That is my understanding as well, Art. However, this particular story specifically says that the latest study contradicts the promising study from June. In fact, there's a link back to the June study. I hope the writer of this news story just has the science wrong and that there is no contradiction.
I don't know if I have benefited from TruNiagen or not, but even if I didn't have PD, I'd be taking it. Like many PwP, if the risk seems low and the science seems legitimate, I'll take just about anything. The problem is that I take so many supplements that it becomes virtually impossible to credit one over the others as far as slowing symptom progression. In addition, there's no way to know how I'd be doing if I were not taking these supplements so any benefit is hard to measure -- EXCEPT that I know I feel better now than in May when I was first diagnosed. I have been taking TruNiagen for approximately three months and I plan to continue with it, at least for now.
Several people pm'd me asking my thoughts. For what it's worth here is one of my responses. Remember I am not a doctor or a researcher. The best person to ask would be Simon. Also for the record I am taking 750 mg of TruNiagen per day and will continue to do so.
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When I saw the headline I groaned. Obviously any study that showed NR was somehow harmful would ruin my day, but then I read the study.
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First and most importantly the study used niacinamide (Nam) not nicotinamide riboside (NR). Second, and this is key, the model they used involved impacting "acetylation". Acetylation is part of the process that makes proteins become toxic in Parkinson's models, and molecules that help block acetylation are on the list of hopeful treatments.
Now this next part is not well understood and has some conflicting research, but so far research indicates that NR is a Sirtuin enhancer and Nam is a Sirtuin inhibitor. Sirtuins act to block acetylation. That means in theory NR would be expected to help with the model of Parkinson's the researchers used in this paper, but Nam would not. It would be great if they repeated the study using NR instead of Nam. Sadly, I do not expect them to do so.
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A quote from the study:
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The toxic effects of nicotinamide’s sirtuin inhibition are associated with exacerbation of behavioural motor based symptoms, the neuropathological progression of the model as detected through MRI, and nigral dopaminergic neurodegeneration. These changes were accompanied by reversal of lactacystin induced histone hypoacetylation resulting in histone hyperacetylation and an upregulation of neuroprotective and neurotrophic factors. Such upregulations however did not translate to neuroprotection, rather exacerbated neurodegeneration suggestive that the histone hyperacetylation observed may have also increased expression of neurotoxic factors not studied here. These findings therefore highlight the importance of target specificity within this class of HDACs and demonstrate the contrasting effects of sirtuin inhibition upon cell survival in this, compared to other animal models of PD.
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The very last line actually makes me wonder if the researchers even realize that NR is a Sirtuin activator and therefore different from Nam in a fundamental way.
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