Oxidative Stress and Cancer an overview by Dr. Nathan Goodyear.
Everyone has to deal with oxidation as we age. We have breakdown in the body, we have damage. Why is that important? Oxidative stress and cancer are related, and we’ll discuss why in this article.
This is part of our weekly in-house Team Oasis educational staff program. Our doctors help educate our Care Team during our Plan of Care meeting. The Oasis Care Team is comprised of;
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We review and have discussions on new and related cancer topics. We review our comprehensive cancer care program and the impact it has on our patients and their healing. We do this so
people can learn from a professional and experienced medical doctor who is informed on the latest studies, research and results in cancer care.
Dr. Nathan Goodyear covers various topics week to week including; vitamin c, cancer stem cells, hormones, and many others related to alternative cancer treatment. We invite you to share
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Oxidative stress is exactly what’s going on in cancer.
We’ve been talking about things that we’ve talked about here recently, where we’ve talked about the acid-base environment around the tumor. We’ve talked about vitamin C. We’ve talked about all of these things. Understand that the foundation of all these things is redox reactions. Redox, reducing agents, oxidation, oxidizing agents; oxidizing requires oxygen.
What is rust? It’s iron, plus oxygen. What happens in cancer cells? Cancer cells are a high oxidative state environment or reactive, oxygenation species. There’s also reactive nitrogen species, but
we’ll leave that aside because it’s too much of a variable and stay on the topic of reactive oxygenation species.
Reactive oxygenation species is in part high oxidative stress because of the high metabolic demand of cancer. The constant turnover of cancer is generating this massive oxidative process that primarily is driven through the electron transport chain.
In some ways, we feel this is why glycolysis may be favored because the oxidative is too much that way. It actually shifts to glycolysis. This high oxidative environment, be it things like hydrogen peroxide, superoxide anions, hydroxyl free radicals are where we’re working every day.
We are trying to induce massive oxidative stress in cancer and not in the rest of the cells.
When you induce oxidative damage, if the cell has the capacity to reduce that, it balances it out. There are no negative effects. That’s why you can give vitamin C in high doses and it’s oxidative to cancer and yet it’s anti-oxidative to healthy cells.
It’s using hydrogen peroxide as a secondary messenger, not as a primary oxidative tool, but as a secondary messenger to go inside the cell and turn on highly oxidative processes and basically create all kinds of damage; DNA, DNA repair, et cetera.
In healthy cells, that doesn’t happen. Why? Well, it doesn’t happen because there are lots of enzymes to reduce them, to break them down, to neutralize them. In cancer cells, they don’t really have that function.
Things like catalase and glutathione perioxidates are deficient in cancer cells. You can get oxidative stress, a lot of oxidation, a lot of cellular rust inside the cancer cells and yet, there’s no means to buff it out. There’s no means to clean it up.
Compare this to a car that’s been left out in the rain for years. That creates that creaky door, that engine that doesn’t turn over, that fuel injection problem, but this is happening on
the inside of the cancer cells. I wanted to bring to light that picture of oxidative rust because that is really what we’re doing from an image perspective inside the cancer cell.
We’re trying to work in that reduction oxidative balance to induce cell death.
We’ve talked about how cancer stem cells and cancer cells lack stemness, high oxidative and high oxidation in cancer cells that lack stem activity appears to be self-destructive, but in cancer stem cells, it appears to be that they have low oxidative stress.
Low oxidative potential, because cancer stem cells have a high capacity to handle it. The more we learn, the more we realize the more complex it is. The idea that you can just look at a particular type of cancer and assume all cancer cells within that, whether they’re the heterogeneous mass in the tumors, whether they’re cancer stem cells, that they’re all going to be similar is just not true. Not true at all.
What we’re dealing with, though is oxidative potential. How can the cells handle it? That’s why vitamin C can be anti-oxidative. It can be an antioxidant. Anti-oxidation in healthy cells because they have the ability to reduce it with those enzymes.
Whereas with cancer cells, it can be pro-oxidative. It’s simply the environment to which the vitamin C is introduced. Vitamin C is really, if you think about it, just a delivery mechanism. It’s a delivery mechanism to the proper environment to then induce a signal with hydrogen peroxide to trigger the internal oxidative rust that then damages the cell beyond a point to which it can’t return.
That’s what we’re really trying to do with things like Vitamin C. That’s what we’re trying to do with IPT. We’re inducing oxidative damage.
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