Regenerative aesthetic medicine increasingly draws upon advances in cellular biology, longevity science and metabolic medicine. As understanding of the biological mechanisms that underpin ageing continues to evolve, it has become clear that many visible changes in skin quality and tissue resilience reflect deeper alterations in cellular metabolism, mitochondrial function and repair capacity. 

One molecule that has attracted growing scientific interest within this context is nicotinamide adenine dinucleotide (NAD+). NAD+ is a ubiquitous coenzyme present in all living cells and plays a central role in mitochondrial energy metabolism, DNA repair and intracellular signalling pathways that regulate cellular stress responses and ageing.1 

Declining intracellular NAD levels are now recognised as an important feature of biological ageing. Reduced NAD+ availability can impair mitochondrial efficiency, alter inflammatory signalling and limit the activity of enzymes involved in genomic maintenance and metabolic regulation.2 

For clinicians working in regenerative aesthetics, these processes are particularly relevant. Many contemporary aesthetic interventions rely on the body’s intrinsic capacity for tissue repair and remodelling. Understanding the metabolic environment in which these regenerative processes occur may therefore have increasing clinical significance. 

In my own clinical practice, interest in NAD+ developed through this broader biological perspective: the recognition that cellular energy metabolism represents a fundamental determinant of tissue function, recovery and resilience. 

NAD+ and cellular metabolism  

NAD+ functions as a central coenzyme within cellular metabolism and plays a critical role in maintaining cellular homeostasis. Its primary biological function relates to its involvement in mitochondrial oxidative phosphorylation, where it facilitates electron transfer during cellular respiration and supports the production of adenosine triphosphate (ATP), the principal energy currency of the cell.3 

Beyond its role in energy metabolism, NAD+ also serves as an essential substrate for several enzyme systems that regulate key biological processes, including: 

• DNA repair mechanisms: NAD+ is required for the activity of poly (ADP-ribose) polymerase (PARP) enzymes involved in repairing DNA damage and maintaining genomic stability.4 

• Epigenetic and metabolic regulation: NAD+ acts as a cofactor for sirtuin enzymes, which regulate gene expression, mitochondrial biogenesis and metabolic homeostasis. Sirtuins also promote DNA repair and genomic stability, in addition to influencing cellular stress responses and metabolic adaptation.5 

• Cellular stress responses: NAD+ participates in signalling pathways that regulate oxidative stress, inflammatory responses and cellular adaptation to metabolic stress.5 

Through these interconnected pathways, NAD+  plays an important role in cellular energy metabolism and repair processes. Consequently, alterations in NAD+ availability have attracted increasing attention within ageing biology and may have implications for tissues with high metabolic activity, including the skin. 

NAD+ decline and ageing biology  

A substantial body of research has reported reductions in intracellular NAD+ concentrations with age, with human studies demonstrating lower NAD+metabolite levels in older adults compared with younger individuals.6 However, emerging perspectives suggest that this relationship may be more complex than initially understood. In metabolically healthy individuals, NAD+ levels may remain relatively stable over time, while reductions in NAD+ appear more closely associated with factors such as chronic inflammation, metabolic dysfunction, sleep disruption and systemic disease. As these processes become more prevalent with advancing age, the observed decline in NAD+ may reflect the cumulative impact of these stressors rather than ageing itself in isolation. 

Reduced NAD+ availability has important biological consequences. Lower intracellular NAD+ concentrations can impair mitochondrial oxidative phosphorylation, reduce ATP generation and diminish the activity of NAD+-dependent enzymes involved in DNA repair and metabolic regulation.7 

These processes contribute to several recognised features of ageing biology, including increased oxidative stress, impaired cellular repair mechanisms and altered inflammatory signalling pathways.7 

From a physiological perspective, declining NAD+ availability may therefore influence how tissues respond to injury, stress and regenerative stimuli. 

Relevance to cutaneous biology and regeneration  

Although much of the NAD+ literature originates from research into systemic ageing and metabolic disease, several of the underlying mechanisms are directly relevant to cutaneous biology. 

Dermal fibroblasts are metabolically active cells that require substantial mitochondrial energy production to maintain extracellular matrix synthesis and support tissue repair.8 

Mitochondrial dysfunction has been identified as an important contributor to cutaneous ageing, influencing collagen production, oxidative stress responses and the development of cellular senescence.9 

Experimental studies have demonstrated that reduced intracellular NAD+ availability can impair mitochondrial function and increase oxidative stress within skin cells, processes that may contribute to diminished collagen synthesis and impaired tissue repair.10 

Conversely, restoration of NAD+ availability in experimental models has been associated with improvements in mitochondrial function and enhanced DNA repair activity following cellular stress.7 These findings have generated increasing interest in the potential role of NAD+ metabolism in maintaining tissue resilience and regenerative capacity. 

Within regenerative aesthetic medicine, where many interventions aim to stimulate endogenous repair pathways, understanding these metabolic processes may therefore have increasing clinical relevance. 

Forms of NAD+ administration  

Strategies aimed at influencing NAD+ metabolism can broadly be divided into approaches that support endogenous NAD+ synthesis and those that involve direct administration of NAD+ itself. 

Oral supplementation strategies are widely used within longevity medicine and typically involve compounds that support endogenous NAD+ synthesis, including precursors such as nicotinamide riboside (NR), nicotinamide mononucleotide (NMN) or related metabolic cofactors.¹¹ 

In clinical settings, intravenous administration of NAD+ is also utilised. Intravenous delivery allows NAD+ to enter the systemic circulation directly under medical supervision and has historically been explored in several medical contexts, including neurological recovery and addiction medicine. However, intravenous protocols typically require prolonged infusion times, often lasting several hours. 

A further approach involves subcutaneous administration, in which smaller doses are delivered gradually. This route allows NAD+ to be introduced into the systemic circulation while avoiding the extended infusion times associated with intravenous therapy. 

In my own practice, I have found subcutaneous administration to be particularly practical for patients with demanding schedules. Many individuals seeking NAD+ therapy within a longevity-focused clinical setting are professionals or athletes with limited availability for prolonged clinic-based treatments. The ability to administer smaller doses over time therefore provides a more flexible approach while still allowing NAD+ delivery through a parenteral route. For these reasons, subcutaneous administration has become my preferred method when incorporating NAD+ therapy into clinical practice. 

Product purity and molecular stability  

Alongside considerations regarding route of administration, the quality and stability of the NAD+ preparation itself represent important practical considerations in clinical practice. NAD+ is a chemically sensitive molecule that can degrade if manufacturing, storage or reconstitution processes are not carefully controlled.2,3 

The molecular integrity of NAD+ is particularly relevant because its biological activity depends on the presence of the intact coenzyme structure. Degradation during production or storage can result in reduced concentrations of active NAD+ or the presence of breakdown products, which may limit the intended biological activity of the preparation.2,3 

Before introducing NAD+ therapy into my practice, I arranged independent laboratory analysis of several commercially available NAD+ preparations. These samples were anonymised and analysed in a laboratory specialising in NAD+ chemistry in order to assess their purity. 

Among the products tested, the preparation manufactured under the VIVE-NAD+ brand demonstrated the highest measured purity, with laboratory analysis indicating approximately 99.7% purity.12 

Given the inherent instability of the molecule, ensuring the integrity of the preparation prior to administration is likely to be an important factor in maintaining the intended biological activity of NAD+. For this reason, manufacturing standards and product quality remain key considerations when incorporating NAD+ therapy into clinical practice. 

Clinical experience in practice  

My interest in NAD+ within clinical practice developed initially through personal exposure to the therapy, which prompted further exploration of the biological mechanisms underlying NAD+ metabolism and its potential relevance to longevity-focused medicine. Over time, I began incorporating NAD+ administration into a broader clinical framework within my practice. 

In clinical use, NAD+ therapy delivered through the VIVE-NAD+ system is typically administered in small subcutaneous doses of approximately 50mg per injection. Treatment protocols often begin with a short introductory phase in which injections are administered daily for the first few days, followed by a maintenance schedule of administration every other day. In some cases, clinicians may temporarily increase dosing frequency during periods of increased physiological stress or illness.  

Courses of subcutaneous NAD+ may be undertaken continuously or alternating months. Other administration schedules can be applied depending on clinical goals and practitioner guidance. As with any injectable therapy, treatment should be undertaken within recommended dosing parameters and under appropriate clinical supervision.  

It is important to emphasise that the reflections described here represent observations from clinical practice rather than outcomes derived from controlled clinical trials. 

Within my patient cohort, several consistent themes have emerged in patient-reported experiences following NAD+ therapy. One of the most frequently described observations relates to sleep quality, with individuals reporting deeper or more restorative sleep after beginning treatment. 

Improvements in perceived cognitive clarity are also commonly reported, with some patients describing reductions in symptoms often characterised as “brain fog”, a concern frequently encountered in peri-menopausal patient populations. 

Some individuals additionally report improvements in perceived energy levels and resilience during periods of physical or professional demand. In addition, a number of patients presenting with inflammatory musculoskeletal complaints, including tendinopathies, have reported reductions in symptoms after initiating NAD+ therapy. 

While these observations remain anecdotal and should be interpreted cautiously, they reflect patterns that have prompted increasing clinical interest in the relationship between cellular metabolism, mitochondrial function and physiological resilience. 

Future directions  

 Interest in NAD+ reflects a broader shift in medicine towards understanding the biological mechanisms that underpin ageing and tissue regeneration. As research in longevity science continues to expand, increasing attention is being directed towards metabolic pathways that influence cellular resilience, mitochondrial function and repair processes. 

Within aesthetic medicine, this perspective is particularly relevant. Many regenerative interventions rely on the body’s intrinsic capacity to repair and remodel tissue. Cellular metabolism therefore represents an important component of the biological environment in which these treatments occur. 

While NAD+ has been extensively studied within the fields of ageing biology and metabolic medicine, clinical research examining its role in aesthetic or regenerative practice remains limited. Future studies will be required to determine whether modulation of NAD+ metabolism can influence treatment outcomes, tissue regeneration or recovery following aesthetic procedures. 

Implications for regenerative aesthetic practice  

Nicotinamide adenine dinucleotide (NAD+) occupies a central position within cellular metabolism, supporting mitochondrial energy production, DNA repair and a range of signalling pathways that influence cellular resilience. Declining NAD+ availability has been identified as a feature of biological ageing and may contribute to the metabolic changes that occur within ageing tissues. 

Although the majority of current research has focused on systemic ageing and metabolic disease, the biological processes regulated by NAD+ are also directly relevant to tissue repair and regeneration. For clinicians working in regenerative aesthetics, this raises important questions about the relationship between cellular metabolism, tissue resilience and treatment outcomes. 

As research into ageing biology continues to evolve, NAD+ metabolism is likely to remain an important area of investigation. Understanding how cellular energy pathways influence tissue health may ultimately provide new insights into how regenerative aesthetic treatments can be supported by broader biological optimisation. 

Disclaimer: Dr Van der Aa is the Chief Medical Officer at InsideOut Biotech, the manufacturer of VIVE-NAD+.