We’ll, I’ve made the point that the LDL from rapamycin must be viewed in the context of all of the other risk factors.
We also disagree about “ safely “ in the context of lipid lowering meds.
I think that it’s apparent that we’re just not going to agree on this, but the debate has been lively and has drawn alot of interest.
I’m glad that we’ve had this discussion because it’s an important topic and deserved a deeper look. We’ll know more about rapamycin and it’s cardiovascular implications in the future.
Again, let’s look at the larger picture. A meta-analysis detected no effect on cognition.
“CONCLUSIONS
Statin therapy was not associated with cognitive impairment in RCTs. These results raise questions regarding the continued merit of the FDA warning about potential adverse effects of statins on cognition.”
These cohort studies tell very little. People that don’t eat breakfast have a higher mortality rate than people that do. [So intermittent fasting is bad.] If you are above 65, then you live longer if you are overweight than if you are at a normal weight. [We should all gain weight.]. People that drink alcohol live longer than people that don’t drink. [Alcohol is healthy.] If you try to draw meaningful conclusions from any of these studies, you do so at your peril. Because you will reach the wrong conclusion each time.
The Dr was looking at more than LDL-C, but she was right not to ignore it. That patient might have had a CAC score of zero. But that also tells very little. She did a coronary angiogram. And a CAC doesn’t begin to compare with a cath. There is a lot of misinformation out there.
Cholesterol and the particles that contain cholesterol are two different things. This is why doctors who are up to date measure ldl-p (not to be confused with ldl-c) and / or ApoB. Total cholesterol itself, does not say much with regard to CVD risk.
I am sorry, I don’t quite understand the need for an ApoB test.
Can you cite any studies where ApoB was very divergent from the LDL-C and VLDL cholesterol test results?
On my latest Quest Diagnostics comprehensive metabolic panel, the lipid portion now includes VLDL cholesterol along with LDL-C in the lipid panel results. This was not provided in previous tests so I only have one VLDL cholesterol data point.
So it would surprise me if there was a significant divergence between these two tests and ApoB
I’d consider cholesterol measurement to be the unnecessary expense, to tell the truth. ApoB gives you the number of atherogenic particles, which is a more direct assessment of atherogenecity compared to the lump sum of how much cholesterol is in all those particles without telling you how many particles there are (i.e. LDL-C).
I would do a poor job explaining but Peter Attia has a lot good information on the subject (Ford Brewer also). Here is one of the many. The test costs $48.
"Started patient on high intensity statin immediately " atherosclerotic plaques literally take decades to form, you are not doing anything by putting them on a statin immediately…
Oh well at least she unblocked her which she did after I pointed out how preposterous high carb diets are. How could a diet which would literally rot the teeth out of our mouths (especially without modern dental care) be any good for the rest of our bodies? Really MDs have no clue about anything related to teeth and I should know because I was an MD before I became dentist…
In this commentary in The Lancet a good argument is made for Apo b over LDL. Note that high LDL is associated with Increased longevity and less diabetes risk. Not so with Apo b.
It’s possible, however, that ApoB may be U shaped like everything else. Several studies have suggested a protective role of both LDL and ApoB in preventing and fighting infections. This study of trauma patients supports such a protective mechanism.
This is particularly important for those of us on rapamycin.
No association between LDL and severe infection risk in this study. Also, we don’t see higher risk of infection when pharmacologically lowering LDL with meds, so again this seems to me like a correlation without causation.
So you’ve posted a causation study while arguing against causation studies.
Here’s one on over 37,000 patients and it’s the same theme. LDL lowering cardiovascular mortality while increasing total mortality, and more specifically infection risk.
This requires more than a casual dismissal in rapamycin users who May already have such an increased risk ( though I’m somewhat skeptical).
Heart disease caused by the buildup of plaque takes literally decades to form and literally decades to undo. So starting someone on intensive statins absolutely does something. You’re starting the process of undoing the harm. I’m not sure I understand the logic here.
Here’s a detailed look at the physiological mechanisms involved in the role of lipids in protecting us from infections.
U shaped like everything else and something to certainly consider before Extreme lipid lowering.
My take away is that if you live in Bangladesh, India, Nepal, Sudan, Ethiopia, and Brazil or are otherwise prone to a certain parasitic infection, then high levels of LDL may be helpful against that infection and equally unhelpful for other common types of infections. I didn’t find that study very compelling. But is anyone advocating extreme lipid lowering? I thought we were concerned about elevated levels of lipids.
atherosclerotic plaques literally take decades to form, you are not doing anything by putting them on a statin immediately…