jejunum and DNA-binding assays experimental_model: Isx, Bco1, Bco2 and Scarb1 mouse mutants; promoter binding and controlled diets. limitations: Tissue-specific regulation, not suppression in every organ. exposure: Isx genotypes and promoter-binding experiments. outcome: ISX bound upstream SCARB1 regulatory motifs and repressed intestinal SCARB1 expression. evidence_location: Abstract [va-widjajaadhi-2015] A genetic dissection of intestinal fat-soluble vitamin and carotenoid absorption (2015). https://pmc.ncbi.nlm.nih.gov/articles/PMC4424956/ DOI: 10.1093/hmg/ddv072
Complete structured claim and evidence
Blocking SR-BI with an extracellular antibody or BLT1 reduced RRR-alpha-tocopherol uptake by human Caco-2 TC7 cells.
Scavenger receptor class B type 1 / SCARB1 → Intestinal alpha-tocopherol uptake source_derived_draftungraded
Experimental context and source evidence
cross_nutrient
false
experimental_model
Differentiated Caco-2 TC7 monolayers
exposure
60-min pretreatment: antibody 3.75 µg/mL or BLT1 10 µM; 40 µM micellar RRR-alpha-tocopherol for 60 min.
limitations
Inhibitor/antibody evidence; contribution under these conditions is not the sole absorption route.
nutrient_topic
Vitamin E research collection; topical membership is not evidence of a direct dietary effect. · Vitamin E
organism
Homo sapiens
plain_language
SR-BI helped these intestinal cells take up vitamin E.
primary_references
[reboul2006] Scavenger receptor class B type I (SR-BI) is involved in vitamin E transport across the enterocyte. (2006). https://pubmed.ncbi.nlm.nih.gov/16380385/ DOI: 10.1074/jbc.m509042200
tissue_or_cell_type
Intestinal epithelial cell model
Vitamin E: transport, membrane protection and nutrient interactions (2026-09-17) · lines 181–192
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Differentiated Caco-2 TC7 monolayers · source_derived_draft · unverified_draft
### ve-transport-scarb1-uptake Blocking SR-BI with an extracellular antibody or BLT1 reduced RRR-alpha-tocopherol uptake by human Caco-2 TC7 cells. Condition category: normal nutrient_topic: Vitamin E research collection; topical membership is not evidence of a direct dietary effect. plain_language: SR-BI helped these intestinal cells take up vitamin E. organism: Homo sapiens tissue_or_cell_type: Intestinal epithelial cell model experimental_model: Differentiated Caco-2 TC7 monolayers limitations: Inhibitor/antibody evidence; contribution under these conditions is not the sole absorption route. exposure: 60-min pretreatment: antibody 3.75 µg/mL or BLT1 10 µM; 40 µM micellar RRR-alpha-tocopherol for 60 min. cross_nutrient: false [reboul2006] Scavenger receptor class B type I (SR-BI) is involved in vitamin E transport across the enterocyte. (2006). https://pubmed.ncbi.nlm.nih.gov/16380385/ DOI: 10.1074/jbc.m509042200
Complete structured claim and evidence
Human NPC1L1 overexpression increased alpha-tocopherol uptake, which was inhibited by ezetimibe.
Human Niemann-Pick C1-like protein 1 / NPC1L1 → Intestinal alpha-tocopherol uptake source_derived_draftungraded
Experimental context and source evidence
cross_nutrient
false
experimental_model
Human NPC1L1 overexpression uptake assay
exposure
NPC1L1 expression with alpha-tocopherol and ezetimibe; dose/time not reported in abstract.
limitations
Cell experiment does not establish a clinical vitamin E deficiency from ezetimibe.
nutrient_topic
Vitamin E research collection; topical membership is not evidence of a direct dietary effect. · Vitamin E
organism
Human protein in cultured cells
plain_language
The cholesterol transporter NPC1L1 can also take up vitamin E.
primary_references
[narushima2008] Niemann-pick C1-like 1 mediates alpha-tocopherol transport. (2008). https://pubmed.ncbi.nlm.nih.gov/18403720/ DOI: 10.1124/mol.107.043034
tissue_or_cell_type
Cellular uptake model
Vitamin E: transport, membrane protection and nutrient interactions (2026-09-17) · lines 207–218
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Human NPC1L1 overexpression uptake assay · source_derived_draft · unverified_draft
### ve-transport-npc1l1-uptake Human NPC1L1 overexpression increased alpha-tocopherol uptake, which was inhibited by ezetimibe. Condition category: normal nutrient_topic: Vitamin E research collection; topical membership is not evidence of a direct dietary effect. plain_language: The cholesterol transporter NPC1L1 can also take up vitamin E. organism: Human protein in cultured cells tissue_or_cell_type: Cellular uptake model experimental_model: Human NPC1L1 overexpression uptake assay limitations: Cell experiment does not establish a clinical vitamin E deficiency from ezetimibe. exposure: NPC1L1 expression with alpha-tocopherol and ezetimibe; dose/time not reported in abstract. cross_nutrient: false [narushima2008] Niemann-pick C1-like 1 mediates alpha-tocopherol transport. (2008). https://pubmed.ncbi.nlm.nih.gov/18403720/ DOI: 10.1124/mol.107.043034
Complete structured claim and evidence
Expression of NPC1L1 in HEK cells increased cholecalciferol uptake, and its corresponding inhibitor reduced this uptake.
Human Niemann-Pick C1-like protein 1 / NPC1L1 → Intestinal cholecalciferol uptake source_derived_draftungraded
Experimental context and source evidence
cross_nutrient
false
evidence_location
Primary abstract, Methods and results; exact incubation concentrations/durations unavailable in abstract.
experimental_model
Transfected HEK-cell uptake assay; intestinal relevance tested separately
exposure
Transporter transfection and selective-inhibitor co-incubation; exact dose/time absent from abstract.
limitations
HEK overexpression is not intact human intestine; inhibitors and uptake assays do not establish clinical deficiency. In-vivo ezetimibe effect in mice was nonsignificant.
nutrient
Vitamin D2 and D3 · Vitamin D2 and D3
nutrient_topic
Vitamin D2 and D3 research collection; topical membership is not evidence of a direct dietary effect. · Vitamin D2 and D3
organism
Homo sapiens
plain_language
NPC1L1 can contribute to vitamin D3 entry into cells.
primary_references
[reboul2011] Vitamin D intestinal absorption is not a simple passive diffusion: evidences for involvement of cholesterol transporters. (2011). https://pubmed.ncbi.nlm.nih.gov/21280209/ DOI: 10.1002/mnfr.201000553
tissue_or_cell_type
HEK cell model of a candidate intestinal uptake mechanism
Vitamin D2 and D3: mechanisms, deficiency and nutrient interactions (2026-09-17) · lines 196–209
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Transfected HEK-cell uptake assay; intestinal relevance tested separately · source_derived_draft · unverified_draft
### vd-act-npc1l1-uptake Expression of NPC1L1 in HEK cells increased cholecalciferol uptake, and its corresponding inhibitor reduced this uptake. Condition category: normal nutrient_topic: Vitamin D2 and D3 research collection; topical membership is not evidence of a direct dietary effect. plain_language: NPC1L1 can contribute to vitamin D3 entry into cells. organism: Homo sapiens tissue_or_cell_type: HEK cell model of a candidate intestinal uptake mechanism experimental_model: Transfected HEK-cell uptake assay; intestinal relevance tested separately limitations: HEK overexpression is not intact human intestine; inhibitors and uptake assays do not establish clinical deficiency. In-vivo ezetimibe effect in mice was nonsignificant. exposure: Transporter transfection and selective-inhibitor co-incubation; exact dose/time absent from abstract. cross_nutrient: false evidence_location: Primary abstract, Methods and results; exact incubation concentrations/durations unavailable in abstract. nutrient: Vitamin D2 and D3 [reboul2011] Vitamin D intestinal absorption is not a simple passive diffusion: evidences for involvement of cholesterol transporters. (2011). https://pubmed.ncbi.nlm.nih.gov/21280209/ DOI: 10.1002/mnfr.201000553
Complete structured claim and evidence
Expression of SR-BI in HEK cells increased cholecalciferol uptake, and its corresponding inhibitor reduced this uptake.
Scavenger receptor class B type 1 / SCARB1 → Intestinal cholecalciferol uptake source_derived_draftungraded
Experimental context and source evidence
cross_nutrient
false
evidence_location
Primary abstract, Methods and results; exact incubation concentrations/durations unavailable in abstract.
experimental_model
Transfected HEK-cell uptake assay; intestinal relevance tested separately
exposure
Transporter transfection and selective-inhibitor co-incubation; exact dose/time absent from abstract.
limitations
HEK overexpression is not intact human intestine; inhibitors and uptake assays do not establish clinical deficiency. In-vivo ezetimibe effect in mice was nonsignificant.
nutrient
Vitamin D2 and D3 · Vitamin D2 and D3
nutrient_topic
Vitamin D2 and D3 research collection; topical membership is not evidence of a direct dietary effect. · Vitamin D2 and D3
organism
Homo sapiens
plain_language
SR-BI can contribute to vitamin D3 entry into cells.
primary_references
[reboul2011] Vitamin D intestinal absorption is not a simple passive diffusion: evidences for involvement of cholesterol transporters. (2011). https://pubmed.ncbi.nlm.nih.gov/21280209/ DOI: 10.1002/mnfr.201000553
tissue_or_cell_type
HEK cell model of a candidate intestinal uptake mechanism
Vitamin D2 and D3: mechanisms, deficiency and nutrient interactions (2026-09-17) · lines 166–179
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Transfected HEK-cell uptake assay; intestinal relevance tested separately · source_derived_draft · unverified_draft
### vd-act-scarb1-uptake Expression of SR-BI in HEK cells increased cholecalciferol uptake, and its corresponding inhibitor reduced this uptake. Condition category: normal nutrient_topic: Vitamin D2 and D3 research collection; topical membership is not evidence of a direct dietary effect. plain_language: SR-BI can contribute to vitamin D3 entry into cells. organism: Homo sapiens tissue_or_cell_type: HEK cell model of a candidate intestinal uptake mechanism experimental_model: Transfected HEK-cell uptake assay; intestinal relevance tested separately limitations: HEK overexpression is not intact human intestine; inhibitors and uptake assays do not establish clinical deficiency. In-vivo ezetimibe effect in mice was nonsignificant. exposure: Transporter transfection and selective-inhibitor co-incubation; exact dose/time absent from abstract. cross_nutrient: false evidence_location: Primary abstract, Methods and results; exact incubation concentrations/durations unavailable in abstract. nutrient: Vitamin D2 and D3 [reboul2011] Vitamin D intestinal absorption is not a simple passive diffusion: evidences for involvement of cholesterol transporters. (2011). https://pubmed.ncbi.nlm.nih.gov/21280209/ DOI: 10.1002/mnfr.201000553
Complete structured claim and evidence
SR-BI antibody or BLT1 inhibited all-E and 5Z lycopene uptake by up to 60% in Caco-2 monolayers.
Scavenger receptor class B type 1 / SCARB1 → Lycopene source_derived_draftungraded
Experimental context and source evidence
evidence_span
{"source_cache": "artifacts/lycopene-research/18641187.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "7c71fd4fd3be9d14176bceb3c2104143269a788587feec232350a6f1c5913e3d", "start_char": 0, "end_char": 1557, "text_sha256": "7c71fd4fd3be9d14176bceb3c2104143269a788587feec232350a6f1c5913e3d"}
experimental_model
Transporter inhibition in Caco-2 cells; intestinal SR-BI transgenic mice
exposure
All-E and 5Z lycopene; mice received 0.25 g/kg diet for one month
limitations
Partial uptake inhibition is not proof of a sole transporter. Ezetimibe result is a cell assay, not a clinical drug-interaction trial.
nutrient_topic
Lycopene research collection; topical membership is not evidence of a direct dietary effect. · Lycopene
organism
Human Caco-2 cells
plain_language
One intestinal lipid transporter helps lycopene enter these cells.
primary_references
[lycopene-p18641187] Lycopene absorption in human intestinal cells and in mice involves scavenger receptor class B type I but not Niemann-Pick C1-like 1. (2008). https://pubmed.ncbi.nlm.nih.gov/18641187/ DOI: 10.1093/jn/138.8.1432
tissue_or_cell_type
Intestinal epithelium and plasma
Lycopene: absorption, metabolism, nutrient connections and human outcomes (2026-09-17) · lines 104–115
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Transporter inhibition in Caco-2 cells; intestinal SR-BI transgenic mice · source_derived_draft · unverified_draft
### lycopene-srbi-uptake SR-BI antibody or BLT1 inhibited all-E and 5Z lycopene uptake by up to 60% in Caco-2 monolayers. Condition category: normal nutrient_topic: Lycopene research collection; topical membership is not evidence of a direct dietary effect. plain_language: One intestinal lipid transporter helps lycopene enter these cells. organism: Human Caco-2 cells tissue_or_cell_type: Intestinal epithelium and plasma experimental_model: Transporter inhibition in Caco-2 cells; intestinal SR-BI transgenic mice limitations: Partial uptake inhibition is not proof of a sole transporter. Ezetimibe result is a cell assay, not a clinical drug-interaction trial. exposure: All-E and 5Z lycopene; mice received 0.25 g/kg diet for one month evidence_span: {"source_cache": "artifacts/lycopene-research/18641187.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "7c71fd4fd3be9d14176bceb3c2104143269a788587feec232350a6f1c5913e3d", "start_char": 0, "end_char": 1557, "text_sha256": "7c71fd4fd3be9d14176bceb3c2104143269a788587feec232350a6f1c5913e3d"} [lycopene-p18641187] Lycopene absorption in human intestinal cells and in mice involves scavenger receptor class B type I but not Niemann-Pick C1-like 1. (2008). https://pubmed.ncbi.nlm.nih.gov/18641187/ DOI: 10.1093/jn/138.8.1432
Complete structured claim and evidence
NPC1L1 antibody and ezetimibe did not significantly reduce all-E or 5Z lycopene uptake in Caco-2 cells.
Human Niemann-Pick C1-like protein 1 / NPC1L1 → Intestinal epithelial lycopene uptake source_derived_draftungraded
Experimental context and source evidence
evidence_span
{"source_cache": "artifacts/lycopene-research/18641187.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "7c71fd4fd3be9d14176bceb3c2104143269a788587feec232350a6f1c5913e3d", "start_char": 0, "end_char": 1557, "text_sha256": "7c71fd4fd3be9d14176bceb3c2104143269a788587feec232350a6f1c5913e3d"}
experimental_model
Transporter inhibition in Caco-2 cells; intestinal SR-BI transgenic mice
exposure
All-E and 5Z lycopene; mice received 0.25 g/kg diet for one month
limitations
Partial uptake inhibition is not proof of a sole transporter. Ezetimibe result is a cell assay, not a clinical drug-interaction trial.
nutrient_topic
Lycopene research collection; topical membership is not evidence of a direct dietary effect. · Lycopene
organism
Human Caco-2 cells
plain_language
A transporter used by other lipids was not necessary in this particular assay.
primary_references
[lycopene-p18641187] Lycopene absorption in human intestinal cells and in mice involves scavenger receptor class B type I but not Niemann-Pick C1-like 1. (2008). https://pubmed.ncbi.nlm.nih.gov/18641187/ DOI: 10.1093/jn/138.8.1432
tissue_or_cell_type
Intestinal epithelium and plasma
Lycopene: absorption, metabolism, nutrient connections and human outcomes (2026-09-17) · lines 117–128
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Transporter inhibition in Caco-2 cells; intestinal SR-BI transgenic mice · source_derived_draft · unverified_draft
### lycopene-npc1l1-null NPC1L1 antibody and ezetimibe did not significantly reduce all-E or 5Z lycopene uptake in Caco-2 cells. Condition category: normal nutrient_topic: Lycopene research collection; topical membership is not evidence of a direct dietary effect. plain_language: A transporter used by other lipids was not necessary in this particular assay. organism: Human Caco-2 cells tissue_or_cell_type: Intestinal epithelium and plasma experimental_model: Transporter inhibition in Caco-2 cells; intestinal SR-BI transgenic mice limitations: Partial uptake inhibition is not proof of a sole transporter. Ezetimibe result is a cell assay, not a clinical drug-interaction trial. exposure: All-E and 5Z lycopene; mice received 0.25 g/kg diet for one month evidence_span: {"source_cache": "artifacts/lycopene-research/18641187.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "7c71fd4fd3be9d14176bceb3c2104143269a788587feec232350a6f1c5913e3d", "start_char": 0, "end_char": 1557, "text_sha256": "7c71fd4fd3be9d14176bceb3c2104143269a788587feec232350a6f1c5913e3d"} [lycopene-p18641187] Lycopene absorption in human intestinal cells and in mice involves scavenger receptor class B type I but not Niemann-Pick C1-like 1. (2008). https://pubmed.ncbi.nlm.nih.gov/18641187/ DOI: 10.1093/jn/138.8.1432
Complete structured claim and evidence
Purified human BCO1 cleaved all-trans-beta-carotene centrally to all-trans-retinal.
Beta-carotene oxygenase 1 / BCO1 → All-trans-retinal source_derived_draftungraded
Experimental context and source evidence
evidence_location
Figure 3
experimental_model
Purified human BCO1 expressed in E. coli; substrate incubations and HPLC.
exposure
20 micromolar beta-carotene, 500 ng enzyme/200 microliters, 37 C, 15 minutes.
limitations
Purified-enzyme rates do not determine dietary conversion efficiency.
nutrient_topic
Vitamin A research collection; topical membership is not evidence of a direct dietary effect. · Vitamin A
organism
Homo sapiens protein expressed in Escherichia coli
outcome
Purified human BCO1 cleaved all-trans-beta-carotene centrally to all-trans-retinal.
plain_language
BCO1 turns a carotenoid precursor into retinal.
primary_references
[va-delasena-2013] Substrate specificity of purified recombinant human beta-carotene 15,15'-oxygenase (BCO1) (2013). https://pubmed.ncbi.nlm.nih.gov/24187135/ DOI: 10.1074/jbc.M113.507160
tissue_or_cell_type
Cell-free enzyme
Vitamin A: forms, mechanisms, deficiency and excess (2026-09-17) · lines 131–143
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Purified human BCO1 expressed in E. coli; substrate incubations and HPLC. · source_derived_draft · unverified_draft
### va-bco1-central-cleavage Purified human BCO1 cleaved all-trans-beta-carotene centrally to all-trans-retinal. Condition category: normal nutrient_topic: Vitamin A research collection; topical membership is not evidence of a direct dietary effect. plain_language: BCO1 turns a carotenoid precursor into retinal. organism: Homo sapiens protein expressed in Escherichia coli tissue_or_cell_type: Cell-free enzyme experimental_model: Purified human BCO1 expressed in E. coli; substrate incubations and HPLC. limitations: Purified-enzyme rates do not determine dietary conversion efficiency. exposure: 20 micromolar beta-carotene, 500 ng enzyme/200 microliters, 37 C, 15 minutes. outcome: Purified human BCO1 cleaved all-trans-beta-carotene centrally to all-trans-retinal. evidence_location: Figure 3 [va-delasena-2013] Substrate specificity of purified recombinant human beta-carotene 15,15'-oxygenase (BCO1) (2013). https://pubmed.ncbi.nlm.nih.gov/24187135/ DOI: 10.1074/jbc.M113.507160
Complete structured claim and evidence

Availability and dependencies

Each situation shows the normal role first, then what the sources report under a specific condition. A shortfall in the diet, a fault in the machinery, and a low blood reading are kept separate because they are not the same thing.

Blocking RPE65 reduces meso-zeaxanthin formation

Condition: machinery_impairment · Pharmacological RPE65 inhibition during chicken eye development

Normal role: RPE65 supports lutein isomerization.

Recorded consequence: Less meso-zeaxanthin formation

Scope: Chicken developmental experiment; not established human lutein deficiency

Low HDL can block retinal delivery despite higher intake

Condition: machinery_impairment · WHAM ABCA1 mutation with severe HDL reduction

Normal role: Lipoproteins participate in tissue lutein delivery.

Recorded consequence: Retinal lutein remains low despite increased dietary supply

Scope: Chicken model plus separately scoped mouse protein experiment; not a human treatment threshold

Absent dietary xanthophylls reduce foveal protection

Condition: nutrient_deficiency · Lifelong xanthophyll-free diet

Normal role: Macular xanthophylls contribute to regional photoprotection.

Recorded consequence: Absent macular pigment and lost relative foveal protection in laser challenge

Scope: Rhesus depletion experiment; no human diagnostic cutoff

A blocked SR-BI tunnel loses selective uptake

Condition: machinery_impairment · C384Y tunnel-blocking mutation

Normal role: SR-BI supports preferential xanthophyll uptake in the expression system.

Recorded consequence: Loss of the observed uptake advantage

Scope: Engineered human HEK293 cells; not a dietary lutein shortage

Lowest dietary intake subgroup had a different cataract estimate

Condition: biomarker_context · Lowest quintile of reported dietary L+Z

Normal role: Lutein/zeaxanthin intake varies among participants.

Recorded consequence: Lower cataract-surgery estimate in this subgroup

Scope: AREDS2 secondary analysis; low reported intake is not proven tissue deficiency

The sources

Every document behind this chapter is preserved word for word. Open one to read it in full with its recorded conflicts marked in place.

Lutein: metabolism, signaling and nutrient connections (2026-09-17)AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · unverified_draftRead preserved source
Lycopene: absorption, metabolism, nutrient connections and human outcomes (2026-09-17)AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · unverified_draftRead preserved source
Pectin: metabolism, signaling and nutrient connections (2026-09-17)AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · unverified_draftRead preserved source
Vitamin A: forms, mechanisms, deficiency and excess (2026-09-17)AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · unverified_draftRead preserved source
Vitamin D2 and D3: mechanisms, deficiency and nutrient interactions (2026-09-17)AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · unverified_draftRead preserved source
Vitamin E: transport, membrane protection and nutrient interactions (2026-09-17)AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · unverified_draftRead preserved source

Recorded disagreements

Where two sources say different things, both are kept and the difference is explained. You can discuss a disagreement or propose a mechanism that might account for it.

Is human BCO2 inactive, or does its preparation conceal activity?The 2014 paper interpreted absent activity as human BCO2 inactivity explaining macular pigment retention. Later primary papers explicitly challenged that general conclusion and demonstrated activity after changes to targeting-sequence processing, expression and assay conditions. This is a published mechanistic disagreement, not a correction to ledger prose.Read the recorded disagreement

Open questions in this collection

Questions the curators could not answer from the sources in front of them, kept here with the reason each one is still open. These are gaps in this collection, not findings or proof that no one has studied them.

How much lutein does each processed human BCO2 isoform cleave in living retinal cells?Recombinant competence and regional protein abundance do not measure physiological substrate flux.
Which Aster family members and partner stoichiometries control lutein delivery to BCO2 in each retinal cell type?The indexed 2025 evidence does not resolve every member; a family node is retained rather than guessing a gene.
Which effects in combined L+Z and AREDS formulas belong to lutein alone?Component coadministration and background nutrients prevent simple single-ingredient attribution.
Do selected cognitive-task improvements translate into reliable clinical cognitive benefit?Small task-specific studies and the larger AREDS2 null finding use different populations, measurements and analyses; neither proves dementia prevention.
How much do transport competition and meal composition change long-term retinal delivery in people?Post-meal AUC, cultured-cell uptake and macular pigment are different endpoints; no universal spacing rule follows.
Does vitamin A status alter human lutein delivery through ISX–SCARB1 regulation?The graph connects existing regulatory and uptake experiments; a combined clinical causal effect is not established.
What lutein tissue concentration is sufficient for each human retinal function?Animal depletion, plasma measures and macular optical density do not establish one clinical deficiency cutoff.

Chapters are assembled from supplied drafts and curated literature summaries. Statements remain unverified against the primary studies, and the ledger is not medical advice.

Evidence, AI assistance and curation standards

Lutein

The mechanisms

Recombinant human StARD3 bound lutein selectively, with dissociation constant 0.45 micromolar.

SR-BI antibody and BLT1 reduced lutein transport by approximately 30% and 57%, respectively.

Overexpressed human RPE65 supported conversion of lutein into meso-zeaxanthin in cultured cells.

High-lutein feeding left WHAM retinal lutein near 6% of controls despite increases in plasma, liver and heart.

Co-incubated lutein reduced alpha-tocopherol uptake in Caco-2 TC-7 cells.

Removing the mitochondrial targeting sequence improved human BCO2a solubility and enabled carotenoid-cleavage activity.

Primary L+Z versus placebo comparison gave HR 0.90 (98.7% CI 0.76–1.07; P=0.12).

Exploratory L+Z versus beta-carotene comparison gave late-AMD HR 0.82 (95% CI 0.69–0.96).

L+Z improved photostress recovery time versus placebo.

L+Z produced no significant difference in yearly cognitive composite change: 0.03 (99% CI −0.14 to 0.19; P=0.66).

The study distinguishes GSTP1-associated zeaxanthin binding from StARD3-associated lutein binding.

Chicken RPE65 overexpression supported meso-zeaxanthin production from lutein.

RPE65 inhibition reduced meso-zeaxanthin biosynthesis during chicken eye development.

Mouse RPE65 supported lutein isomerization in cultured cells despite mice not normally concentrating meso-zeaxanthin in the eye.

RPE65 E148Q substitution did not reduce meso-zeaxanthin yield in the reported cultured-cell experiments.

Lutein quenched singlet oxygen in the solution assay comparing individual macular carotenoids and mixtures.

The equal-ratio meso-zeaxanthin, zeaxanthin and lutein mixture quenched more singlet oxygen than each individual pigment at the same total concentration.

Lutein protected cells against hydroxyl-radical challenge across the oxygen concentrations tested.

The 2014 expression assay detected zeaxanthin cleavage by mouse BCO2 but not human BCO2.

Human BCO2 binding to tested macular carotenoids was 10–40-fold weaker than mouse BCO2 in the 2014 comparison.

The BCO2a targeting sequence directed a reporter to mitochondria in ARPE-19 cells; this experiment establishes mitochondrial import, not precise membrane topology.

Human BCO2 associated with the inner mitochondrial membrane in cell-line experiments.

Expression temperature and detergent choice affected recombinant BCO2 binding and xanthophyll turnover, including meso-zeaxanthin.

Human donor retina had higher BCO2 protein expression peripherally than centrally.

Activity assays indicated interaction between BCO2 and intracellular carotenoid-transporting Aster proteins.

WHAM chickens with ABCA1 E89K had over 90% lower plasma HDL.

The analogous mouse ABCA1 E89K substitution impaired intracellular trafficking, leaving little transporter at the cell surface.

WHAM chicks had retinal lutein around 6% of control levels.

High-lutein feeding increased plasma lutein greatly in WHAM chicks.

Lifelong xanthophyll-free animals had no detectable macular pigment.

The foveal protection observed in controls was absent in xanthophyll-free animals.

Lutein or zeaxanthin supplementation restored foveal protection after deprivation.

Low n-3 intake increased parafoveal damage sensitivity relative to adequate n-3 intake.

Co-incubated beta-carotene reduced lutein absorption by approximately 20% in this cell model.

Lycopene did not significantly reduce lutein uptake in the same mixed-micelle assay.

Ezetimibe-sensitive lutein uptake supported a contribution from NPC1L1 in Caco-2 cells.

Ezetimibe reduced lutein accumulation by up to 40% in Caco-2 monolayers.

Adding lutein reduced the postprandial beta-carotene response, more strongly when lutein predominated.

The retinyl-ester response suggested no apparent inhibition of beta-carotene cleavage despite reduced absorption.

Lutein rose 207% with the high-fat spread versus 88% with the low-fat spread during lutein-ester supplementation.

The high-egg salad meal increased lutein/zeaxanthin lipoprotein AUC about four- to fivefold versus salad without egg.

The high-lutein/zeaxanthin diet increased circulating xanthophylls approximately two- to threefold in both groups.

After the high-xanthophyll diet, HDL carried 52% of measured plasma lutein; LDL carried approximately 22%.

LDL delivery produced the greatest lutein uptake in the tested ARPE-19 system.

HDL most effectively delivered zeaxanthin and meso-zeaxanthin; SR-BI inhibition suppressed zeaxanthin delivery.

This ARPE-19 delivery experiment detected no lutein conversion to meso-zeaxanthin.

SR-BI expression increased lutein and zeaxanthin uptake preferentially over beta-carotene.

Hepatic lipase increased carotenoid uptake in HDL-treated SR-BI-expressing cells, favoring lutein/zeaxanthin over beta-carotene.

Adding HDL reduced cellular lutein in the HEK293 assay despite preferential retention relative to beta-carotene.

SR-BI C384Y abolished the preferential lutein/zeaxanthin uptake effect observed with wild-type receptor.

Lung cancers occurred in 2.0% with beta-carotene versus 0.9% without, predominantly among former smokers.

The corresponding neovascular-AMD HR was 0.78 (95% CI 0.64–0.94).

Central geographic atrophy HR was 0.94 (95% CI 0.70–1.26), without a significant difference.

Ten-year analysis by original L+Z assignment gave late-AMD HR 0.91 (95% CI 0.84–0.99).

L+Z assignment had lung-cancer OR 1.15 (95% CI 0.79–1.66), without a significant increase.

Overall cataract-surgery HR was 0.96 (95% CI 0.84–1.10; P=0.54).

In the lowest dietary L+Z quintile, cataract-surgery HR was 0.68 (95% CI 0.48–0.96; P=0.03).

L+Z increased macular pigment optical density versus placebo at all measured eccentricities.

L+Z improved the tested chromatic-contrast threshold versus placebo.

Glare disability did not improve significantly in the treated group despite correlation with pigment density.

The young-adult trial reported improved visual memory associated with supplementation.

Attention and reasoning improvements were observed in analyses requiring significant macular-pigment increases.

Lutein AUC was reduced with the tested fibers, including pectin.

FeSO4 restored chelator-inhibited RPE65 isomerohydrolase activity in bovine microsomes and recombinant assays; ferric salts did not.

Recombinant RPE65 catalyzed conversion of all-trans-retinyl esters to 11-cis-retinol in visual-cycle reconstitution.

ZnCl2 did not restore isomerohydrolase activity after metal chelation in the bovine RPE assay, whereas FeSO4 did.

Retinoic-acid receptor signaling increased intestinal ISX expression.

ISX bound upstream SCARB1 regulatory motifs and repressed intestinal SCARB1 expression.

Blocking SR-BI with an extracellular antibody or BLT1 reduced RRR-alpha-tocopherol uptake by human Caco-2 TC7 cells.

Human NPC1L1 overexpression increased alpha-tocopherol uptake, which was inhibited by ezetimibe.

Expression of NPC1L1 in HEK cells increased cholecalciferol uptake, and its corresponding inhibitor reduced this uptake.

Expression of SR-BI in HEK cells increased cholecalciferol uptake, and its corresponding inhibitor reduced this uptake.

SR-BI antibody or BLT1 inhibited all-E and 5Z lycopene uptake by up to 60% in Caco-2 monolayers.

NPC1L1 antibody and ezetimibe did not significantly reduce all-E or 5Z lycopene uptake in Caco-2 cells.

Purified human BCO1 cleaved all-trans-beta-carotene centrally to all-trans-retinal.

Availability and dependencies

The sources

Recorded disagreements