Strange day for me. I start by rewatching the Peter Attia (where he says CAC doesn’t really matter) videos, go to get my CAC done again (a little over a year ago it was 323) and the new value comes up as 303!!!
I’m going in the right direction in spite of having:
LDL of 148 (which they color bright red)
apoB=100
It moved around quite a bit, which makes me wonder what’s going on. LM went from 173 to 29 and LAD from87 to 228, which is a bad thing for sure. But it makes me wonder if it’s moving around so much why it’s so hard to get it to go away.
My wife may be suffering from atherosclerosis. What tests should she run? All she has done is a treadmill test which may indicate atherosclerosis. She has been postponing seeing the doctor as she thinks things will go away after taking Rapamycin, but I think she needs to be a bit more proactive as she was walking yesterday and got short of breath. That should not have happened and I am quite concerned. She is also concerned it may be lung cancer as her last chest X-ray did have a “shadow” and she was recommended to take another chest X-ray at a different angle. This episode has convinced her to see a cardiologist and get another X-ray. However, I want to make sure that all the proper tests are done, so if you could recommend the proper ones, I can make sure the cardiologist assigns them. Thanks in advance for any advice.
Wait he said it doesn’t matter, because LDL and apoB is what’s important (according to Peter), but you seem satisfied with “bright red” LDL and 100 apoB?
“I just don’t see a reason to have an ApoB ever north of 60 milligrams per deciliter.”
—Peter Attia
Yes you have repeated that point and it has been debunked every time with reference to genetic and mendelian randomization studies. Showing benefits in “low risk” patients, because a “low risk” patient is just someone who hasn’t had a long exposure to above optimal apoB. Because age (time) is de facto strongest contributor to risk.
That article is just hilarious. Completely ignoring the totality of evidence including mendelian randomization. It’s like a time capsule to a time before these new methods.
Are you going to keep cherry picking?
You have not yet mustered a response to the mendelian randomization and genetic studies.
Historically, before Rapa and Keto, it was in the 180 area. That’s LDL. And my Trigs were high too, like 145. I just wasn’t worried about it because I believed I was bulletproof. Little misguided there. My diet included lots of junk, also some good.
I took a CAC and it was 285, so went on keto and lost 25 lbs. It’s still gone after 2 years… When I increased my dosage of Rapa the lipids went so high my doctor insisted on statin and I even got a few doses of Rapatha (I think, is that the one you inject?) The statin didn’t really agree and I was worried about the side effects. I have a lot of pain anyway and didn’t need any more. So I quit those and reduced the Rapa and rode it out. Next year CAC was 323. I was worried, so went on 1200 garlic extract and increased my niacin until I could take 3 grams a day.
This brings it down to only a little above 140, which is what Lustgarten says is optimal for all cause mortality. I’m 62 and I can run 2 miles in about 17 minutes. I do that and weights 3 times a week and my work is pretty physical too.
The only reason I considered a statin and tried it for awhile is because I trust Chris Masterjohn, and I know he’s smarter than me. Otherwise I think LDL is doing important work and should be left alone. I know it’s correlated with ASCVD, and lowering it may slow the progression, but I don’t think it’s the cause. I like treating the cause and the LDL should go down by itself. That’s not what I’m doing, but that’s what I’m aiming for.
Improved diet (keto)
improved microbiome (I take all the biotics, including post)
exercise
improved hygiene (oral and skin, postbiotics take care of gut barrier)
I like your passion, but you should read Lustgarten’s free book if you haven’t. It’s called Microbial Burden, and what we can do to fight back. It really opened my eyes about what’s going on. It’s very short.
No, LDL causes heart disease as all of the randomized controlled trials and genetic studies show.
The higher your LDL is above optimal the more you’re increasing your own causal risk for heart attack. Even reducing LDL from 70 mg/dl to 30 mg/dl reduces events. Over a longer time period a higher reduction.
That’s the data. That’s reality. It’s really simple.
The rest is just stories and storytelling.
These 8 life style factors seem reasonable. I like that it reduced all cause mortality, the only thing that really matters. There was 30 years of follow up. They included sleep which is a real positive. I’d also like to see measures for chronic stress reduction and biomarkers of inflammation included.
You’re linking an association study, you cannot say it “reduced all cause mortality”. “It is associated with lower all cause mortality” is correct. That type of information I think can be found in health and fitness magazines. It’s not groundbreaking or coming close to figuring out what’s real.
Because rapamycin raises LDL and other lipids, people who are taking rapamycin now want to make the case that low LDL is not important, despite the facts. There may in fact be a “sweet spot” for low LDL. But, studies showing that extremely low LDL levels increase all-cause mortality do not take into account all of the confounding variables. I am not an advocate of extremely low LDL levels, but I certainly think we should keep it in the normal range.
A recent article in the very prestigious journal JAMA by cardiologists at the University of California and editors of JAMA Internal Med. They discuss in detail the indications, benefits, and risks of statin usage in primary prevention.
In summary, when it comes to primary prevention of the low risk patient and the life time use of statins, the benefit/ risk ratio favors risk. Or, as they conclude, “ time to curb our enthusiasm “.