Molybdenum for Gout
Verdict: Counter-Evidence
Across 4 PubMed studies, the evidence for Molybdenum in Gout 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 0.44
D
C
B
A
S
← counter-evidence / ineffectiveeffective / strong evidence →
Final grade
D · Counter-Evidence
Confidence
83%
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 = 0.437
- 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 (4)L2 · primary research & systematic reviews
Occupational molybdenum exposure and a gouty electrician (Selden AI et al.; Occup Med, London)
Finding: A young male electrician developed hyperuricemia and gouty arthritis associated with occupational molybdenum exposure; symptoms improved during an exposure-free period and relapsed after an exposure reconstruction. Authors note 'Molybdenum is an essential trace element and a component of xanthine oxidase, which catalyses the formation of urate,' but caution the association 'might also be entirely circumstantial.'
View on PubMed Endemic molybdenosis (gout-like syndrome) in Ankava, Armenia (Kovalskiy GA et al.)
— See PubMed for details
View on PubMed Antioxidative effects of molybdenum and its association with reduced prevalence of hyperuricemia in the adult population (PLoS One)
Finding: At normal dietary/environmental exposure ranges, higher urinary molybdenum was significantly associated with LOWER serum uric acid (beta -0.119, 95% CI -0.148 to -0.090) and reduced hyperuricemia risk (OR 0.73, 95% CI 0.64-0.83, p<0.001), attributed to antioxidant effects. Counter-signal to the toxicological harm data and applies only within physiologic intake, not gout-treatment supplementation.
View on PubMed A systematic review and meta-analysis of the hyperuricemia risk from certain metals
Finding: In pooled biomonitoring data within ordinary exposure ranges, molybdenum was associated with a ~20% LOWER hyperuricemia risk (pooled OR 0.804, 95% CI 0.724-0.975), in contrast to arsenic, cadmium, lead and calcium which raised risk (OR 1.20-1.77). The protective association is at physiologic exposure and does not contradict toxicological evidence that supraphysiologic molybdenum (mg-level) raises urate; it does NOT support molybdenum as a gout treatment.
View on PubMed Regulatory & authoritative positionsL4/L5 · FDA / EMA / NIH ODS / Cochrane / Mayo …
L4a US FDA
Supportive
The DV for molybdenum is 45 mcg for adults and children age 4 years and older. source↗
L4b EU EFSA
Supportive
Molybdenum contributes to normal sulphur amino acid metabolism. source↗
L4c UK NHS
Cautious
Molybdenum is found in many different types of food, such as nuts, canned vegetables, peas, leafy vegetables (like broccoli and spinach), cauliflower and cereals. You should be able to get all the molybdenum you need from your daily diet. source↗
L4d TW TFDA / 衛福部
Neutral
鉬 (Molybdenum) 列於「食品添加物使用範圍及限量暨規格標準」第(七)類營養添加劑，得使用之化合物包括鉬酸鈉 (Sodium molybdate)、鉬酸銨 (Ammonium molybdate)，限用於補充膳食營養之食品 (如錠狀、膠囊狀食品及綜合維生素礦物質產品)，並依使用限量及對象規定添加。 source↗
L4e WHO
Not addressed
Molybdenum is considered to be an essential trace element in both animals and humans. Safe and adequate intake levels have been suggested... namely 0.015-0.04 mg/day for infants, 0.025-0.15 mg/day for children aged 1-10 and 0.075-0.25 mg/day for all individuals above the age of 10. The guideline value of 0.07 mg/litre is consistent with the essential daily requirement for molybdenum. source↗
L5a NIH Office of Dietary Supplements
Supportive
Molybdenum deficiency has not been reported, except in people with a genetic mutation that prevents the synthesis of molybdopterin and therefore of sulfite oxidase. In this rare metabolic disorder, known as molybdenum cofactor deficiency, mutations in one of several genes prevent the biosynthesis of molybdopterin. … Molybdenum is not a standard treatment for any disease or disorder. source↗