Mauritio
Member
- Joined
- Feb 26, 2018
- Messages
- 5,669
Research on Selegiline seems to be picking up and researchers are now using it for all kinds of disorders like fatty liver disease or atherosclerosis, not just Parkinson's and anti-aging.
This study looked the causes of atherosclerosis and if MAO-B has something to do with it. It turned it, it does.
MAO-B causes oxidative stress in the blood vessels, which is central to atherosclerosis. Selegiline was able to reduce those inflammatory markers, by working as an antioxidant.
They noticed that simply putting the animals on a high fat diet was enough to cause the increase in MAO-B and ROS.
I suspect the high fat diet, was also a high PUFA diet, since the MDA levels were increased, which is normally caused by a high PUFA diet, so it looks like PUFA can increase MAO-B and thus serotonin on its own.
They also did an in vivo study showing that selegiline, in normal human doses, can ameliorate atherosclerosis.
They also showed that this amelioration was downstream from a change in the microbiome: Selegiline increased a few beneficial bacterial genera like Akkermansia, which has a lot of its own pro-metabolic effects ( A. Muciniphila Improves Insulin Sensitivity, Lowers Weight+ Cholesterol+reduces Endotoxin Load) and decreased even more some pathological genera.
Here you can see that selegiline decreased total bacteria genera a lot more than the number it increased, so I presume that the total bacteria number went down. Interestingly the bacterium genus that decreased the most was Clostridia. The study about serotonin I quote below shows that Clostridia is among the top serotonin producers in the gut. Reducing clostridia and another genus, lowered serotonin production in the gut by as much as 50%!
" ...in mice, a specific mixture of bacteria, consisting mainly of Turicibacter sanguinis and Clostridia, produces molecules that signal to gut cells to increase production of serotonin. When Hsiao's team raised mice without the bacteria, more than 50% of their gut serotonin was missing."
What I found interesting as well, is that animals on a HFD, had zero Akkermansia bacteria in their gut, just after starting Selegiline they increased, which can be seen here:
So, Selegiline was able to alter the gut microbiome, who would have thought?
Although the effect on the atherosclerosis is downstream of the change in the microbiome, I suspect that the effect on the microbiome is downstream from a reduction in serotonin (through MAO-B inhibition): I posted a study years ago on how serotonin itself can alter the microbiome (Serotonin Itself Alters The Microbiome, Central Role Of Only 2 Bacteria Species) so this might be the root of all evil once again.
- Inhibition of MAOB Ameliorated High-Fat-Diet-Induced Atherosclerosis by Inhibiting Endothelial Dysfunction and Modulating Gut Microbiota
This study looked the causes of atherosclerosis and if MAO-B has something to do with it. It turned it, it does.
MAO-B causes oxidative stress in the blood vessels, which is central to atherosclerosis. Selegiline was able to reduce those inflammatory markers, by working as an antioxidant.
They noticed that simply putting the animals on a high fat diet was enough to cause the increase in MAO-B and ROS.
I suspect the high fat diet, was also a high PUFA diet, since the MDA levels were increased, which is normally caused by a high PUFA diet, so it looks like PUFA can increase MAO-B and thus serotonin on its own.
They also did an in vivo study showing that selegiline, in normal human doses, can ameliorate atherosclerosis.
They also showed that this amelioration was downstream from a change in the microbiome: Selegiline increased a few beneficial bacterial genera like Akkermansia, which has a lot of its own pro-metabolic effects ( A. Muciniphila Improves Insulin Sensitivity, Lowers Weight+ Cholesterol+reduces Endotoxin Load) and decreased even more some pathological genera.
Here you can see that selegiline decreased total bacteria genera a lot more than the number it increased, so I presume that the total bacteria number went down. Interestingly the bacterium genus that decreased the most was Clostridia. The study about serotonin I quote below shows that Clostridia is among the top serotonin producers in the gut. Reducing clostridia and another genus, lowered serotonin production in the gut by as much as 50%!
" ...in mice, a specific mixture of bacteria, consisting mainly of Turicibacter sanguinis and Clostridia, produces molecules that signal to gut cells to increase production of serotonin. When Hsiao's team raised mice without the bacteria, more than 50% of their gut serotonin was missing."
What I found interesting as well, is that animals on a HFD, had zero Akkermansia bacteria in their gut, just after starting Selegiline they increased, which can be seen here:
So, Selegiline was able to alter the gut microbiome, who would have thought?
Although the effect on the atherosclerosis is downstream of the change in the microbiome, I suspect that the effect on the microbiome is downstream from a reduction in serotonin (through MAO-B inhibition): I posted a study years ago on how serotonin itself can alter the microbiome (Serotonin Itself Alters The Microbiome, Central Role Of Only 2 Bacteria Species) so this might be the root of all evil once again.
- Inhibition of MAOB Ameliorated High-Fat-Diet-Induced Atherosclerosis by Inhibiting Endothelial Dysfunction and Modulating Gut Microbiota
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