Could NAD+ Be the Molecule of Healthy Longevity and AntiAging?

By Dr. Marcus Robinson (c) 2025

Doctor of Clinical Hypnotherapy | Integrative Health Practitioner

Health Implications of NAD Depletion in a 50-Year-Old Human

Nicotinamide adenine dinucleotide (NAD+) is a vital coenzyme found in every cell, and its levels decline significantly with age¹. By around age 50, NAD+ concentrations are much lower than in youth, which can impact multiple aspects of health. For example, human skin NAD+ content in middle age (around 51-70 years) was reported to be ~ than in young adults², and skeletal muscle NAD+ levels in older adults may drop by about 30% compared to young individuals³. NAD+ functions like a cellular “battery,” shuttling energy and regulating critical processes¹. When NAD+ is depleted, cells struggle to produce energy, repair damage, and maintain normal metabolism. This structured report examines how reduced NAD+ levels in a 50-year-old affect aging, metabolism, cellular repair, and disease susceptibility, incorporating recent scientific findings.

Aging

Age-related NAD+ depletion is thought to contribute to the hallmarks of aging in multiple ways. NAD+ is required for enzymes (sirtuins and PARPs) that preserve cellular function and genomic stability⁴. As NAD+ declines with age, these protective mechanisms wane, leading to accelerated aging at the cellular and organism level¹. Key effects of NAD+ loss on aging include:

·         Decline in Sirtuin Activity: Sirtuins (SIRT1-SIRT7) are NAD+-dependent enzymes that promote longevity by regulating gene expression, stress resistance, and metabolism⁴. In aging tissues, falling NAD+ means reduced sirtuin activity, which can hasten age-related decline. For instance, diminished NAD+/SIRT1 activity in blood vessels leads to loss of small blood vessels and poorer blood flow with age. Restoring NAD+ in old mice reactivated SIRT1, reversed vascular aging, and improved muscle endurance⁵, highlighting NAD+’s role in maintaining youthfulness.

·         Impaired Mitochondrial Function: NAD+ is essential for mitochondrial energy production. With age, NAD+ drops and sirtuin 3 (SIRT3) activity in mitochondria falls, resulting in accumulated mitochondrial protein acetylation and dysfunction⁶. This contributes to the loss of cellular energy and efficiency seen in older adults. Research indicates that declining NAD+ directly reduces muscle mitochondrial function and exercise capacity. Boosting NAD+ in aged animals restores mitochondrial health: old mice given NAD+ precursors showed 56-80% greater exercise endurance after treatment⁵. This suggests NAD+ depletion is a factor in age-related fatigue and muscle weakness.

·         DNA Damage & Cellular Senescence: NAD+ fuels DNA repair enzymes like PARP-1. During aging, DNA damage accumulates and PARPs consume more NAD+ to fix it¹. If NAD+ is low, repair is incomplete, leading to persistence of DNA lesions. This can trigger cellular senescence or cell death, contributing to tissue aging. Indeed, studies show NAD+ is essential for efficient DNA repair⁴; low NAD+ leads to genomic instability and the buildup of senescent cells that secrete inflammatory factors (driving “inflammaging” - chronic inflammation in aging)⁴. By middle age, the increased demand for NAD+ in DNA repair can outpace supply, accelerating the aging process¹.

·         Oxidative Stress and Inflammation: NAD+ and sirtuins help cells cope with oxidative damage. SIRT1, activated by NAD+, normally dampens inflammatory pathways (like NF-κB) and enhances antioxidant gene expression⁴. NAD+ depletion in older adults thus leads to weaker antioxidant defenses and higher inflammation. This inflammatory state (inflammaging) contributes to tissue damage and age-related disorders⁴. For example, obese individuals (who often have low NAD+ in tissues) show elevated inflammatory markers⁶. Adequate NAD+ is needed to keep oxidative stress in check and maintain normal tissue function as we age.

·         Evidence from Model Organisms: Boosting NAD+ has been shown to slow or reverse aspects of aging in animal models. In mice, raising NAD+ levels via precursors like NMN rejuvenated skeletal muscle and restored blood vessel growth that had been lost with age⁵. Treated old mice ran significantly farther (430 m vs 240 m) than untreated peers⁵. Such findings suggest NAD+ depletion is a driver of aging changes in muscle and possibly other tissues. However, recent evidence shows complexity: a 2025 study in Denmark found that even an 85% NAD+ reduction in adult mice’s muscles did not accelerate apparent aging or frailty³. The NAD-depleted mice maintained normal muscle strength and lifespan, indicating that some tissues can tolerate NAD+ loss without immediate functional decline³. This surprising result implies NAD+’s role in aging may be tissue-specific - critical in some cell types (e.g. neurons, blood vessels) but more adaptable in others like muscle. Overall, most studies support that maintaining NAD+ helps counteract aging, but the impact can vary across different organs and conditions³.

Metabolism

NAD+ is a central mediator of metabolic health, and its depletion by midlife can disrupt normal metabolism and energy balance. As a coenzyme in redox reactions, NAD+ is required to convert nutrients into ATP (cellular energy) in pathways like glycolysis and the TCA cycle⁷. It also regulates metabolic genes via sirtuins. When NAD+ levels fall, cells cannot optimally generate energy or respond to metabolic stress. Key metabolic implications of NAD+ depletion include:

·         Reduced Energy Production: NAD+ functions like a “rechargeable battery” for cells, carrying energy from food to fuel biochemical processes¹. Lower NAD+ means cells have a harder time producing ATP. A 50-year-old with NAD+ depletion may experience lower energy and stamina because muscle and other tissues become less efficient at oxidative metabolism. In fact, muscle NAD+ decline (~30% by old age) was thought to contribute to age-related fatigue³. Cells adapt by shifting to less efficient energy pathways when NAD+ is scarce. This metabolic slowdown can manifest as fatigue, reduced exercise capacity, and slower metabolism.

·         Impaired Glucose Metabolism & Insulin Sensitivity: NAD+ is critical for maintaining normal blood sugar regulation. Sirtuin 1 (SIRT1) in liver and fat, which depends on NAD+, improves insulin sensitivity and glucose homeostasis. NAD+ loss with age or obesity inactivates these pathways. Obesity is associated with low NAD+ levels and sirtuin activity in adipose tissue⁶. In one twin study, the heavier (obese) twins had significantly lower expression of NAD+-producing enzymes (NAMPT, NMNAT) and sirtuins in fat, along with higher NAD-consuming PARP activity⁶. This NAD+/sirtuin suppression correlated with insulin resistance and inflammation in the obese twins⁶. Thus, NAD+ depletion contributes to the metabolic derangements of midlife obesity and type 2 diabetes. Conversely, restoring NAD+ shows benefits: in diabetic mouse models, NAD+ precursor (NMN) supplementation restored NAD+ levels and rescued insulin secretion and sensitivity⁸. These results indicate that maintaining NAD+ can protect against insulin resistance and glucose intolerance as we age.

·         Lipid Metabolism and Weight Gain: NAD+ is a key regulator of lipid metabolism in liver, muscle, and fat. Sufficient NAD+ and sirtuin activity promote fat breakdown and healthy lipid profiles. When NAD+ is low, cells favor storing fat and burning less, contributing to weight gain and dyslipidemia. Studies in rodents show NAD+ depletion in obesity leads to fatty liver and elevated cholesterol⁸. Boosting NAD+ can reverse these trends: in high-fat diet mice, NMN prevented the typical NAD+ decline, which helped suppress weight gain and improved cholesterol levels⁸. Middle-aged mice given long-term NMN stayed leaner and more physically active than controls⁸. For a 50-year-old human, low NAD+ may mean the body is less able to metabolize fats, predisposing to abdominal weight gain and fatty liver. Indeed, disturbances in NAD+-linked energy sensing pathways are implicated in metabolic syndrome⁸. Maintaining NAD+ through diet (niacin, etc.) or lifestyle (exercise increases NAD+) may support healthier weight and lipid metabolism in midlife.

·         Mitochondrial Health and Exercise Metabolism: NAD+ is indispensable for mitochondrial function - it carries electrons for ATP production. NAD+ decline in midlife contributes to mitochondrial inefficiency and reduced aerobic capacity. Muscles of older adults have fewer NAD+ molecules available to sustain prolonged exercise, partly explaining age-related endurance loss⁵. Restoring NAD+ can rejuvenate mitochondria. In aged rats, NAD+ supplementation improved muscle mitochondrial function and oxygen use, which translated into better treadmill endurance⁵. NAD+ also activates PGC-1α via SIRT1, boosting mitochondrial biogenesis. Low NAD+ blunts this adaptive response to exercise. This is why even fit 50-year-olds may notice a decline in performance - their muscles’ “fuel efficiency” is reduced without adequate NAD+. Encouragingly, combining NAD+ boosters with exercise has synergistic effects in animals, greatly enhancing muscle oxidative capacity⁵. However, in the absence of metabolic stress, extra NAD+ might not further enhance performance; studies in healthy adults taking NAD+ precursors have sometimes seen minimal gains in exercise or metabolism³. It suggests NAD+ therapy yields the most benefit when a deficit or metabolic dysfunction is present (as is often the case by age 50 or beyond).

·         Therapeutic Outlook: The link between NAD+ and metabolism has spurred clinical trials in humans around age 50-60 to test NAD+ boosters for metabolic health. Early evidence is mixed. Some trials report improved muscle mitochondrial markers and reduced blood pressure with NAD+ precursor supplementation, while others show no significant improvement in glucose metabolism in non-deficient individuals³. The consensus emerging is that NAD+ decline contributes to age-related metabolic disease, and correcting it may help, but it is not a magic bullet on its own³. Lifestyle remains crucial. Still, keeping NAD+ levels robust (through a healthy diet rich in B3 and exercise, or possibly supplements under medical guidance) could support a 50-year-old’s metabolic health by ensuring the enzymes that govern energy balance remain active⁸.

Cellular Repair

Cells constantly undergo wear-and-tear, and NAD+ is a linchpin of cellular repair mechanisms. When NAD+ is depleted, the ability of cells to fix damage and maintain homeostasis is compromised, which can accelerate aging and lead to disease. Several repair processes are affected:

·         DNA Repair Systems: One of NAD+’s most crucial roles is as a substrate for Poly(ADP-ribose) polymerases (PARPs), enzymes that detect and repair DNA strand breaks⁷. PARP-1 uses NAD+ to form poly(ADP-ribose) chains signaling DNA repair machinery to the damage site⁷. If NAD+ is low, PARP activity is limited, leaving DNA breaks unrepaired. Accumulation of DNA damage can cause mutations and trigger cell senescence or apoptosis. In a 50-year-old, decades of oxidative stress and environmental exposures cause DNA lesions just when NAD+ availability for repair is diminishing. The result is genomic instability, a hallmark of aging and a risk factor for cancer. Studies confirm that NAD+ levels strongly influence DNA repair capacity⁴. In fact, chemically inhibiting PARP to conserve NAD+ in old mice cells improved their function and lifespan by preserving NAD+ for other repairs⁴. This illustrates that NAD+ shortage, whether from age or high PARP demand, can leave the genome vulnerable. By middle age, NAD+ depletion may slow the repair of everyday DNA damage from UV, toxins, or cell division, allowing damage to accumulate in tissues over time.

·         Epigenetic Maintenance: NAD+-dependent sirtuin enzymes (especially SIRT1 and SIRT6) help repair DNA and maintain epigenetic stability. SIRT1 assists in repairing broken DNA strands and modulates gene expression to promote cell survival under stress⁴. SIRT6 specifically is known to repair telomeres and double-strand breaks. Both require NAD+ for their deacetylase activity. With less NAD+, SIRT1/6 activity falls, leading to mistakes in DNA repair and altered epigenetic marks. Over time, this can cause age-related epigenetic drift and genomic instability. Research in mice has shown that increasing NAD+ can activate SIRT1 such that cells better survive oxidative stress and fix DNA damage⁴. Conversely, NAD+ depletion may create a vicious cycle of DNA damage -> activation of PARP consuming more NAD+ -> further NAD+ loss -> even poorer sirtuin function and repair, etc.¹. Breaking this cycle by replenishing NAD+ has been proposed as a strategy to maintain genome integrity in aging cells.

·         Protein and Organelle Quality Control: Cells also need NAD+ for pathways that remove or repair damaged components. For example, NAD+-activated sirtuins stimulate autophagy - the cell’s garbage disposal system. SIRT1 deacetylates proteins that control autophagy and lysosomal function, and SIRT3 helps stabilize mitochondrial proteins⁴. Low NAD+ impairs autophagy, meaning defective proteins and organelles (like mitochondria) accumulate. This can make cells less resilient and prone to dysfunction. In the brain, for instance, NAD+ depletion is linked to a build-up of damaged mitochondria and increased reactive oxygen species (ROS), whereas adding NAD+ reduced mitochondrial damage and ROS in a chronic brain injury model⁹. Similarly, in other tissues, adequate NAD+ triggers repair pathways that clear out junk, whereas NAD+ shortage leads to clutter and stress within cells. For a 50-year-old, declining NAD+ might mean slower turnover of misfolded proteins or less efficient replacement of aged organelles, contributing to tissue aging and stiffening.

·         Cell Survival Under Stress: NAD+ is critical for cell survival mechanisms in the face of stress like oxidative damage, UV exposure, or toxins. NAD+ not only repairs damage but also serves as a signaling molecule for stress responses. For example, when DNA is extensively damaged, excessive PARP activation can completely deplete NAD+ and ATP, causing cell death (this is a mechanism in stroke or severe inflammation injury)⁴. In moderate stress, cells try to increase NAD+ supply via salvage pathways, but at age 50 the enzyme NAMPT (which recycles NAD+ from nicotinamide) is often less expressed (skeletal muscle NAMPT is ~35% lower at age 70 vs 20²). Thus, midlife cells are less equipped to quickly replenish NAD+ during a crisis. This can lead to greater cell loss after an injury. Indeed, experiments show enhancing NAD+ levels (e.g., with NMN) improves cell survival after stress like ischemia or neurotoxins, by providing the energy and signaling needed to endure the stress⁹. Therefore, NAD+ depletion lowers the threshold for cells to undergo apoptosis or senescence when challenged. Important repair crews (sirtuins, PARPs) cannot work effectively, and the cell’s emergency battery is drained. Over years, this means subtle injuries accumulate into noticeable tissue damage or organ degeneration.

In summary, NAD+ is a cornerstone of cellular repair and maintenance. At 50, declining NAD+ leads to slower DNA repair, weaker stress response, and accumulation of cellular damage. This not only drives aging, but also sets the stage for age-related diseases due to unrepaired damage in cells.

Disease Susceptibility

Because NAD+ influences so many fundamental processes (energy production, DNA repair, cell survival, and inflammation), chronically low NAD+ levels can increase susceptibility to a wide range of diseases in midlife and beyond. Researchers note that dysregulated NAD+ metabolism is implicated in aging as well as diseases “ranging from cancer to diabetes and neurodegenerative diseases.”¹ Below are key disease areas where NAD+ depletion in a 50-year-old may elevate risk:

·         Metabolic Diseases: NAD+ depletion contributes to conditions like type 2 diabetes, metabolic syndrome, and fatty liver disease. In addition to causing insulin resistance in tissues⁶, low NAD+ hampers pancreatic β-cells that produce insulin. Studies in mice show NAD+ restoration can revive failing β-cells and improve blood sugar control⁸. Low NAD+ also promotes chronic inflammation in fat (inflammaging), which is a driver of insulin resistance⁶. A 50-year-old with falling NAD+ may develop higher blood glucose and triglycerides, edging toward diabetes. Supporting this, obese humans with metabolic syndrome have diminished adipose NAD+/sirtuin pathways⁶. Boosting NAD+ has potential therapeutic effects: in obese and diabetic rodent models, NAD+ supplementation increased insulin sensitivity, reduced fatty liver, and protected against further metabolic deterioration⁸. While human trials are ongoing, maintaining NAD+ is seen as a strategy to stave off metabolic diseases as we age⁸.

·         Neurodegenerative Diseases: The brain is highly energy-dependent and sensitive to NAD+ levels. NAD+ decline by midlife may increase vulnerability to disorders like Alzheimer’s, Parkinson’s, and other neurodegenerative diseases. Professor Mathias Ziegler notes that NAD+ is critical for both energy metabolism and genomic regulation in neurons, so depleted NAD+ leaves neurons less able to cope with stress, contributing to brain aging and neurodegeneration¹. In aging brains, DNA damage and mitochondrial dysfunction accumulate, and NAD+ loss exacerbates both issues¹. For example, in models of Alzheimer’s and vascular dementia, raising NAD+ levels has yielded promising results: NAD+ supplementation in chronically under-perfused rat brains improved cognitive function and reduced neuroinflammation by protecting mitochondria and lowering oxidative damage⁹. Similarly, a small clinical study in Parkinson’s patients found that giving a NAD+ precursor (NR) improved the patients’ brain NAD+ levels and had beneficial effects on mitochondrial function in cells, hinting at symptom relief. Thus, NAD+ depletion is linked to neuronal injury (partly via energy shortfall and impaired DNA repair in the brain), whereas preserving NAD+ can be neuroprotective. A 50-year-old with low NAD+ might be at higher risk of memory impairment or slower cognitive function in later decades. Conversely, strategies that maintain NAD+ (exercise, diet, possibly NAD+ boosters) are being explored to support brain health and delay neurodegenerative disease onset¹.

·         Cardiovascular Health: NAD+ is emerging as important for the heart and blood vessels. NAD+ decline contributes to endothelial cell aging, hypertension, and heart muscle weakness. Vascular aging - the loss of capillaries and elasticity - is tied to diminished SIRT1 activity due to NAD+ loss. This leads to poor tissue perfusion and can promote conditions like hypertension, atherosclerosis, and heart failure⁵. In mice, NAD+ loss was shown to reduce blood flow and exercise tolerance, whereas restoring NAD+ via NMN stimulated new blood vessel growth and improved cardiac endurance⁵. By age 50, many individuals have early artery stiffening; NAD+ depletion may accelerate this by impairing endothelial repair and increasing oxidative stress in vessels. In the heart, NAD+ is required for sustaining high-energy output. Low myocardial NAD+ can precipitate mitochondrial dysfunction in heart cells, contributing to age-related decline in cardiac output or arrhythmias. On the other hand, raising NAD+ in aged mouse hearts has been linked to enhanced mitochondrial function and resistance to stress (e.g. limiting damage from heart attacks)¹. It’s worth noting that any intervention to boost NAD+ and blood flow must be done cautiously in those with cancer (extra blood supply could feed tumors)⁵. Still, adequate NAD+ is generally beneficial for cardiovascular maintenance: it supports healthy blood pressure, cholesterol processing, and vessel flexibility. NAD+ depletion, conversely, likely increases the risk of cardiometabolic diseases - this is supported by human evidence that low NAD+ status correlates with markers of heart disease and poor metabolic health.

·         Immune Function and Inflammation: A 50-year-old’s immune system (both innate and adaptive) becomes less efficient in a state of NAD+ deficit. NAD+ is required for immune cell metabolism during activation⁷. When an immune cell (like a T cell or macrophage) encounters a pathogen, it must rapidly produce energy and building blocks - processes heavily reliant on NAD+. Low NAD+ can thus blunt the immune response, leading to slower or weaker reactions to infections. Additionally, NAD+-dependent sirtuins regulate inflammation; SIRT1 normally deacetylates and inhibits inflammatory gene regulators, but with low NAD+, this brake is released⁴. The result is higher baseline inflammation (inflammaging) and potentially autoimmune tendencies. Chronic NAD+ depletion has been linked to elevated inflammatory cytokines (like TNF-α, IL-6) which contribute to conditions such as arthritis, atherosclerosis, and neuroinflammation⁹. On the flip side, research shows replenishing NAD+ can calm inflammation: in aged mice, boosting NAD+ reduced pro-inflammatory cytokines and protected tissues from inflammatory damage⁹. NAD+ also plays a role in immune cell longevity - for instance, experiments found that enhancing NAD+ in T cells improved their function (this is being tested to “rejuvenate” aging CAR-T immune cells for cancer therapy). Thus, NAD+ depletion by age 50 may leave one more prone to infections, slower wound healing, and possibly less effective cancer immunosurveillance. Maintaining NAD+ supports a more youthful immune profile, whereas loss of NAD+ tilts the body toward chronic inflammation and immune risk.

·         Cancer Susceptibility: The relationship between NAD+ and cancer is complex. On one hand, NAD+ is critical for fixing DNA damage, so chronically low NAD+ could allow mutations to accumulate, potentially increasing cancer risk over time¹. NAD+-dependent sirtuins like SIRT1 and SIRT6 have tumor-suppressor functions (promoting DNA repair, stabilizing telomeres, regulating oncogenes); their impairment due to NAD+ shortage might remove safeguards against tumor development. Indeed, genomic instability from poor DNA repair is a root cause of cancer, and NAD+ depletion exacerbates that instability⁴. Some studies have noted that elderly people have both low NAD+ and higher cancer incidence, suggesting a connection. On the other hand, cancer cells themselves often have high NAD+ needs to fuel rapid growth, and some therapies try to exploit this by blocking NAD+ synthesis in tumors. Notably, normal cells in a 50-year-old with low NAD+ may struggle to sustain immune surveillance against emerging cancer cells. There is evidence that NAD+ repletion can enhance DNA repair and cell death of damaged cells, potentially preventing malignant transformation⁴. However, if a cancer has already formed, restoring blood NAD+ broadly could theoretically “feed” the tumor as well as healthy cells⁵. Current research is examining NAD+-modulating drugs for cancer prevention and therapy in a nuanced way. For general health, keeping NAD+ at healthy levels likely aids in preventing cancer by maintaining DNA integrity and robust immune function to eliminate precancerous cells. NAD+ depletion, conversely, might leave an individual more exposed to carcinogenic effects of toxins or radiation due to sluggish repair and a less vigilant immune system¹.

In summary, NAD+ depletion at age 50 can heighten the risk or severity of many age-associated diseases. Lower NAD+ undercuts the body’s natural defenses - metabolic balance, neuronal resilience, vascular repair, immune response, and genomic stability - thereby opening the door for disorders to take hold. Conversely, interventions that sustain or boost NAD+ levels are being actively researched as potential therapies to reduce disease risk and improve healthspan in midlife and older adults⁸.

Summary of NAD Depletion Impacts on Health

The table below summarizes key findings on how NAD+ depletion affects each health aspect and the implications for a 50-year-old individual:

Health Aspect	NAD+ Depletion Effects	Health Implications (Age
Aging	NAD+ levels drop with age (e.g. 60%↓ in skin by midlife2), reducing SIRT1/3 activity and DNA repair1. Cells accumulate damage and senescent cells increase. Some tissues (muscle) adapt to NAD+ loss3, but others cannot.	Accelerates aging processes: poorer tissue function, fatigue, and cellular aging. Higher oxidative stress and inflammaging due to low NAD+4. Overall, vitality and resilience decline faster in midlife when NAD+ is low, though effects vary by tissue.
Metabolism	NAD+ is required for energy production, insulin secretion, and metabolic enzyme function8. NAD+ loss reduces ATP generation and impairs metabolic regulation (lower SIRT1 → insulin resistance; less SIRT3 → mitochondrial inefficiency)6.	Leads to sluggish metabolism: fatigue, lower exercise endurance, and propensity for weight gain. Risk of metabolic syndrome rises - insulin resistance, higher blood sugar, and fatty liver in NAD+-depleted individuals8. Elevated risk of type 2 diabetes and dyslipidemia by age 50 if NAD+ is low.
Cellular Repair	NAD+ fuels DNA repair (PARP) and stress response enzymes7. Low NAD+ means DNA breaks persist (genomic instability) and sirtuin-driven repair pathways falter4. Autophagy and antioxidant defenses weaken without NAD+ (SIRT1/SIRT3 inactivity)4.	Accumulation of cellular damage: unrepaired DNA can trigger mutations or senescence, raising cancer risk1. Cells are less able to recover from injury or oxidative stress, contributing to organ aging. Weaker autophagy leads to buildup of misfolded proteins and dysfunctional mitochondria (linked to neurodegeneration and muscle decline).
Disease Risk	Chronic NAD+ depletion is linked to major diseases of aging: neurodegeneration (due to neuron energy failure and DNA damage)9, metabolic diseases (due to insulin resistance/inflammation)6, cardiovascular disease (endothelial dysfunction), and even cancer (genomic instability)1. Immune function also declines as NAD+ falls7.	Increases susceptibility to diseases in midlife and later. Examples: higher risk of Alzheimer’s and Parkinson’s (if brain NAD+ is low), greater chances of type 2 diabetes and obesity-related complications, more heart and blood vessel issues (hypertension, atherosclerosis), and potentially higher cancer risk over time due to DNA repair deficits. Low NAD+ also contributes to chronic inflammation, compounding disease processes4.

Every aspect of health - from cellular vitality to whole-body metabolism - is influenced by NAD+ availability. For a 50-year-old, preserving NAD+ levels (through a healthy lifestyle or emerging therapies) could mean better aging outcomes, more robust metabolism, improved repair capacity, and lower risk of age-related diseases¹. Conversely, unchecked NAD+ depletion acts as a unifying thread linking aging and increased disease susceptibility, underscoring NAD+’s central role in human health.⁴

References

1. Study unveils NAD's link to aging and disease development. https://www.news-medical.net/news/20241223/Study-unveils-NADs-link-to-aging-and-disease-development.aspx

2. Age-Dependent Decline of NAD+-Universal Truth or Confounded ... - MDPI. https://www.mdpi.com/2072-6643/14/1/101

3. Study Finds Huge Drop in NAD+ Doesn’t Affect Aging or Strength. https://www.sciencenewstoday.org/study-finds-huge-drop-in-nad-doesnt-affect-aging-or-strength

4. Cellular Repair and Reversal of Aging: the Role of NAD - CellR4. https://www.cellr4.org/article/852

5. Rewinding the Clock - Harvard Medical School. https://hms.harvard.edu/news/rewinding-clock

6. Obesity Is Associated With Low NAD - Oxford Academic. https://academic.oup.com/jcem/article/101/1/275/2806840

7. NAD + metabolism and function in innate and adaptive immune cells. https://journal-inflammation.biomedcentral.com/articles/10.1186/s12950-025-00457-7

8. NAD+ Supplementation Mitigates Age-Associated Metabolic Diseases like .... https://www.nmn.com/news/nad-supplementation-could-mitigate-age-associated-metabolic-diseases

9. NAD+ improves cognitive function and reduces neuroinflammation by .... https://jneuroinflammation.biomedcentral.com/articles/10.1186/s12974-021-02250-8

📌 About the Author: 

Marcus Robinson, DCH, has been a leader in the human potential and social change movements since 1985. He holds a doctorate in clinical hypnotherapy and is nationally certified as an Integrative Health Practitioner. His work has inspired many, and he is a published author with three books and numerous articles in these fields.

Content Disclaimer: 

Neither the author nor the publisher is engaged in providing advice or services to individual readers. The information in this article is for educational purposes only and should not be construed as medical advice. It is not intended to diagnose or replace qualified medical supervision. For any medical conditions, individuals are encouraged to consult a healthcare provider before using any information, ideas, or products discussed. Neither the author nor the publisher will be responsible for any loss or damage allegedly arising from any information or suggestions made in this article. While every effort has been made to ensure the accuracy of the information presented, neither the author nor the publisher assumes any responsibility for errors.