As discussed in my last post, hydrogen peroxide (H2O2) is our enemy as we age because our antioxidant activity decreases (http://www.alliedacademies.org/articles/total-antioxidant-activity-in-old-age.pdf) and so we are less able to break down H2O2. Besides apparently turning our hair grey (https://www.ncbi.nlm.nih.gov/pubmed/19237503) and possibly contributing to heart disease (http://atvb.ahajournals.org/content/26/9/1931.full), H2O2 appears to be very much a part of Alzheimer's etiology, per this abstract from an article back in 2004 (https://www.ncbi.nlm.nih.gov/pubmed/14960126):
Hydrogen peroxide (H(2)O(2)) is a stable, uncharged and freely diffusable reactive oxygen species (ROS) and second messenger. The generation of H(2)O(2) in the brain is relatively high because of the high oxygen consumption in the tissue. Alzheimer's disease is a neurodegenerative disorder characterised by the appearance of amyloid-beta (Abeta)-containing plaques and hyperphosphorylated tau-containing neurofibrillary tangles. The pathology of Alzheimer's disease is also associated with oxidative stress and H(2)O(2) is implicated in this and the neurotoxicity of the Abeta peptide. The ability for Abeta to generate H(2)O(2), and interactions of H(2)O(2) with iron and copper to generate highly toxic ROS, may provide a mechanism for the oxidative stress associated with Alzheimer's disease. The role of heavy metals in Alzheimer's disease pathology and the toxicity of the H(2)O(2) molecule may be closely linked. Drugs that prevent oxidative stress include antioxidants, modifiers of the enzymes involved in ROS generation and metabolism, metal chelating agents and agents that can remove the stimulus for ROS generation. In Alzheimer's disease the H(2)O(2) molecule must be considered a therapeutic target for treatment of the oxidative stress associated with the disease. The actions of H(2)O(2) include modifications of proteins, lipids and DNA, all of which are effects seen in the Alzheimer's disease brain and may contribute to the loss of synaptic function characteristic of the disease. The effectiveness of drugs to target this component of the disease pathology remains to be determined; however, metal chelators may provide an effective route and have the added bonus in the case of clioquinol of potentially reducing the Abeta load. Future research and development of agents that specifically target the H(2)O(2) molecule or enzymes involved in its metabolism may provide the future route to Alzheimer's disease therapy.
Yet do you know what is in your toothpaste? Your mouthwash? I was looking for a dry mouth mouthwash (brand name Biotene) at the store yesterday that purportedly included lactoperoxidase (a peroxidase contained in fresh milk, but which becomes inactive within a few hours after milking). I was dismayed to see that not only did Biotene's maker change the formulation to take out the lactoperoxidase but two spots away from the Biotene mouthwash was a big-name mouthwash advertising its hydrogen peroxide content. Many toothpastes now include H2O2 to bleach teeth. Do we really value whitened teeth over our health as we age?
Fruits and vegetables are a great source of peroxidases, and scientists regularly use horseradish peroxidase in their research (http://hortsci.ashspublications.org/content/28/1/48.full.pdf). As enzymes, peroxidases tend to like neutral Ph, so pickling them in lactic acid or putting them in vinegar (acetic acid) dampens peroxidase activity (http://www.ehow.com/info_8440237_effects-ph-peroxidase.html). Heating peroxidases also has a negative impact on their activity, but sometimes they can be regenerated up to 50% (https://www.ncbi.nlm.nih.gov/pubmed/15826080). Raw radishes seem to be very good peroxidase sources, but I've never enjoyed the biting taste of them; I guess it's a good thing that taste function declines with age (https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3864165/).
After my disappointment at the oral care section of my local supermarket, I headed over to the farmer's market grocery store (Sprouts) and searched there for oral care products that might be high in peroxidase activity. I wanted them to have extracts of plants that weren't combined with camellia sinensis (I avoid it because I'm LDS), cinnamon (my husband reacts to cinnamon oil), or acids. It was harder to find toothpastes and mouthwashes that fit that description than I would have anticipated. Peroxidation activity in aloe vera leaves is fairly high (https://www.ncbi.nlm.nih.gov/pubmed/11243179) and stable even in commercial gel (https://www.ncbi.nlm.nih.gov/pubmed/11199129), so I ended up buying an aloe vera toothpaste off Amazon.
Ginger has a neuroprotective effect on diabetic mouse brains by upping antioxidant activity (https://www.ncbi.nlm.nih.gov/pubmed/21184796). Ginger also protects diabetic mice from liver and kidney damage by, again, upping antioxidant activity (http://www.sciencedirect.com/science/article/pii/S0308814610009726). That is especially interesting given that Alzheimer's is sometimes called a form of diabetes. If the aloe vera toothpaste is too weird, perhaps I'll try ginger next. Grape pomace (https://www.ncbi.nlm.nih.gov/pubmed/16637228) and maqui berry (https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4369103/) also seem like they'd be good H2O2-fighting additions to the diet. I already eat grapes anyway (just not the ones sprayed with sulfites to a level that requires it be labelled, i.e., 10 ppm or more), but maqui seems rather exotic.
Another way to up peroxidase activity is sufficient intake of selenium, a trace metal that our body incorporates into glutathione peroxidases; being deficient in selenium almost completely wipes out activity by glutathione peroxidases (https://www.ncbi.nlm.nih.gov/pubmed/8391784). Molecular biology findings indicate that selenium plays a decisive role in the pathophysiology of Alzhimer's (https://www.ncbi.nlm.nih.gov/pubmed/21593562). I already drink barley water, a good source of selenium, so I'll just keep on doing that.
I'm just a little over 40, but I occasionally find a gray hair already. Maybe that's my body's signal to me that it needs help breaking down H2O2. Early efforts to increase antioxidant activity appear more likely to bear fruit in preventing Alzheimer's from developing than in stopping Alzheimer's once it's already gotten going (https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3941783/).
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