#82

Are you also taking rapamycin? If so, did you track when the Lp(a) test was relative to the dose?

I’ve found that mine has ranged from 175 to 195 nmol/L depending on the day after the dose. In general, it was higher 7 days after the dose, while on day 4, it tended to be lower. At the same time, LDL-C was higher on day 4 and lower on day 7. It seems like the LDL-C and Lp(a) move in opposite directions as a function of time after a rapa dose, but I’ve never seen any studies on it.

Anyway, your Lp(a) is definitely high. If I could get in repatha, I would. Ezetimibe doesn’t affect it according to what I’ve read.

2 Likes
#83

Seems like a better test just got approved in the U.S.:

1 Like
#84

“nanomoles per liter (nmol/L) as opposed to milligrams per deciliter.”

I’m confused. Both of the testing centers I’ve been using switched to molar units years ago, like maybe 10 years ago(?)

#85

Some labs still use US style units which are unreliable when the molecular weight varies.

#86

I think the test in mol up until this point have not been FDA approved but “investigational” or something like that?

If so, hopefully this approved one will be more precise and have less of the big random variation we have been seeing

1 Like
#87

Perhaps an approach until new anti-LP(a) drugs become available:

1 Like
#88

Yeah, unfortunately, it doesn’t mean that lowering the Lp(a) number translates into less MACE. It might just affect the biomarker, without affecting the outcomes. There are several agents that lower Lp(a), all with the same problem: aspirin, niacin, HRT, several others:

Do We Know When and How to Lower Lipoprotein(a)?

Therapeutic Lowering of Lipoprotein(a): A Role for Pharmacogenetics?

https://www.ahajournals.org/doi/10.1161/CIRCGEN.118.002052

And the story is complicated - genes enter the picture:

Lowering of lipoprotein(a) level under niacin treatment is dependent on apolipoprotein(a) phenotype

https://www.sciencedirect.com/science/article/abs/pii/S1567568815000094

1 Like
#89

Screen Shot 2025-02-20 at 6.37.27 PM
Screen Shot 2025-02-20 at 6.37.27 PM982×836 108 KB

https://www.ahajournals.org/doi/epub/10.1161/JAHA.124.038656

1 Like
#90

Totally agree with Tom here, and it’s super disappointing.

My family doctor looked at me as if I was completely insane when I suggested testing Lp(a).

So I did it myself, outside the system. Turns out, my Lp(a) is 65mg/dl… 2x the definition of “high”. I then found a better doctor and we tested my child when they were 6 years old… came out as 45 mg/dl. So clearly this genetic, and now we know she has a higher CVD risk profile than a typical child, and we can take preventative measures. Ideally that will extend her healthspan and lifespan. All from a single cheap blood test.

These things are not uncommon or rare. The test is not expensive. So the lack of knowledge, or straight-up dismissal of evidence by doctors is really appalling IMO.

4 Likes
#91

I am getting some material variations in lp(a) as i vary my interventions. I have not yet tried to control it, but I find it varies. As i keep detailed records i expect at some stage to be able to work out what is affecting it.

2 Likes
#92

Interesting John.
Id be interested in what you think causes variation in Lp(a) once you have enough data points. So much noise to signal though. Ive had two tests (less easy to get in UK on NHS) and was 180 and 195 so probably within margin of error.

#93

Two years ago no one was talking about Lp(a). Then came Peter Attia’s book and over night it’s a thing. Fascinating how quickly things can catch fire. Makes you wonder what else is not being measured because we don’t (yet) know what to do about it.

And, turns out there are things you can do about Lp(a) even before we get the drugs like Pelacarsen that are in trials now: reduce inflammation and take Repatha.

#94

Randox do it as part of their standard test

1 Like
#95

My lp(a) went from 186 to 134 from repatha

And to your post @RapAdmin, it wasn’t until my 3rd cardiologist that anyone tested it.

3 Likes
#96

My doctors have never suggested I get tested for Lp(a). I just did it myself. Fortunately I don’t have this issue. One less thing.

1 Like
#97

Took aspirin, niacin etc for which there is low grade evidence for lowering Lpa but made no difference. I dont qualify for a PCSK9i until I have a CV ‘event’ (MI or stroke) as only secondary prevention in the UK.
My CAC last week came back at 31 so not too bad for calcified plaque so far :crossed_fingers:t2:

#98

It seems that SGLT2/1 inhibitors reduce Lpa. Has anyone tested this before and after starting a flozin?

2 Likes
#99

That’s a really good point. I think Attia brought it to “widespread” attention, at least in our enthusiast demographic. Then you look back at the literature, and people have been saying this for 10 years!

Is that mg/dl? Mine was red flagged at 65 mg/dl, since the target is less than 30.

Sad to say, but the UK NHS is simply not equipped enough to handle the sort of preventative medicine that you’re trying to do. I do everything “out of system” now - private prescriptions, self-paid medications etc. It’s completely pathetic that they’ll wait for you to have a heart attack before they’ll agree to try and prevent you from having a heart attack…

They’ll tell you things are “normal”, but the “normal” guy in the UK dies at 78, and their last decade is spent in very poor health. No thanks.

And the CAC score of 31 is either decent, or very bad, depending on your age and other risk factors.

2 Likes
#100

I should have included that, whoops. Here is the scale we use

Lipoprotein (a)

nmol/L

134High

Reference Range <75 Risk: Optimal <75 Moderate 75-125 High >125

1 Like
#101

Yes, nmol/L as in the UK.

My CAC at 31 was for a 60yr old male.

With my FH of ASCVD (all men either dead or needing CABGs in 50’s) I was expecting a CAC of >100