N1-Methylnicotinamide

cross_nutrient

true

evidence_span

{"source_cache": "artifacts/niacin-consumption-sources/nnmt2013.txt", "locator": "Full text, normalized paragraph 33", "start_char": 18035, "end_char": 19275, "file_sha256": "7d88fd656ba772962185234a9bd021e40a9b83f9156db836f723eba06b68acca", "text_sha256": "efcd23e962441fae2b1fb3602db6a6d820ad2d17a511651b3950a2499df2fa02"}

experimental_model

Deuterated metabolite tracing and LC-MS

exposure

Deuterated N1-methylnicotinamide for 24 hours; labeled nicotinamide comparison

limitations

Engineered human cancer-cell culture, not healthy-human niacin repletion. SAM consumption does not establish systemic methyl depletion or a need for folate/B12 supplements. Non-detection is assay-limited and does not establish absolute irreversibility or whole-body clearance.

nutrient_topic

Niacin research collection; topical membership is not evidence of a direct dietary effect. · Niacin (vitamin B3)

organism

Human

plain_language

The methylated product was relatively stable during this cell-culture experiment.

primary_references

[b3-cons-nnmt2013] NNMT promotes epigenetic remodeling in cancer by creating a metabolic methylation sink. (2013). https://pubmed.ncbi.nlm.nih.gov/23455543/ DOI: 10.1038/nchembio.1204

tissue_or_cell_type

Human 769P renal carcinoma cells

Niacin: NAD metabolism, deficiency and nutrient interactions (2026-09-17) · lines 817–829

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Deuterated metabolite tracing and LC-MS · source_derived_draft · unverified_draft

### b3-cons-mna-stability After 24 hours of labeled N1-methylnicotinamide exposure, cancer-cell tracing did not detect conversion to other labeled metabolites. Condition category: normal nutrient_topic: Niacin research collection; topical membership is not evidence of a direct dietary effect. plain_language: The methylated product was relatively stable during this cell-culture experiment. organism: Human tissue_or_cell_type: Human 769P renal carcinoma cells experimental_model: Deuterated metabolite tracing and LC-MS limitations: Engineered human cancer-cell culture, not healthy-human niacin repletion. SAM consumption does not establish systemic methyl depletion or a need for folate/B12 supplements. Non-detection is assay-limited and does not establish absolute irreversibility or whole-body clearance. exposure: Deuterated N1-methylnicotinamide for 24 hours; labeled nicotinamide comparison cross_nutrient: true evidence_span: {"source_cache": "artifacts/niacin-consumption-sources/nnmt2013.txt", "locator": "Full text, normalized paragraph 33", "start_char": 18035, "end_char": 19275, "file_sha256": "7d88fd656ba772962185234a9bd021e40a9b83f9156db836f723eba06b68acca", "text_sha256": "efcd23e962441fae2b1fb3602db6a6d820ad2d17a511651b3950a2499df2fa02"} [b3-cons-nnmt2013] NNMT promotes epigenetic remodeling in cancer by creating a metabolic methylation sink. (2013). https://pubmed.ncbi.nlm.nih.gov/23455543/ DOI: 10.1038/nchembio.1204

cross_nutrient

true

evidence_span

{"source_cache": "artifacts/niacin-consumption-sources/nnmt2013.txt", "locator": "Full text, normalized paragraph 8", "start_char": 2396, "end_char": 4508, "file_sha256": "7d88fd656ba772962185234a9bd021e40a9b83f9156db836f723eba06b68acca", "text_sha256": "fc5cdd48751fa59656f5c16e70c31ab3f36788c265267d7cb57f269bb1848fc6"}

experimental_model

Human cancer-cell enzyme activity and metabolomics study

exposure

Nicotinamide substrate and NNMT expression/activity comparisons

limitations

Engineered human cancer-cell culture, not healthy-human niacin repletion. SAM consumption does not establish systemic methyl depletion or a need for folate/B12 supplements.

nutrient_topic

Niacin research collection; topical membership is not evidence of a direct dietary effect. · Niacin (vitamin B3)

organism

Human

plain_language

Nicotinamide methylation uses a methyl group from SAM.

primary_references

[b3-cons-nnmt2013] NNMT promotes epigenetic remodeling in cancer by creating a metabolic methylation sink. (2013). https://pubmed.ncbi.nlm.nih.gov/23455543/ DOI: 10.1038/nchembio.1204

tissue_or_cell_type

769P, OVCAR3, MUM2C and comparison cell models

Niacin: NAD metabolism, deficiency and nutrient interactions (2026-09-17) · lines 747–759

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Human cancer-cell enzyme activity and metabolomics study · source_derived_draft · unverified_draft

### b3-cons-nnmt-methyl-transfer NNMT transfers a methyl group from SAM to nicotinamide, yielding N1-methylnicotinamide and S-adenosylhomocysteine. Condition category: normal nutrient_topic: Niacin research collection; topical membership is not evidence of a direct dietary effect. plain_language: Nicotinamide methylation uses a methyl group from SAM. organism: Human tissue_or_cell_type: 769P, OVCAR3, MUM2C and comparison cell models experimental_model: Human cancer-cell enzyme activity and metabolomics study limitations: Engineered human cancer-cell culture, not healthy-human niacin repletion. SAM consumption does not establish systemic methyl depletion or a need for folate/B12 supplements. exposure: Nicotinamide substrate and NNMT expression/activity comparisons cross_nutrient: true evidence_span: {"source_cache": "artifacts/niacin-consumption-sources/nnmt2013.txt", "locator": "Full text, normalized paragraph 8", "start_char": 2396, "end_char": 4508, "file_sha256": "7d88fd656ba772962185234a9bd021e40a9b83f9156db836f723eba06b68acca", "text_sha256": "fc5cdd48751fa59656f5c16e70c31ab3f36788c265267d7cb57f269bb1848fc6"} [b3-cons-nnmt2013] NNMT promotes epigenetic remodeling in cancer by creating a metabolic methylation sink. (2013). https://pubmed.ncbi.nlm.nih.gov/23455543/ DOI: 10.1038/nchembio.1204

evidence_access

Primary full text

experimental_model

Same 11-person human pilot.

limitations

Not a quantitative map of every tissue uptake route or evidence of rejuvenation.

nutrient_topic

NAD+ collection; molecular form, preparation, species, exposure and manipulation remain explicit. · NAD+

plain_language

Some infused material is broken down or excreted.

primary_references

A Pilot Study Investigating Changes in the Human Plasma and Urine NAD+ Metabolome During a 6 Hour Intravenous Infusion of NAD. · 2019 · https://pubmed.ncbi.nlm.nih.gov/31572171/ · DOI 10.3389/fnagi.2019.00257

NAD+: compartmental supply, consumption and cross-nutrient mechanisms (2026-09-19) · lines 292–298

AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Same 11-person human pilot. · source_derived_draft · unverified_draft

## nad-plus-iv-metabolites Some infused material is broken down or excreted. The six-hour NAD+ infusion altered circulating breakdown products and urinary NAD/metabolite excretion, demonstrating substantial handling of administered material. Model: Same 11-person human pilot. Limitations: Not a quantitative map of every tissue uptake route or evidence of rejuvenation. Evidence access: Primary full text A Pilot Study Investigating Changes in the Human Plasma and Urine NAD+ Metabolome During a 6 Hour Intravenous Infusion of NAD. · 2019 · https://pubmed.ncbi.nlm.nih.gov/31572171/ · DOI 10.3389/fnagi.2019.00257

availability_state

biomarker_context Imported condition classification; unverified.

evidence_access

Primary abstract

experimental_model

Same five-day randomized trial; primary analysis n=50.

limitations

Catabolite concentration changes are consistent with metabolism but are not direct quantitative flux measurements or proof of intact uptake.

nutrient_topic

NAD+ collection; molecular form, preparation, species, exposure and manipulation remain explicit. · NAD+

plain_language

Blood compartments and breakdown products can move differently.

primary_references

Oral LNAD+ rapidly elevates whole blood intracellular NAD and metabolic flux without elevating plasma NAD: evidence from a randomized controlled trial. · 2026 · https://pubmed.ncbi.nlm.nih.gov/42530810/ · DOI 10.1007/s11357-026-02399-1

trigger_kind

biomarker_context Imported condition classification; unverified.

NAD+: compartmental supply, consumption and cross-nutrient mechanisms (2026-09-19) · lines 316–322

AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Same five-day randomized trial; primary analysis n=50. · source_derived_draft · unverified_draft

## nad-plus-oral-formulation-plasma Blood compartments and breakdown products can move differently. The same LNAD+ trial found unchanged plasma NAD while methyl-nicotinamide and 2PY increased. Model: Same five-day randomized trial; primary analysis n=50. Limitations: Catabolite concentration changes are consistent with metabolism but are not direct quantitative flux measurements or proof of intact uptake. Evidence access: Primary abstract Oral LNAD+ rapidly elevates whole blood intracellular NAD and metabolic flux without elevating plasma NAD: evidence from a randomized controlled trial. · 2026 · https://pubmed.ncbi.nlm.nih.gov/42530810/ · DOI 10.1007/s11357-026-02399-1

availability_state

nutrient_deficiency Imported condition classification; unverified.

cross_nutrient

Nicotinamide (challenge_substrate); N1-methylnicotinamide (methylated_product)

evidence_span

{"source_cache": "artifacts/niacin-clinical-sources/swendseid1987.abstract.txt", "locator": "Indexed primary abstract", "file_sha256": "9a410f57b23d220c2f97bf589b82b31e6e6f6ca2a7b680c2720e1881a0a71b74", "start_char": 0, "end_char": 1188, "text_sha256": "9a410f57b23d220c2f97bf589b82b31e6e6f6ca2a7b680c2720e1881a0a71b74"}

experimental_model

Sequential controlled diets; five men aged 25–32 years

exposure

10-day ordinary diet; 14 days at 285 mg methionine/day; 7 days at 725 mg/day; end-period nicotinamide challenge 102 micromol/kg

limitations

Methylated metabolite outputs, not all methylation reactions or tissue SAM, were measured. Four participants achieving final-period nitrogen balance contributed the reported comparison. Short exposure, very small study; no inference of unlimited methyl capacity.

nutrient_topic

Niacin research collection; topical membership is not evidence of a direct dietary effect. · Niacin (vitamin B3)

organism

Homo sapiens

plain_language

Using methyl groups to dispose of nicotinamide did not automatically exhaust that capacity during this short low-methionine study.

primary_references

[nia-clin-swendseid1987] Methylated niacin derivatives in plasma and urine after an oral dose of nicotinamide given to subjects fed a low-methionine diet. (1987). https://pubmed.ncbi.nlm.nih.gov/2957911/ DOI: 10.1093/ajcn/46.3.496

tissue_or_cell_type

Urine, plasma and nitrogen balance

trigger_kind

nutrient_deficiency Imported condition classification; unverified.

Niacin: NAD metabolism, deficiency and nutrient interactions (2026-09-17) · lines 1177–1189

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Sequential controlled diets; five men aged 25–32 years · source_derived_draft · unverified_draft

### nia-clin-methionine-output-preserved After the nicotinamide challenge, urinary and plasma methylated-metabolite outputs were similar across ordinary, low-methionine and adequate-methionine periods despite negative nitrogen balance during restriction. Condition category: nutrient_deficiency nutrient_topic: Niacin research collection; topical membership is not evidence of a direct dietary effect. plain_language: Using methyl groups to dispose of nicotinamide did not automatically exhaust that capacity during this short low-methionine study. organism: Homo sapiens tissue_or_cell_type: Urine, plasma and nitrogen balance experimental_model: Sequential controlled diets; five men aged 25–32 years limitations: Methylated metabolite outputs, not all methylation reactions or tissue SAM, were measured. Four participants achieving final-period nitrogen balance contributed the reported comparison. Short exposure, very small study; no inference of unlimited methyl capacity. exposure: 10-day ordinary diet; 14 days at 285 mg methionine/day; 7 days at 725 mg/day; end-period nicotinamide challenge 102 micromol/kg cross_nutrient: Nicotinamide (challenge_substrate); N1-methylnicotinamide (methylated_product) evidence_span: {"source_cache": "artifacts/niacin-clinical-sources/swendseid1987.abstract.txt", "locator": "Indexed primary abstract", "file_sha256": "9a410f57b23d220c2f97bf589b82b31e6e6f6ca2a7b680c2720e1881a0a71b74", "start_char": 0, "end_char": 1188, "text_sha256": "9a410f57b23d220c2f97bf589b82b31e6e6f6ca2a7b680c2720e1881a0a71b74"} [nia-clin-swendseid1987] Methylated niacin derivatives in plasma and urine after an oral dose of nicotinamide given to subjects fed a low-methionine diet. (1987). https://pubmed.ncbi.nlm.nih.gov/2957911/ DOI: 10.1093/ajcn/46.3.496

availability_state

biomarker_context Imported condition classification; unverified.

cross_nutrient

L-Tryptophan (measured_precursor); N1-methylnicotinamide (measured_metabolite)

evidence_span

{"source_cache": "artifacts/niacin-clinical-sources/bouma2016.abstract.txt", "locator": "Indexed primary abstract", "file_sha256": "1c1db5a8c0880ceda2066e1fcf23020ab293689782b99402d9913ff326917497", "start_char": 0, "end_char": 1869, "text_sha256": "1c1db5a8c0880ceda2066e1fcf23020ab293689782b99402d9913ff326917497"}

experimental_model

Retrospective serotonin-producing NET cohort; 42 baseline and 34 paired samples; 133 healthy urine references

exposure

Patients selected for low tryptophan and/or pellagra-associated symptoms; prescribed oral niacin mean 144 mg/day

limitations

No randomized comparator or direct tracer measurement of tryptophan diversion. Biomarker normalization does not establish symptom cure. Indexed abstract does not unambiguously specify the administered chemical form; retain niacin rather than guessing nicotinamide.

nutrient_topic

Niacin research collection; topical membership is not evidence of a direct dietary effect. · Niacin (vitamin B3)

organism

Homo sapiens

plain_language

In some serotonin-producing tumor patients, low tryptophan was accompanied by a low niacin marker.

primary_references

[nia-clin-bouma2016] Niacin (Vitamin B3) Supplementation in Patients with Serotonin-Producing Neuroendocrine Tumor. (2016). https://pubmed.ncbi.nlm.nih.gov/26335390/ DOI: 10.1159/000440621

tissue_or_cell_type

Plasma and urine

trigger_kind

biomarker_context Imported condition classification; unverified.

Niacin: NAD metabolism, deficiency and nutrient interactions (2026-09-17) · lines 1263–1275

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Retrospective serotonin-producing NET cohort; 42 baseline and 34 paired samples; 133 healthy urine references · source_derived_draft · unverified_draft

### nia-clin-net-low-marker In the selected NET cohort, mean plasma tryptophan was 31.8 micromol/L and 45% had urinary N1-methylnicotinamide below the study reference range. Condition category: biomarker_context nutrient_topic: Niacin research collection; topical membership is not evidence of a direct dietary effect. plain_language: In some serotonin-producing tumor patients, low tryptophan was accompanied by a low niacin marker. organism: Homo sapiens tissue_or_cell_type: Plasma and urine experimental_model: Retrospective serotonin-producing NET cohort; 42 baseline and 34 paired samples; 133 healthy urine references limitations: No randomized comparator or direct tracer measurement of tryptophan diversion. Biomarker normalization does not establish symptom cure. Indexed abstract does not unambiguously specify the administered chemical form; retain niacin rather than guessing nicotinamide. exposure: Patients selected for low tryptophan and/or pellagra-associated symptoms; prescribed oral niacin mean 144 mg/day cross_nutrient: L-Tryptophan (measured_precursor); N1-methylnicotinamide (measured_metabolite) evidence_span: {"source_cache": "artifacts/niacin-clinical-sources/bouma2016.abstract.txt", "locator": "Indexed primary abstract", "file_sha256": "1c1db5a8c0880ceda2066e1fcf23020ab293689782b99402d9913ff326917497", "start_char": 0, "end_char": 1869, "text_sha256": "1c1db5a8c0880ceda2066e1fcf23020ab293689782b99402d9913ff326917497"} [nia-clin-bouma2016] Niacin (Vitamin B3) Supplementation in Patients with Serotonin-Producing Neuroendocrine Tumor. (2016). https://pubmed.ncbi.nlm.nih.gov/26335390/ DOI: 10.1159/000440621

availability_state

biomarker_context Imported condition classification; unverified.

cross_nutrient

N1-methylnicotinamide (measured_metabolite)

evidence_span

{"source_cache": "artifacts/niacin-clinical-sources/bouma2016.abstract.txt", "locator": "Indexed primary abstract", "file_sha256": "1c1db5a8c0880ceda2066e1fcf23020ab293689782b99402d9913ff326917497", "start_char": 0, "end_char": 1869, "text_sha256": "1c1db5a8c0880ceda2066e1fcf23020ab293689782b99402d9913ff326917497"}

experimental_model

Retrospective serotonin-producing NET cohort; 42 baseline and 34 paired samples; 133 healthy urine references

exposure

Patients selected for low tryptophan and/or pellagra-associated symptoms; prescribed oral niacin mean 144 mg/day

limitations

No randomized comparator or direct tracer measurement of tryptophan diversion. Biomarker normalization does not establish symptom cure. Indexed abstract does not unambiguously specify the administered chemical form; retain niacin rather than guessing nicotinamide.

nutrient_topic

Niacin research collection; topical membership is not evidence of a direct dietary effect. · Niacin (vitamin B3)

organism

Homo sapiens

plain_language

Supplementation improved the measured niacin-status marker for most deficient patients in this series.

primary_references

[nia-clin-bouma2016] Niacin (Vitamin B3) Supplementation in Patients with Serotonin-Producing Neuroendocrine Tumor. (2016). https://pubmed.ncbi.nlm.nih.gov/26335390/ DOI: 10.1159/000440621

tissue_or_cell_type

Plasma and urine

trigger_kind

biomarker_context Imported condition classification; unverified.

Niacin: NAD metabolism, deficiency and nutrient interactions (2026-09-17) · lines 1277–1289

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Retrospective serotonin-producing NET cohort; 42 baseline and 34 paired samples; 133 healthy urine references · source_derived_draft · unverified_draft

### nia-clin-net-supplement-marker Urinary N1-methylnicotinamide rose into the high-normal range in 86% of initially niacin-deficient patients after supplementation in this retrospective series. Condition category: biomarker_context nutrient_topic: Niacin research collection; topical membership is not evidence of a direct dietary effect. plain_language: Supplementation improved the measured niacin-status marker for most deficient patients in this series. organism: Homo sapiens tissue_or_cell_type: Plasma and urine experimental_model: Retrospective serotonin-producing NET cohort; 42 baseline and 34 paired samples; 133 healthy urine references limitations: No randomized comparator or direct tracer measurement of tryptophan diversion. Biomarker normalization does not establish symptom cure. Indexed abstract does not unambiguously specify the administered chemical form; retain niacin rather than guessing nicotinamide. exposure: Patients selected for low tryptophan and/or pellagra-associated symptoms; prescribed oral niacin mean 144 mg/day cross_nutrient: N1-methylnicotinamide (measured_metabolite) evidence_span: {"source_cache": "artifacts/niacin-clinical-sources/bouma2016.abstract.txt", "locator": "Indexed primary abstract", "file_sha256": "1c1db5a8c0880ceda2066e1fcf23020ab293689782b99402d9913ff326917497", "start_char": 0, "end_char": 1869, "text_sha256": "1c1db5a8c0880ceda2066e1fcf23020ab293689782b99402d9913ff326917497"} [nia-clin-bouma2016] Niacin (Vitamin B3) Supplementation in Patients with Serotonin-Producing Neuroendocrine Tumor. (2016). https://pubmed.ncbi.nlm.nih.gov/26335390/ DOI: 10.1159/000440621

cross_nutrient

Nicotinamide adenine dinucleotide, oxidized (coenzyme); PBMC NAD+ content (separate_compartment_marker); N1-methylnicotinamide (muscle_metabolite)

evidence_span

{"source_cache": "artifacts/niacin-clinical-sources/yoshino2021.txt", "locator": "Primary full report; exact character range, zero-based and end-exclusive", "file_sha256": "e4999dc5b9d3392d8180280727c424044b35249bb24c999c3bc863cd23e6c856", "start_char": 4842, "end_char": 6119, "text_sha256": "bb73c5ac9d2ac503143ede8627aaa6be34763fdd501bf48a32528a332b89016c"}

experimental_model

Randomized double-blind trial; 25 overweight or obese postmenopausal women with prediabetes completed

exposure

NMN 250 mg/day for 10 weeks; 13 NMN and 12 placebo participants

limitations

Small selected female cohort. Tissue NAD concentration, NAD turnover and clinical outcomes differ. No lifespan or diabetes-prevention endpoint. Positive muscle findings do not establish whole-body or cross-population benefit.

nutrient_topic

Niacin research collection; topical membership is not evidence of a direct dietary effect. · Niacin (vitamin B3)

organism

Homo sapiens

plain_language

More NAD-related activity did not necessarily mean a larger standing NAD pool in muscle.

primary_references

[nia-clin-yoshino2021] Nicotinamide mononucleotide increases muscle insulin sensitivity in prediabetic women. (2021). https://pubmed.ncbi.nlm.nih.gov/33888596/ DOI: 10.1126/science.abe9985

tissue_or_cell_type

Skeletal muscle, PBMCs, liver and adipose insulin sensitivity

Niacin: NAD metabolism, deficiency and nutrient interactions (2026-09-17) · lines 1515–1527

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Randomized double-blind trial; 25 overweight or obese postmenopausal women with prediabetes completed · source_derived_draft · unverified_draft

### nia-clin-nmn-muscle-nad Muscle NAD+ content did not rise after NMN even though PBMC NAD+ and muscle methylated niacin metabolites increased; authors interpreted the latter as consistent with increased turnover. Condition category: normal nutrient_topic: Niacin research collection; topical membership is not evidence of a direct dietary effect. plain_language: More NAD-related activity did not necessarily mean a larger standing NAD pool in muscle. organism: Homo sapiens tissue_or_cell_type: Skeletal muscle, PBMCs, liver and adipose insulin sensitivity experimental_model: Randomized double-blind trial; 25 overweight or obese postmenopausal women with prediabetes completed limitations: Small selected female cohort. Tissue NAD concentration, NAD turnover and clinical outcomes differ. No lifespan or diabetes-prevention endpoint. Positive muscle findings do not establish whole-body or cross-population benefit. exposure: NMN 250 mg/day for 10 weeks; 13 NMN and 12 placebo participants cross_nutrient: Nicotinamide adenine dinucleotide, oxidized (coenzyme); PBMC NAD+ content (separate_compartment_marker); N1-methylnicotinamide (muscle_metabolite) evidence_span: {"source_cache": "artifacts/niacin-clinical-sources/yoshino2021.txt", "locator": "Primary full report; exact character range, zero-based and end-exclusive", "file_sha256": "e4999dc5b9d3392d8180280727c424044b35249bb24c999c3bc863cd23e6c856", "start_char": 4842, "end_char": 6119, "text_sha256": "bb73c5ac9d2ac503143ede8627aaa6be34763fdd501bf48a32528a332b89016c"} [nia-clin-yoshino2021] Nicotinamide mononucleotide increases muscle insulin sensitivity in prediabetic women. (2021). https://pubmed.ncbi.nlm.nih.gov/33888596/ DOI: 10.1126/science.abe9985

availability_state

nutrient_deficiency Imported condition classification; unverified.

cross_nutrient

N1-methylnicotinamide (measured_metabolite)

evidence_span

{"source_cache": "artifacts/niacin-clinical-sources/jacob1989.abstract.txt", "locator": "Indexed primary abstract", "file_sha256": "749fc69d8d6cb1ba79a0b17e38e9300611713e3939224ba9ac809cef91c7a64c", "start_char": 0, "end_char": 1463, "text_sha256": "749fc69d8d6cb1ba79a0b17e38e9300611713e3939224ba9ac809cef91c7a64c"}

experimental_model

Controlled metabolic-unit feeding of young men for 11 weeks

exposure

6.1–32 NE/day; oral nicotinamide test doses

limitations

Small controlled male metabolic-unit study. Erythrocytes are not every tissue; historical adequate intake is not a current recommendation. Jacob and Fu reports may describe related participants and are not counted as independent trials. Historical NMN abbreviation means N1-methylnicotinamide, not nicotinamide mononucleotide. Urinary output is not a universal diagnostic cutoff.

nutrient_topic

Niacin research collection; topical membership is not evidence of a direct dietary effect. · Niacin (vitamin B3)

organism

Homo sapiens

plain_language

Less niacin intake left less methylated niacin waste in urine; the study threshold belongs to this particular experiment.

primary_references

[nia-clin-jacob1989] Biochemical markers for assessment of niacin status in young men: urinary and blood levels of niacin metabolites. (1989). https://pubmed.ncbi.nlm.nih.gov/2522982/ DOI: 10.1093/jn/119.4.591

tissue_or_cell_type

Urine and plasma

trigger_kind

nutrient_deficiency Imported condition classification; unverified.

Niacin: NAD metabolism, deficiency and nutrient interactions (2026-09-17) · lines 1149–1161

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Controlled metabolic-unit feeding of young men for 11 weeks · source_derived_draft · unverified_draft

### nia-clin-urine-mna-restriction Urinary N1-methylnicotinamide below 1.2 mg/day identified the lowest 6.1-NE/day intake in this experiment and was more responsive than 2PY to the 10.1-NE/day diet. Condition category: nutrient_deficiency nutrient_topic: Niacin research collection; topical membership is not evidence of a direct dietary effect. plain_language: Less niacin intake left less methylated niacin waste in urine; the study threshold belongs to this particular experiment. organism: Homo sapiens tissue_or_cell_type: Urine and plasma experimental_model: Controlled metabolic-unit feeding of young men for 11 weeks limitations: Small controlled male metabolic-unit study. Erythrocytes are not every tissue; historical adequate intake is not a current recommendation. Jacob and Fu reports may describe related participants and are not counted as independent trials. Historical NMN abbreviation means N1-methylnicotinamide, not nicotinamide mononucleotide. Urinary output is not a universal diagnostic cutoff. exposure: 6.1–32 NE/day; oral nicotinamide test doses cross_nutrient: N1-methylnicotinamide (measured_metabolite) evidence_span: {"source_cache": "artifacts/niacin-clinical-sources/jacob1989.abstract.txt", "locator": "Indexed primary abstract", "file_sha256": "749fc69d8d6cb1ba79a0b17e38e9300611713e3939224ba9ac809cef91c7a64c", "start_char": 0, "end_char": 1463, "text_sha256": "749fc69d8d6cb1ba79a0b17e38e9300611713e3939224ba9ac809cef91c7a64c"} [nia-clin-jacob1989] Biochemical markers for assessment of niacin status in young men: urinary and blood levels of niacin metabolites. (1989). https://pubmed.ncbi.nlm.nih.gov/2522982/ DOI: 10.1093/jn/119.4.591