I’m really interested to hear what experience, words of warning, and personal good/bad, apart from the wallet biopsy of the expense, people have had with 5-amino-1MQ.
There is a lot of hype and discussion around optimization of NAD, and this seems like an interesting method with a nicotinamide N-methyltransferase agent.
Furthermore, how would you choose to use it with Rapamycin - in recovery (e.g. day 3-7) or during the time your MTORC1 is maximally inhibited, or continuously? And if you have an opinion, what is the rationale?
There are multiple suppliers, I suspect I can find some that are properly confirmed for human use on my side, as I know some doctors are prescribing it.
I’m curious in the setting of NAD optimization (whether through this mechanism, NMN,NR or others), whether individuals are approaching this in a cyclic fashion with their rapamycin, and if so are they doing it in recovery from MTORC1 inhibition or continuously or on some other basis?
I heard some functional medicine doctors in a talk have an extensive discussion around how excellent this peptide was … and the literature is interesting.
I’m hoping to hear from someone even in regard to their approach to NAD boosters, regardless of type and their rationale and pattern of use of these agents in conjunction with Rapamycin.
The 2 are certainly used commonly together, and there are some smart folks on this board, there must be some ideas in this space.
I take a NAD booster, 1 g of NMN powder (DNA) mixed in EVOO daily. It provides an energy boost and prevents a lot of fatigue. When I travel (usually 21+ hours) I take it when I land and I don’t experience any jetlag. It’s an amazing substance for healthspan as I rarely feel fatigued when I am not sick. The jury is still out for lifespan.
I believe you want higher NAD, but not too high. The rationale can be found here:
Also, Niacin assists in creatine supplementation (depending on your MTHFR) : creatine synthesis uses S-Adenosyl Methionine (SAMe) as a methyl donor. SAMe is critical for methylation processes in the body. When you supplement with creatine, it can reduce the demand for endogenous creatine synthesis, potentially leading to an excess of SAMe and consequently, an overmethylated state. Niacin can help regulate this balance. After donating a methyl group, SAMe becomes homocysteine. Niacin contributes to the conversion of homocysteine back into methionine, which can then be transformed into SAMe again, helping to maintain a balance in the methylation cycle.
How often are you dosing? Study is 750-1000 mg qd. Is the flushing not worse with non qd dosing? Does niacin really affect the atherogenic potential of lipids for the negative? Great find thanks for posting.
Hi @Jeff_A, welcome to the forum! For a detailed exploration of NMN vs Niacin, I recommend Dr. Brad Stanfield’s summary, which you can find here: NMN vs Niacin.
As for my personal regimen, I’m currently taking 100mg of niacin daily, specifically in its nicotinic acid form. This variant is well-known for causing a “flush,” a response due to its effect on prostaglandin signaling, which leads to vasodilation.
However, a key point to consider is that niacin, particularly at higher doses, utilizes a biochemical pathway that involves methylation, a crucial process in which methyl groups are transferred for various critical physiological functions. To support this pathway and maintain a healthy balance of methyl donors in the body, I supplement with 500-1000mg of Trimethylglycine (TMG), especially on days when I am not training.
On workout days, my routine includes creatine supplementation. Creatine is not only beneficial for muscle energy but also acts as a methyl donor (through pathway, which I have described above). Due to this property of creatine, it helps in replenishing the body’s methyl pool, thereby reducing the necessity for additional TMG on these days.
Thank you for the response, the welcome and the share. I take TMG 3 gm po qd, creatine 5 gm resistance training days, LEF Homocysteine Assist, niacinamide at 50 mg and have 1 copy MTHFR. Your dose is only 1/8-1/10 of the dose listed in the study. Have you had your NAD+ levels tested at 100 mg? Any evidence that 100 mg nicotinic acid has efficacy in restoring NAD+?
@Jeff_A, valid point. You’re right to point out that my current dose is substantially lower than what’s cited in the study. I haven’t tested my NAD+ levels at the 100 mg dose, so I can’t confirm its efficacy at this level.
Regarding NAD+ and longevity, I have some personal skepticism. There’s a lack of conclusive evidence in current longevity studies about the direct impact of NAD+ supplementation to max/median lifespan. My approach is more intuitive. I believe in the importance of a healthy lifestyle, including exercise, balanced diet, and sun exposure moderation, to naturally support NAD+ levels.
In study, the level of whole blood NAD+ was increased by supplementation by 7.1-fold in the study group and 5.7 in the control group after 4 months compared to the participants’ baseline. While my dose is much smaller, I’m inclined to think that even a minor systemic supplement of nicotinic acid might help maintain NAD+ levels to a certain degree. If an opportunity arises to test my NAD+ levels, I’ll consider it and may adjust my dose based on the findings.
If you will find some insights to dosage/impact in future: would appreciate your feedback.
I guess we just should quit being lazy and measure, LOL. I measure everything else. But I agree w/ both your skepticism and intuitive approach thus greatly appreciate the feedback. I haven’t measured either honestly because I’m not sold.
