Vitamin D and Parkinson's disease—A hypothesis

Abstract

Parkinson's disease (PD), a common disease of the elderly, is a movement disorder characterized by tremor, akinesia, and loss of postural reflexes, leading to immobility and frequent falls. It results from selective loss (death) of dopaminergic neurons in the substantia nigra region of the brain, largely developed prior to clinical diagnosis, and continuous after diagnosis, despite use of current therapeutic modalities. In PD in the United States the cause and mechanism of continued neuron cell death in the substantia nigra is currently unknown. We hypothesize, based upon several lines of evidence, that documented chronically inadequate vitamin D intake in the United States, particularly in the northern states and particularly in the elderly, is a significant factor in the pathogenesis of PD. This hypothesis implies that dietary aid for prevention and therapy for PD is possible.

Low Serum 25(OH)D Levels in Parkinson ’s Disease; a Non Specific Marker of Neurodegeneration?

“…Low vitamin D is frequently found in PD. Similar findings were described efficaciously in previous studies [20,27,28]. However, at odds with other contributions [29,30], we failed to detect correlations between vitamin D levels and PD symptom severity, as measured by both H&Y and UPDRS part III.…”

An estimate of the global reduction in mortality rates through doubling vitamin D levels

“…This idea was hypothesized on the basis of higher rates in northern US states (Newmark and Newmark, 2007). Perhaps the strongest evidence is from a study of outdoor work and risk of Parkinson's disease in Denmark.…”

Oral phycocyanobilin may diminish the pathogenicity of activated brain microglia in neurodegenerative disorders

“…[100][101][102] The efficacy of this effect will presumably be proportional to the concentration of 25-hydroxyvitamin D in brain parenchyma; there is some evidence that risk for Alzheimer's and Parkinson's correlates positively with latitude, and poor vitamin D status is a frequent concomitant of these disorders. [103][104][105] To the extent that optimal vitamin D status can decrease, if perhaps only to a minor degree, microglial iNOS activity, it should collaborate with PCB in suppressing peroxynitrite production in regions of the brain challenged by inflammatory neuropathology.…”