Component
B12-associated neuropsychiatric impairment
Independent substance, clinical endpoint or measured readout; study context is retained with each finding.
2 recorded relationships. Experimental role, claim status and evidence remain attached to each record.
How nutrients influence it
Every nutrient with a recorded effect on this component, credited to the nutrient that acted rather than the chapter that recorded it. Open a nutrient to see the findings and the conditions they were measured under.
Other things that act on it
Enzymes, hormones, genes, and other components with a recorded effect. These are not nutrients, so they do not count toward the arrows above. Each finding names the chapter that recorded it.
How nutrients reach it in more than one step
Chains of two or more recorded steps that end here, grouped by the nutrient they start from. Each step is a separate finding, so a chain is a route a mechanism could take, not proof that it does.
Tracing routes…
What it does
Every recorded relationship this component is part of, grouped by its role. Plain wording comes first; the technical statement follows.
What acts on it
Of 141 neurologic B12-deficiency patients, 34 had normal hematocrit, 25 normal mean cell volume, and 19 both; 40 lacked at least one of these two abnormalities.
Experimental context and source evidence
- availability_state
- nutrient_deficiency Imported condition classification; unverified.
- experimental_model
- Clinical series: 141 consecutive patients with neuropsychiatric abnormalities attributed to cobalamin deficiency; 40 lacked anemia or macrocytosis.
- exposure
- Clinical evaluation and cobalamin replacement; observational response series.
- limitations
- The reported 28% is not the percentage with both tests normal. Selected patients do not estimate population prevalence.
- nutrient_topic
- Vitamin B12 research collection; topical membership is not evidence of a direct dietary effect. · Vitamin B12 (cobalamins)
- organism
- Homo sapiens
- plain_language
- Normal red-cell size or hematocrit did not exclude the neurologic presentation.
- primary_references
- [b12-lindenbaum1988] Neuropsychiatric disorders caused by cobalamin deficiency in the absence of anemia or macrocytosis (1988). https://pubmed.ncbi.nlm.nih.gov/3374544/ DOI: 10.1056/nejm198806303182604
- tissue_or_cell_type
- Human blood or whole-person endpoints
- trigger_kind
- nutrient_deficiency Imported condition classification; unverified.
Vitamin B12: mechanisms, deficiency and nutrient interactions (2026-09-17) · lines 1426–1436
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Clinical series: 141 consecutive patients with neuropsychiatric abnormalities attributed to cobalamin deficiency; 40 lacked anemia or macrocytosis. · source_derived_draft · unverified_draft
### b12-neuro-normal-blood-counts Of 141 neurologic B12-deficiency patients, 34 had normal hematocrit, 25 normal mean cell volume, and 19 both; 40 lacked at least one of these two abnormalities. Condition category: nutrient_deficiency nutrient_topic: Vitamin B12 research collection; topical membership is not evidence of a direct dietary effect. plain_language: Normal red-cell size or hematocrit did not exclude the neurologic presentation. organism: Homo sapiens tissue_or_cell_type: Human blood or whole-person endpoints experimental_model: Clinical series: 141 consecutive patients with neuropsychiatric abnormalities attributed to cobalamin deficiency; 40 lacked anemia or macrocytosis. limitations: The reported 28% is not the percentage with both tests normal. Selected patients do not estimate population prevalence. exposure: Clinical evaluation and cobalamin replacement; observational response series. [b12-lindenbaum1988] Neuropsychiatric disorders caused by cobalamin deficiency in the absence of anemia or macrocytosis (1988). https://pubmed.ncbi.nlm.nih.gov/3374544/ DOI: 10.1056/nejm198806303182604
Complete structured claim and evidenceTwelve of 419 recognized B12-deficient patients had serum cobalamin above 200 pg/mL; five had prominent neurologic involvement that responded to therapy.
Experimental context and source evidence
- availability_state
- biomarker_context Imported condition classification; unverified.
- experimental_model
- Maintenance-relapse observations plus a review of 419 recognized B12-deficient patients.
- exposure
- Serum cobalamin, MMA and total homocysteine measurements; clinical response used in diagnosis.
- limitations
- Retrospective diagnostic attribution; no estimate of specificity in unselected patients. Potential cohort overlap with related reports.
- nutrient_topic
- Vitamin B12 research collection; topical membership is not evidence of a direct dietary effect. · Vitamin B12 (cobalamins)
- organism
- Homo sapiens
- plain_language
- A single circulating B12 measurement is not a complete picture of function.
- primary_references
- [b12-lindenbaum1990] Diagnosis of cobalamin deficiency: II. Relative sensitivities of serum cobalamin, methylmalonic acid, and total homocysteine concentrations (1990). https://pubmed.ncbi.nlm.nih.gov/2339684/ DOI: 10.1002/ajh.2830340205
- tissue_or_cell_type
- Human blood or whole-person endpoints
- trigger_kind
- biomarker_context Imported condition classification; unverified.
Vitamin B12: mechanisms, deficiency and nutrient interactions (2026-09-17) · lines 1500–1510
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Maintenance-relapse observations plus a review of 419 recognized B12-deficient patients. · source_derived_draft · unverified_draft
### b12-serum-normal-recognized-cases Twelve of 419 recognized B12-deficient patients had serum cobalamin above 200 pg/mL; five had prominent neurologic involvement that responded to therapy. Condition category: biomarker_context nutrient_topic: Vitamin B12 research collection; topical membership is not evidence of a direct dietary effect. plain_language: A single circulating B12 measurement is not a complete picture of function. organism: Homo sapiens tissue_or_cell_type: Human blood or whole-person endpoints experimental_model: Maintenance-relapse observations plus a review of 419 recognized B12-deficient patients. limitations: Retrospective diagnostic attribution; no estimate of specificity in unselected patients. Potential cohort overlap with related reports. exposure: Serum cobalamin, MMA and total homocysteine measurements; clinical response used in diagnosis. [b12-lindenbaum1990] Diagnosis of cobalamin deficiency: II. Relative sensitivities of serum cobalamin, methylmalonic acid, and total homocysteine concentrations (1990). https://pubmed.ncbi.nlm.nih.gov/2339684/ DOI: 10.1002/ajh.2830340205
Complete structured claim and evidence
The events it takes part in
A mechanism often involves more than two components. These are the full events, with every participant and its role.
Situations it appears in
Low-supply and faulty-machinery situations recorded in the chapters where this component plays a part.
In the sources
Preserved passages that mention this component, quoted exactly. Open one to read it in context.
Open hypotheses
Proposed ideas that involve this component. They are labeled as hypotheses and do not change any recorded statement.
This is a research prototype built from draft material. It is not medical advice, and its statements still await verification against the original studies.