Vitamin B12 for Masld
Verdict: Counter-Evidence
Across 6 PubMed studies, the evidence for Vitamin B12 in Masld grades Tier D — counter-evidence. High-quality evidence indicates it is not effective (or is harmful) for this use.
D 🔴 D Counter-Evidence Counter-Evidence
Why this grade7-layer evidence engine
⚖️
Scoring transparency
All scores computed by a 7-layer evidence engine — fully auditableRaw score 0.47
D
C
B
A
S
← counter-evidence / ineffectiveeffective / strong evidence →
Final grade
D · Counter-Evidence
Confidence
90%
Highly consistent evidence
Evidence level
E3
Single high-quality meta-analysis
▸View the full decision path (audit trail)
- compute_raw_score — 加權公式: L2×0.30 + L3×0.25 + L5×0.25 + L11×0.10 + L1×0.10 = 0.465
- tier_from_score — 依分數區間映射至 tier letter
- apply_hec_rules — 無高階證據可裁決
- tier_strict_requirement_check — Tier 條件達標，未降階
- detect_disputes — 偵測到 0 個 hard + 0 個 soft dispute
- decide_status — 依 tier + dispute 結果決定 status
PubMed studies (6)L2 · primary research & systematic reviews
Bi-directional causal effect between vitamin B12 and non-alcoholic fatty liver disease: Inferring from large population data
Finding: Genetically predicted higher vitamin B12 was associated with INCREASED NAFLD risk (combined OR 1.30, 95% CI 1.13-1.48, p<0.001 per SD), with reverse causality also seen (NAFLD liability raised B12, beta 0.08, p=0.034).
View on PubMed The effects of vitamin B12 supplementation on metabolic profile of patients with non-alcoholic fatty liver disease: a randomized controlled trial
Finding: B12 significantly lowered the surrogate marker homocysteine vs placebo (median -2.1 vs -0.003 umol/L, p=0.038), but between-group differences in liver steatosis, ALT and fasting glucose were NOT significant.
View on PubMed Use of a Micronutrient Cocktail to Improve Metabolic Dysfunction-Associated Steatotic Liver Disease (MASLD) in Adults with Obesity: A Randomized, Double-Blinded Pilot Clinical Trial
Finding: The B12-containing cocktail reduced CAP by 4% and TE by 7.8% vs placebo (both p<0.05), but B12 was co-administered with folate, betaine, omega-3 and choline so its independent effect cannot be isolated.
View on PubMed Associations of serum folate and vitamin B12 levels with all-cause mortality among patients with metabolic dysfunction associated steatotic liver disease: a prospective cohort study
Finding: Higher serum B12 was associated with LOWER all-cause mortality (Q3 HR 0.58, 95% CI 0.39-0.86, p=0.008; Q4 HR 0.72, 95% CI 0.54-0.96, p=0.026), but this is observational and likely confounded by reverse causation (low B12 marking sicker patients).
View on PubMed The Association between Non-Alcoholic Fatty Liver Disease (NAFLD) and Advanced Fibrosis with Serological Vitamin B12 Markers: Results from the NHANES 1999-2004
Finding: Functional B12-pathway markers were associated with advanced fibrosis (homocysteine OR 2.76, 95% CI 1.49-5.11; methylmalonic acid OR 1.41, 95% CI 1.10-1.80), indicating impaired B12 metabolism tracks with worse disease rather than B12 being protective.
View on PubMed The Role of Vitamins in Non-Alcoholic Fatty Liver Disease: A Systematic Review
Finding: Narrative review of 17 studies concluded vitamin deficiency associates with NAFLD and that B12 shows 'promise', but found no quantitative pooled effect and explicitly stated more well-designed human trials are needed.
View on PubMed Regulatory & authoritative positionsL4/L5 · FDA / EMA / NIH ODS / Cochrane / Mayo …
L4a US FDA
Supportive
NUTRIENT SUPPLEMENT source↗
L4b EU EFSA
Supportive
a cause and effect relationship has been established source↗
L4c UK NHS
Supportive
Adults aged 19 to 64 need about 1.5 micrograms a day of vitamin B12. source↗
L4d TW TFDA / 衛福部
Supportive
維生素B12之足夠攝取量(AI)成人為每日2.4微克 source↗
L4e WHO
Supportive
Vitamin B12 or folate supplementation during pregnancy is not recommended as an intervention to improve maternal and infant health outcomes source↗
L5a NIH Office of Dietary Supplements
Supportive
Vitamin B12 supplementation appears to have no beneficial effect on performance in the absence of a nutritional deficit. source↗