In this context, I wonder if there are really any downsides to leaning in towards having a diet with more fiber and unsaturated fat such as olive oil or avocado oil? Such interventions have been shown to reduce LDL-C, and they seem to have other benefits too, or are generally harmless.
This is a great point! It is a slippery slope of how much do we believe data and how much do we believe numbers that we can manipulate. If Rapamycin helps you live longer then who cares what your lipid panel does? Not all associations correlate with causation.
Did you use on of the Moroccan high polyphenol oils? Did you have any blood sugar changes that can alter your ratios. I am about to check my levels and am worried about bumping up what I am trying to bring down.
I agree that with everything it’s the dose. With my over priced, but extremely high oleocanthal EVOO, I only need a tblsp per day. More like a drug than a food.
I remember when I was a kid and my father gave me a tbls of cod liver oil every day, believe me it was more like a drug.
I’ve switched back and forth between high oleocanthal greek/cyprus varieties. There are good products from other places, just need to try to ascertain the quality/chemical analysis.
I did a classic one variable intervention study…swapping out high dose EVOO for another one of my plant fats, avocado/nuts to try and keep fat macro calories approx the same, before and after blood panel…it was the EVOO (for n=1 me). I continue to consume EVOO, it (the phenols) has a plethora of beneficial pathways, including inflammation, blunting oxLDL lipids. It’s a staple in mediterranean diets.
It is very interesting to hear about the different responses to EVOO. I had been taking EVOO for a long time before I started taking rapamycin. I swallow 1 - 2 tbs. a day with lemon juice; a small glass and take like a shot of tequila with a water chaser. As I have posted my results over time showing that my lipid levels ranged from good to excellent while taking EVOO every day before starting on rapamycin. Even after using a high-dose rapamycin regimen, my lipids were only mildly over the normal range in certain areas. (IMO)
I had even stopped taking a low dose once daily atorvastatin. I will start taking atorvastatin again to get them back in range. I have been taking atorvastatin for decades and have never had any problems with it. I certainly would not recommend statins to anyone who can avoid them while keeping their lipids under control.
There seem to be two camps in this discussion. One says: You are taking rapamycin and rapamycin extends lifespan, so higher lipid levels must be okay.
My camp says: Maybe rapamycin will extend lifespan even more if you keep your lipids in check.
I have no idea which is right.
I think we’ve progressed a little more definitively (on rapamycin/CVD thread), essentially accepting that rising lipids on rapamycin is not benevolent (and not just LDL, but atherogenic TG and TG/HDL, APOB, an important distinction).
You know rapamycin is “working” if disrupting mTOR to some degree when lipids and some minor side effects emerge. Those who have zero changes in blood panel and/or typical side effects are likely at insufficient steady state trough sirolimus levels: this is a fact of every clinical trial with mTOR inhibitors. So if you’re in CVD risk (CAC >>100, metabolic syndrome markers) AND atherogenic lipids risk rise, take a statin or other lifestyle intervention to bring them to a lower level, therefore, allowing the benefits of continued rapamycin to accrue. But if you’ve got essentially a zero (say < 100) CAC and no other CVD and other risk factors, you have significant runway to continue dosing, but monitor.
Personally I’ve eliminated all fiber from my diet (I’ve been doing carnivore for several years) and it just feels so much better: no more bloating, zero flatulence, no more hard or painful stools, no more anal fissures, no more GERD just a completely regular small and easy to void stool