22 LONGEVITY Keratinocyte-melanocyte models have
shown senescent melanocytes can cause a DNA damage response in surrounding keratinocytes, reduce their proliferation, and result in a thinner epidermis.8
and fibroblasts, showed increasing levels of senescent fibroblasts led to skin thinning and barrier disruption.9
The new paradigm: uniting traditional with longevity While the new evidence highlighting the hallmarks of ageing opens new modes of treatment, what about all the existing modes of treatment? Retinoids have decades of research elucidating their mechanisms of action, strong clinical benefits, and are among the most consumer accepted ingredients available. Peptides as a category have countless mechanisms of action across growth factor mimics to anti-inflammatory solutions to matrikines, all with clinical validation. The strength of evidence supporting these treatments is currently well above new longevity approaches, mainly because they have been studied longer and more thoroughly. They may not directly impact the hallmarks of ageing to the extent new longevity approaches do, but this leads us to our next key question: if the end clinical result is the same, does it matter how we get there? This is especially relevant considering the
limited economic space and routine share for consumers. Consumers are deeply habituated to traditional actives that have likely worked for years. Especially with the rise of agentic commerce
and AI-assisted queries, the competition between actives and the importance of their track record will only increase with time. Do consumers spend the extra money to also incorporate longevity actives? Do they change their routines to replace traditional actives with these new approaches? While there are many potential answers
to these questions, I believe the most potent response is best exemplified by invoking our previous analogy of the Hindu deity Shiva. The prior balance of anti-ageing actives is being incinerated and from their ashes a new harmony is being built. The new age, targeting well ageing and preventative care, involves identifying modes of synergy between both approaches.
A new harmony: Bakuchiol NAD+ BCR
Bakuchiol NAD+ BCR – hereafter, the bakuchiol NAD+ ester - is a new ingredient that was designed exactly with this in mind. It is the fusion of a traditional anti-ageing active (bakuchiol) with an NAD+ precursor to target longevity (nicotinic acid) into one ester with powerful synergy (bakuchiyl nicotinate).
Another model, this time keratinocytes
Figure 1: The hallmarks of ageing paper often cited as a review of ageing research condensed into one mental model3
Ester fusion technology allows consumers
to receive the benefits of both worlds without the additional economic or routine inflating burden. The identification of one key molecule also provides greater track record for AI-assisted queries and agentic commerce over extracts that may obfuscate results since extracts can vary significantly in efficacy. Nicotinic acid has been shown to convert
to NAD+ through the Preiss Handler pathway in multiple cell types, including keratinocytes.10,11 NAD+ plays a key role in energy production, DNA repair, epigenetic regulation, and inflammation. NAD+ accepts electrons from various processes
breaking down nutrients and transfers those electrons required for optimal energy production. Sirtuins and PARPs utilize NAD+ for their activities and release niacinamide as a byproduct. For all these reasons and more, NAD+ is a central target in longevity. NAD+ levels decline with age for several
reasons, three main ones to highlight: chronic inflammation, overwhelmed DNA repair systems, and reduced NAD+ production efficiency. Chronic
low-grade inflammation is a known quality of ageing skin, aptly termed ‘inflammaging’.12 Inflammatory signalling compounds such
as CD38 break down NAD+ for their activities, this means that over time more NAD+ is utilized for inflammation and less is available to keep cells ‘young/effective’. Concurrently, the stress defence systems of cells (including DNA repair) get overwhelmed with time. This is especially the case with photoageing,
highlighting the importance of sunscreens. Sirtuins and PARPs are important examples; both compounds are pivotal for DNA repair and regulating the epigenome/proteome to maintain youthful skin. When these systems are overwhelmed by
their damage mitigation faculties, it further shrinks the amount of resources placed on maintaining the orderly biological information necessary for youthfulness. Finally, the efficiency of NAD+ production
shrinks with time. One of the main ways NAD+ is produced in cells is through recycling of Niacinamide, NAMPT is the limiting factor enzyme
Figure 2: A theoretical framework for one route how ageing might occur based on known hallmarks PERSONAL CARE MAGAZINE May 2026
www.personalcaremagazine.com
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