zazim
#2872
I would posit that even the most dedicated bio hacker would not find it valuable to retest. Obviously if you’re doing something like aphaeresis it would change, but absent that none of these other interventions are clinically relevant. For these trials to be successful, they will need a reduction of something like greater than 70%. If you test high, you are high, and there’s really nothing you can do about it for now other than optimize every other risk factor. Hence, my PCSK9 inhibitor.
2 Likes
How high is ruinously high? Mine is 157 nmol/L. High, but I don’t think I win a prize.
Neo
#2874
Maybe not. Here is my data from Quest on Lp(a)
And here is my data from LabCorp:
without being on any cholesterol related med:
(Have a few other data points around that level from LabCorp)
—
And here is from when being on a half dose of Repatha:
From the last two data points there was enough data for my cardiologist and me to ask ourselves if it might be worth trying a full dose of Repatha instead of the half dose. (A half dose lowered my Lp(a) 25%). This is an experiment we are doing right now.
But what if the only Lp(a) blood test we took was the Quest Diagnostics one from October 2 or 6 2023 where the levels were ~55? Those were BOTH from a period when I had not been on PCSK9i or any cholesterol med for many months.
Either I had found some magical way to lower my Lp(a) via diet or exercise or supplemented that there were no know Lp(a) benefits from… or much more likely those two tests has testing errors.
But if we only had one (or even both of those data points) and thought they was my baseline (a) we would be less concern and I may not have pushed for taking PCSK9i and (b) when we then looked at the Quest datapoints from when I was on PCSK9i in November and December at levels around 75 or so, we could have concluded based on data that PCSK9i increased my Lp(a) level by 35-40%….
Clearly when we see all the data points it’s almost certainly that I’m around 85-100 when on no medication, and it goes down by perhaps 25% to 70ish whenever I do decreases level PCSK9i.
This is just one example of why we should rely on more than one data point when gathering data to make decisions on.
There is always an error bar around any blood test, so you have to think about any one data point as being within a confidence interval that generally can be quite wide.
3 Likes
Neo
#2875
It seems that the Phase 2 data and pre-clinical data makes that very likely to be the case. The bigger question mark I think is was the disease outcome impacts will be from lowering it that much.
Only one of my labs tests for lp(a). I have glanced at this and it is quite low . I have not been recording it in my spreadsheet, but I could go through and see what variability it has if people would find that helpful. There is quite a bit of work in doing this, however, so I am not enthusiastic. Would people find it useful?
I will extract the page for curiosity. I don’t fast for the test and don’t worry about the LDL-C because it bounces around the Uk threshold which is 3 mmol/L.
2 Likes
Neo
#2877
I agree that we do not know what is clinically relevant, but a lot of the best guys in the world on Lp(a) to think that lowering in by 20-40% may be helpful and hence fight for PCSK9i for their patients. So I do not think you can say that it is not clinical relevant.
In fact as discussed on one of the Lp(a) threads on this forum you can see that there is clinical data that seem to show that PCSK9i are having benefits in people with higher Lp(a) that goes beyond the LDL lowering effects.
And where there is an option to avoid having Lp(a) up from statin use (in your case perhaps via Bempedoic Acid instead of statin given your cholesterol balance test and experience that Eze does not have any real impact for you) they often try that path out. So for that is a case where one might also want to measure Lp(a) changed - to understand whether the statin increased Lp(a) or not in a given individual.
This for me is the difference of precision medicine that a dedicated health optimizer/biohacker can pursue. I understand that most patients and physicians don’t have the energy or often cannot or do want to prioritize the time and/or resources to approach things this way.
Neo
#2878
Thanks John. From my perspective, given how low yours is it would probably be more interesting to see how much it bounced around with someone who has higher / more concerning levels.
Neo
#2879
What is the H-FABP test btw?
adssx
#2880
I had a bad experience with Randox: when I got the results, my PTH was too high (8.5 pmol/L), while calcium and vitamin D were OK. I went to see my endocrinologist. He told me that I was the third person this month coming from Randox with an elevated PTH but normal calcium and vitamin D. He redid the test for all of us with an accredited lab, and they came back normal (4.6 pmol/L). So I’m afraid Randox is not reliable. Too bad because it’s the cheapest…
2 Likes
adssx
#2881
Super low Lp(a), normal ApoB but high LDL: how common is that, and what are the potential consequences/risks (if any)?
1 Like
Neo
#2882
Since cardiovascular disease - and heart disease stroke alone - are the by far biggest killers and drivers of awful disability - in the western world, I think one has to see normal Apo B as one of one’s largest risks (even if healthy, exerciser, etc).
Not until you have optimal Apo B should you be satisfied if health and longevity optimization is your goal.
Especially in the context that there are powerful meds with side effects profiles that are good.
4 Likes
I dont know what this is.
I not researched this. Most recently i have been working on getting my rhr and bp dpwn following a metabolic boost. I now am back to a hr just over 50, but with a higher stroke volume. I am curious about these figures, but they dont seem a priority.
I do weekly tests so can compare labs. I have no reason to doubt randox, but they do a broader test.
1 Like
Neo
#2886
I the last test in the bloodwork summary that you shared:
1 Like
adssx
#2887
Long-term safety profile of statins does not look 100% good to me unfortunately… Rilmenidine vs Telmisartan or other BP meds for Longevity - #29 by adssx
1 Like
Neither RCTs nor MR studies have shown any negative effect of statins on dementia rates.
I may still get an occasional full cholesterol test. But, in light of more recent studies.
ApoB is a better indicator of future cardiovascular outcomes.
This has been debated before in this and other threads. I was on the fence on this but I have changed my mind so that I like ApoB better than an ordinary lipid panel test.
Because I like to keep my supplement stack as low as possible, I would also like to keep my blood tests as few as possible while still maintaining the health information to make decisions in my diet etc. So, for the most part, I will just get my ApoB tested and not a cholesterol panel.
“The risk of myocardial infarction was best predicted by APOB levels, independent of LDL-C or triglycerides”
These studies may have already been posted, but I just got around to reading them.
This a large cohort study The primary study outcome was incident myocardial infarction (MI).
“Of the 389 529 individuals in the primary prevention group, 224 097 (58%) were female, and the median (IQR) age was 56.0 (49.5-62.5) years. Of the 40 430 patients with established atherosclerosis”
(“Patients with established atherosclerosis” would include just about everybody over the age of 30 because it starts quite early in life)
https://sci-hub.se/10.1016/j.cca.2020.05.001
5 Likes
adssx
#2890
No but several longitudinal + MR studies showed that there seems to be a causal relationship between high cholesterol and lower risk of PD: Lipids, Apolipoproteins, and the Risk of Parkinson Disease - PubMed
And RCT of statins in PD failed.
1 Like
adssx
#2891
And actually there are MR showing detrimental effects: Mendelian Randomization Study of PCSK9 and HMG-CoA Reductase Inhibition and Cognitive Function
In contrast, we observed adverse neurocognitive effects related to HMGCR inhibition, which may well be outweighed by the cardiovascular benefits of statin use, but nonetheless may warrant pharmacovigilance.
There seems to be a tradeoff between CVD, AD, and PD 
2 Likes
