I'm just putting together two things that caught my attention (If you are not familiar with my posts, I am not a smart man so please don't embrace my speculation).
Our findings supported that lots of clinical and epidemiological data observed lower UA levels in PD patients. Manipulation of UA or its precursors’ concentration could be effective to treat or prevent PD. However, it is still suspectable that higher UA levels are better enough to PD patients. Furthermore, for the complex nature of PD and its heterogeneous genetic and environmental influences, it is inadequate for just manipulating UA in treating the disease.
Not at the top of my interesting supplements list. But on my list now.
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Well written park_bear. Now I'm going to make it look like I did not learn a thing
Oxidative Stress in Parkinson’s Disease: Potential Benefits of Antioxidant Supplementation 2020 hindawi.com/journals/omcl/2...
3.1.3. Urate
High levels of urate have been associated with a lower risk for PD [162], and changes in urate levels can predict the development of PD in animal models of the disease [163]. Coolen et al. [164], in a study with daily oral supplementation of 5000 mg of ATP in humans, identified that there was an increase in uric acid. In parallel, Andreadou et al. [165] detected the presence of reduced serum levels of this antioxidant molecule in patients with PD and suggested the potential use of this molecule in the therapy of the disease. Indeed, feeding a 1% uric acid diet to rats reversed PD symptoms [166], effects that may be related to NF-E2-related factor 2 (Nrf2) bound to the antioxidant response element (Nrf2-ARE) pathway [167]. Moreover, administration of inosine, a urate precursor, was safe and promoted improvement of PD symptoms in humans [168].
This is the study it references. It is from 2017:
One year safety and efficacy of inosine to increase the serum urate level for patients with Parkinson's disease in Japan
The question they did not answer was if there were benefits
Results
We did not observe any adverse events requiring termination or reduction of the study drug, although uric acid crystalluria was transiently observed in a single subject. An inosine dosage of 1070 (SD = 501) mg/day significantly raises the urate level from 3.5 (0.84) mg/dl at baseline to 6.68 (1.11) mg/dl at the 52nd week.
Conclusions
Inosine was safely used for one year and effectively raised urate levels in a small group of subjects. Our study is the first report to use inosine for patients with PD in an Asian population.
The final word on the matter was the futility halt of the phase III study that had been undertaken because of the kind of data you cited.. My writing from the link I provided:
"An extensive controlled phase 3 study was then undertaken – only to be halted for futility. A futility halt means the study was abandoned prior to completion because it was determined it would not show any advantage for the treatment [or possibly was causing harm]. This negative result demonstrates that the observed association between uric acid levels and Parkinson's was just that - association, not causation."
It takes observation over many years and a large number of subjects to detect the adverse impact of high urate levels. The trials of raising urate levels were of insufficient duration and size to detect this issue. Again from my writing, for example:
" All of the studies in this review [that found adverse effects] followed patients for more than 24 months and eight of them followed patients for more than 10 years. The relative risk (RR) of stroke of 1.47 that the review found is extremely high."
Do not be fooled. Raising urate levels does no good and invites disaster.
Agree - plus uric acid can cause gout. My husband has swollen feet and ankles (not heart related) and doctor gave him water pills. Then, after a few weeks tested his uric acid and it was high - borderline for gout. A case where one RX pill helps one issue but causes another issue.
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