This single-author perspective proposes that low molybdenum intake, by lowering activity of the molybdenum-dependent enzyme xanthine oxidase-dehydrogenase, lets certain dietary purines reach and accumulate in the brain, and that this could start Parkinson’s disease with dementia. The argument extrapolates from sheep studies and from diet and soil figures taken from other work. It presents an untested hypothesis, not new data.
Key numbers
- Average daily diet molybdenum content, calculated by the author from earlier surveys: 0.07 ppm (United States) and 0.04 ppm (United Kingdom) (Abstract, p. 1; Molybdenum deficiency section, p. 3).
- Central nervous system disease occurs in molybdenum-deficient sheep ingesting dietary purines when dietary molybdenum falls below 0.04 ppm (p. 3; secondary, sheep data).
- Soils of southern Guam food gardens: mean molybdenum 0.85 ppm (range 0.1 to 1.6, n = 24), compared with 4.3 ppm in one limestone-derived soil sample (p. 4; secondary).
- Annual incidence of Parkinsonism-dementia complex on Guam peaked at 57 per 100,000 (males, 1960 to 1964) and 28 per 100,000 (females, 1970 to 1974), falling to 16 and 8 by 1995 to 1999 (p. 4; secondary).
Methods (brief)
Narrative perspective. No experiments, sampling or statistical analysis were performed; figures are taken or calculated from cited surveys and sheep studies.
Evidence fitness
Useful only as context for the idea that molybdenum deficiency, rather than excess, may carry risk, and for the role of molybdenum in xanthine oxidase-dehydrogenase. It does not establish that molybdenum deficiency causes Parkinson’s disease, and it reports no new measurements.
Limitations
Single author, hypothesis-generating. Relies on extrapolation from sheep, which share purine salvage with humans per the author, and on ecological correlation in Guam. The author declares no competing financial interests.
Related evidence
Update history
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