I have approached the arterial health question with two minds. First, as a person with a less than ideal genetic profile and second as a scientist attempting to sort out what I believe is still a messy empirical field. The common goal of both mindsets is to arrive at an optimum plan to preserve arterial health.
My current plan focuses on maintaining very low inflammation (multiple strategies) and reducing Apo(b) as the most beneficial metrics to manage. I think this plan is transitional. I believe a better model is out there waiting to be discovered.
While this new Medscape article is not comprehensive, I found it a good read when combined with the comments.
Even in this article there is a strong theme of “statin side effects are probably not real but if you really are upset there are alternatives.” I wonder if it relates to a lack of connection between statin “experts” and personal experience with maintaining physical fitness. Attia stopped using a statin. Did he ever say why? I’m quitting because atorvastatin and rosuvastatin make me ache and make me weak. I say that having denied it in my own mind for a year. I blamed every other drug and supplement before settling on what should have been easier to identify…the statin.
I will use Bempedoic acid to keep my apoB levels low. I am also doing everything else I can to get my mitochondria healthy and my arteries healthy to limit the effect of apoB particles on my arteries.
I started taking 5mg of Manganese about 8 months ago. In combination with my weight management protocol I’ve seen my PWV, pulse wave velocity drop. That is a good thing, the dropping part
@Joseph_Lavelle. I found the article naively condescending; to call statins “settled science” is fundamentally out of touch with the meaning of scientific evidence. The comments were better than usual and, among other things, added strength to the inflammation model of explaining arterial damage.
Vyvyane Loh MD does a good job explaining more of the details that get glossed over or ignored in most discussions and arguments over this truly complicated topic.
Here is one of her episodes
I will have an episode on this general area with Dr Twyman coming out very soon.
It could be that statins are not the best, and something like PCKS9i, siRNA, ezetimibe, bempedoic acid, or later on CETPi are. There isn’t just a lot of data for the other treatments and they tend to be expensive and not widely available.
Did you switch to something else, or if I remember correctly CoQ10 helped with your side effects?
I’m experimenting with atorvastatin now but yeah I had muscle aches from rosuvastatin until supplementing with ubiquinol. But lately I’ve had side effects from ubiquinol so I had to stop that for the time being.
The horse we are betting on is the genetic, mendelian randomization data, so method of lowering apoB probably doesn’t matter that much. It’s typical to switch around until someone finds a statin which works best for them (or other drug, or even supplement(s)).
I used to use berberine before statins and it probably lowered my apoB a bit, but it made one of my hands feel weird, and one toe like gout almost. Crestor I don’t think I had noticed any side effects. Atorvastatin might’ve snapped a tendon a little bit in one of my fingers.
Modification is without sacrifice for most but not all.
The key is to find something which you can tolerate or pay no price, at least in the short term.
Well, I haven’t read your attachment, but I’ll comment on rapamycin and arterial health.
I’m 67 and, at 61, had serious kidney failure and complications of non-alcoholic fatty-liver cirrhosis (hepatorenal syndrome, hepatic encephalopathy, 12 rounds of dialysis) prior to a liver transplant.
A year or so post transplant, already back in good cardio-shape, I had a coronary artery Calcium scan. Gadzooks: CACS score of 1126. That’s 95th %-tile bad, for my cohort. So the cardiologist did a treadmill EKG stress-test, and they stopped the test when my HR got to 170, but I was still going strong. There was no stenosis, or narrowing of the lumen (flow-restriction).
Vascular smooth muscle cells (VSMCs) occupy the middle thickness of arterial walls, and contract or relax, to control blood pressure and flow.
Unlike skeletal or cardiac muscle, the VSMC are not terminally differentiated. Because blood vessels have to respond to injuries, the VSMC can still replicate, and even MORPH! into other cell types, including cartilage and even bone (some coronary autopsies have found bone marrow growing in calcified arteries).
So, various changes in the metabolic milieu change the epigenetic expression of a VSMC (and it’s descendants) towards specific other cell-types. I don’t know if epigenetic damage also creates random mutations and chaotic cell types. Kidney disease is known for it’s mineral imbalances and calcium deposits, and probably strongly influences the VSMC’s fate.
My thesis is that my high CAC-Score is not from atherosclerotic placque in the lining of the arteries, but rather from calcified VSMCs. Furthermore, I hope that vitamin K2, natto and nattokinase, exercise and rapamycin may be able to roll back the CAC-Score. That would be unusual, but not unheard of.
So that’s my conjecture about cardio and rapamycin. BTW, save for a smidge of residual kidney disease (CKD-3), I now believe I am in better “shape” and health than most men half my age.
@Joseph_Lavelle , I don’t know if you tried CoQ10 (or ubiquinol) first, but I saw that you were taking GG (geranylgeraniol). Apparently that didn’t solve your problems with statins but could you comment?
My recent tests showed quite high Lp(a) levels at 2 different labs so I’ve been studying up on atherosclerosis. My other lipid scores are OK but LDL-C and ApoB definitely need to come down so I started atorvastatin and ezetimibe and supplemented with ubiquinol. @Virilius , what problem did you have with ubiquinol?
I’ll probably get a CAC score because it’s not too expensive. And I’ll probably order bempedoic acid (and ezetimibe) from India.
From my reading, the big picture is important - so not just Lp(a) and ApoB (or ApoB/ApoA1 ratio) but especially HsCRP, blood pressure, HbA1c (and HOMA-IR) and BMI (body fat). Two new tests that I’d like to get are GlycA for inflammation and LP-IR for insulin resistance.
Two issues I’m concerned with are whether ezetimibe restricts the absorption of Omega 3s, particularly EPA which has a pharmaceutical version that can be very helpful for artherosclerosis. My OmegaQuant score was 9.27%, so good. Also Vit D helps and there my blood test also showed normal levels. The other issue is whether I should consider PCSK9 inhibitors, but I hate injections.
After watching the youtube of “The Proof” interview with Dr William Cromwell, he’s my favored expert (Dayspring is old-school). But I will look into Sam Tsimikas.
I took coq10 from day 1 of statins. I didn’t notice any problems with rosuvastatin at first. I switch from atorvastatin due to muscle aches after lifting. But then i started feeling an ache after lifting with rosuvastatin. I switched to EOD dosing which solved it. What wasn’t solved was a falling power output on my bike that I didn’t connect to the statin. I tried GG after watching a YouTube presentation that I’ve posted here that convinced me it might be the statin. My power came roaring back. A miracle. I’m getting off the statin all together now to avoid all the unknown damage the statin is causing. My Bempedoic acid has just arrived to keep my apoB down.
Hmmmm, don’t say that to @AnUser (hope he’s not listening)…I’ll see how I feel, I guess. I don’t look forward to being on statins (or anything) for the rest of my life.
Based on what I remember, it wasn’t the EPA that was being blocked it was the ALA. It seems it may only have an effect on a subset of fat-soluble substances. The only two I have seen data about are vitamin K and alpha lipoic acid (ALA).
Then again, how much does it affect absorption? 5%? 10%? 50%? I wouldn’t worry about the first two, but if it was the last, I would do something about it.
I too have bad genetics specifically, homozygous (C;C) for the risk allele on 9p21 (the “heart attack gene”). So what is the mechanism? seems it leads to greater inflammatory response in the artery wall coupled with deficiency in ability to repair damage. So I started thinking more about inflammation being the underlying bad operator. Then came across more studies suggesting that if inflammation is very low, the impact of having higher Lp(a) (which I also have) is reduced. I don’t know if the Lp(a) and the 9p21 gene are one and the same or separate agents working in tandem, but it is clear that inflammation is a major player. This has refocused my efforts and choices. Though still want to get APOB down, I am viewing most of my efforts through the lens of inflammation reduction.
