Inside the NAD for Health Conference in Copenhagen: Key Takeaways from the World's Leading NAD+ Researchers
Key Takeaways
- A rare gathering of minds: The NAD for Health 2026 conference brought together the world's leading NAD+ researchers and clinicians in Copenhagen for a rigorous and honest assessment of where the science truly stands—and where it needs to go.
- The science is promising, but still catching up: Early clinical signals are real and compelling, particularly in disease states with documented NAD+ deficiency, but large-scale human trials are still needed to guide everyday clinical practice.
- Blood levels only tell part of the story: The evidence that oral NAD+ precursors raise blood NAD+ levels is solid, but blood levels may not fully reflect what is happening in specific tissues—one of the field’s most important near-term challenges to resolve.
- Lifestyle comes first: Exercise is one of the most potent known stimulators of NAD+ metabolism, and data presented at the conference suggests it may work even better in combination with supplementation.
- Mechanism shouldn’t slow clinical progress: There is strong consensus among researchers that mechanistic uncertainty should not delay large phase III clinical trials—both tracks should and can run simultaneously.
- IV NAD+ is more complex than its marketing suggests: The molecule can’t cross cell membranes intact, which is why some researchers view precursor-based approaches as a more direct route for intravenous applications.
- The field and the market are out of sync: The consumer market is advancing faster than the clinical evidence, and the research community is aligned on its most pressing obligation.
In late March 2026, some of the world’s leading researchers in metabolism, aging, and clinical medicine gathered inside the Royal Danish Academy of Sciences and Letters in Copenhagen, an institution whose membership roll across the centuries has included Albert Einstein, Charles Darwin, Marie Skłodowska-Curie, and Niels Bohr himself. They were there for three days to do something the NAD+ field needed: have an honest conversation.
The event was called NAD for Health: Opportunities and Challenges, a conference centered on NAD+, or nicotinamide adenine dinucleotide, an essential coenzyme present in every cell in the body. Organized by Dr. Jonas Treebak and Dr. Vilhelm Bohr (a descendant of Dr. Niels Bohr) of the University of Copenhagen, the conference brought together scientists, physician-trialists, and clinicians working across research and the wellness industry. The closing session was a two-hour panel discussion livestreamed globally, and this article summarizes that conversation. The full two-hour panel discussion is available to watch on the conference website.
If you follow wellness at all, you have likely encountered an influx of NAD+ content: podcasts, intravenous (IV) drip clinics, and influencers promising it will reverse aging, restore energy, and add decades to your life. The supplement market, and most recently, the IV and injection markets, for NAD-related compounds are enormous and growing fast. The Copenhagen conference was, in many ways, a three-day reckoning with exactly how far the science has, and hasn’t, kept up.
Biology of NAD+: What We Know Today, and What We Don’t
The panel opened by establishing a foundation—how did the field arrive at the idea that boosting NAD+ might be beneficial in the first place, and what do we actually understand about how it works?
The most compelling early evidence came from preclinical research into mitochondrial myopathy, a group of serious muscle diseases driven by mitochondrial mutations. Through a broad screening of metabolites, researchers identified NAD+ as the primary metabolite that changed in diseased mouse muscle tissue.¹ When they intervened with nicotinamide riboside (NR), a vitamin B3-derived NAD+ precursor, the results were striking; the pathological features of the disease improved significantly in mouse models.
These findings translated into human studies, in which patients who had been living with mitochondrial myopathy for decades began gaining muscle strength after increasing NAD+. Some patients using it for seven years now have experienced continued improvement, with some progressing from walking only a few hundred meters to covering two or even ten kilometers. For a field looking for proof of concept in humans, this was a landmark moment.
On the mechanistic side, the panel was candid about how much remains unresolved. Several precursor molecules can be converted into NAD+, among them nicotinamide, niacin, NR, and nicotinamide mononucleotide (NMN)—and while they differ in how they enter the synthesis pathway, recent findings suggest both NR and NMN may be partially broken down by the gut microbiome into simpler precursors before absorption. That said, two recent head-to-head clinical studies comparing the two directly found some advantages for NR over NMN—results that align with earlier preclinical evidence and offer a meaningful directional signal, even as the broader science continues to evolve.
The evidence that these compounds raise NAD+ in whole blood is solid.² Whether those elevated blood levels reflect what is happening in specific tissues, such as the muscle, brain, liver, or in the precise subcellular compartments where NAD+ does its work, is far less clear. For example, blood levels have been shown to behave quite differently from tissue levels with age: muscle and skin NAD+ declines,³'⁴ while blood NAD+ often doesn’t. That disconnect is one of the central scientific tensions the field is grappling with.
Bridging Scientific Research and Clinical Practice: Key Challenges
With the biological foundation laid, the discussion turned to what it takes to move that knowledge into clinical practice, and where the biggest gaps lie. Across perspectives from clinicians, scientists, and translational researchers, a coherent picture emerges of a field rich in potential but still lacking the methodological foundations required for confident medical use.
The most immediate challenge is the absence of a standardized clinical framework. No universally accepted standard of care exists for NAD-related therapies. Much of current clinical practice is driven by anecdote, informal protocols, or commercial trends rather than rigorous, placebo-controlled trials. This has created a credibility gap in which interventions are widely marketed despite insufficient evidence on efficacy, dosing, or patient selection. The result is a disconnect between scientific discovery and clinical implementation, with the market in some cases advancing faster than the science itself.
The panel was unified, however, on one critical point: mechanistic uncertainty should not delay large clinical trials. Clinically meaningful outcomes–walking speed, VO₂ max, brain health–can be measured now, and the safety profile observed to date provides no justification for waiting. The path forward is to run both tracks simultaneously: rigorous mechanistic research in parallel with well-designed human studies in conditions where early signals already exist, such as peripheral artery disease, Friedreich’s ataxia, and mild cognitive impairment.
There was also urgency beyond the purely scientific. With the consumer market moving fast and public claims outpacing the evidence, generating rigorous data quickly is the field’s most effective tool for keeping the narrative grounded. If that vacuum isn’t filled with good science, it will continue to be filled by marketing.
A recurring and important distinction throughout this section was the difference between two quite different populations: patients with documented, disease-driven NAD+ deficiency, and healthy individuals seeking general optimization. The evidence base, clinical rationale, and research strategy are different for each, and conflating them serves neither well.
NAD+ Boosting in Healthy Individuals: Promise vs. Prudence
This section was perhaps the most practically relevant for a general audience, and the panel’s views formed a spectrum rather than a consensus, which is itself informative.
The one point of universal agreement was that lifestyle foundations come first. Exercise is among the most potent known stimulators of NAD+ metabolism, and data presented at the conference suggested the combination of exercise and NAD+ supplementation may be more effective than either alone. Supplementation is not a substitute for healthy behavior; at best, it is an adjunct to it.
Beyond that baseline, the panel was more divided. Some expressed cautious openness to supplementation in healthy individuals given the favorable short-term safety profile, particularly at standard oral doses. Others advocated for a more targeted approach: identify why an individual’s energy or function is suboptimal, measure NAD+ status where possible, and treat supplementation as a specific correction rather than a general tonic. One useful framing from the discussion: if someone requires continuous supplementation to maintain normal function, that may signal an underlying issue worth investigating rather than indefinitely compensating for.
The panel also raised an important safety note. At very high doses, NAD+ precursors behave more like pharmacological agents than dietary supplements, with known risks including liver toxicity, for example, at extreme niacin doses.⁵ The supplement framing can obscure the fact that these are potent metabolic modifiers that warrant clinical context and appropriate dosing.
Clinical Measurement and Monitoring of NAD+
Underpinning every other discussion was a more fundamental challenge: how do you reliably measure NAD+ status in a human, and how do you know if an intervention is actually working?
The honest answer, as the panel laid it out, is that the field doesn’t have great tools for this yet. Whole blood NAD+ measurement is the most accessible approach, but it is an imperfect proxy. Blood and tissue levels diverge–muscle NAD+ declines with age while blood levels often do not–making blood measurements a potentially misleading surrogate for what is happening in the tissues that matter most. More direct methods, such as magnetic resonance spectroscopy and muscle biopsy, exist but are not scalable for routine clinical use.
What the field needs as a foundation is a standardized reference range for NAD+ across different ages, sexes, and health states—the kind of baseline that exists for vitamin D or cholesterol, against which individual values can be meaningfully interpreted. Without it, clinicians have no clear framework for what “low” or “optimal” actually means.
The panel also made a strong case for moving beyond purely biochemical markers. Validated functional measures, such as VO₂ max, cognitive assessments, and walking speed, which are free to administer, capture both mitochondrial and vascular function, and are a strong predictor of adverse outcomes, offer practical alternatives that don’t require sophisticated lab infrastructure.
Wearable-derived digital biomarkers represent another promising avenue, particularly for capturing real-world effects on sleep, activity, and autonomic function. Combining biological, functional, and digital measures is likely to give a far richer picture of whether an intervention is improving health, not just moving a number on a lab report.
Therapeutic Strategies and Interventions
The panel then addressed the practical question of how to deliver NAD-boosting interventions and whether the choice of form matters.
On oral supplementation, the primary candidates remain NR and NMN alongside simpler forms like nicotinamide and niacin. Despite significant marketing investment in positioning NR and NMN as superior, the clinical trial evidence comparing them directly doesn’t yet support strong conclusions either way, although recent head-to-head clinical studies demonstrate NR’s superiority over NMN.
The question of IV NAD+ delivery received considerable attention. IV NAD+ has a long history in addiction medicine—particularly for opioid and alcohol detoxification—and has more recently moved into the wellness market as a premium longevity treatment. The original rationale—bypassing first-pass liver metabolism—is logical, but the biochemistry is more complicated.
NAD+ has difficulty crossing cell membranes, so IV-administered NAD+ does not raise intracellular levels in the way oral precursors do through gradual metabolic conversion. The actual mechanism involves extracellular effects, particularly breakdown into smaller NAD+ precursors, or conversion to adenosine, a signaling molecule with anti-inflammatory properties. This may explain the acute effects patients report, and the panel flagged it as a genuinely interesting and underexplored mechanistic area.
An important counterpoint also emerged: oral supplementation appears to positively influence the gut microbiome,⁶ a benefit that IV delivery bypasses entirely. Whether that trade-off is clinically meaningful is an open question that deserves direct study.
On the cancer question, raised from the audience as a concern that surfaces regularly in clinical trial safety discussions, the panel’s view was measured. The concern is biologically plausible, as cancer cells are metabolically active and heavily reliant on NAD+. The weight of available human evidence, however, including long-term niacin studies and a phase III trial on nicotinamide in skin cancer prevention, does not show increased risk. Adding further nuance, a growing body of preclinical work suggests that NAD+ precursors, including NR, may actually support the cancer-fighting capacity of T cells, with multiple studies demonstrating improved T cell mitochondrial health⁷ and cancer-killing ability⁸—a finding that complicates any straightforward assumption of harm. The appropriate response is informed caution for individuals with cancer history or strong genetic predisposition, rather than alarm for the general population.
Societal Impact, Communication, and the Road Ahead
The final section stepped back from the molecular details to address something equally important: how the field communicates what it knows, how the public makes decisions in the meantime, and what the path forward looks like.
The central concern was what one panelist described as the risk of losing the narrative. An enormous commercial infrastructure has formed around NAD+ that is advancing faster than the science. If the research community does not generate clear, accessible, evidence-based guidance, that vacuum will continue to be filled by those with different incentives—and the field’s credibility will suffer for it. Conferences like Copenhagen, which placed basic scientists, clinicians, and industry in the same room, were held up as a model for the kind of cross-sector dialogue that can align priorities and produce more coherent public communication.
Looking ahead, the panel’s priorities were consistent: large phase III randomized controlled trials in conditions with the strongest existing signals, standardized NAD+ reference ranges in human populations, validated biomarker frameworks, and head-to-head comparisons of precursor molecules and delivery methods. The longer-term vision is a precision medicine approach to NAD+—matching the right intervention, at the right dose, to the right individual based on their biological profile, much the way insulin is titrated to glucose in diabetes management.
Closing Reflections: Where the NAD+ Field Goes Next
At the close of the session, panelists were asked what, if anything, would change in their work as a result of the conference. The responses were telling. One clinician planned to add microbiome data collection to an upcoming peripheral artery disease trial. A scientist expressed new excitement about investigating the adenosine mechanism of IV NAD+, newly connected to clinical collaborators who could help. Others left with expanded collaboration networks and plans to study NAD+ reference ranges across broader populations and disease contexts.
Perhaps the most resonant closing thought was simpler: that gatherings like this one, where scientists sit alongside clinicians, alongside industry, alongside the people communicating science to the public, need to happen more often. The science of NAD+ is advancing. Whether the public understanding of it keeps pace depends on exactly that kind of coordinated, honest dialogue.
The Bottom Line
The Copenhagen panel didn't arrive with easy answers, and it didn't leave with them either. What it did was model something the field critically needs: rigorous, honest engagement with where the science of NAD+ actually stands, and what it will take to move it forward.
The biology is compelling, the early clinical signals are real, and the safety profile for oral supplementation at reasonable doses is reassuring. But the clinical evidence needed to guide practice remains underdeveloped. Bigger studies, better biomarkers, and more disciplined public communication are not aspirational goals–they are the concrete next steps the field must take. The public is already making decisions about NAD+ without that clarity, and generating it is the research community’s most important obligation.
That is ultimately what Copenhagen was about—not hype, not dismissal, but the necessary work of figuring out what is real.
This blog post is based on the recorded panel discussion from the inaugural NAD for Health: Opportunities and Challenges 2026 conference, hosted by the University of Copenhagen at the Royal Danish Academy of Sciences and Letters, March 23-25, 2026. The full panel recording can be viewed here.
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