ProdromeNeuro™ Improves Oxidative Stress Biomarkers in Cognitively Impaired Persons (C106)

Supplementation with ProdromeNeuro was observed to elevate blood DHA-plasmalogen levels. The increase in blood DHA-plasmalogens correlated with a decrease in malondialdehyde levels (r=-0.5, p=7.2e-07) and an increase in catalase activity (r=0.28, p=0.008). Superoxide dismutase activity was increased in persons with low baseline activity (p=0.017). 

To access the FREE seminars with full presentations and videos please visit Dr. Goodenowe’s resource site here. This is the article for seminar C106, Supplements (Series C).

ProdromeNeuro is a plasmalogen supplement designed to specifically elevate DHA plasmalogen levels. An escalating dose study was performed in 22 persons (11M/11F) diagnosed with various degrees of cognitive impairment to determine the optimal dose for elevating blood plasmalogen levels. 

In addition to clinical evaluations of cognition and mobility, blood samples were collected at baseline and after each month of supplement dosing for biomarker analyses.  

The escalating dosing of ProdromeNeuro was performed as follows: 

Month 1 – 1ml/day (900mg/day – one bottle of ProdromeNeuro) 

Month 2 – 2ml/day (1800mg/day – two bottles of ProdromeNeuro) 

Month 3 – 2ml/day (1800mg/day – two bottles of ProdromeNeuro) 

Month 4 – 4ml/day (3600mg/day – four bottles of ProdromeNeuro) 

Month 5 – 0ml/day (0mg/day – zero bottles of ProdromeNeuro) 

Blood DHA-Plasmalogen levels were observed to be increased in all participants in a dose-dependent manner. After month 1 there was a 30% increase, after months 2 and 3 there was a 60% increase and after month 4 there was a 90% increase in the target DHA-plasmalogen levels. Persons with low baseline DHA-plasmalogen levels (quartiles 1 and 2) experienced a greater increase in blood DHA-plasmalogen levels (50%, 90%, and 120%, respectively).  When blood DHA-plasmalogen levels were expressed relative to an endogenous non-DHA phosphatidylethanolamine, the relative increase in the target DHA plasmalogen levels was more pronounced. 

The oxidative stress cascade begins with the formation of the superoxide radical resulting from a cellular insufficiency in recycling NADH back to NAD by the mitochondrial electron transport chain. A build-up of NADH beyond the intracellular capacity to recycle NADH by alternative, non-oxidative, anaerobic mechanisms leads to the export of free electrons to the extracellular environment by NAD(P)H oxidase (NOX). These electrons combine with molecular oxygen to form the superoxide radical. Superoxide is neutralized to molecular oxygen and hydrogen peroxide by superoxide dismutase both inside and outside of the cell. Hydrogen peroxide, in turn, is neutralized into molecular oxygen and water by multiple mechanisms such as catalase, glutathione peroxidase or by chemical neutralization by plasmalogens. The failure of the antioxidant system to neutralize hydrogen peroxide results in hydrogen peroxide reacting with superoxide to form the hydroxyl free radical. The hydroxyl free radical reacts with polyunsaturated fatty acids in biological membranes to form lipid peroxides. These lipid peroxides are the primary chemoattractants for inflammatory immune cells. Malondialdehyde is a biomarker of lipid peroxidation and thus represents and quantifies the oxidative stress load on biological systems. In order to assess the effect of elevating blood DHA-plasmalogens on the oxidative stress load on the participants in the trial, malondialdehyde levels, catalase and superoxide dismutase activity and C-reactive protein levels were measured in all participants at baseline and at the end of months 3-5. Although these biomarkers are quantitatively measured, they each have biological floor levels that represent a “healthy state” which cannot reasonably be improved upon. Accordingly, in addition to evaluating the effect of ProdromeNeuro on all participants, participants were also grouped into either low (Q1,Q2) or high (Q3,Q4) subgroups and evaluated accordingly. 

ProdromeNeuro supplementation reduced malondialdehyde levels in all participants by 32% (p=0.028) and by 46% (p=0.002) in persons with high baseline malondialdehyde levels. Overall, malondialdehyde levels were negatively correlated with blood DHA-plasmalogen levels (r=-0.5, p=7.2e-07) 

ProdromeNeuro supplementation increased catalase activity to 186% (p=0.014) of baseline levels in participants and to 240% (p=0.02) in persons with low baseline catalase activity. Overall, catalase activity was positively correlated with blood DHA-plasmalogen levels (r=0.28, p=0.008) 

ProdromeNeuro supplementation increased superoxide dismutase activity (p=0.017) only in persons with low baseline superoxide dismutase activity. 

Of the 22 participants, only 4 had baseline C-reactive protein levels greater than 1.0. All four of these participants had low baseline DHA-plasmalogen levels. All four of these participants exhibited a decrease in CRP by greater than 0.5 units and in two of the participants CRP levels decreased to less than 0.5. 

The results of the oxidative stress biomarker analyses indicate that increasing blood DHA-plasmalogen levels using ProdromeNeuro has a profound positive effect on oxidative stress biomarkers. 

ProdromeNeuro was well tolerated at all dosages and no adverse reactions were observed or reported. 

Dr. Goodenowe explains the trial design and biomarker analyses in detail in C106 – ProdromeNeuro improves oxidative stress biomarkers in cognitively impaired persons.

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