IL6

availability_state

biomarker_context Imported condition classification; unverified.

evidence_span

{"source_cache": "artifacts/iron-research/15124018.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "f2ed307ef57c255917685bb7bfb1f02f3a6481c732cc2ee41ad1f338e2a2a830", "start_char": 0, "end_char": 578, "text_sha256": "f2ed307ef57c255917685bb7bfb1f02f3a6481c732cc2ee41ad1f338e2a2a830"}

experimental_model

Human liver-cell, mouse and human-volunteer inflammation experiments

exposure

IL-6 and inflammatory stimulation

limitations

IL-6 dependence applies to the tested inflammatory models, not every possible inflammatory iron pathway.

nutrient_topic

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

organism

Humans and mice

plain_language

Inflammation can turn up the hormone that restricts iron release.

primary_references

[iron-p15124018] IL-6 mediates hypoferremia of inflammation by inducing the synthesis of the iron regulatory hormone hepcidin. (2004). https://pubmed.ncbi.nlm.nih.gov/15124018/ DOI: 10.1172/jci20945

tissue_or_cell_type

Liver and circulation

trigger_kind

biomarker_context Imported condition classification; unverified.

Iron: absorption, trafficking, iron-dependent enzymes and nutrient interactions (2026-09-17) · lines 875–886

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Human liver-cell, mouse and human-volunteer inflammation experiments · source_derived_draft · unverified_draft

### iron-il6-hepcidin IL-6 induced hepcidin in the tested human liver-cell, mouse and volunteer systems. Condition category: biomarker_context nutrient_topic: Iron research collection; topical membership is not evidence of a direct dietary effect. plain_language: Inflammation can turn up the hormone that restricts iron release. organism: Humans and mice tissue_or_cell_type: Liver and circulation experimental_model: Human liver-cell, mouse and human-volunteer inflammation experiments limitations: IL-6 dependence applies to the tested inflammatory models, not every possible inflammatory iron pathway. exposure: IL-6 and inflammatory stimulation evidence_span: {"source_cache": "artifacts/iron-research/15124018.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "f2ed307ef57c255917685bb7bfb1f02f3a6481c732cc2ee41ad1f338e2a2a830", "start_char": 0, "end_char": 578, "text_sha256": "f2ed307ef57c255917685bb7bfb1f02f3a6481c732cc2ee41ad1f338e2a2a830"} [iron-p15124018] IL-6 mediates hypoferremia of inflammation by inducing the synthesis of the iron regulatory hormone hepcidin. (2004). https://pubmed.ncbi.nlm.nih.gov/15124018/ DOI: 10.1172/jci20945

cell_type

Hepatocytes

experimental_model

Human hepatocyte cultures

limitations

Adaptive withholding untested; acute illness can coexist with true deficiency.

organism

Homo sapiens

Selenium: literature corrections and mechanism additions · lines 1408–1418

Metabolic Ledger literature curation, 17 September 2026; primary papers linked individually · supports · Human hepatocyte cultures · secondary_verified · secondary_verified

## il6-selenop Inflammation can reduce selenium-carrier production independently of intake. IL-6 lowers hepatic SELENOP expression and secretion in human hepatocyte cultures. Organism: Homo sapiens Cell type: Hepatocytes Experimental model: Human hepatocyte cultures Limitations: Adaptive withholding untested; acute illness can coexist with true deficiency. Primary reference: [Gene-specific regulation of hepatic selenoprotein expression by interleukin-6](https://pubs.rsc.org/en/content/articlelanding/2015/mt/c5mt00211g)

cross_nutrient

Folic acid was given to both arms; no biochemical B6–folate synergy established.

experimental_model

Single-blind randomized cointervention in 35 RA patients: 15 control and 20 B6.

exposure

Both groups folic acid 5 mg/day; B6 group also 100 mg/day for 12 weeks. Reported cytokine result is within-group change.

limitations

The accessed abstract reports within-group significance, not a demonstrated between-group change contrast. Plasma concentration differs from cytokine production; no automatic contradiction with 2005.

nutrient_topic

Vitamin B6 research collection; topical membership is not evidence of a direct dietary effect. · Vitamin B6

organism

Homo sapiens

plain_language

A different trial found a cytokine signal under a different exposure and measurement design.

primary_references

[b6-huang2010] Vitamin B(6) supplementation improves pro-inflammatory responses in patients with rheumatoid arthritis (2010). https://pubmed.ncbi.nlm.nih.gov/20571496/ DOI: 10.1038/ejcn.2010.107

tissue_or_cell_type

Human blood and whole-body measurements

Vitamin B6: mechanisms, deficiency and nutrient interactions (2026-09-17) · lines 1510–1521

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Single-blind randomized cointervention in 35 RA patients: 15 control and 20 B6. · source_derived_draft · unverified_draft

### b6-ra-cointervention-cytokine-signal In the 2010 cointervention trial, plasma IL-6 and TNF declined within the B6-plus-folic-acid group over 12 weeks. Condition category: normal nutrient_topic: Vitamin B6 research collection; topical membership is not evidence of a direct dietary effect. plain_language: A different trial found a cytokine signal under a different exposure and measurement design. organism: Homo sapiens tissue_or_cell_type: Human blood and whole-body measurements experimental_model: Single-blind randomized cointervention in 35 RA patients: 15 control and 20 B6. limitations: The accessed abstract reports within-group significance, not a demonstrated between-group change contrast. Plasma concentration differs from cytokine production; no automatic contradiction with 2005. exposure: Both groups folic acid 5 mg/day; B6 group also 100 mg/day for 12 weeks. Reported cytokine result is within-group change. cross_nutrient: Folic acid was given to both arms; no biochemical B6–folate synergy established. [b6-huang2010] Vitamin B(6) supplementation improves pro-inflammatory responses in patients with rheumatoid arthritis (2010). https://pubmed.ncbi.nlm.nih.gov/20571496/ DOI: 10.1038/ejcn.2010.107

availability_state

biomarker_context Imported condition classification; unverified.

experimental_model

Double-blind randomized placebo-controlled RA trial: 36 recruited, 33 baseline completers, 28 low-PLP patients eligible for supplementation.

exposure

Pyridoxine hydrochloride 50 mg/day or placebo for 30 days; historical trial exposure, not a regimen recommendation.

limitations

Small short trial; a null finding is not proof that no population can respond. The CRP/ESR/RF table-versus-narrative reporting ambiguity is retained separately as an open question.

nutrient_topic

Vitamin B6 research collection; topical membership is not evidence of a direct dietary effect. · Vitamin B6

organism

Homo sapiens

plain_language

Correcting the vitamin measurements did not resolve the measured inflammation.

primary_references

[b6-chiang2005-trial] Pyridoxine supplementation corrects vitamin B6 deficiency but does not improve inflammation in patients with rheumatoid arthritis (2005). https://pubmed.ncbi.nlm.nih.gov/16277693/ DOI: 10.1186/ar1839

tissue_or_cell_type

Human blood and whole-body measurements

trigger_kind

biomarker_context Imported condition classification; unverified.

Vitamin B6: mechanisms, deficiency and nutrient interactions (2026-09-17) · lines 1485–1495

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Double-blind randomized placebo-controlled RA trial: 36 recruited, 33 baseline completers, 28 low-PLP patients eligible for supplementation. · source_derived_draft · unverified_draft

### b6-ra-no-cytokine-suppression The 2005 trial found no suppression of IL-6 or TNF production despite improved B6 markers. Condition category: biomarker_context nutrient_topic: Vitamin B6 research collection; topical membership is not evidence of a direct dietary effect. plain_language: Correcting the vitamin measurements did not resolve the measured inflammation. organism: Homo sapiens tissue_or_cell_type: Human blood and whole-body measurements experimental_model: Double-blind randomized placebo-controlled RA trial: 36 recruited, 33 baseline completers, 28 low-PLP patients eligible for supplementation. limitations: Small short trial; a null finding is not proof that no population can respond. The CRP/ESR/RF table-versus-narrative reporting ambiguity is retained separately as an open question. exposure: Pyridoxine hydrochloride 50 mg/day or placebo for 30 days; historical trial exposure, not a regimen recommendation. [b6-chiang2005-trial] Pyridoxine supplementation corrects vitamin B6 deficiency but does not improve inflammation in patients with rheumatoid arthritis (2005). https://pubmed.ncbi.nlm.nih.gov/16277693/ DOI: 10.1186/ar1839

evidence_access

Primary abstract

experimental_model

Human respiratory epithelial-cell exposure to Suwannee River/Nordic reference fulvic fractions; comparison with smoke water-soluble fractions.

limitations

Abstract access; exposure concentration and duration require full-method verification. Increased iron import is consistent with compensatory iron stress, not direct quantification of every intracellular available-iron pool. These are airway-cell exposures, not an oral trial.

nutrient_topic

Fulvic acid collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · Fulvic acid (heterogeneous humic fraction)

plain_language

Direct airway-cell exposure stimulated inflammatory mediators.

primary_references

A Fulvic Acid-like Substance Participates in the Pro-inflammatory Effects of Cigarette Smoke and Wood Smoke Particles. · 2020 · https://pubmed.ncbi.nlm.nih.gov/32191033/ · DOI 10.1021/acs.chemrestox.0c00036

Fulvic acid: mixture identity, mineral chemistry, signaling and cross-nutrient mechanisms (2026-09-19) · lines 220–226

AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Human respiratory epithelial-cell exposure to Suwannee River/Nordic reference fulvic fractions; comparison with smoke water-soluble fractions. · source_derived_draft · unverified_draft

## fulvic-acid-airway-inflammation Direct airway-cell exposure stimulated inflammatory mediators. Reference fulvic fractions increased IL-6 and IL-8 release from respiratory epithelial cells. Model: Human respiratory epithelial-cell exposure to Suwannee River/Nordic reference fulvic fractions; comparison with smoke water-soluble fractions. Limitations: Abstract access; exposure concentration and duration require full-method verification. Increased iron import is consistent with compensatory iron stress, not direct quantification of every intracellular available-iron pool. These are airway-cell exposures, not an oral trial. Evidence access: Primary abstract A Fulvic Acid-like Substance Participates in the Pro-inflammatory Effects of Cigarette Smoke and Wood Smoke Particles. · 2020 · https://pubmed.ncbi.nlm.nih.gov/32191033/ · DOI 10.1021/acs.chemrestox.0c00036

evidence_span

{"source_cache": "artifacts/glucan-research/28736555.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "9e9388d9e8263db85cdd17df9a497d9867627097a09ff8a0d630e5733e591e54", "start_char": 0, "end_char": 1128, "text_sha256": "9e9388d9e8263db85cdd17df9a497d9867627097a09ff8a0d630e5733e591e54"}

experimental_model

Comparison of large and small beta-glucan particles on human dendritic cell cytokine output

exposure

Large against small particulate beta-glucans, with assessment of phagocytosis

limitations

Human primary cells with a size comparison. The abstract reports the cytokine differences and the role of phagocytosis and IL-1beta; it does not report an oxidase dependence, so no claim here rests on that.

nutrient_topic

Beta-glucan research collection; topical membership is not evidence of a direct clinical effect, and each preparation is recorded as its own entity with no family link joining any pair. · Beta-glucan

organism

Human

plain_language

Bigger particles pulled three inflammatory signals out of the same cells; two other signals did not care about size at all.

primary_references

[bg-p28736555] β-Glucan Size Controls Dectin-1-Mediated Immune Responses in Human Dendritic Cells by Regulating IL-1β Production. (2017). https://pubmed.ncbi.nlm.nih.gov/28736555/ DOI: 10.3389/fimmu.2017.00791

tissue_or_cell_type

Monocyte-derived dendritic cell

Beta-glucan: a structural family rather than an agent, what decides whether a bound glucan actually signals, the complement route that a cereal and a yeast preparation share, and the unequal human evidence behind each (2026-09-22) · lines 177–188

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Comparison of large and small beta-glucan particles on human dendritic cell cytokine output · source_derived_draft · unverified_draft

### bg-particle-size-sets-the-cytokines Beta-glucans differ greatly in size, structure and ability to activate effector immune responses from dendritic cells and small particulate beta-glucans are thought to be poor activators of innate immunity, and large beta-glucan-stimulated human dendritic cells generate significantly more IL-1beta, IL-6 and IL-23 compared to those stimulated with the smaller beta-glucans, while in marked contrast the secretion of TSLP and CCL22 were found to be insensitive to beta-glucan particle size, with the capacity to induce phagocytosis and the relative IL-1beta production determined by beta-glucan size regulating the composition of the cytokine milieu. Condition category: normal nutrient_topic: Beta-glucan research collection; topical membership is not evidence of a direct clinical effect, and each preparation is recorded as its own entity with no family link joining any pair. plain_language: Bigger particles pulled three inflammatory signals out of the same cells; two other signals did not care about size at all. organism: Human tissue_or_cell_type: Monocyte-derived dendritic cell experimental_model: Comparison of large and small beta-glucan particles on human dendritic cell cytokine output limitations: Human primary cells with a size comparison. The abstract reports the cytokine differences and the role of phagocytosis and IL-1beta; it does not report an oxidase dependence, so no claim here rests on that. exposure: Large against small particulate beta-glucans, with assessment of phagocytosis evidence_span: {"source_cache": "artifacts/glucan-research/28736555.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "9e9388d9e8263db85cdd17df9a497d9867627097a09ff8a0d630e5733e591e54", "start_char": 0, "end_char": 1128, "text_sha256": "9e9388d9e8263db85cdd17df9a497d9867627097a09ff8a0d630e5733e591e54"} [bg-p28736555] β-Glucan Size Controls Dectin-1-Mediated Immune Responses in Human Dendritic Cells by Regulating IL-1β Production. (2017). https://pubmed.ncbi.nlm.nih.gov/28736555/ DOI: 10.3389/fimmu.2017.00791

availability_state

nutrient_deficiency Imported condition classification; unverified.

cross_nutrient

Interleukin 4 (measured_cytokine); interleukin 6 (measured_cytokine); Interleukin 10 (measured_cytokine)

evidence_location

Indexed primary abstract.

evidence_span

{"source_cache": "artifacts/zinc-clinical-sources/beck1997.abstract.txt", "locator": "Primary indexed abstract; complete local file", "file_sha256": "f731be20460b3ded18a253c1d1595c48849db9c09ef164f8a7d03a552e5619dd", "utf8_bytes": 1106}

experimental_model

Experimental dietary zinc restriction and repletion in humans

exposure

Baseline, end of zinc restriction, and following repletion were assessed.

limitations

Indexed abstract only; no sample size, intake, duration, assay stimulus or repletion effect size is invented. Changes in selected cytokines do not quantify overall infection risk.

nutrient_topic

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

organism

Homo sapiens

plain_language

Zinc shortage did not suppress every cytokine in the same way.

primary_references

[zn-clin-beck1997] Changes in cytokine production and T cell subpopulations in experimentally induced zinc-deficient humans. (1997). https://pubmed.ncbi.nlm.nih.gov/9227444/ DOI: 10.1152/ajpendo.1997.272.6.e1002

tissue_or_cell_type

T lymphocytes and cytokine production

trigger_kind

nutrient_deficiency Imported condition classification; unverified.

Zinc: transport, enzyme loading, deficiency and nutrient interactions (2026-09-17) · lines 1392–1405

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Experimental dietary zinc restriction and repletion in humans · source_derived_draft · unverified_draft

### zn-clin-depletion-th2-null Production of IL4, IL6 and IL10 was unchanged during the reported zinc-deficiency experiment, unlike the TH1-associated cytokines. Condition category: nutrient_deficiency nutrient_topic: Zinc research collection; topical membership is not evidence of a direct dietary effect. plain_language: Zinc shortage did not suppress every cytokine in the same way. organism: Homo sapiens tissue_or_cell_type: T lymphocytes and cytokine production experimental_model: Experimental dietary zinc restriction and repletion in humans limitations: Indexed abstract only; no sample size, intake, duration, assay stimulus or repletion effect size is invented. Changes in selected cytokines do not quantify overall infection risk. exposure: Baseline, end of zinc restriction, and following repletion were assessed. cross_nutrient: Interleukin 4 (measured_cytokine); interleukin 6 (measured_cytokine); Interleukin 10 (measured_cytokine) evidence_location: Indexed primary abstract. evidence_span: {"source_cache": "artifacts/zinc-clinical-sources/beck1997.abstract.txt", "locator": "Primary indexed abstract; complete local file", "file_sha256": "f731be20460b3ded18a253c1d1595c48849db9c09ef164f8a7d03a552e5619dd", "utf8_bytes": 1106} [zn-clin-beck1997] Changes in cytokine production and T cell subpopulations in experimentally induced zinc-deficient humans. (1997). https://pubmed.ncbi.nlm.nih.gov/9227444/ DOI: 10.1152/ajpendo.1997.272.6.e1002

evidence_access

Primary abstract

experimental_model

Human respiratory epithelial-cell exposure to Suwannee River/Nordic reference fulvic fractions; comparison with smoke water-soluble fractions.

limitations

Abstract access; exposure concentration and duration require full-method verification. Increased iron import is consistent with compensatory iron stress, not direct quantification of every intracellular available-iron pool. These are airway-cell exposures, not an oral trial. This is not a recommendation to supplement iron or proof of systemic iron deficiency.

nutrient_topic

Fulvic acid collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · Fulvic acid (heterogeneous humic fraction)

plain_language

Adding iron altered the inflammatory response in this experiment.

primary_references

A Fulvic Acid-like Substance Participates in the Pro-inflammatory Effects of Cigarette Smoke and Wood Smoke Particles. · 2020 · https://pubmed.ncbi.nlm.nih.gov/32191033/ · DOI 10.1021/acs.chemrestox.0c00036

Fulvic acid: mixture identity, mineral chemistry, signaling and cross-nutrient mechanisms (2026-09-19) · lines 228–234

AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Human respiratory epithelial-cell exposure to Suwannee River/Nordic reference fulvic fractions; comparison with smoke water-soluble fractions. · source_derived_draft · unverified_draft

## fulvic-acid-airway-iron-rescue Adding iron altered the inflammatory response in this experiment. Iron co-exposure reduced fulvic-associated IL-6/IL-8 release in the tested cells. Model: Human respiratory epithelial-cell exposure to Suwannee River/Nordic reference fulvic fractions; comparison with smoke water-soluble fractions. Limitations: Abstract access; exposure concentration and duration require full-method verification. Increased iron import is consistent with compensatory iron stress, not direct quantification of every intracellular available-iron pool. These are airway-cell exposures, not an oral trial. This is not a recommendation to supplement iron or proof of systemic iron deficiency. Evidence access: Primary abstract A Fulvic Acid-like Substance Participates in the Pro-inflammatory Effects of Cigarette Smoke and Wood Smoke Particles. · 2020 · https://pubmed.ncbi.nlm.nih.gov/32191033/ · DOI 10.1021/acs.chemrestox.0c00036

evidence_span

{"source_cache": "artifacts/cold-research/8925815.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "ca491f2f549a1e245e952978c0df82c4075622affdf114a70315c0cce8583ff4", "start_char": 0, "end_char": 1732, "text_sha256": "ca491f2f549a1e245e952978c0df82c4075622affdf114a70315c0cce8583ff4"}

experimental_model

Athletic young men given a single immersion and then repeated immersions over six weeks

exposure

14 degrees C for 1 hour, three times a week for six weeks

limitations

The authors themselves state the biological significance of the changes remains to be elucidated. Most immune measures did not change.

nutrient_topic

Cold water immersion research collection; topical membership is not evidence of a direct clinical effect, and a therapeutic exposure is not a dietary intake. · Cold water immersion

organism

Human

plain_language

Six weeks of repetition nudges a few immune markers, and leaves most untouched.

primary_references

[cold-p8925815] Immune system of cold-exposed and cold-adapted humans. (1996). https://pubmed.ncbi.nlm.nih.gov/8925815/ DOI: 10.1007/bf00242274

tissue_or_cell_type

Immune system

Cold water immersion: cold sensing, heat production, the catecholamine axis and what repeated exposure changes (2026-09-19) · lines 715–726

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Athletic young men given a single immersion and then repeated immersions over six weeks · source_derived_draft · unverified_draft

### cold-repeated-immersion-immune With immersions continued three times a week for six weeks, a small but significant increase appeared in the proportions of monocytes and of lymphocytes expressing the IL-2 receptor CD25, and in plasma tumour necrosis factor alpha, with increases in haptoglobin and haemopexin, while interleukin-1 beta, C-reactive protein, immunoglobulins, complement and total leucocyte counts showed no significant change. Condition category: normal nutrient_topic: Cold water immersion research collection; topical membership is not evidence of a direct clinical effect, and a therapeutic exposure is not a dietary intake. plain_language: Six weeks of repetition nudges a few immune markers, and leaves most untouched. organism: Human tissue_or_cell_type: Immune system experimental_model: Athletic young men given a single immersion and then repeated immersions over six weeks limitations: The authors themselves state the biological significance of the changes remains to be elucidated. Most immune measures did not change. exposure: 14 degrees C for 1 hour, three times a week for six weeks evidence_span: {"source_cache": "artifacts/cold-research/8925815.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "ca491f2f549a1e245e952978c0df82c4075622affdf114a70315c0cce8583ff4", "start_char": 0, "end_char": 1732, "text_sha256": "ca491f2f549a1e245e952978c0df82c4075622affdf114a70315c0cce8583ff4"} [cold-p8925815] Immune system of cold-exposed and cold-adapted humans. (1996). https://pubmed.ncbi.nlm.nih.gov/8925815/ DOI: 10.1007/bf00242274

evidence_span

{"source_cache": "artifacts/dihydrocapsaicin-research/36007275.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "b04a74a345c83df1454aa34ad591c7cefd04325de39cde8d5118bbea005aba3b", "start_char": 0, "end_char": 1605, "text_sha256": "b04a74a345c83df1454aa34ad591c7cefd04325de39cde8d5118bbea005aba3b"}

experimental_model

Primary human endothelial cells stimulated with tumour necrosis factor alpha, with viability, adhesion and radical scavenging assays

exposure

Dihydrocapsaicin from below 50 up to 500 micromolar, against capsaicin and vitamin C

limitations

The only head-to-head cytotoxicity comparison in this collection. Concentrations of 100 micromolar and above are far higher than any plasma level reported here.

nutrient_topic

Dihydrocapsaicin research collection; topical membership is not evidence of a direct clinical effect, and dihydrocapsaicin is recorded separately from capsaicin. · Dihydrocapsaicin

organism

Human

plain_language

Below the toxic range it calms the inflamed vessel lining and stops immune cells sticking to it.

primary_references

[dhc-p36007275] Beneficial effects of capsaicin and dihydrocapsaicin on endothelial inflammation, nitric oxide production and antioxidant activity. (2022). https://pubmed.ncbi.nlm.nih.gov/36007275/ DOI: 10.1016/j.biopha.2022.113521

tissue_or_cell_type

Vascular endothelium

Dihydrocapsaicin: the second capsaicinoid, the hypothermia it is used to induce, what the gut and liver do to it, and what it does without TRPV1 (2026-09-21) · lines 673–684

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Primary human endothelial cells stimulated with tumour necrosis factor alpha, with viability, adhesion and radical scavenging assays · source_derived_draft · unverified_draft

### dhc-endothelial-anti-inflammatory Tumour necrosis factor alpha induced Ser536 phosphorylation of p65 NF-kappa-B, expression of vascular cell adhesion molecule 1 and intercellular adhesion molecule 1, and interleukin 6 production in primary human endothelial cells, and these effects were robustly abrogated by dihydrocapsaicin, which also led to a marked reduction in tumour-necrosis-factor-mediated monocyte adhesion to endothelial cells. Condition category: normal nutrient_topic: Dihydrocapsaicin research collection; topical membership is not evidence of a direct clinical effect, and dihydrocapsaicin is recorded separately from capsaicin. plain_language: Below the toxic range it calms the inflamed vessel lining and stops immune cells sticking to it. organism: Human tissue_or_cell_type: Vascular endothelium experimental_model: Primary human endothelial cells stimulated with tumour necrosis factor alpha, with viability, adhesion and radical scavenging assays limitations: The only head-to-head cytotoxicity comparison in this collection. Concentrations of 100 micromolar and above are far higher than any plasma level reported here. exposure: Dihydrocapsaicin from below 50 up to 500 micromolar, against capsaicin and vitamin C evidence_span: {"source_cache": "artifacts/dihydrocapsaicin-research/36007275.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "b04a74a345c83df1454aa34ad591c7cefd04325de39cde8d5118bbea005aba3b", "start_char": 0, "end_char": 1605, "text_sha256": "b04a74a345c83df1454aa34ad591c7cefd04325de39cde8d5118bbea005aba3b"} [dhc-p36007275] Beneficial effects of capsaicin and dihydrocapsaicin on endothelial inflammation, nitric oxide production and antioxidant activity. (2022). https://pubmed.ncbi.nlm.nih.gov/36007275/ DOI: 10.1016/j.biopha.2022.113521

evidence_locator

Abstract

experimental_model

Mouse B-cell/dendritic-cell systems and vitamin A-deficient mice.

exposure

RA with IL-6 or IL-5

limitations

Cannot generalize to every IgA-switching pathway.

nutrient_topic

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

organism

Mus musculus

plain_language

IgA output required additional immune signals in this experiment.

primary_references

[va-mora-2006] Generation of gut-homing IgA-secreting B cells by intestinal dendritic cells (2006). https://pubmed.ncbi.nlm.nih.gov/17110582/ DOI: 10.1126/science.1132742

tissue_or_cell_type

B-cell cultures

Vitamin A: forms, mechanisms, deficiency and excess (2026-09-17) · lines 1227–1238

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Mouse B-cell/dendritic-cell systems and vitamin A-deficient mice. · source_derived_draft · unverified_draft

### va-sig-ra-cytokine-iga RA alone was insufficient for IgA secretion but cooperated with IL-6 or IL-5 to induce it. Condition category: normal nutrient_topic: Vitamin A research collection; topical membership is not evidence of a direct dietary effect. plain_language: IgA output required additional immune signals in this experiment. organism: Mus musculus tissue_or_cell_type: B-cell cultures experimental_model: Mouse B-cell/dendritic-cell systems and vitamin A-deficient mice. limitations: Cannot generalize to every IgA-switching pathway. evidence_locator: Abstract exposure: RA with IL-6 or IL-5 [va-mora-2006] Generation of gut-homing IgA-secreting B cells by intestinal dendritic cells (2006). https://pubmed.ncbi.nlm.nih.gov/17110582/ DOI: 10.1126/science.1132742

evidence_locator

Abstract

experimental_model

Mouse naive T-cell differentiation under TGF-beta and inflammatory cytokine conditions.

exposure

RA with IL-6/TGF-beta

limitations

New lineage induction differs from established intestinal Th17 effector function.

nutrient_topic

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

organism

Mus musculus

plain_language

The cytokine environment determines which T-cell differentiation program RA modifies.

primary_references

[va-mucida-2007] Reciprocal TH17 and regulatory T cell differentiation mediated by retinoic acid (2007). https://pubmed.ncbi.nlm.nih.gov/17569825/ DOI: 10.1126/science.1145697

tissue_or_cell_type

Naive T-cell cultures

Vitamin A: forms, mechanisms, deficiency and excess (2026-09-17) · lines 1266–1277

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Mouse naive T-cell differentiation under TGF-beta and inflammatory cytokine conditions. · source_derived_draft · unverified_draft

### va-sig-ra-th17-differentiation Added RA inhibited IL-6-driven Th17 induction in the tested TGF-beta context. Condition category: normal nutrient_topic: Vitamin A research collection; topical membership is not evidence of a direct dietary effect. plain_language: The cytokine environment determines which T-cell differentiation program RA modifies. organism: Mus musculus tissue_or_cell_type: Naive T-cell cultures experimental_model: Mouse naive T-cell differentiation under TGF-beta and inflammatory cytokine conditions. limitations: New lineage induction differs from established intestinal Th17 effector function. evidence_locator: Abstract exposure: RA with IL-6/TGF-beta [va-mucida-2007] Reciprocal TH17 and regulatory T cell differentiation mediated by retinoic acid (2007). https://pubmed.ncbi.nlm.nih.gov/17569825/ DOI: 10.1126/science.1145697

availability_state

biomarker_context Imported condition classification; unverified.

evidence_span

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experimental_model

Human liver-cell, mouse and human-volunteer inflammation experiments

exposure

IL-6 and inflammatory stimulation

limitations

IL-6 dependence applies to the tested inflammatory models, not every possible inflammatory iron pathway.

nutrient_topic

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

organism

Humans and mice

plain_language

Low blood iron during inflammation is a distribution response, not by itself proof of low total-body stores.

primary_references

[iron-p15124018] IL-6 mediates hypoferremia of inflammation by inducing the synthesis of the iron regulatory hormone hepcidin. (2004). https://pubmed.ncbi.nlm.nih.gov/15124018/ DOI: 10.1172/jci20945

tissue_or_cell_type

Liver and circulation

trigger_kind

biomarker_context Imported condition classification; unverified.

Iron: absorption, trafficking, iron-dependent enzymes and nutrient interactions (2026-09-17) · lines 888–899

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Human liver-cell, mouse and human-volunteer inflammation experiments · source_derived_draft · unverified_draft

### iron-inflammatory-low-serum The IL-6–hepcidin axis mediated inflammation-associated hypoferremia in the studied systems. Condition category: biomarker_context nutrient_topic: Iron research collection; topical membership is not evidence of a direct dietary effect. plain_language: Low blood iron during inflammation is a distribution response, not by itself proof of low total-body stores. organism: Humans and mice tissue_or_cell_type: Liver and circulation experimental_model: Human liver-cell, mouse and human-volunteer inflammation experiments limitations: IL-6 dependence applies to the tested inflammatory models, not every possible inflammatory iron pathway. exposure: IL-6 and inflammatory stimulation evidence_span: {"source_cache": "artifacts/iron-research/15124018.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "f2ed307ef57c255917685bb7bfb1f02f3a6481c732cc2ee41ad1f338e2a2a830", "start_char": 0, "end_char": 578, "text_sha256": "f2ed307ef57c255917685bb7bfb1f02f3a6481c732cc2ee41ad1f338e2a2a830"} [iron-p15124018] IL-6 mediates hypoferremia of inflammation by inducing the synthesis of the iron regulatory hormone hepcidin. (2004). https://pubmed.ncbi.nlm.nih.gov/15124018/ DOI: 10.1172/jci20945

evidence_access

Primary abstract

experimental_model

Human adipocytes, stromal-vascular cells and adipose explants.

limitations

Culture concentrations and cell mixtures limit extrapolation.

nutrient_topic

CLA collection; isomer, preparation, species, exposure and manipulation remain explicit. · Conjugated linoleic acid / CLA isomer family

plain_language

The response could signal to neighboring cells.

primary_references

Conjugated linoleic acid promotes human adipocyte insulin resistance through NFkappaB-dependent cytokine production. · 2005 · https://pubmed.ncbi.nlm.nih.gov/16155293/ · DOI 10.1074/jbc.M508159200

Conjugated linoleic acid: isomers, signaling, nutrient interactions and discovery (2026-09-19) · lines 134–140

AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Human adipocytes, stromal-vascular cells and adipose explants. · source_derived_draft · unverified_draft

## cla-cytokines The response could signal to neighboring cells. CLA treatment increased IL-6 and IL-8 secretion from the human adipose culture systems. Model: Human adipocytes, stromal-vascular cells and adipose explants. Limitations: Culture concentrations and cell mixtures limit extrapolation. Evidence access: Primary abstract Conjugated linoleic acid promotes human adipocyte insulin resistance through NFkappaB-dependent cytokine production. · 2005 · https://pubmed.ncbi.nlm.nih.gov/16155293/ · DOI 10.1074/jbc.M508159200

evidence_span

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experimental_model

Mendelian randomisation meta-analysis of 56 studies and 261,991 individuals

exposure

The ADH1B rs1229984 variant as an instrument for alcohol exposure

limitations

Genetic instrument design, which avoids the confounding and reverse causation of consumption questionnaires. It cannot speak to drinking patterns the variant does not affect.

nutrient_topic

Alcohol research collection; topical membership is not evidence of a direct clinical effect, and ethanol is recorded separately from the acetaldehyde it becomes. · Ethanol

organism

Human

plain_language

The gene variant that makes people drink less also gives them less heart disease, including among light drinkers.

primary_references

[alcohol-p25011450] Association between alcohol and cardiovascular disease: Mendelian randomisation analysis based on individual participant data. (2014). https://pubmed.ncbi.nlm.nih.gov/25011450/ DOI: 10.1136/bmj.g4164

tissue_or_cell_type

Cardiovascular system

Alcohol: ethanol clearance, acetaldehyde, the channels it binds, organ injury and nutrient collisions (2026-09-21) · lines 566–577

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Mendelian randomisation meta-analysis of 56 studies and 261,991 individuals · source_derived_draft · unverified_draft

### alcohol-mendelian-cardiovascular Carriers of the ADH1B rs1229984 A-allele consumed 17.2% fewer units per week, had lower systolic blood pressure, interleukin-6, waist circumference and body mass index, and had lower odds of coronary heart disease (odds ratio 0.90), with the protective association the same across all categories of alcohol consumption. Condition category: normal nutrient_topic: Alcohol research collection; topical membership is not evidence of a direct clinical effect, and ethanol is recorded separately from the acetaldehyde it becomes. plain_language: The gene variant that makes people drink less also gives them less heart disease, including among light drinkers. organism: Human tissue_or_cell_type: Cardiovascular system experimental_model: Mendelian randomisation meta-analysis of 56 studies and 261,991 individuals limitations: Genetic instrument design, which avoids the confounding and reverse causation of consumption questionnaires. It cannot speak to drinking patterns the variant does not affect. exposure: The ADH1B rs1229984 variant as an instrument for alcohol exposure evidence_span: {"source_cache": "artifacts/alcohol-research/25011450.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "d8f5f9f8c57fc5e32e827d8db1f212ebb427553d9b9f59db611a622bd99c4a10", "start_char": 0, "end_char": 1978, "text_sha256": "d8f5f9f8c57fc5e32e827d8db1f212ebb427553d9b9f59db611a622bd99c4a10"} [alcohol-p25011450] Association between alcohol and cardiovascular disease: Mendelian randomisation analysis based on individual participant data. (2014). https://pubmed.ncbi.nlm.nih.gov/25011450/ DOI: 10.1136/bmj.g4164