Seeking Advice on High LP(a) Levels: Any Insights or Personal Experiences?

The latest Attia podcast (5/22/23) is an interview with a lipidologist/scientist in charge of clinical trials of the CETP inhibitor obicetrapib, a pill which at a dose of 10mg cuts LDL by 50% and also drops Lp(a) by 56%, so far with essentially zero side effects in phase 1 and phase 2 trials (phase 3 trials with larger #patients yet to be completed). It also may drop risk of diabetes and Alzheimer’s (again, yet to be shown but seems to hold great potential). Also a really great discussion on why the earlier CETP inhibitors failed and why this one is different (in a nutshell, HDL is worthless and it’s all about LDL/ApoB, and the first CETP inhibitor killed patients because it raised blood pressure, a side effect unrelated to CETP inhibition or lipid changes).

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I don’t mean to be difficult here, but that study used extended release niacin (1.5-2 g/day) and a statin and ezetimbe whatever it takes to get ldl<40.

It’s too complicated for me to be sure of anything, but the smartest and most independent people I know still are posting links to studies like this:

https://sci-hub.se/10.1126/scitranslmed.3004445

I take 2 or 3 grams of IR Niacin daily and have faith that it is helping my heart disease. Maybe it’s a placebo, or maybe it’s the faith but my CAC this year improved quite a bit. My LDL and Trigs are much lower and I feel great. LDL~140 = Perfect.

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FWIW

Most people do not read published papers/material. or change what was used.

They use immediately release nician.

NOT time/slow release nician.

Repeating;

Their is a PDF copy of Parsons book, titled "Cholesterol Control Without Diet!”. Posted on this forum in another thread. At no cost, all the information required and references are in that book.

I was taking a statin to keep my lipid levels under control while taking rapamycin. I stopped taking a statin and started taking extended-release niacin. I haven’t had any blood tests since I started but I am hoping it works as well as the statin.

"therapy with niacin (nicotinic acid) is unique in that it improves all lipoprotein
abnormalities
.

“Extended-release niacin, also given once daily, has an absorption rate intermediate between the other formulations and is associated with fewer flushing and gastrointestinal symptoms without increasing hepatotoxic risk.”

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Desertshores, what was your reason for stopping the statin? Also, what dose and what brand of Niacin you taking?

I don’t recommend to anyone currently on statins to stop taking them if they have no side effects. You can also add niacin to your statin if the statin is not doing the job. The reason I am taking niacin is because it treats a broader spectrum of lipid disorders. I don’t have any brand preference I just buy whatever generic brand that is on the shelf labeled “extended-release” Amazon has the NOW brand of extended-release and I consider NOW brand supplements to be legit.

As I previously quoted from the paper I cited, this is just one of many that say essentially the same thing: “therapy with niacin (nicotinic acid) is unique in that it improves all lipoprotein abnormalities.”

I don’t know if this is personally true yet because I started on a relatively low dose (.5g) to get used to it. I am going to up the dose to 1g for a few weeks then I will get my lipids checked to see how they compare to when I was taking a statin.

The other advantage of taking niacin is that it raises NAD levels. I also take tryptophan in doses large enough to raise NAD levels. This is an added benefit of these two supplements.

This citation also lists the dangers and side effects of niacin supplementation.

“Once absorbed, physiologic amounts of niacin are metabolized to NAD”
“Most dietary niacin is in the form of nicotinic acid and nicotinamide, but some foods contain small amounts of NAD and NADP. The body also converts some tryptophan, an amino acid in protein, to NAD, so tryptophan is considered a dietary source of niacin.”

Thank you Desertshores. This info is very helpful.

Yes, most people here believe in and are doing a lot of lifestyle related things - going to great lengths in those regards even.

The main point is that the framework for someone who is doing all of those type of things and also has goals of living healthily beyond their 70s is very different from the limited ways current cardiologists were trained to weigh things or medical guidelines that only focus on 10 year risk assessments.

It is NOT about being on top of controllable and modifiable risk factors for something that will impact anyone who lives long enough (such as number one killer, cardiovascular disease and clearly causal impacts of Apo B and Lp(a) OR life style. It IS about AND and BOTH.

Anyone hear taking Rouvastatin along with Niacin? When I run an interaction check I see some issues. Thoughts?

I wouldn’t take niacin with a statin due to increased risk of rhabdomyolysis, especially given the lack of benefit on CVD outcomes adding niacin to statins:

https://www.ahajournals.org/doi/10.1161/CIR.0000000000000626

There is always this uncertainty, luck if I may call it that or bad luck, that exists and doing everything might not prevent things from happening and does not give you total control. In both directions, lifestyle or medicines. ANd sometimes also too much of good can become bad.

And I have not suggested anywhere that if your risk assessment is high you should not aggressively lower lipids. I was merely stating that risk assessment is necessary before you aggressively prevent something. In medicine important ethical guideline is first do no harm.

If you point me to some in depth scientific reading (date, studies, papers…) where would I get more of this perspective you are trying to present I would be most grateful. I guess I am not as progressive as I thought or maybe people I talk to in medical field are too conservative and cautious.

My last LDL reading was 81. I just started taking citrus bergamot and I feel a bit weird. Can you have too low LDL cholesterol?

My triglycerides are 132 though. That seems high in relation to my LDL?

My doctor just says they’re fine but gives no further information. Not sure if she even knows anything other than ‘too high’!

It’s difficult as there’s people with genetic mutations in the tens and they are completely normal and healthy. Children and toddlers also have very low LDL’s.

The problem using supplements that have no data to lower LDL is you might get… side effects that no one knows about… from the supplement. I think I got gout pain from berberine, for example. Something felt weird with my joints.

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Which units?

I have just started to read Clinical Lipidology, quite interesting read so far. There are distinct phenotypes in different dyslipidemias, might be worth wile looking into this. But in the first chapters there is a strong emphasis on triglycerides promoting inflammation and contribute causally to atherosclerotic risk.

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The book or the Journal?

Regarding too low LDL, see Cholesterol: the race to the bottom | European Heart Journal | Oxford Academic

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Good video lecture by Penn Medicine:

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Was having a discussion over email, here are some extracts from that

  • More and more leading doctors believe that lowering LDL/Apo B cholesterol aggressively, and keeping it low throughout life, could essentially prevent people from dying of cardiovascular disease

“The lower the LDL, the better,” says Professor Eugene Braunwald, MD, distinguished Hersey Professor of Medicine at Harvard Medical School, faculty dean for academic programs at Mass General Brigham and cardiovascular medicine specialist at Brigham and Women’s Hospital. “You can’t have too low an LDL." (quote from recent feature in MIT Technology Review)

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Here’s a few cases with literally exactly 0 apoB/LDL etc genetically. Of course that’s too low as it messes with the fat soluble vitamin absorption, which these patient somewhat has managed with high vitamin doses. One did an angiogram and it was normal.

Forty year follow-up of three patients with complete absence of apolipoprotein B-containing lipoproteins

https://www.lipidjournal.com/article/S1933-2874(22)00030-7/fulltext

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