In your view
A person posting on a forum is
of very little value mostly useless.
The two people in the link video are medical doctors, Lustig
is Professor emeritus of Pediatrics in the Division of Endocrinology at the University of California, San Francisco. What he has to say is highly valuable.
I meant as a citation, a youtube video as evidence on its own is useless. You need to find papers too, that’s why it’s more useful to write out your arguments and finding scientific papers to back up your position as well. The totality of evidence and the quality of that evidence matters.
Papers are useful, but so is a renowned doctor giving the benefit of his experience. Don’t get me wrong. I love reading papers. We all try to read these papers with varying degrees of success, but I don’t think anybody would have much success reading a few papers and formulating judgments in my profession. I suspect it is similar in the medical field.
While it is true that rapamycin has been associated with increased lipids, the claim that rapamycin causes heart disease as a side effect is not supported by the available evidence.
In fact, studies have suggested that TORC1 inhibition may have cardioprotective effects by reducing inflammation and oxidative stress in the heart, which are key drivers of heart disease. For example, a study published in the journal Aging Cell in 2019 found that rapamycin treatment reduced cardiac fibrosis and improved cardiac function in aged mice.
Furthermore, the claim that the lipid number is all that matters when assessing the risk of heart disease is also not entirely accurate. While elevated lipids are a risk factor for heart disease, they are not the only factor. Other risk factors such as hypertension, smoking, and diabetes also play important roles in the development of heart disease. Therefore, simply controlling lipid levels may not completely nullify the risk of heart disease in individuals
I think both of those statements are are accurate… I don’t want to repeat the cardiovascular disease thread discussion here, just saying that higher APOB trends are something I’m going to watch/measure and work to reduce. Nobody knows yet how the beneficial effects of rapamycin on the heart balance out against any possible lipid increases, in humans.
The data of people with genetically PCSK9 loss-of-function says otherwise.
Yes it is, it increases atherogenic lipoprotein concentration, hence it causes heart disease. You’d have to show practically impossible evidence that it would counter negative effects from the increase in atherogenic lipoproteins. Mice studies cannot counter RCT’s and genetic data in humans, that would make no sense.
If a fallacious appeal to authority argument is going to be used, it should be done for an expert lipidologist like Allan Sniderman or Thomas Dayspring. Not a pediatric endocrinologist. In an earlier video that was linked of Lustig, he literally confused a table of studies with a meta analysis. The paper which also argued against meta analysis as a method.
I also doubt Joseph understands what apoB is, since Lustig seems to be fond of measuring triglycerides, which apoB also measures the lipoprotein concentration of.
ASCVD and heart disease and risk is really easy to understand, just people like Lustig wants to be Lustig (It’s Swedish for funny) and do a reverse Occam’s razor and muddy the waters.
Forgive me. I didn’t realize you were an MD. If yes then, of course, the studies would mean more to you than to me. If you were not a cardiologist, I would take the views of a pediatric endocrinologist over yours any day of the week.
I think you missed the part where I said it was a fallacy.
Arguments and evidence stand on their own two feet.
I mentioned Thomas Dayspring and Allan Sniderman.
If you’re not going to read any science papers yourself, why not listen to Sniderman instead?
Oh yeah, humans are WAY more vulnerable to cardiovascular disease than mice, which barely die of it.
ApoB is mostly bad when oxidized/glycated - thus reductions in inflammation/ROS [with BOTH rapamycin+metformin+taurine+carnosine] should reduce much of the risk associated with increased lipids.
Citation needed, and mechanistic speculations isn’t high quality evidence, it is actually next to the lowest on the evidence hierarchy. Until there is (1) genetic studies showing significance of inflammation/ROS (2) randomized controlled trial of a drug via the same mechanism, then it is too early to say.
And if that was the case, just take the drug proven in a randomized controlled trial.
To gamble on mitigating causal risk with increased lipoprotein concentration via other mechanisms, is just an unnecessary gamble imo. When there are safe drugs to lower said lipoprotein concentration.
Randomized controlled trials for cardiovascular disease are meaningless. They are too short. I could send you a link, but why bother?
As I have shamelessly posted many times from "Rapamycin for longevity: opinion article" by
Mikhail V. Blagosklonny
“If you wait until you are ready, it is almost certainly too late.” ~ Seth Godin
No, they establish a baseline which you can extrapolate from using genetic studies.
And short term CVD trials do show beneficial effects.
But this discussion is done because I don’t think you’re serious.
Are you using ChatGPT? That paper doesn’t exist.
A couple weeks ago I was doing research on Trametinib using ChatGPT and I asked it for academic references. I spent the next hour trying to find any of the references it quoted. I couldn’t, they were all made up.
I had the same experience - it makes up papers! Really makes you wonder about it.
According to Dr. Lustig and most of the other experts, avoiding sugar plays the most important role in prevention of atherosclerosis and heart disease. Insulin resistance affects development or worsening of hyperlipidemia. Low carb diet is probably the most reasonable.
Sugar only plays a role in as far as it reduces apoB, the vast majority of apoB is due to saturated fat, so for most people a low carb diet will have the opposite result.
apoB measures all atherogenic lipoproteins, including those with triglycerides.
But it’s possible to have a healthy low carb diet, replacing saturated fat for polyunsaturated or monounsaturated fat. And measuring apoB every now and then to make sure things are (or are going) in the right direction.
Search “LDL” on the keto subreddit for some morbid wednesday reading 
“We still have LDL denialists out there”
“It’s one of the most dangerous things I see, actually”
I have a friend who did keto and had sky-high apoB. Tbf it was meat-based keto, not MUFA-based keto
Jose Ricon also speculated that the increasing prevalence of keto may increase heart disease risks in people in the future
I tried plant-based keto for like a month and while my panels weren’t terrible, they were still elevated a bit. Even olives and nuts have SOME saturated fat in them, and the unsaturated fats don’t increase HDL that much (HDL seems more genetically determined)