Tumor necrosis factor

evidence_access

Primary abstract

experimental_model

Substance-P or IgE/anti-IgE mast-cell experiments.

limitations

Not a clinical comparison of oral treatments.

nutrient_topic

Luteolin collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Luteolin / 3′,4′,5,7-tetrahydroxyflavone

plain_language

It affected another mediator besides histamine.

primary_references

The novel flavone tetramethoxyluteolin is a potent inhibitor of human mast cells. · 2015 · https://pubmed.ncbi.nlm.nih.gov/25498791/ · DOI 10.1016/j.jaci.2014.10.032

Luteolin: metabolism, immune signaling, redox chemistry and cross-nutrient mechanisms (2026-09-19) · lines 396–402

AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Substance-P or IgE/anti-IgE mast-cell experiments. · source_derived_draft · unverified_draft

## luteolin-mast-tnf It affected another mediator besides histamine. Luteolin inhibited preformed TNF secretion from activated human LAD2 mast cells. Model: Substance-P or IgE/anti-IgE mast-cell experiments. Limitations: Not a clinical comparison of oral treatments. Evidence access: Primary abstract The novel flavone tetramethoxyluteolin is a potent inhibitor of human mast cells. · 2015 · https://pubmed.ncbi.nlm.nih.gov/25498791/ · DOI 10.1016/j.jaci.2014.10.032

evidence_span

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experimental_model

Dectin-1 and Toll-like receptor co-expression with phagosome recruitment and cytokine measurement

exposure

Beta-glucan-containing zymosan particles on cells expressing dectin-1 with and without Toll-like receptor signalling

limitations

The particle is zymosan, which carries mannan and other yeast wall components as well as glucan, so a response to zymosan is not by itself a response to purified beta-glucan.

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

Mouse

plain_language

The glucan receptor does not work alone; paired with a bacterial sensor the same particle produces far more than either would.

primary_references

[bg-p12719479] Collaborative induction of inflammatory responses by dectin-1 and Toll-like receptor 2. (2003). https://pubmed.ncbi.nlm.nih.gov/12719479/ DOI: 10.1084/jem.20021787

tissue_or_cell_type

Macrophage and 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 190–201

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Dectin-1 and Toll-like receptor co-expression with phagosome recruitment and cytokine measurement · source_derived_draft · unverified_draft

### bg-dectin1-works-with-tlr2 Dectin-1 is recruited to phagosomes containing zymosan particles but not to phagosomes containing immunoglobulin G-opsonised particles, dectin-1 expression enhances Toll-like receptor-mediated activation of nuclear factor kappa B by beta-glucan-containing particles, and in macrophages and dendritic cells dectin-1 and Toll-like receptors are synergistic in mediating production of cytokines such as interleukin 12 and tumour necrosis factor alpha, while dectin-1 triggers production of reactive oxygen species, an inflammatory response that is primed by Toll-like receptor activation. 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: The glucan receptor does not work alone; paired with a bacterial sensor the same particle produces far more than either would. organism: Mouse tissue_or_cell_type: Macrophage and dendritic cell experimental_model: Dectin-1 and Toll-like receptor co-expression with phagosome recruitment and cytokine measurement limitations: The particle is zymosan, which carries mannan and other yeast wall components as well as glucan, so a response to zymosan is not by itself a response to purified beta-glucan. exposure: Beta-glucan-containing zymosan particles on cells expressing dectin-1 with and without Toll-like receptor signalling evidence_span: {"source_cache": "artifacts/glucan-research/12719479.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "297eb222223ff6861d6890a273716f4cfb3f3c14f887c57c057c2af524f8b425", "start_char": 0, "end_char": 1588, "text_sha256": "297eb222223ff6861d6890a273716f4cfb3f3c14f887c57c057c2af524f8b425"} [bg-p12719479] Collaborative induction of inflammatory responses by dectin-1 and Toll-like receptor 2. (2003). https://pubmed.ncbi.nlm.nih.gov/12719479/ DOI: 10.1084/jem.20021787

evidence_span

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experimental_model

Neoglycolipid oligosaccharide microarrays built from three glucan polysaccharides and screened against 187 sequence-defined probes

exposure

Dectin-1 binding to oligosaccharide probes generated from a soluble yeast glucan, curdlan and pustulan

limitations

A binding assignment on arrayed probes rather than on a cell surface. The clustered-ligand test uses liposomes and a Dectin-1-expressing cell line.

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

Recombinant protein and a macrophage cell line

plain_language

The receptor reads only one linkage, needs a run of about ten sugars to grip at all, and needs them clustered to fire.

primary_references

[bg-p16371356] Ligands for the beta-glucan receptor, Dectin-1, assigned using "designer" microarrays of oligosaccharide probes (neoglycolipids) generated from glucan polysaccharides. (2006). https://pubmed.ncbi.nlm.nih.gov/16371356/ DOI: 10.1074/jbc.m511461200

tissue_or_cell_type

Cell-free microarray and cultured cells

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 125–136

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Neoglycolipid oligosaccharide microarrays built from three glucan polysaccharides and screened against 187 sequence-defined probes · source_derived_draft · unverified_draft

### bg-only-beta-1-3-oligomers-bind Dectin-1 lacks residues involved in calcium ligation that mediates carbohydrate-binding by classical C-type lectins, and among 187 diverse sequence-defined oligosaccharide probes together with designer microarrays from a neutral soluble glucan from S. cerevisiae, curdlan from Alcaligenes faecalis and pustulan from Umbilicaria papullosa, Dectin-1 binding is detected exclusively to 1,3-linked glucose oligomers, the minimum length required for detectable binding being a 10- or 11-mer, and 11-13 gluco-oligomers in clustered form displayed on liposomes mimic the macromolecular beta-glucans and compete with zymosan binding and triggering of tumour necrosis factor alpha secretion. 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: The receptor reads only one linkage, needs a run of about ten sugars to grip at all, and needs them clustered to fire. organism: Recombinant protein and a macrophage cell line tissue_or_cell_type: Cell-free microarray and cultured cells experimental_model: Neoglycolipid oligosaccharide microarrays built from three glucan polysaccharides and screened against 187 sequence-defined probes limitations: A binding assignment on arrayed probes rather than on a cell surface. The clustered-ligand test uses liposomes and a Dectin-1-expressing cell line. exposure: Dectin-1 binding to oligosaccharide probes generated from a soluble yeast glucan, curdlan and pustulan evidence_span: {"source_cache": "artifacts/glucan-research/16371356.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "dd98941694dedd8e3e85766c0c299b54fbc29ca8cce7c61a333efceee796867f", "start_char": 0, "end_char": 1911, "text_sha256": "dd98941694dedd8e3e85766c0c299b54fbc29ca8cce7c61a333efceee796867f"} [bg-p16371356] Ligands for the beta-glucan receptor, Dectin-1, assigned using "designer" microarrays of oligosaccharide probes (neoglycolipids) generated from glucan polysaccharides. (2006). https://pubmed.ncbi.nlm.nih.gov/16371356/ DOI: 10.1074/jbc.m511461200

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 THP-1 cells; antibody perturbation.

limitations

This is an explained stimulus difference, not a contradiction or proof of a clinical immune benefit.

nutrient_topic

Stevia collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · Stevia

plain_language

The same compound can stimulate resting cells while suppressing an already stimulated response.

primary_references

Anti-Inflammatory and Immunomodulatory Activities of Stevioside and Its Metabolite Steviol on THP-1 Cells. · 2006 · https://pubmed.ncbi.nlm.nih.gov/16448183/ · DOI 10.1021/jf0523465

Stevia: glycoside metabolism, taste, ion channels and cross-nutrient mechanisms (2026-09-19) · lines 330–336

AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Human THP-1 cells; antibody perturbation. · source_derived_draft · unverified_draft

## stevia-immune-resting The same compound can stimulate resting cells while suppressing an already stimulated response. In unstimulated THP-1 cells, stevioside induced TNF, IL-1beta and nitric oxide release; anti-TLR4 antibody partially neutralized TNF release. Model: Human THP-1 cells; antibody perturbation. Limitations: This is an explained stimulus difference, not a contradiction or proof of a clinical immune benefit. Evidence access: Primary abstract Anti-Inflammatory and Immunomodulatory Activities of Stevioside and Its Metabolite Steviol on THP-1 Cells. · 2006 · https://pubmed.ncbi.nlm.nih.gov/16448183/ · DOI 10.1021/jf0523465

evidence_access

Primary abstract

experimental_model

Human monocyte-derived cell line with LPS stimulation.

limitations

High direct exposure is not demonstrated after dietary sweetener use; pathway inhibition does not establish direct protein binding.

nutrient_topic

Stevia collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · Stevia

plain_language

The inflammatory state changes what the compound does.

primary_references

Anti-Inflammatory and Immunomodulatory Activities of Stevioside and Its Metabolite Steviol on THP-1 Cells. · 2006 · https://pubmed.ncbi.nlm.nih.gov/16448183/ · DOI 10.1021/jf0523465

Stevia: glycoside metabolism, taste, ion channels and cross-nutrient mechanisms (2026-09-19) · lines 322–328

AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Human monocyte-derived cell line with LPS stimulation. · source_derived_draft · unverified_draft

## stevia-immune-stimulated The inflammatory state changes what the compound does. Stevioside at 1 mM suppressed LPS-induced TNF and IL-1beta release in human THP-1 cells, with suppression of IKKbeta and NF-kappaB activation. Model: Human monocyte-derived cell line with LPS stimulation. Limitations: High direct exposure is not demonstrated after dietary sweetener use; pathway inhibition does not establish direct protein binding. Evidence access: Primary abstract Anti-Inflammatory and Immunomodulatory Activities of Stevioside and Its Metabolite Steviol on THP-1 Cells. · 2006 · https://pubmed.ncbi.nlm.nih.gov/16448183/ · DOI 10.1021/jf0523465

availability_state

nutrient_deficiency Imported condition classification; unverified.

cross_nutrient

Tumor necrosis factor (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 reduced tumor necrosis factor alpha production in the tested immune cells.

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 1377–1390

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-tnf Experimental human zinc restriction reduced tumor necrosis factor alpha production, contributing to the selective decline in the tested TH1-associated cytokine response. Condition category: nutrient_deficiency nutrient_topic: Zinc research collection; topical membership is not evidence of a direct dietary effect. plain_language: Zinc shortage reduced tumor necrosis factor alpha production in the tested immune cells. 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: Tumor necrosis factor (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_span

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experimental_model

Jurkat T cells stimulated through the T-cell receptor with transcription factor reporter assays

exposure

AM404 applied to CD3 and CD28-stimulated cells, with fatty acid amide hydrolase independence tested

limitations

Identifies a target of the metabolite that has nothing to do with pain. Cell line work at concentrations that are not related here to those reached in a person.

nutrient_topic

Paracetamol research collection; topical membership is not evidence of a direct clinical effect, and the drug is recorded separately from the metabolites NAPQI and AM404. · Paracetamol

organism

Human cells

plain_language

The metabolite also switches off a transcription factor that immune cells use, by a route unrelated to the enzyme that made it.

primary_references

[apap-p17196940] The acetaminophen-derived bioactive N-acylphenolamine AM404 inhibits NFAT by targeting nuclear regulatory events. (2007). https://pubmed.ncbi.nlm.nih.gov/17196940/ DOI: 10.1016/j.bcp.2006.12.001

tissue_or_cell_type

T lymphocytes

Paracetamol: the enzyme it reduces rather than blocks, the isoform that turned out not to exist, the metabolite that carries the analgesia, and the metabolite that destroys the liver (2026-09-22) · lines 389–400

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Jurkat T cells stimulated through the T-cell receptor with transcription factor reporter assays · source_derived_draft · unverified_draft

### apap-am404-blocks-nfat AM404 was a potent inhibitor of T-cell-receptor-mediated T-cell activation, specifically inhibiting interleukin-2 and tumour necrosis factor alpha gene transcription and tumour necrosis factor alpha synthesis in stimulated Jurkat T cells in a fatty acid amide hydrolase independent way, inhibiting both the binding to DNA and the transcriptional activity of endogenous nuclear factor of activated T cells without affecting early steps such as calcium mobilization or dephosphorylation, and without interfering with the pathways leading to AP-1 or nuclear factor kappa B activation. Condition category: normal nutrient_topic: Paracetamol research collection; topical membership is not evidence of a direct clinical effect, and the drug is recorded separately from the metabolites NAPQI and AM404. plain_language: The metabolite also switches off a transcription factor that immune cells use, by a route unrelated to the enzyme that made it. organism: Human cells tissue_or_cell_type: T lymphocytes experimental_model: Jurkat T cells stimulated through the T-cell receptor with transcription factor reporter assays limitations: Identifies a target of the metabolite that has nothing to do with pain. Cell line work at concentrations that are not related here to those reached in a person. exposure: AM404 applied to CD3 and CD28-stimulated cells, with fatty acid amide hydrolase independence tested evidence_span: {"source_cache": "artifacts/paracetamol-research/17196940.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "adb730eafbac5bf2eeb05418523f3f943b2b4f0ffb83e8e80cdc97c6f0ce27e9", "start_char": 0, "end_char": 1544, "text_sha256": "adb730eafbac5bf2eeb05418523f3f943b2b4f0ffb83e8e80cdc97c6f0ce27e9"} [apap-p17196940] The acetaminophen-derived bioactive N-acylphenolamine AM404 inhibits NFAT by targeting nuclear regulatory events. (2007). https://pubmed.ncbi.nlm.nih.gov/17196940/ DOI: 10.1016/j.bcp.2006.12.001

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