#61

I found out I had atherosclerosis accidentally, because I developed tinnitus and it showed up on a scan done for that complaint

It seems to me that this should be an embarrassment to the doctors at Kaiser. Seems to me there might be some standard early detection test at least, when there’s still time to take mitigating actions. But that’s probably just my ignorance talking, what do I know? The three lipid panels taken over the the prior thirteen years were ‘perfect’, what more do I want?

It is said that a large percentage of people first find out they have cardiovascular disease when they die from it.

One of my PCPs on atherosclerosis: ‘Lots of old people have that.’ Beginning and end of discussion.

I think inaction is also rooted in financial perspectives.

Regarding LP(a).

Mine is 157/nmol/L. On the high side. I tested it through LabCorp.

I emailed my Kaiser doc, just as FYI. The nurse/message screener repolied, ‘If you have some concern you’d like to express, set up an appointment.’ I’m not sure the doc ever saw the message.

I’m confident that when LP(a)-lowering medicines are approved in a couple years, Kaiser won’t cover them. They don’t cover PCSK9 inhibitors.

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#62

Frankly I don’t know enough about it to make such definite statements. This is not my field. Great question for a cardiologist or cardiovascular surgeon.

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#63

You’re absolutely right - but like all current healthcare providers, their focus is once you have the disease, not on prevention and early identification.

I love Kaiser for what they do, but they are definitely still sick care.

The biggest sign of this is when the CEO dies of a heart attack at age 60:

Look on the bright side… You’re getting better care than the CEO of Kaiser :wink:

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#64

I won’t and cannot even try to get in to the enormous amount of detail missing in your case to make any judgement whether your case was handled appropriately.

However I can tell you for certain that the great majority of CAD, metabolic disorders, etc. is due to the INACTION of the patient in terms of their lifestyle.

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#65

I’m happy to stipulate that my having cardiovascular disease is 100% my fault, and if I was a better person I wouldn’t have it. Like the girl in the short skirt, I asked for it.

Still seems like they could have given me a heads up a bit sooner. There is the remote possibility I might have repented of my sins.

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#66

I’m learning that we have a very, very different world view

Above might be technically true. But I’m not sure why that was introduced in the context of @anon16510610 post

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#67

spend 25 years in the medical field and you would be very enlightened

Above might be technically true. But I’m not sure why that was introduced in the context of @anon16510610 post

Because it’s not technically the truth, it is the truth and the more people realize it the less doctors they will need to see. So instead griping about doctor’s relative inaction, an individual should focus on their own inaction as that will have a far greater impact on their health than anything than modern medicine can possibly provide.

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#68
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#69

Nice find! I hope they will send to UK.

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#70

Is this your org’s website?

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#71

Elizabeth, thank you for the info on that product. I assume you suggest taking one capsule a day as the bottle suggests?

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#72

If I remember properly, niacin was the go-to standard of care for treating arteriosclerosis before statins. However, they found that even though cholesterol levels were reduced with niacin, deaths due to heart disease did not go down.

Then statins were invented and everything changed.

It seems a bit backward going back to Niacin which looks great at first, but in the end doesn’t work to reduce mortality.

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#73

As I understand it, the consensus of experts no longer recommends niacin. Even if something lowers Lp(a), the side effects can still be greater —> does not reduce mortality. I have high Lp(a).

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#74

From the Atherosclerosis Journal. Published:January 31, 2024

https://www.atherosclerosis-journal.com/article/S0021-9150(24)00029-7/abstract?uuid=uuid%3A30707e9d-e11d-472e-9071-53625fb208e1

Methods

Participants of the Dallas Heart Study (DHS), a multi-ethnic cohort of ambulatory individuals at low-intermediate risk for future atherosclerotic cardiovascular disease (ASCVD), who had their blood tested for 31 biomarkers reflecting multiple pathophysiological pathways, underwent 2 serial non-contrast computed tomography assessments for CAC a median ∼7 years apart. The collected biomarkers were explored for association with CAC incidence or progression using univariate and multivariate analysis.

Results

A total of 1424 participants were included; mean age 43 years, 39 % male, and nearly half African-American. Over a 7-year interval between the two CAC measurements, 340 participants (23.9 %) had CAC incidence or progression, 105 (7.4 %) with incident CAC, and 309 (21.7 %) with CAC progression. Although several plasma biomarkers were associated with CAC incidence or progression in a univariate model, only soluble intercellular adhesion molecule-1 (sICAM-1), related to atherosclerosis by the inflammatory pathway, remained independently associated in a multivariate model adjusted for traditional risk factors.

Conclusions

Further studies are needed to characterize the role of sICAM-1 in CAC evolvement to establish whether it has a pivotal mechanistic contribution or is rather an innocent bystander. Alternate measures of coronary atherosclerosis may be needed to elucidate contributors to atherosclerosis incidence or progression.

The studies I reference, above and this one, involved human subjects, and CVD incidence. The first compared data between healthy men (14,916 healthy participants in the Physicians’ Health Study), and men who had an MI (474 men with confirmed MI during the nine-year follow-up period). This second study compared 31 biomarkers (sICAM, among the 31) among patients whose CAC scores did not progress, versus those whose CAC scores progressed.

The study that started this thread analyzed the vascular endothelium of mice.They connect that to niacin in a roundabout way. Niacin elevates 4PY among humans. 4PY elevates sVCAM among humans. So they treat mice with 4PY, not niacin, then analyze the vascular endothelium of the mice.

Lastly, treatment with physiological levels of 4PY, but not its structural isomer 2PY, induced expression of VCAM-1 and leukocyte adherence to vascular endothelium in mice.

As Dr Bart observes: “Yes it’s correlation study in humans but the proof of concept study on mice is convincing.”

In the absence of human data, I read mouse studies, because they may predict human outcomes. But when contrary human data is presented, mouse data (to me) becomes useless.

As both the human studies conclude, it is sICAM, not sVCAM that is associated with CVD risk.

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#75

I think the reason this thread was started is to discuss whether it makes sense in a high Lp(a) context.

For someone with high Lp(a) there are still basically zero options and Lp(a) is a massive and different, independent from Apo B / LDL risk factor.

Is your comment meant for the context of high Apo B/LDL (for that I100% agree with your comment) or are you (also) talking about the context of someone with high Lp(a) (I’m not sure how to weigh things as Lp(a) is such a bad risk factor and if you have such a clear view on that trade-off I’d love to hear more)?

deaths due to heart disease did not go down
Is that for LDL lowering or HDL increasing trials or for Lp(a) lowering trials?

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Is anyone having significant side effects from Bempedoic Acid?
#76

Thanks @JuanDaw very much appreciate your analysis

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#77

The impact of Niacin on Lp(a) might also differ depending on what type of apolipoprotein phenotype a person has and/or LPA genetics:

  1. This might help stratify the risk/reward decision for someone with high Lp(a) further.

  2. we recommend genetic testing for patients with elevated Lp(a) and to consider Niacin therapy in a patient-to-patient case based on genetic profile

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

Abstract

Background

Lipoprotein(a) [Lp(a)] is a cardiovascular risk factor; in addition to being a low-density lipoprotein (LDL)-like particle, it contains highly heterogeneous apolipoprotein(a) [apo(a)]. No prior studies have evaluated extended-release (ER) niacin effect on Lp(a) level depending on apo(a) phenotype.

Methods

For this 24-week, prospective, open-label clinical trial we recruited 30 men (mean age 46.2 ± 7.5 years) with Lp(a) levels >20 mg/dL. No participant had previously received lipid lowering therapy, and started ER niacin 500 mg with stepwise dose increasing up to 1.5–2.0 g. Subjects were evaluated for Lp(a), lipids, high-sensitivity C-reactive protein, lipoprotein-associated phospholipase A2 (Lp-PLA2), and fibrinolytic markers (plasminogen activator inhibitor-1, tissue plasminogen activator/plasminogen activator inhibitor-1 complex, plasmin–antiplasmin complex). Patients were divided into two groups with major low- (LMW) or high-molecular weight (HMW) apo(a) isoforms determined by sodium dodecyl sulfate-polyacrylamide gel electrophoresis of plasma under reducing conditions followed by immunoblotting.

Results

At baseline, groups were comparable in age, lipid, inflammatory and fibrinolytic biomarkers levels. There was a significant difference in baseline Lp(a) concentrations: 92 ± 29 mg/dL versus 54 ± 46 mg/dL in LMW and HMW apo(a) groups, respectively, p < 0.01. During the course of niacin treatment Lp(a) decreased by 28% (p < 0.003), Lp-PLA2 by 22% (p < 0.001), C-reactive protein by 24% (p = 0.07)*** in LMW apo(a) group***, whereas no changes in Lp(a) and biomarkers levels were obtained in HMW apo(a) group.

Conclusion

High-dose ER niacin declines elevated Lp(a) level in male subjects with low- but not high-molecular weight apo(a) phenotype.

https://www.sciencedirect.com/science/article/abs/pii/S1567568815000094#:~:text=Niacin%20is%20effective%20not%20only,7]%2C%20[8].

Niacin decreases Lpa(a) by 20%. However, there has been cases reported in the literature with 60-80% reduction in Lp(a) levels by Niacin alone based on Lp(a) isoform. The following case presents a patient with reduction of Lp(a) levels by 68% with Niacin.

62-year-old male with past medical history of CAD with elevated calcium score 254 and elevated Lp(a). Patient presented to the cardiologist office to establish care and at that time Lp(a) was 325.7 nmol/L not on any lipid reducing agents. Patient was started on high dose Rosuvastatin and 6 months later, repeat Lp(a) level was persistently high 313 nmol/L (3.9% reduction). Patient was started on Niacin 500 mg daily and 5 months later Lp(a) levels significantly reduced to 115 nmol/L (63% reduction).

Recent studies have shown that reduction of Lp(a) by Niacin could be related to Apolipoprotein(a) isoform size, which normally confers rate of Lp(a) anabolism and catabolism as well as structural and functional properties of Lp(a). However, apart from apo(a) isoform size, Niacin also binds to the LPA gene promoter region. Our patient underwent genetic testing, he had rs3798220 variant in LPA gene.Research has shown that the presence of such sequence variants near the promoter region, can affect niacin regulation and furthermore can explain the difference of Niacin effectivity among patients.
Conclusion

Based on these findings, we recommend genetic testing for patients with elevated Lp(a) and to consider Niacin therapy in a patient-to-patient case based on genetic profile.

https://www.jacc.org/doi/10.1016/S0735-1097(23)03757-9

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CVD and high Lp(a) levels
#78

$40/ 30 pills. Has to come from Poland? Wonder if they’ll ship to US.

I’ve been worried about megadosing the Niacin, cut back to 250 morning and night a few months ago. Now pretty much counting on the magic crystals (if cyclodextrins are actually crystals) Lol.

Guns, Bible, and Magic crystals.

#79

Seems it is a Polish startup and they have patented it if I understood correctly some articles I skimmed.

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#80

Perspective on how the potential cautions for the paper might (or might not) matter (from the context of people taking NAD or NAD precursors):

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