#29

Hello @Dr.Bart, Are you talking about LDL or Lp(a)?

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#30

My LDL is in good range. It is the LPa that diet has not impacted and thus the reason I take Niacin to lower.

#31

Lpa test is not covered and not easily amenable, personally I have quite unremarkable family history of CAD. I rather concentrate on LDL which I can easily obtain and affect with my lifestyle. I live my life adhering to Stephen Covey’s circle of influence rule.

#32

@Dr.Bart - crucial, crucial

They are fundamentally different independent risk factors and one cannot be used for a proxy of the other.

Quite a lot of people with non optimal Lp(a) levels have low LDL

And versa versa

And crucially, while diet, exercise can have a somewhat material effect on LDL, those things have virtually always hardly any impact on Lp(a) which is extremely determined by genetics.

Can I suggest that you edit your comments above so people are not led astray that you were able to lower your Lp(a) via lifestyle in such a way (even if it is impressive that you succeeded in having such an impact on your LDL)

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#33

Btw, because Lp(a) is genetically determined - you only have to test it once or twice in your life. So in that sense the cost is not that high (like 25 USD with Ulta Labs I think).

Only if you then use prescribed medicine (or niacin) to try and lower your Lp(a) would you need to re-test

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#34

My current feeling is that it may or may not be something to worry about. Especially in the context of the opening post about what to do with high Lp(a).

For someone with not optimal Lp(a) those risks may strongly outweigh the unclear risks from this paper of associations to higher niacin (that correlated to more processed food intake for instance and could be one driver of the human association) - that seems to go against the net (weak) signals for other papers.
(Until next gen Lp(a) lowering meds hopefully start becoming approved the next 3-5 years or other stronger data comes out on Niacin being worse than high Lp(a)).

For someone with low Lp(a), but who wants to lower LDL, there are other more optimal medicines than niacin so not need to try and evaluate how bad niacin could be, when rather just use some other Apo B lowering medicine(s).

For someone taking NMN, NR or Niacin to increase NAD+, I’d strongly consider testing NAD+ levels so that one at least is not increasing NAD+ more than needed via those supplements and risks the potentially negative VCAM effects from the figure you included and that others have discussed above.

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CVD and high Lp(a) levels
#35

That is the quandary I’m facing. Which is the path will the most rewards given I have high LPa without Niacin. The path that involves taking Niacin to lower LPa or the path to not take Niacin and live with high LPa given this recent negative research on Niacin. I guess there is not a clear cut answer.

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#36

Done anyone know the answer to this:

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#37

The effects in this study were with very high niacin doses (1.5-2.0g). I recall Lustgarten was using 50-100mg in his tests to boost NAD. Maybe I won’t throw out the baby with the bath water.

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#38

A high Lp(a) is very bad so work on getting that down. IIRC Lp(a)-apoB is 6 times more atherogenic than LDL-apoB.

Lipoprotein(a) Is Markedly More Atherogenic Than LDL: An Apolipoprotein B-Based Genetic Analysis, 2024

It just doesn’t seem reasonable to me that niacin would somehow be worse than the Lp(a) it reduces if you get no side effects. But I have not done that analysis or looked at this in detail.

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CVD and high Lp(a) levels
#39

For someone with not optimal Lp(a) those risks may strongly outweigh the unclear risks from this paper of associations to higher niacin

I would be careful making this statement, because you making it seem like the Niacin is CLEARLY mitigating the the risks of Lp(a), which is not the case.
In fact I believe that even though Niacin can lower Lp(a), it has no effect on ischemic events and death.

So you are dealing with dubious benefit vs potential risk of using high dose Niacin.

Do no harm.

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#40

As you quoted me:

For someone with not optimal Lp(a) those risks may strongly outweigh the unclear risks from this paper of associations to higher niacin

I’m sorry if it came across as it clearly does, I was truly trying to convey that it may.

Can you explain how may in my sentence does not mean may but comes across as clearly so I can be more careful in my posts in the future?

#41

I think the statement " may strongly outweigh" does make it seem like you’re saying or at least suggesting it at least outweighs, and perhaps strongly outweighs… when compared to “unclear” risks from this paper…

Anyway, I get the points that both of you are making.

Given the many ways to reduce risks in the lipid/cardio area, I tend to go with the ones most tested and validated. This tends to be the pharmaceuticals simply because they have more money to do the RCTs that the FDA requires.

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#42

Harm can be done via action or inaction

In this case we know that inaction could have a very large potential harm given how bad high Lp(a) can be.

I personally don’t know how to weigh the risks.

So I can understand where you are coming from, do you believe the following [in bold] is correct or not correct:

#43

I am on facuty for SSRP which is a cellular MEdicine educational organization and we have been preaching the risks of oversupplementation of niacin, and especially NAD and its precursors with disease states!! This finding is not news since excess contributes to higher levels of aldehyde oxidase which has end products of 2 and 4 pyridones which have been shown for years to increase CV risk. The other problem is the upregulation of the enzyme NNMT, which contributes to helping cancer cells, fat cells, and senescent cells. NNT blockers are being researched extensively to help cancer and metabolic disease as well as long covid and yet many people are taking lots of NAD and its precursors and upregulating this enzyme!!!. Bad news! It is hard to know how much is too much! ANd it likely depends on disease states and levels of AOX and NNMT. Likely low intermittent dosing is OK. But, We finally have access to a much better option recently available from Europe called 1MNA. 1 MNA blocks NNMT and increases SIRT. It has the benefits of niacin and other NAD precursors and NAD and not the risks since it controls the formation of these bad metabolites by blocking NNMT and being excreted directly into the urine to control oxidative stress. It has been shown to have marked antiinflammatory, CV and metabolic health benefits!

Song Z, Zhong X, Li M, Gao P, Ning Z, Sun Z, Song X. 1-MNA Ameliorates High Fat Diet-Induced Heart Injury by Upregulating Nrf2 Expression and Inhibiting NF-κB in vivo and in vitro . Front Cardiovasc Med. 2021 Oct 12;8:721814. doi: 10.3389/fcvm.2021.721814. PMID: 34712707; PMCID: PMC8545986.

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NMN/NR worth taking for longevity?
5 Amino 1 MQ - Thoughts
#44

Thanks. I’ll reflect on it and try to be more clear in future communications.

To help clarify what I mean/believe:

  • I think there is a lot of uncertainty here
  • I think bad Lp(a) is really, really risky, really, really bad
  • I know that there are no good medicines for Lp(a) (yet)
  • I think the odds are meaningfully better than 50/50 that the risk/downside of Niacin in someone with high Lp(a) that responded well to Niacin and where it crushed Lp(a) levels are smaller than the risks of the Lp(a) as among the largest risk factors for the largest killer, cardiovascular disease
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CVD and high Lp(a) levels
#45

Thank you. Will look into this.

Do you have a perspective in the context of high Lp(a) and the associated materially increased cardiovascular risks where there are no good alternatives (and not just in the context NAD+ “optimization”)?

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#46

There are two problems with your statement: First of all the problem is not “may”, it’s the use of “strongly”… Strongly implies that there is good evidence that Niacin mitigates the risk of Lp(a). I am not aware of any such evidence. Maybe you are then you can share it.
Second you label the risk of Niacin “unclear” and yet you put NO such a label on the purported benefit of the Niacin - which is even farther from clear.

So by doing using “strongly” for potential benefit and using “unclear” risk of Niacin you give the appearance that there may be a net benefit over the risk ratio of using Niacin with Lp(a) risk- which is absolutely unsupported by any evidence.

I think you are conflating "lowering Lp(a) with positive clinical outcomes, which is a common mistake. In medicine it’s the outcomes that really matter, affecting data point without positively affecting the outcomes is of little clinical significance.

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#47

Niacin is an FDA approved drug?

#48

https://pubmed.ncbi.nlm.nih.gov/22085343/
[Here is a direct quote from this relevant paper - Niacin reduces lipoprotein (a) by 15% to 25%, but does not reduce death or ischemic cardiovascular events [[42]

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