First of all, oxidative stress does look to be an issue.
Second, "the activity of the endogenous antioxidant system decreased proportionally to the disease severity." I think this means that as Parkinson's progresses, the antioxidant system itself stops working as well.
Third, some of their measures of oxidative damage DO appear to be worse for people who have been taking anti-Parkinsonian medication as compared to people who have been unmedicated.
For people at the same stage of the disease, those who had been treated with antiparkinsonian medication had: higher levels of lipid hydroperoxides and a reduced (less active?) endogenous antioxidant system when compared to unmedicated patients. Both of these findings were statistically significant. The treated patients also had a higher maximum intensity of lipid peroxidation than untreated patients, but this difference was not statistically significant.
At any rate, their take-home message is this:
"These data confirm the concept of the significance of oxidative stress in the pathogenesis of PD and indicate the advisability of using antioxidant drugs in complex therapy of PD."
Antioxidant drugs appear to be quite important for everyone, and perhaps even more so if you are taking antiparkinsonian medication.
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ElliotGreen
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Makletsova, Marina G., et al. "Polyamines in Parkinson’s Disease: Their Role in Oxidative Stress Induction and Protein Aggregation." Journal of Neurology Research 9.1-2 (2019): 1-7.
I'm beginning to build up a vague picture in my mind that the cause of PD and it's progression could be initiated by oxidative stress, aggravated by inflammation, followed by death of dopamine-producing neurons.
If this is the case, at any stage of the disease, I would imagine that impacted neurons could be classified into at least 3 groups:
1) fairly healthy or healthy neurons that are doing the hard work in helping us to function and don't need much externally sourced dopamine.
2) moderately damaged neurons, not yet condemned, producing some dopamine, but also capable of using dopamine available via medication
3) severely damaged or dying neurons that produce very little or no dopamine and are so damaged as to be largely incapable of taking up and using dopamine available through medication.
If this situation is caused by oxidative stress, and this stress was aggravated by diet over many years and is still continuing since we have not changed our habits (yes, that's a lot of ifs), then we should explore a strategy that covers:
a) damage limitation,
b) damage control,
c) damage reversal.
Damage limitation means not eating significant quantities of food that are reported to create oxidative stress or inflammation. These include carbohydrates, sugar, processed foods, dairy products, ice cream, canned fruit, fried foods, red meat (contains too much iron), etc.
Damage control means eating lots of foods containing antioxidants to combat the oxidants that arise naturally through various metabolic pathways. These foods include lots of fresh, and preferably raw, fruit and vegs, especially red fruit, berries, tomatoes, green leafy vegs, cabbage, broccoli, peppers, celery, avocados, nuts and fish.
The aim here is to protect stage 1 and stage 2 neurons from further damage.
Damage reversal means providing the means whereby stage 2 neurons can recover and reach a more healthy state resembling stage 1.
Damage reversal may be more difficult but it can only considered once damage limitation and damage control have been achieved.
I see damage reversal being helped by supplements or drugs, that help the recovery of brain cells damaged by any cause, not just PD : injury, drugs, stroke etc. high dose omega3 fish oils could be a possibility.
The recent article by Dr Laurie Mischley on diet related progression of PD made me think about this idea.
I have now been putting this low oxidative stress diet into practice since the beginning of August. The data from Dr Mischley's review is convincing, especially at the extremes where the p values are low, less than 0.05 and the effects are high. Remember, this survey only fixed rather modest levels for the consumption of foods that have a good effect on PD progression, e.g. ½ cup of fresh vegs or fresh fruit per day, but the impact was strong and the p value = 0.000.
To actively counter PD we can do much better than that: fruit for breakfast, fresh vegs and fresh fruit at every other meal. Fish rather than meat, low carbs, low sugar, no dairy, no canned foods, no sodas, and no red meat. This is easy to do and takes us well beyond the modest limits of Dr Mischley's review.
PD takes years to do its dirty work on our neurons, so we should not expect quick results to counter this effect. I don't expect to see any positive signs for months, maybe years, but I would expect to see more negative signs if I were to ignore this information and I don't want to go down that road.
I can't say that I have. I mean, I'm trying. I'm still trying to figure out what that means.
Nutritionally, I'm trying to stay away from sugar and refined carbs. I'm trying to stay away from red meat and animal fat and dairy. I guess I should be eating more fresh vegetables.
I am confused about how to increase glutathione. It seems like direct supplementation is expensive and doesn't work very well. I started trying NAC again today, but the last time I tried, it caused stomach pain. I'm trying to dilute it in water substantially, but my stomach is still hurting a little bit. I purchased some Amla on the basis of another recent thread, but I am somewhat skeptical. I do believe that it is a significant antioxidant itself, but it seems like it reduces the activity of one of glutathione's helper enzymes.
Concerning omega 3 fish oil supplements, Dr Arne Reimers recommends going high dose = 3g of omega 3 per day. Make sure these oils are high in the antioxidants EPA and DHA. These molecules are made by algae that are eaten by small sea animals: krill, shrimps, shellfish, small fish etc. Large fish get this by eating small fish, so it's better to eat small wild caught oily fish such as sardines. Farmed fish are now sometimes fed cheaper non-fish food and so contain less omega 3 than wild caught fish.
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