So Dr Sinclair and the paper above* in the context of Niacin have now pointed us to two different genetic variants that we might want to weigh in context of Niacin and/or NAD precursor supplementation.

Does anyone know how to easily check our status of those two?

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Another perspective for those trying to understand this stuff

NMN Probably Won't Make You Live Forever?

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NMN has some specific uses, but is not beneficial for all. Based on my research the following people may find NMN useful:

  1. Overweight
  2. Sleep deprived
  3. Jet lagged

So, IMHO, most people here should not be taking NMN. Unfortunately I am all 3 above, so I’m in the sweet spot. :stuck_out_tongue:

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Interesting. NAD+ also seems like a good thing to test and then make decisions depending on where one’s levels are in relation to one’s age group and overall percentile.

Establishment medicine has been anti niacin for decades. Same old message.

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Just a thought that occurred to me, but could it be that Niacin’s beneficial effects on lipoproteins is countered by its detrimental breakdown products (2PY & 4PY) and that’s why you see no overall effect on cardiovascular events and deaths ?

Also interestingly, in humans 2PY (and I’m assuming the same is true for 4PY) increases with age 2.6 fold

Blockquote

The mean plasma 2PY concentration in young (5-16 years old) healthy subjects was 0.39 +/- 0.22 micromol/l while in old healthy subjects (50-90 years old) it was approximately 2.6-fold higher. No gender differences was found in plasma 2PY concentration.

Blockquote

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As an aside, Niacin was tested by @ConquerAging and it provided the worst epigenetic age tests he has had this year by a longshot. So, Niacin doesn’t seem all that it’s cracked up to be for longevity.

Use Bempedoic Acid, Ezetemibe or a statin instead.

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Hey @ConquerAging , what do you think of this product?

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This was true for higher dose niacin (500mg?) as I recall. He has since decreased the dosage (50mg?) to still get a NAD boost. Did I recall correctly?

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As mentioned - I 100% agree with you on this for Apo B optimization (and don’t think there has been hardly any disagreement about that on this thread).

But @DeStrider - how do we use those medicines instead for Lp(a)? What to do in the context of high Lp(a) is or at least was the genesis/purpose of this thread.

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Indeed Neo, thanks for keeping the discussion focused on my initial question. The focus is not on LDL or APOB but rather the focus is on Niacin or alternatives for Lp(a).

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If you use Niacin to treat Lp(A), you may be affecting your epigenetic age. Unfortunately I am not aware of anything currently available to treat Lp(A). There are a few therapies under development and may be ready in a few years time.

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He might be talking about average lowering here

not the ~50% lower that was in the case of our forum member colleague that started this thread

Importantly note that PCSK9i impacting Lp(a) seems to occur at lower lowering levels.

What are your thoughts on this last piece?

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Based on reading Sam Tsimikas page, I would use niacin to reduce my Lp(a), but I would check later whether the failed niacin trials didn’t find a stat sig effect (possibly because underpowered), or if it was a stat sig effect but no decrease. If experts disagree I’d look at the expert with possibly more knowledge about the topic, which is Sam in this case, if I didn’t know anything.

Since my Lp(a) was tested below 10 nmol/L I am not going to use niacin however to increase my HDL.

I didn’t know X was this useful to find information.

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Seems different doctor’s say different things. Will be interesting to get Dr. Tsimikas’s input when I visit with him. on Friday. My current view is I should stop the Niacin even thought it lowered my LPa significantly (I’m the author of this original post). Will be interest to see what Dr. T says.

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1 daily unless treating disease stated. Then 2 or 3

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“Disease stated”? Please clarify!