By Dr. Charles Kamen, MD — Board-Certified Neurologist, LiveWell21, Las Vegas, NV
Albert Einstein College of Medicine (MD, 2011) | Yale-New Haven Hospital Internship (2011–2012) | Loma Linda University Neurology Residency (2015–2018) | ABPN Board Certified
The longevity research field has a credibility problem. For every serious finding published in a peer-reviewed journal, there are a dozen supplement companies making claims that outrun the evidence by miles. NAD+ sits right at the center of this tension — it is one of the most legitimately studied molecules in aging biology, and simultaneously one of the most overhyped by the wellness industry.
As a board-certified neurologist who prescribes NAD+ IV therapy at my Las Vegas practice, I have a professional obligation to draw the line clearly between what the science has established, what it strongly suggests, and what remains unproven. This post is my honest attempt to do that, drawing on the research landscape as it stands in 2026.
The decline of NAD+ with aging is one of the most reproducible findings in metabolic research. It has been documented in mice, rats, worms, and humans across multiple tissues. A landmark 2015 paper by Eric Verdin at the Buck Institute, published in Science, established the framework: NAD+ levels fall approximately 50% between the ages of 40 and 60, and this decline is causally connected to multiple hallmarks of aging.1
The primary drivers of this decline are now well characterized:
This is established biochemistry, not speculative. The decline is real, measurable, and mechanistically understood.
Sirtuins (SIRT1 through SIRT7) are a family of enzymes that have been at the center of aging research since Leonard Guarente's lab at MIT first connected them to lifespan extension in yeast in the late 1990s. Every sirtuin requires NAD+ as a co-substrate to function. When NAD+ levels fall, sirtuin activity falls with it — regardless of how much sirtuin protein is present.3
What sirtuins do when they are active:
The connection between NAD+ depletion, reduced sirtuin activity, and the specific functional decline we associate with aging — mitochondrial dysfunction, accumulated DNA damage, chronic inflammation, metabolic dysregulation — is not theoretical. It is a well-mapped molecular pathway with thousands of supporting studies.
Multiple randomized controlled trials have now confirmed that oral NMN and NR supplementation meaningfully increases circulating NAD+ levels in humans. This was not guaranteed — a molecule that works in mice does not always translate to humans. But the human pharmacokinetic data is clear: NMN at doses of 250–1200 mg/day produces sustained, dose-dependent increases in blood NAD+ levels.4
IV NAD+ administration achieves even higher concentrations, with 100% bioavailability and rapid tissue distribution. The pharmacokinetics of IV delivery are well established from decades of clinical use in addiction medicine settings.
The human clinical trial landscape for NAD+ precursors has matured substantially. Key findings through 2026:
These are real, peer-reviewed, placebo-controlled findings. They are not case reports or testimonials.
This is where I want to be particularly careful. There are several areas where the preclinical (animal model) data is compelling but the human evidence is not yet definitive.
In Alzheimer's disease mouse models, NAD+ restoration reduces amyloid plaque burden, decreases tau phosphorylation, improves mitochondrial function in neurons, and extends survival. The work by Fang et al. published in Proceedings of the National Academy of Sciences in 2019 was particularly striking — NMN treatment reduced neuroinflammation and improved cognitive function in AD mice through a mitophagy-dependent mechanism.7
Human trials evaluating NAD+ precursors in Alzheimer's and mild cognitive impairment are underway but have not yet reported definitive results. I follow this research closely, given my neurology background. The mechanistic rationale is strong. But I do not tell patients that NAD+ therapy prevents or treats Alzheimer's disease. That claim would be ahead of the evidence.
NAD+ restoration in aged mice has been shown to improve vascular function, reduce arterial stiffness, and enhance cardiac contractility. These findings suggest a role for NAD+ in cardiovascular aging, but large-scale human cardiovascular outcome trials have not been completed.
NAD+ precursors have extended lifespan in worms, flies, and some mouse strains. Whether this translates to meaningful lifespan extension in humans is unknown and may take decades to determine. I think it is more accurate — and more clinically useful — to focus on healthspan: the period of life spent in good health, with preserved physical and cognitive function. The evidence that NAD+ restoration improves healthspan markers in humans is already real.
In the interest of the credibility I think this field needs, here is what NAD+ research has not established:
I share these gaps because I think patients deserve to make decisions based on complete information. The science supporting NAD+ therapy is strong and getting stronger. But it is not complete, and pretending otherwise would be dishonest.
At LiveWell21, I position NAD+ therapy as one component of an evidence-based longevity strategy — not a standalone anti-aging treatment. For patients in the Las Vegas metro — Henderson, Summerlin, and surrounding areas — who are interested in proactive aging management, my approach integrates NAD+ with:
The goal is not to chase a single molecule. It is to address aging systematically, using every evidence-supported tool available, calibrated to each patient's biology.
I want to close with something that is particularly relevant to my specialty. Neurons are postmitotic — they do not divide. A neuron you were born with will serve you for your entire life, accumulating DNA damage every day for 70, 80, or 90 years. The only thing standing between that accumulated damage and neuronal death is the DNA repair machinery — and the most important DNA repair enzymes in neurons (PARPs and sirtuins) are entirely dependent on NAD+.
When I trained in neurology at Loma Linda University, the prevailing view of neurodegenerative disease was largely fatalistic — neurons die, they do not regenerate, and there is little we can do about it. The NAD+ research has complicated that narrative in a hopeful way. It has shown that neuronal resilience is not fixed; it is modifiable. The repair and maintenance systems that protect neurons from age-related damage can be supported, and NAD+ repletion is one of the most direct ways to do that.
I do not prescribe NAD+ therapy as a treatment for neurological disease. But I do prescribe it as a rational, evidence-supported strategy for neurological resilience — and I think that distinction matters enormously for patients who want to protect their brain health as they age.
If you have read this far, you are probably the kind of patient who wants real information, not marketing copy. Here is my summary:
If you are in the Las Vegas area and want to discuss whether NAD+ therapy makes sense for your aging and longevity goals, I am available for a thorough consultation.
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This content is for educational purposes and does not constitute medical advice. Consult a qualified physician before beginning any supplementation or IV therapy program. Statements about NAD+ therapy have not been evaluated by the FDA for disease prevention or treatment. Individual results vary.