Wow... every time I see you explain the complex systems I'm amazed at the complexity and further amazed that someone figured this out. How is this stuff deciphered? That would be a good topic.
Long back it was discovered that drinking fresh pomegranate juice or drinking tea made from boiling dried pomogranate seeds(anardana) daily, decreased arterial plaques.Not sure whether the same mechanism is at play.
Amazing and well explained lecture as always. But the cancer cell part was confusing, the explanation was a bit contradictory. This is because initially there was a lot of reactive oxygen species produced by the dysfunctional mitochondria of the cancer cell (38 min mark) and when the mitochondria is repaired by Urolithin a and it produces I guess less relative oxygen species because it is more healthier why does this cause more oxidative stress and apoptosis because previously when the cancer cell had dysfunctional mitochondria it was producing more reactive oxygen species and was still stable
This is a good question and with a complex answer (hence I had skipped explaining too much, but you caught it). Cancer cells have increased ROS because of the dysfunctional mitochondria, and also because of metabolic pathway shifting towards glycolysis that further strains mitochondria causing them to produce ROS. Finally the NADPH oxidase (NOS) are overexpressed in the cancer cells producing ROS as well. Local immune cells produce ROS to combat the cancer cells creating a high ROS environment around the cancer cells. These ROS also spill into the cancer cells. Pro-inflammatory cytokines also trigger cancer cells to generate ROS. Cancer cells' ER also is under stress to produce a huge amount of proteins resulting in ROS production, and more... Top the above conditions with reduced antioxidant capacity of the cancer cells. Now, when we administer UA it triggers mitophagy. During the initial phase of mitophagy the mitochondria produces a burst of ROS as well. This burst of ROS tips the already ROS filled cell and apoptotic signals get triggered. So the ROS increase is due to mitochondrial dysfunction, metabolic pathway changes, organelle over-function, over-expression of NOX, and reduced anti-oxidant capacity. Administering UA tips the balance towards even more ROS leading to apoptosis. If a cancer cell could survive this initial ROS burst then in theory mitochondrial function restoration and clearance of damaged mitochondria could lead to less ROS. But, hopefully the cell dies before then.
Well there's studies that show that increasing proteins, like taking whey, may decrease CRP. So in that case mTOR must go up, and yet there is less inflammation, thanks to increased glutathione or whatever.
Going back to your talk on EBV reactivation in Long Covid, you mentioned reducing ROS via glutathione and NAC. Seems like Urolithin A can also aid in this? Also, blocking mTOR can also be immuno-supportive or immunomodulating in the same way Rapamycin can helps with T cell function or production?
Are PINK1 and BNIP3 activated independent of mTOR inhibition by AMPK? Is it possible to have high mTOR to stimulate muscle growth and tissue regeneration and the same time activate autophagy to clean up the cell of all the debris generated?
Please please i had to interfere for this video. Sorry i did not watch it but the first phrase was enough to make a comment. Urolithin A has no medical benefit. I have followed this product for the last few years, written to the company in Switzerland and challenged their human clinical results without much of an answer. None of the benefits were statistically significant. Maybe it does something in animal studies but human benefits are not demonstrated. Can you share your credentials.
The body is truly amazing! I saw a shirt that that said “make mitochondria great again”!
How cute!
WOW
Nice
😂😂😂😂
There is another one and it says Make native america great again.
Wow... every time I see you explain the complex systems I'm amazed at the complexity and further amazed that someone figured this out. How is this stuff deciphered? That would be a good topic.
Thank you, Dr. Been🙏
You are welcome!
Excellent clarity, helping put the pieces together! Thank you Mobeen!
My pleasure!
Beautiful lecture! Would love to see an interview with Thomas Seyfried!
Thanks!
Welcome!
Well done thank you for time
Incredible ❤ you are amazing!
Thank you so much!!
Very informative!! I tried explaining some of this to my neighbor, but all she wanted me to ask you was, " Can it fix my crepey skin?"
Thanks! Very informative.
Thank you. 🙏
Thank you
Thank you for your lectures ❤
You're most welcome!
another difference: the pomegranates may be different - more or less ripe, organic or not, over-ripe, unripe, different in size, etc.
True
Long back it was discovered that drinking fresh pomegranate juice or drinking tea made from boiling dried pomogranate seeds(anardana) daily, decreased arterial plaques.Not sure whether the same mechanism is at play.
Very interesting and informative thank you.
Do you know if PINK1 and BNIP3 activated independent of mTOR inhibition by AMPK?
Glad you enjoyed it!
Wow, what an amazing lecture. Thank you.
Glad you enjoyed it!
Amazing.
Thank you 👍
You are welcome
Thank you
You're welcome
So what steps can one take to keep mitochondria functioning optimally? Urolithin A is very pricy !! And not affordable by everyone?
Amazing and well explained lecture as always. But the cancer cell part was confusing, the explanation was a bit contradictory. This is because initially there was a lot of reactive oxygen species produced by the dysfunctional mitochondria of the cancer cell (38 min mark) and when the mitochondria is repaired by Urolithin a and it produces I guess less relative oxygen species because it is more healthier why does this cause more oxidative stress and apoptosis because previously when the cancer cell had dysfunctional mitochondria it was producing more reactive oxygen species and was still stable
This is a good question and with a complex answer (hence I had skipped explaining too much, but you caught it). Cancer cells have increased ROS because of the dysfunctional mitochondria, and also because of metabolic pathway shifting towards glycolysis that further strains mitochondria causing them to produce ROS. Finally the NADPH oxidase (NOS) are overexpressed in the cancer cells producing ROS as well. Local immune cells produce ROS to combat the cancer cells creating a high ROS environment around the cancer cells. These ROS also spill into the cancer cells. Pro-inflammatory cytokines also trigger cancer cells to generate ROS. Cancer cells' ER also is under stress to produce a huge amount of proteins resulting in ROS production, and more...
Top the above conditions with reduced antioxidant capacity of the cancer cells.
Now, when we administer UA it triggers mitophagy. During the initial phase of mitophagy the mitochondria produces a burst of ROS as well. This burst of ROS tips the already ROS filled cell and apoptotic signals get triggered.
So the ROS increase is due to mitochondrial dysfunction, metabolic pathway changes, organelle over-function, over-expression of NOX, and reduced anti-oxidant capacity. Administering UA tips the balance towards even more ROS leading to apoptosis. If a cancer cell could survive this initial ROS burst then in theory mitochondrial function restoration and clearance of damaged mitochondria could lead to less ROS. But, hopefully the cell dies before then.
Wonderful
Thank you
DrBean, could you please look into, and do a discussion on C15, the recently discovered essential fatty acid?
Will do
Thank you. You have made a real difference in my family's life.
You are welcome. Glad my work is helpful 🙏
Thank u
Well there's studies that show that increasing proteins, like taking whey, may decrease CRP. So in that case mTOR must go up, and yet there is less inflammation, thanks to increased glutathione or whatever.
Yes. There are many inflammatory pathways that can operate independent of each other.
Consider a show with dr Angus Dalglish, an oncologist keeping lethal cancer patients alive for decades.
I went to Substack to follow you there and could not find you anywhere. Where are you? Could you provide a link?
Here: mobeensyedmd.substack.com/
Going back to your talk on EBV reactivation in Long Covid, you mentioned reducing ROS via glutathione and NAC. Seems like Urolithin A can also aid in this? Also, blocking mTOR can also be immuno-supportive or immunomodulating in the same way Rapamycin can helps with T cell function or production?
Can you feel like your detoxing when taking UA?
Could it be that our body, in trying to get rid of excess glucose cells, develops cancer cells that will gobble up the glucose?
I haven't come across this mechanism.
Interesting
Are PINK1 and BNIP3 activated independent of mTOR inhibition by AMPK? Is it possible to have high mTOR to stimulate muscle growth and tissue regeneration and the same time activate autophagy to clean up the cell of all the debris generated?
Yes to your first question. Second question needs a discussion.
Will this be good for stage 4 pancreatic cancer patient??
where does one get urolithin A? I must have missed it.
Pomegranate
Supplement
Please please i had to interfere for this video. Sorry i did not watch it but the first phrase was enough to make a comment. Urolithin A has no medical benefit. I have followed this product for the last few years, written to the company in Switzerland and challenged their human clinical results without much of an answer. None of the benefits were statistically significant. Maybe it does something in animal studies but human benefits are not demonstrated. Can you share your credentials.
Thank you Dr. Been! ❤