How Building NAD will be the 2026 Wellness Trend and the Different Delivery Systems

NAD, short for nicotinamide adenine dinucleotide, has become a familiar term in longevity clinics and supplement aisles, often framed as a direct “top up” for energy. The biology is real, but the language around it is frequently sloppy. NAD is a coenzyme found in every cell, constantly being made, used, recycled and broken down. Most interventions marketed as “NAD” are not a straightforward intake of NAD itself. They are, more often, ways of feeding the pathways that help the body build NAD inside cells.

What NAD is, and why cells care

NAD exists in two main forms: NAD⁺ (oxidised) and NADH (reduced). In basic metabolic terms, NAD⁺ is the workhorse that accepts electrons during processes such as glycolysis and the citric acid cycle, becoming NADH. NADH then donates those electrons into mitochondrial oxidative phosphorylation, which supports ATP production. That redox cycling is why NAD is linked to energy metabolism in almost every tissue.

NAD⁺ also acts as a substrate for enzyme systems that sit at the heart of cellular maintenance. Sirtuins use NAD⁺ in signalling related to stress response and gene regulation. PARPs use NAD⁺ during DNA damage response signalling. CD38 is another major NAD-consuming enzyme, often discussed in the context of age-related NAD decline because it can accelerate NAD breakdown. Together, these pathways explain why NAD is discussed in the same breath as cellular resilience, DNA repair signalling and inflammatory regulation, even if the clinical translation is still being worked out in humans.

The misconception: “taking NAD” versus making NAD

The consumer shorthand is “NAD intake”. Biochemically, that framing rarely holds. The most robust human evidence for raising NAD status comes from supplying building blocks and measuring the downstream rise in NAD or the wider NAD metabolome, usually in blood. Nicotinamide riboside (NR), nicotinamide mononucleotide (NMN), nicotinamide (NAM) and nicotinic acid (niacin) are all vitamin B3 related precursors that feed into NAD salvage pathways, enabling cells to synthesise NAD internally.

Even with NAD⁺ given by injection or infusion, “direct” does not automatically mean “into cells”. Outside cells, NAD⁺ can be broken down by enzymes such as CD38 into smaller components that are then taken up and rebuilt. This complicates the popular narrative that an infusion necessarily equals straightforward tissue repletion.

Delivery systems, and what they typically deliver

IV infusions (like the ones at NADClinic and Get a Drip) are sold as the “fast lane” because they deliver rapid systemic exposure. From a strict delivery standpoint, that is accurate. The unresolved question is efficiency in the sense that matters to biology: how much exposure translates into meaningful intracellular NAD⁺ in relevant tissues, for long enough to change outcomes that patients can feel or clinicians can measure.

Home injections (think NADClinic SQx Pen), usually subcutaneous systems, are positioned as maintenance or ongoing optimisation. They share the same core scientific question as IV NAD⁺: the gap between administration and intracellular NAD⁺ in target tissue, and the scarcity of independent, head-to-head outcome data versus oral precursors.

Oral supplements (available from Nuchido and ARTAH) are the most evidence-dense category in humans for reliably shifting NAD biomarkers. NR and NMN lead on repeatability in published human work. NAM and niacin are older and widely used, but dosing constraints and tolerability matter, particularly flushing with niacin and broader safety considerations at high doses.

A clinic viewpoint on purity and protocols

Iain de Havilland, Founder and CEO of NADclinic, argues that route is only part of the story, with manufacturing standards playing a decisive role, “outcomes depend heavily on quality because not all NAD+ is produced to the same standards. Purity, source and manufacturing controls influence safety, bioavailability and results, whatever the route. IV infusions remain the most direct and efficient option for rapid uptake, while subcutaneous delivery can be an effective option for ongoing optimisation and maintenance when manufactured to rigorous standards and used within a structured protocol.”

Which options look best for delivery and efficiency, on current evidence

If “best delivery” means the most reliable, repeatable evidence in humans for raising NAD-related biomarkers, oral precursors sit at the front of the queue. NR and NMN have the clearest published record for shifting blood NAD measures, and NMN has shown a clinically relevant metabolic signal in a defined cohort. For many consumers, that combination of evidence, convenience and lower procedural overhead makes oral supplementation the most defensible starting point.

If “best delivery” means fastest systemic exposure, IV administration is hard to beat. What remains less certain is whether that speed translates into superior intracellular NAD⁺ repletion in target tissues and into durable, clinically meaningful outcomes across indications. That distinction matters, because the market often treats intensity as proof. Home subcutaneous delivery can be appealing for continuity, but as an evidence proposition it is still behind oral precursors, largely because independent, comparative human outcome data are limited.

The cleanest way to evaluate any NAD offering is to ask a blunt question: did it move a biomarker only, or did it shift an endpoint that matters, in a population like yours, for long enough to be persuasive. That is where NAD stops being a trend and starts behaving like a clinical proposition.