Dr. Cory Goldberg connects oxidative stress to asthma, arthritis, kidney disease, and aging. He explains how sirtuins and epigenetic repair pathways link cellular damage to disease, then argues that raising endogenous superoxide dismutase through compounds like glycitin offers a preventive approach to reduce that damage.
Hi, everybody. Corey Goldberg here. And welcome back to the fifth installment of our mini series on oxidative stress, its consequences and ways that we have to combat it. Up until now, we've talked about the oxygen species that damage our cells, the protein and DNA within it. We've talked about some of the sources of that from outside our body, including UV and dietary sources. We've got talked about dietary sources of antioxidants and why they're not nearly as powerful as our own SOD and enzymatic forms of combating oxidative stress. We've talked about this molecule, glycitin, which increases our own levels of SOD and help us to combat this oxidative stress. I'd like to talk a little bit about the disease states related to this issue, this oxidative stress, because it's not just in our skin. Yes, I'm a plastic surgeon. Yes, the skin is the heaviest, largest organ in our body. And yes, ultraviolet radiation and all these other sources outside of us of oxidative stress absolutely damage our skin and make us look older and have all kinds of disease states involving the skin. But reactive oxygen species involves our entire body. Our own biochemistry, our own energy production produces these things. This results in all sorts of disease states. And in fact, most disease states have some relation to inflammation caused by oxidative stress. This involves things like lungs and asthma. It involves our joints cells such as arthritis, autoimmune disease like lupus, our kidneys, heart disease, cardiovascular disease. All of these disease processes have one thing in common, and that is they're related to oxidative stress, which ultimately causes inflammation and the disease process. If we can reduce the reactive oxygen species, this oxidative stress, we can actually reduce the effect of these diseases and in some cases, even treat them. Now, the other thing about the reactive oxygen species and oxidative stress, the overall aging of our cells, the theory which has been, you know, at this point, well proven and is being well researched around the world, called the information theory of aging. One of the researchers who's pioneered this is Dr. David Sinclair of Harvard, and he talks about these cellular mechanisms that we have to repair and undo the damage to the information in our cells, the epigenetics. He talks about sirtuin and mtor, or mammalian target of rapamycin. These genetic mechanisms are ways that we have of repairing damage to our DNA, our cells that is part of the process of aging. However, a large source of the damage caused to our cells is the oxidative stress that they undergo. The oxidative stress that results in damage to the DNA and the epigenetics. And this ultimately is a source of disease states, but it is also a source of the damage that is the primary cause of aging, based on this information theory of aging. So the use of glycidin and increasing our own superoxide dismutase levels is a way of preventing this damage to our cells and therefore leaving our cells with less damage that it has to clean up and repair after the fact. So up until now, we've talked about the reactive oxygen species and the effect us and ways of combating it. I'm going to try and put this all together in our last episode coming up. I look forward to seeing you there. Take care.
