I’m not sure where to put this post, but I guess it has most to do with CVD.

Lustgarten talked a lot about oral bacteria becoming the plaque in your arteries. His book is all about microbial burden. In the bloodstream, in the mouth, even on the skin and in the gut. And your ability to fight it becoming worse with age. This has me thinking.

Was it Matt Kaeberlein that talked about oral bacteria or some kind of oral hygiene relative to Rapamycin? Where did I hear that? Is there anything about Rapamycin’s ability to decrease the microbial burden in the gut or in the mouth?

It seems to me that if you are inhibiting TORC1 in your system, then the microbial burden is also exposed to this and I just am wondering what effect it has. Does Rapa kill bacteria in your bloodstream and mouth?

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There’s this:

I believe Jonathan An is running a study on humans as well.

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Yes, thank you for finding that. And it does support the idea that fixing the microbial burden in the mouth could also fix inflammation in the arteries.

This is probably obvious to you guys, but the large dose every couple weeks probably has a huge effect on the microbial burden overall in the body. Maybe the lipids go up because there is a die off of things in the bloodstream and they have to clean up the mess. Later, the mess is gone and if you keep treating then the burden stays low. The lipids go back down.

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Yes, there is a study at the UW Dept of Dentistry on rapamycin & oral health. I think it’s in people, though all I find is about mice.

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I’m a little surprised Rapa has this effect of altering the bacterial load in the oral. It’s not an antibiotic. I don’t understand it, but I still think it is very important after reading Lustgartens book. By what mechanism and in what way does it alter the microbial load?

Also this:

“LDL acts as a carrier for LPS and is involved in mechanisms to inactivate it. Collectively, these data provide further support for the hypothesis that aging and the progression of CVD are associated with increased microbial burden.” This is Lustgarten again.

He then shows how a greater load of LPS causes HDL to increase.

LPS is lipopolysaccharide, which I understand to be a chunk of the cell wall of your microbial burden. LPS could also be thought of as “Little Pieces of Shit”. This stuff is bad news and he goes to great lengths to explain it.

So, to take one more swing at it here, your LPS will increase if Rapa kills off a bunch of microbial burden. This will drive up both LDL and HDL, because their job is to clean up the mess. As time goes on the mess will be cleaned up, the microbial burden will stay low and your lipids should decrease to normal. I think this explains it, but my problem is that nobody is really talking about it and Rapa is not a big killer of bacteria. Though it’s presence may push on the scale in favor of the friendlier bacteria. Why is nobody looking at this?

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It’s all very interesting. Here’s a look at the role of cholesterol and its sub components in fighting and preventing infections in layman’s terms.

The risk of infections could explain the increased mortality rates seen in large population studies associated with low LDL levels. It’s possible that as a modulator, rapamycin may be setting lipids at an optimal level according to circumstances. This response isn’t fixed but tends to be in flux.
All of this supports my assertions that we basically don’t know what we’re doing when it comes to a very complex system like the human body. This is even true of TC and LDL where it’s very possible to go overboard.

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Fantastic article and discussion. Most of the research in Lustgarten’s book came from 20 or 30 years ago.

Very complex subject, thanks again.

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NIce! this article makes me feel my current LDL-C of 141 is protective when you take it with a zero CT Coronary Calcium Score. Was as high as 179 in late April of this year. Rapamycin tends to push it up too.

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Don’t count on it forever. No, disrespect, but people like to find ways around facts that don’t agree with their current beliefs.


Statin Denial: An Internet-Driven Cult With Deadly Consequences

ACP Journals

There Is Urgent Need to Treat Atherosclerotic Cardiovascular Disease Risk Earlier, More Intensively, and with Greater Precision. A Review of Current Practice and Recommendations for Improved Effectiveness. - ScienceDirect

There’s also no question about the role of inflammation in the development and progression of CAD.

It’s very conceivable that chronic inflammation is necessary for the detrimental effects of lipids , and in your case a low level of inflammation may be very protective.

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So now people who question the usage and side effects of statins are “ an internet driven cult”.

Seems a little narrow minded and harsh.

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I would be ignoring my LDL, which is between 140 and 175, if not for Chris Masterjohn. Most of the stuff I read and watch says 140 is optimal and for an old person, the higher the better. Instead I’m taking 3 or 4 grams of Niacin a day plus garlic pills and it is getting under control.

So now I’m worried that I am unintentionally increasing my microbial burden.

I’ve been reading Chris Masterjohn for years, since when he used to write for WAPF. When he had no academic, I should say he had a BS in history. I know this guy pretty well and he is as objective as a person can be. Problem is that he believes papers and many of the papers on statins were done by pharmaceutical companies and they were trying to sell statins.

If you have an increased microbial burden due to loose junctions in your gut or bacteria in your mouth, then you need higher lipids to control this. Thus higher lipids. Control the lipids and it makes the problem worse. Lustgarten says to use xylitol gum or mouth rinse plus flax oil through the teeth to kill bacteria.
As for the loose junctions, you need soluble fiber or Inulin. It sounds like Acarbose works too. All these things produce gas like crazy. Because you are feeding your gut buddies and this is what happy gut buddies do.
Heart disease may go up with lipids because lipids increase with the microbial burden that causes heart disease. Statins do all kinds of stuff that helps, apparently. They also have nasty effects. So that is a separate issue. Killing off your microbial burden is a win win.

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Exactly - my extensive GlycanAge blood test showed no or minimal inflammation - one of the reasons my biological age was 37 - this reduction in inflammation I attribute to the 2 years of rapamycin.

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Just, say’n :laughing:
Not harsh at all. Too many people just choose to ignore the preponderance of the evidence because it doesn’t fit in with their present beliefs.
I see it time and again on this forum where people just simply refuse to believe the evidence and attribute the evidence they don’t like to “Big Pharma” etc.

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No, I’m suggesting that the authors are overly harsh and opinionated when they suggest that those who disagree with them regarding statins are an internet cult.

At one point in the article they argue for aggressive intervention for LDL levels shortly after birth. Maybe they’re part of a statin cult.

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So now I’m worried that I am unintentionally increasing my microbial burden.

Microbes are not inherently bad. We need a healthy microbial environment for our own health. The science doesn’t have the knowledge of how to make it happen (despite people talking about pre- & pro-biotics), but killing bacteria in & of itself isn’t a good idea.
End of rant … :slight_smile:

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“Maybe they’re part of a statin cult”
I have no horse in this race. I am not on statins, just pointing out the facts.

Too many people just choose to ignore the preponderance of the evidence because it doesn’t fit in with their present beliefs.

The current point I am attacking is: Rapamycin raised my LDL-C, but rapamycin extends life so higher LDL-C must be okay.

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Cigarettes have a preponderance of evidence which is why no one is saying that it’s okay to smoke while on rapamycin. LDL, not so much, and statins definitely not so clear cut.

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I don’t really mind rants if it helps understand what’s going on. I appreciate your input.

If you read Lustgarten’s book, which is a free ebook if you have a kindle. I read through an app on my phone:

He spends the entire first part of the book going over the problem with microbial burden, and does it much as an engineer would. How many in the blood, how many WBCs, how we know…what they do. If you inject LPS into a person they will get type 2 diabetes. They did it. You should read the book, it takes about 4 hours. Of course I had to read it 4 times, so maybe 16 for me.

So maybe microbes in the gut are good. In the blood we have several lines of defense and still a burden. If you manage to clean them out it will lengthen your life and make you feel better. I don’t know how it does this but Rapa manages to reduce the burden both orally and in the blood. I kinda think this could be a big part of the magic of Rapa.

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Are you saying that my high (145) glucose level is ok whilst taking Rapamycin and that I shouldn’t medicate it? Prior to Rapamycin my glucose level was around 100

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