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Search complete. 9 mentions across 7 episodes found for "SOD2".

Sep 9, 2026

Anthony JayGUEST
13:25
But it's important because if you have a gene-- Like, I literally just got off the phone with somebody who has a hemochromatosis gene, and they have a superoxide dismutase gene.
Anthony JayGUEST
13:37
It's called SOD2.
Sarah KleinerHOST
13:39
Hmm.
Anthony JayGUEST
13:39
And that SOD2 gene is a tenfold higher risk of heart disease if your iron is high.
Anthony JayGUEST
13:45
It's only a risk-
Sarah KleinerHOST
13:46
Wow
Justin HarrisHOST
12:00
I think peptides are a great example of that as well, because everybody's on them, everybody's talking about them, and they're kind of just doing it in this Wild West format where it's just like, "I heard this works for this.
Justin HarrisHOST
12:12
Let's give it a shot." Well, we can be a lot more detailed, right? We can go into a genetic report and say, "Hey, I have a suboptimal mitochondrial pathway," right? We look at genes like SOD2, GPX, CAT, which is this catalase enzyme.
Justin HarrisHOST
12:27
So if you have underlying genetics that are suboptimal there, that can be a bit of an indicator that, hey, maybe I should guide my toolkit towards mitochondrial health.
Justin HarrisHOST
12:37
You should probably do it with a clinician's guidance, you should do it with lab work and things like that, but it lets you know that this is a pathway that at a baseline requires some support.
Yuan ZhaoHOST
4:29
The researchers also observed changes in proteins involved in antioxidant defense, mitochondrial regulation, and apoptosis.
Yuan ZhaoHOST
4:38
VPS13C knockdown reduced SOD1, SOD2, NRF2, PGC1-alpha, and the anti-apoptotic protein Bcl-2 while increasing the pro-apoptotic protein Bax.
Yuan ZhaoHOST
4:51
Treatment with the three herbal extracts significantly reversed these changes.
Yuan ZhaoHOST
4:56
The extracts also increased mitochondrial membrane potential and mitochondrial mass while reducing mitochondrial superoxide production.
Yuan ZhaoHOST
5:04
Quote, "Depletion of VPS13C leads to mitochondrial dysfunction." End quote.
Yuan ZhaoHOST
5:10
These results suggest several possible mechanisms underlying the observed cellular protection.
Yuan ZhaoHOST
5:16
Increased SOD1 and SOD2 may strengthen antioxidant defenses, while NRF2 and PGC1-alpha are involved in responses to oxidative stress and regulation of mitochondrial function and biogenesis.
Yuan ZhaoHOST
5:30
Changes in Bcl-2 and Bax are also consistent with reduced susceptibility to apoptotic cell death.
Mike BelkowskiHOST
31:09
Then we have good old mitochondrial quality control, whereby humanin has been shown after TBI to normalize disruptions in mitochondrial fusion, fission, mitophagy, and biogenesis, including pathways involving PGC1 alpha.
Mike BelkowskiHOST
31:28
Oxidative stress protection, whereby humanin influenced antioxidant defenses such as SOD2 or SOD2 and has a broader literature supporting protection against oxidative stress and mitochondrial injury.
Mike BelkowskiHOST
31:43
Then we have anti-apoptotic and neuronal survival signaling, whereby humanin is well-characterized as a cytoprotective and anti-apoptotic peptide and has been studied for protecting neurons from multiple forms of cellular stress.
Mike BelkowskiHOST
32:02
And then last but certainly not least, we have neurodegenerative resilience, whereby human was originally identified through its ability to protect neurons from Alzheimer's-associated insults, and subsequent research has explored roles in amyloid toxicity, neuroinflammation, autophagy, and mitochondrial dysfunction.
Kashif KhanGUEST
4:46
... taking in excess oxygen, then you're making more soot without the ability to neutralize it into water and pee it out, which is what happens through hydrogen oxide, peroxide synthesis.
Kashif KhanGUEST
4:56
So that's the SOD2 gene pathway.
Kashif KhanGUEST
4:58
So that was one thing he had going on.
Kashif KhanGUEST
5:01
Now, after we know it's accumulating because of the excess oxidation of his habit of exercise and the genetics of not being able to process the oxidation, there's a second pathway that uses glutathione, this molecule that we all talk about, this, uh, detox tool, to remove whatever got left over, and that gene he was missing.
speaker_1HOST
18:25
It actually upregulated the cell's own endogenous antioxidant enzymes.
speaker_0HOST
18:29
It forced the cell to produce more of its own internal bomb squad enzymes like GPX-1 and SOD-2 to prepare for the next attack.
speaker_1HOST
18:36
Precisely.
speaker_1HOST
18:37
It neutralized the immediate threat, recycled the debris to repair the damage, and then trained the cell's internal army to be stronger for tomorrow.
Sam ShayGUEST
26:29
You need janitors to run around and put out the sparks so the building doesn't catch on fire.
Sam ShayGUEST
26:32
You've got three genes, MNSOD, GPX1, CAT, that are the three main janitors of the mitochondria, and if you've got red and yellow versions, or bad or slower janitors, they can't catch all of the sparks, therefore you're at higher risk of your factory catching on fire.
Sam ShayGUEST
26:45
That's the easiest way to think about it.
Sam ShayGUEST
26:47
Now, one thing that's unique about Fitgenes testing is that these drivers are in a order of priority.

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