People try NAD+ for five reasons that each have real evidence behind them. There is also one honest reason for doubt: raising NAD+ has been much easier to prove than making anyone feel or function better because of it.
Longevity
Published by Astra, which offers some of the treatments discussed. Educational, not medical advice.
The starting fact behind the whole NAD+ movement is that levels of the coenzyme fall as people age. This is not a theory extrapolated from mice. It has been measured directly in human tissue. A study of human tissue samples across the lifespan found age-associated changes in NAD+ metabolism alongside markers of oxidative stress, with older tissue carrying less of the coenzyme than younger tissue 2. A widely cited 2021 review of NAD+ metabolism in aging summarizes the same pattern across skin, blood, and other tissues, and lays out the mechanistic case for why the decline could matter: NAD+ is a required cofactor for the sirtuin and PARP enzyme families that run DNA repair and metabolic signalling, and a shrinking supply of it constrains what those enzymes can do 1.
That is the evidence in favor. There is also a serious critique of how confidently this story gets told, and it deserves equal space. A 2021 review titled bluntly asks whether the age-dependent decline of NAD+ is a universal truth or a confounded consensus, and argues for the latter more than the field usually admits 9. Its point is not that NAD+ never falls. It is that the literature supporting the decline is a patchwork of different tissues, different measurement methods, different age ranges, and often small sample sizes, assembled after the fact into a tidier narrative than the underlying data supports. Some tissues and some studies show a clear fall. Others show a much smaller change or none at all.
The honest summary is that NAD+ decline with age is a real, measured phenomenon in specific human tissues, but it is not the single, universal, cleanly quantified decline that supplement marketing implies. Reason one holds up. It should hold up with a footnote.
Whatever the exact shape of the decline, the second reason people try NAD+ is that oral precursors demonstrably raise it. This part of the story is on firmer ground than the decline itself. A randomized trial of nicotinamide riboside (NR) in healthy middle-aged and older adults found the supplement well tolerated and reported it elevated NAD+ levels in blood, with a dose-dependent pattern across the doses tested 3. That is a real human RCT, not a cell-culture inference.
The same holds in tissue that matters more directly for physical function. A study giving NR to older adults measured the aged human skeletal muscle NAD+ metabolome directly and found NR supplementation raised it, alongside changes in gene expression consistent with reduced inflammation 7. Together these two trials answer the narrow biochemical question cleanly: yes, an oral precursor taken by an older adult increases the amount of NAD+ measurable in their blood and their muscle.
This is the most solid rung in the entire NAD+ ladder, and it is worth being precise about what it does and does not establish. It establishes that the pipe works: precursor in, more coenzyme in tissue. It says nothing yet about what having more of that coenzyme changes for the person carrying it. That is a separate question, and the next two sections are about how that question has actually been answered.
Here is the reason for skepticism, presented as its own numbered item rather than buried at the end, because it deserves to be read with the same weight as the reasons to try NAD+.
In 2024, a randomized, placebo-controlled trial gave nicotinamide riboside to older adults with mild cognitive impairment 4. The trial confirmed the biochemistry worked exactly as the earlier studies predicted: NAD+ levels rose roughly 2.5-fold in the treated group. Then it measured what actually mattered to the people in the study, cognitive performance, and found no improvement in the NR group compared to placebo.
This is the cleanest test the NAD+ hypothesis has had in humans to date, because it did the thing so much of the rest of the field skips: it confirmed the biomarker moved, in the population that plausibly stood to benefit most, and then it looked for a clinical result and did not find one. A 2.5-fold rise in NAD+ is not a subtle change. If raising NAD+ straightforwardly improved brain function in people with measurable cognitive decline, this is close to the trial that should have shown it. It did not.
That result does not prove NAD+ precursors do nothing for anyone. It proves that raising the coenzyme is not automatically the same as fixing the downstream problem people hope it fixes, at least for cognition in this population, over the trial's timeframe. Anyone selling NAD+ on the strength of the decline-and-precursor story owes their customers this trial in the same paragraph.
The cognition trial is not the whole outcome record, and it would be its own kind of dishonesty to stop there. Nicotinamide mononucleotide (NMN), the other major precursor, was tested in a randomized trial of prediabetic women and improved muscle insulin sensitivity in the treated group 6. That is a specific, metabolically plausible, positive human result in a defined population: women with prediabetes, not a mixed healthy-adult sample, treated with NMN and followed for a metabolic outcome that moved in the right direction.
That result sits alongside a much less favorable systematic review. A 2025 systematic review and meta-analysis pooled the trial evidence for NMN and NR on skeletal muscle mass and function specifically, and found the case unconvincing across the pooled data 8. Put next to each other, the picture is not one of blanket failure or blanket success. It is a scattered field: one well-designed trial finds a real signal in a narrow metabolic outcome in a narrow population, while the broader muscle-outcome literature, pooled and scrutinized, does not hold up as well.
This is what an honest middle looks like. NAD+ precursors are not a proven treatment for aging, and they are not nothing. They are a class of supplement with at least one credible positive trial in a specific population and outcome, sitting inside a larger body of evidence that mostly has not replicated that kind of result elsewhere.
Astra offers compounded NAD+ injection, so this next part is the one that costs us to say plainly, and we're saying it anyway because that is the deal with this library.
The published human evidence specific to intravenous NAD+ is one study: a pilot investigation of 11 people receiving a 6-hour intravenous infusion of NAD+, which measured how NAD+ and related metabolites changed in plasma and urine over the course of the infusion 5. That is a pharmacokinetic study. Its job was to characterize how the infused compound moves through and out of the body, not to test whether the infusion improved energy, cognition, mood, recovery, or any other outcome people buy NAD+ injections hoping to change. It had no placebo arm and no clinical endpoint, and it enrolled 11 people.
Nothing about that study is disqualifying on its own; pharmacokinetic pilots are a normal and necessary early step in understanding a compound. What it is not is proof that intravenous NAD+ produces a clinical benefit worth paying for. As of this writing, there is no published randomized, placebo-controlled outcomes trial of intravenous NAD+ in humans. Everything past the pharmacokinetics, in this specific delivery route, is inference borrowed from the oral precursor literature above, which itself just delivered a null cognition result in the trial best positioned to find something.
We think that's worth knowing before you start, whether you start with us or somewhere else. If you decide the rest of the case, the measured decline, the reliable biomarker response, the one positive metabolic trial, is compelling enough to try, that is a reasonable position to hold. It should just be held with eyes open about which part of the pyramid is solid and which part is still one small pilot study deep.
Every precursor trial that measures NAD+ finds more of it. The trials that measure a person, not a molecule, are far less convinced. That gap is the entire NAD+ story.
Astra Editorial, reviewing the current human trial record
Yes, in measured human tissue samples, but the size and consistency of that decline across different tissues and studies is debated. A 2021 review argues the field has overstated how universal the decline is, even while affirming it occurs in specific tissues studied so far 29.
Yes. Randomized trials of nicotinamide riboside in healthy middle-aged and older adults, and in aged human skeletal muscle specifically, both found NAD+ levels rose with supplementation. This is one of the more solidly established facts in the field 37.
Not necessarily. A 2024 randomized placebo-controlled trial in older adults with mild cognitive impairment raised NAD+ roughly 2.5-fold using nicotinamide riboside and found no improvement in cognition compared to placebo. Raising the biomarker and improving the outcome are separate questions 4.
Yes, in a narrow case. A randomized trial of NMN in prediabetic women found improved muscle insulin sensitivity in the treated group. That is a real clinical-outcome signal, though it is one trial in one population and one outcome, not a general result 6.
A 2025 systematic review and meta-analysis pooling NMN and NR trials for skeletal muscle mass and function found the evidence unconvincing overall, even though isolated positive results, like the insulin sensitivity finding, exist within the broader literature 8.
One published pharmacokinetic pilot study of 11 people receiving a 6-hour intravenous NAD+ infusion, which tracked plasma and urine metabolite changes. It did not test any clinical outcome, had no placebo group, and is not an efficacy trial 5.
Because some adults want to try it despite that gap, on the strength of the broader precursor and mechanistic literature, and we would rather supervise that decision with a licensed physician and a state-licensed US compounding pharmacy than have it happen unsupervised. We think the honest thing is to say clearly that injectable NAD+ has one small pharmacokinetic study behind it, not an outcomes trial, and let you decide from there.
Astra's compounded NAD+ injection program is prescribed and supervised by a licensed physician and dispensed by a state-licensed US compounding pharmacy. It is not FDA-approved, and the injectable-specific evidence is a single 11-person pharmacokinetic pilot, not an outcomes trial. Read the case above, then decide with that context.
This guide is educational and is not medical advice. Compounded medications are not FDA-approved. Speak with a licensed physician about your own care.