NAD+ is one of those molecules you keep hearing about in longevity and “cellular energy” conversations. But what is it really – and why does everyone say it drops as we get older?
This article gives a clear, research-based answer in plain language.
What is NAD+?
NAD+ (nicotinamide adenine dinucleotide) is a coenzyme found in every cell in your body.
You can think of it as:
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a key helper for turning food into cellular energy (ATP) in the mitochondria
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a co-factor for enzymes that repair DNA
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a signal molecule used by longevity-related proteins like sirtuins and PARPs
Recent reviews in leading medical journals describe NAD+ as a central node that connects many “hallmarks of aging”: mitochondrial dysfunction, DNA damage, impaired stress responses, and chronic inflammation.
When NAD+ is low, these systems struggle to perform optimally.
What does NAD+ actually do?
The main roles, simplified:
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Energy production
NAD+ shuttles electrons in reactions that generate ATP. Without enough NAD+, your mitochondria can’t produce energy efficiently. PubMed -
DNA repair and genome stability
NAD+ fuels enzymes (like PARPs and sirtuins) that detect and repair DNA damage and help maintain chromosome integrity. PubMed -
Cellular stress responses and “longevity pathways”
Sirtuins, often called “longevity proteins,” depend on NAD+ to regulate metabolism, inflammation, mitochondrial quality control and cellular stress resistance. PubMed -
Metabolic and immune regulation
Changes in NAD+ influence insulin sensitivity, inflammatory signaling and immune cell function – all crucial for healthy aging. Nature
Because NAD+ touches so many systems, even moderate changes in its levels can have broad effects.
Does NAD+ really decline with age?
In short: yes – but it’s tissue-specific and more complex than a simple straight line.
Animal and cell studies
Multiple studies in mice and other models show a clear age-related decrease in NAD+ in tissues such as skeletal muscle, liver, adipose tissue and brain. Restoring NAD+ in these models often improves healthspan and delays features of aging.
Human data
Human data is newer but growing:
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Imaging studies of healthy adults using advanced MRI/MRS techniques suggest whole-brain NAD+ levels fall by roughly 10–25% from young adulthood to older age.
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Clinical and ex vivo studies indicate that NAD+ can decline with age in some tissues (e.g. skeletal muscle, skin, possibly liver), while remaining more stable in others.
A 2025 review on NAD+ dynamics in human ageing concluded that age-related NAD+ decline is real but not uniform: it depends on the tissue, individual health status and environmental factors.
There is still debate – one 2021 review even asked whether “age-dependent NAD+ decline” is a universal truth or context-dependent phenomenon – but the consensus is moving toward: In many people and tissues, NAD+ availability tends to fall with age and chronic disease.
Why does NAD+ decline as we age?
Current evidence points to several overlapping mechanisms:
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Increased NAD+ consumption
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DNA damage accumulates with age → PARP enzymes use more NAD+ for repair.
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Chronic low-grade inflammation activates CD38 and other NAD-consuming enzymes on immune cells.
Result: more NAD+ is burned just to keep up with stress.
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Reduced NAD+ production / recycling
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The salvage pathway (recycling vitamin B3 forms back to NAD+) becomes less efficient in some tissues.
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Changes in key enzymes (like NAMPT) and nutrient availability can impair this recycling.
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Overnutrition, inactivity, obesity and metabolic disease increase oxidative stress and inflammation, which further drive NAD+ consumption and impair synthesis.
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Disease-specific factors
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Neurodegeneration, cardiovascular disease, fatty liver and kidney disease have all been associated with disturbed NAD+ metabolism in human and animal studies.
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In other words, aging + modern lifestyle = higher NAD+ demand and lower NAD+ supply in many tissues.
Why does this matter for longevity?
Because NAD+ is involved in:
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mitochondrial energy
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DNA repair
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inflammation control
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cell survival and stress resilience
most experts now see NAD+ homeostasis as one of the key biological levers in aging.
So the most evidence-based message today is:
Keeping NAD+ pathways healthy – through lifestyle and targeted supplementation under professional guidance – is a promising way to support cellular resilience and healthy aging, but not yet a guaranteed “anti-aging cure.”
References:
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Chini CCS, et al. NAD metabolism: role in senescence regulation and aging. Aging Cell. 2024. PubMed+2Wiley Online Library+2
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Lautrup S, et al. Roles of NAD+ in Health and Aging. Cold Spring Harb Perspect Med. 2024;14(1):a041193. perspectivesinmedicine.cshlp.org+2PubMed+2
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McReynolds MR, et al. Age-related NAD+ decline. Mech Ageing Dev. 2020. PMC
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Yusri K, et al. The role of NAD+ metabolism and its modulation in aging and chronic disease. Nat Rev Bioeng. 2025. Nature
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Iqbal T, et al. The therapeutic perspective of NAD+ precursors in age-related diseases. Biochim Biophys Acta Gen Subj. 2024. ScienceDirect+1
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Peluso A, et al. Age-dependent decline of NAD+—universal truth or confounded artifact? Nutrients. 2021. MDPI
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Khatri S, et al. Clinical evidence for the use of NAD+ precursors to slow aging. GeroMedicine. 2025. sciexplor.com+1
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Dean G. Whole-Brain NAD+ Levels Decline with Age, New Study Shows. NAD.com News, 2024. NAD.com+1