Nicotinamide mononucleotide (NMN) - Educational material

Nicotinamide mononucleotide (NMN) was first discovered in 1963. But it came to attention as an anti-aging compound around 2011, when various studies showed its ability to improve blood sugar control in laboratory animals.

What is NMN?

Structurally, NMN is a nucleotide derived from ribose and nicotinamide, a form of vitamin B3. Specifically, it consists of a nicotinamide molecule linked to a ribose sugar and a phosphate group, making it an essential intermediate in various biological processes. Studies indicate that NMN supports the function of various organs, including the kidneys, liver, heart, skeletal muscle and nervous system. It also helps reduce inflammation and strengthens the immune system

NMN acts as an essential precursor of nicotinamide adenine dinucleotide (NAD⁺ ), an important coenzyme present in every living cell. NAD⁺ is fundamental to energy metabolism, enabling redox reactions that produce cellular energy. In addition to its role in energy production, NAD⁺ plays a significant role in a variety of important cellular functions, such as DNA repair, regulation of gene expression and maintenance of circadian rhythms. By increasing NAD+ levels, NMN is considered both safe and beneficial in the treatment and prevention of age-related diseases.

Dietary sources and supplementation

NMN is found in small amounts in a variety of foods, including:

• Fruits and vegetables: Such as broccoli, cabbage, cucumbers and avocados.
• Animal products: This includes raw beef and shrimp, although usually in lower concentrations compared to plant sources.

Despite its presence in foods, NMN concentrations are relatively low, which has led to increased interest in NMN supplementation as a way to reach therapeutic levels for potential health benefits.

Pharmacological and therapeutic applications

In addition to its role in aging, NMN has been studied for its potential benefits in various health conditions, including:

• Metabolic disorders: Such as type 2 diabetes and obesity.
• Neurodegenerative diseases: This includes Alzheimer's disease.
• Cardiovascular health: It helps prevent heart failure and other heart-related conditions.
• Inflammatory conditions: By reducing inflammation and strengthening the immune system.

Potential health benefits of NMN

Based on human testing and preliminary studies, NMN offers the following health benefits and offers anti-aging effects.

NMN increases NAD+ levels

As a precursor to nicotinamide adenine dinucleotide (NAD+), NMN has been widely studied for its potential to improve health outcomes and increase NAD+ levels in the body. Yi et al (2023) conducted a randomized, double-blind, placebo-controlled study evaluating NMN supplementation in 80 healthy middle-aged adults for 60 days. Participants received 300 mg, 600 mg or 900 mg of NMN daily [1]. The study showed a significant increase in blood NAD+ levels in all NMN-treated groups, with the highest levels observed at the 600 mg and 900 mg doses. It is noteworthy that physical performance, as assessed by a six-minute walk test, improved significantly in the NMN groups, especially at the higher doses. NMN was well tolerated and no adverse effects were reported, with the 600 mg/day dose providing maximum efficacy. These results suggest a potential role for NMN in promoting NAD+ levels and physical performance.

In addition, Yamaguchi et al (2024) evaluated the effect of an 8-week regimen of 250 mg/day of NMN in 11 healthy middle-aged Japanese men [2]. It is noteworthy that NAD+ levels in peripheral blood mononuclear cells increased steadily, demonstrating the ability of NMN to increase NAD+ biosynthesis. In participants with hyperinsulinemia, NMN slightly reduced postprandial insulin levels, suggesting a potential metabolic benefit. NMN was safe and well tolerated, and no adverse effects were observed. This study highlights the use of NMN in mitigating age-related metabolic risks. In addition, Igarashi et al (2022) examined the effects of 250 mg/day of NMN for 6 to 12 weeks in healthy older men [3]. The study showed a significant increase in blood NAD+ levels and a slight improvement in muscle function, including gait speed and grip strength. These findings suggest the potential of NMN in dealing with low NAD+ levels and aging-related muscle decline.

Moreover, Okabe et al (2022) conducted a 12-week randomized, placebo-controlled study involving 30 participants receiving 250 mg/day NMN or placebo [4]. NMN significantly increased levels of NAD+ and related metabolites without side effects. The study confirmed that NMN is a safe and effective strategy for increasing NAD+ levels in humans. In addition, Yamane et al (2023) evaluated the effects of NMN supplementation in a 12-week study involving 11 healthy volunteers [5]. Participants took 250 mg of NMN daily, which resulted in a significant increase in plasma NAD+ and NMN levels. In addition, postprandial serum insulin levels were elevated, although responses varied among individuals. Importantly, no adverse effects were reported, confirming the safety of NMN supplementation. These results suggest that NMN improves metabolic health by increasing NAD+ levels and insulin secretion without compromising safety.

In another study, Pencina et al (2023) examined MIB-626, a microcrystalline preparation of beta-NMN, in a randomized, placebo-controlled trial involving 32 overweight or obese adults aged 55-80 years [6]. Participants received 1000 mg of MIB-626 once or twice daily for 14 days. The study showed a significant dose-dependent increase in blood levels of NAD+ and NMN, with a 1.7- to 3.7-fold increase in NAD+ compared to placebo. MIB-626 was well tolerated and no significant adverse events were reported. These results indicate that MIB-626 (beta-nmn) is a safe and effective formulation for increasing NAD+ levels in the body.

NMN supplementation shows anti-aging potential

Nicotinamide mononucleotide (NMN), a precursor to NAD+, has shown significant potential in counteracting age-related declines in cardiovascular, metabolic, cognitive and tissue function. By replenishing NAD+ levels, NMN restores cellular repair mechanisms and strengthens essential pathways for maintaining health during aging. Huang et al (2022) conducted a double-blind, randomized, controlled study involving 66 adults aged 40-65 years who received 300 mg/day of NMN (Uthever) for 60 days [7]. NAD+/NADH levels increased by 38%, and walking endurance improved significantly in the NMN group. While the reduction in blood pressure was minimal, insulin sensitivity remained stable, in contrast to a 30.6% increase in HOMA-IR in the placebo group. NMN was well tolerated and no serious side effects were reported. These results suggest that NMN is a promising intervention to improve metabolic health and delay aging-related changes.

In addition, Kim et al (2022) conducted a 12-week randomized controlled trial to examine the effects of NMN supplementation on sleep, fatigue and physical performance in 108 older adults [8]. Participants were divided into four groups: NMN (250 mg) or placebo, taken in the morning or afternoon. The NMN_PM group (afternoon intake) showed the greatest improvement in sleep quality, reduced fatigue and physical performance. Sleep indicators, such as sleep latency and daytime dysfunction, improved significantly, with an effect size of up to 0.80. It is noteworthy that elements of fatigue, including lethargy and instability, were significantly reduced, and physical tests , such as the 5-Times Sit-to-Stand and Timed Up and Go tests, showed improvements in lower limb function. These findings suggest that afternoon intake of NMN is a promising intervention to mitigate age-related decline in sleep and physical performance.

With age, the heart experiences deterioration in function, including reduced mitochondrial efficiency and increased protein acetylation. Whitson et al (2022) studied NMN at a dose of 400 mg/kg in aged mice and found improved diastolic and systolic cardiac function [9]. NMN reduced mitochondrial protein acetylation and oxidative stress while improving fractional shortening and diastolic filling capacity. These results indicate the potential of NMN to restore cardiac function by targeting mitochondrial health and protein regulatory pathways. In addition, aging affects blood vessels, leading to poor blood flow and increased risk of heart disease. A study by Kiss et al (2019) showed that NMN restores blood vessel health in aged mice [10, 11]. It improved blood flow, reduced oxidative stress and helped blood vessels behave like those in younger animals. NMN also activated certain genes to protect against damage and inflammation. These findings suggest that NMN may help people maintain healthier blood vessels as they age, potentially reducing the risk of diseases such as high blood pressure and atherosclerosis. Importantly, aging stiffens arteries, reducing their ability to carry blood efficiently. NMN supplementation reversed this effect in older mice, according to de Picciotto et al. (2016). Mice treated with NMN (300 mg/kg/day) showed improved vascular elasticity and better blood flow [12]. NMN also reduced oxidative stress and activated SIRT1, a cell-protecting enzyme. These results suggest that NMN may help reduce the risk of heart disease in aging adults.

In addition, taking NMN supplements can improve gut health and reduce the effects of aging. A study by Niu et al. (2021) found that NMN increases the number of beneficial gut bacteria, such as Helicobacter i Faecalibacterium, which help with digestion and overall health [13]. It also enhanced metabolic processes and improved telomere length, which protects cells from aging. In both mice and volunteers (aged 45-60), NMN increased telomere length in blood cells, a marker of cellular health. This shows NMN's potential in delaying aging, while also being safe because it does not affect weight or appetite.

In addition, long-term use of NMN may protect against the negative effects of an unhealthy diet. Zhou et al (2024) studied mice fed a high-fat diet and gave them NMN (400 mg/kg/day) for seven months [14]. NMN helped prevent weight gain, improved the way their bodies processed sugar and fat, and reduced inflammation. It also helped improve kidney and muscle function. This suggests that NMN may be a useful supplement in the fight against aging caused by poor diet. Gut health often deteriorates with age, leading to problems such as poor nutrient absorption and inflammation. Gu et al (2024) showed that NMN (400 mg/kg/day) strengthened the intestinal lining, reduced inflammation and promoted the growth of good bacteria such as Akkermansia muciniphila [15].. It also activated proteins that promote intestinal regeneration and repair. These improvements helped extend the lifespan of aging mice, demonstrating the benefits of NMN for improving gut health and overall vitality.

Aging affects myocardiocytes (heart cells) by disrupting oxidative phosphorylation, NAD+ metabolism and autophagy. Marzoog (2024) found that NMN corrects intracellular imbalances, promotes autophagy and reduces oxidative stress in aging heart cells [16]. By activating sirtuins and promoting a protective "dormant" state, NMN preserved myocardial function and alleviated ischemic injury. These findings suggest that NMN is a potential anti-aging strategy for maintaining heart health. In addition, oxidative stress contributes to vascular aging and endothelial dysfunction. Nakajo et al (2023) showed that NMN reduces oxidative damage in endothelial cells through activation of the SIRT1/NQO-1 pathway [17]. NMN attenuated cytotoxicity, reduced reactive oxygen species (ROS) levels and prevented cellular aging. These vasoprotective effects position NMN as a promising intervention in age-related cardiovascular disease.

Aging leads to structural and functional decline in the neurovascular unit, contributing to cognitive impairment. Kiss et al (2020) administered NMN to aging mice at a dose of 500 mg/kg/day for two weeks and observed significant improvements in cerebral blood flow, neurovascular coupling and mitochondrial function [18]. Transcriptomic analysis showed that NMN restored 204 genes in the neurovascular unit to youthful levels, promoting mitochondrial rejuvenation and anti-inflammatory effects. The study linked these molecular changes to improved neurovascular and cognitive outcomes, suggesting that NMN is a promising intervention for VCI and age-related dementia.

Aging impairs metabolic functions such as insulin sensitivity, energy metabolism and mitochondrial function. Mills et al (2016) administered 300 mg/kg NMN daily to aging mice for 12 months [19]. This long-term intervention inhibited age-related weight gain, improved glucose tolerance, enhanced lipid profiles and promoted physical activity. In addition, NMN promoted mitochondrial oxidative metabolism and reduced mitonuclear protein imbalance in skeletal muscle, which is important for energy homeostasis. Importantly, supplementation showed no toxicity, highlighting its safety for chronic use. Long-term administration (300 mg/kg/day) preserved muscle mass, increased insulin sensitivity and improved metabolic pathways in multiple tissues, demonstrating the comprehensive anti-aging potential of NMN.

Interestingly, NMN has also shown promise in reversing androgen-induced hair loss. Xu et al (2024) studied the effects of NMN in mice exposed to dihydrotestosterone (DHT), a compound that induces hair follicle thinning and atrophy [20]. At doses of 100 mg/kg, NMN promoted hair follicle regeneration by reducing inflammatory markers such as IL-6 and TNF-α, alleviating oxidative stress and increasing vascular endothelial growth factor (VEGF) expression. These findings suggest that NMN is a potential treatment for androgenetic alopecia by improving hair follicle immunity and vascular support.

Aging-induced cognitive decline is associated with mitochondrial dysfunction and neuronal apoptosis. Hosseini et al. (2019) found that NMN and melatonin, both alone and in combination, alleviated memory impairment in aged rats [21]. The combination therapy significantly increased ATP production, reduced ROS levels and stabilized mitochondrial membranes. In addition, the simultaneous administration of NMN and melatonin showed improved anti-apoptotic effects, making it a promising strategy for treating age-related cognitive impairment by improving mitochondrial function and reducing oxidative stress.

NMN improves cardiometabolic health in aging adults

In another study, Pencina et al (2023) evaluated MIB-626 (NMN) in 30 overweight or obese adults aged ≥45 years [22]. Participants received 1000 mg of MIB-626 twice daily for 28 days. Treatment significantly reduced body weight (1.9 kg), diastolic blood pressure (7.01 mmHg) and cholesterol levels, including LDL cholesterol (18.73 mg/dl). NAD+ levels also increased significantly. While muscle strength and insulin sensitivity remained unchanged, the cardiometabolic improvement underscores the potential of NMN (MIB-626) to safely and effectively address health challenges associated with aging. In another study, Katayoshi et al (2023) evaluated the effects of 12-week NMN supplementation (250 mg / day) on cardiovascular health in a double-blind study involving 36 healthy middle-aged adults [23]. NMN significantly increased serum levels of NAD+ metabolites and showed a tendency to reduce arterial stiffness, as indicated by pulse wave velocity. The study confirmed the safety and tolerability of NMN at the dose administered, highlighting its potential as a safe intervention to promote vascular health in middle age.

In addition, Kimura et al (2022) evaluated the effects of intravenous NMN in 10 healthy adults [24]. NMN administration significantly increased blood NAD+ levels and decreased triglycerides without affecting vital signs or metabolic markers of the liver, heart, pancreas or kidney. These findings highlight intravenous NMN as a potential therapeutic option for treating triglyceride-related conditions and promoting metabolic health. In another study, Zhong et al (2022) analyzed 40 clinical trials involving 14,750 participants to evaluate the effects of NAD+ precursors, including NMN, on lipid and glucose metabolism [25]. They observed significant reductions in triglycerides (SMD: -0.35), total cholesterol (SMD: -0.33) and LDL (SMD: -0.38), with an increase in HDL (SMD: 0.66). However, plasma glucose levels increased moderately (SMD: 0.27), especially for nicotinic acid (NA). NMN showed limited effects on lipid metabolism in healthy individuals, but precursors were more effective in populations with cardiovascular or metabolic disease.

NMN improves energy and physical performance

Studies have shown that NMN increases energy and aerobic capacity. Liao et al (2021) examined the effects of NMN supplementation on aerobic capacity in amateur runners during a six-week training program [26]. Participants received 300 mg, 600 mg or 1200 mg of NMN daily. The medium (600 mg) and high (1200 mg) dose groups showed significant improvements in oxygen uptake and power at ventilatory thresholds, enhancing exercise performance. The results suggest that NMN increases oxygen utilization in skeletal muscle, making it a valuable addition to exercise to enhance cardiovascular performance. In another study, Morifuji et al (2024) conducted a 12-week study in elderly subjects administering 250 mg/day of NMN [27]. NMN supplementation increased blood NAD+ levels, reduced daytime dysfunction scores and significantly improved walking speed. A negative correlation was observed between improved walking speed and increased NAD+ levels, suggesting a direct relationship. As mentioned above, Kim et al (2022) also found significant improvements in fatigue and physical performance [7]. Sleepiness was reduced, and improvements in sleep duration, quality and daytime dysfunction were observed in the NMN-treated group. These findings suggest that taking NMN improves lower limb function and reduces fatigue, suggesting the potential of NMN as a promising intervention to improve physical performance and alleviate age-related fatigue.

NMN for cardiovascular health

Mitochondrial dysfunction plays a key role in heart failure, especially in conditions of NAD+ deficiency. Zhang et al (2017) studied KLF4-deficient mice that exhibit mitochondrial protein hyperacetylation and NAD+ deficiency [28]. Short-term NMN supplementation preserved mitochondrial ultrastructure, reduced oxidative stress and inhibited cell death in the stressed heart. NMN also increased fatty acid oxidation in cardiomyocytes, improving cardiac energy metabolism without affecting pyruvate oxidation. These findings suggest NMN's ability to restore mitochondrial function and prevent heart failure under conditions of NAD+ deficiency, positioning it as a promising therapy for heart diseases associated with mitochondrial dysfunction.

In addition, doxorubicin (DOX), a chemotherapeutic agent, causes dose-dependent cardiotoxicity, leading to treatment discontinuation. Wan et al (2021) found that NMN alleviated DOX-induced cardiac damage by reducing oxidative stress, suppressing the NLRP3 inflamasome, and preventing apoptosis and fibrosis [29]. NMN enhanced antioxidant defense and reduced pro-inflammatory cytokines, indicating its potential to protect the heart during DOX-based chemotherapy. In addition, doxorubicin often causes severe cardiac damage. Khosroshahi et al (2022) showed that the combination of NMN (100 mg/kg/day) and troxerutin (TXR, 150 mg/kg/day) significantly reduced DOX-induced cardiac damage in rats [30]. The therapy restored mitochondrial membrane potential, reduced reactive oxygen species and increased ATP production. NMN and TXR also increased the expression of mitochondrial biogenesis proteins (PGC-1α, NRF1, TFAM) and decreased inflammatory cytokines (TNF-α, IL-1β, IL-6). The combination therapy was superior to individual treatment, showing a synergistic effect in preventing DOX-associated cardiac damage.

Moreover, in another study, Margier et al (2022) examined the protective effect of nicotinamide mononucleotide against doxorubicin-induced cardiotoxicity [31]. Using acute and chronic mouse models, NMN supplementation (180-500 mg/kg/day) significantly improved survival rates, attenuated weight loss and protected against doxorubicin-induced cardiac damage. NMN preserved mitochondrial function, reduced oxidative stress, and inhibited apoptosis and inflammation in heart tissue. In addition, NMN alleviated physical dysfunction caused by chronic exposure to Doxo. Transcriptomic analysis showed that NMN counteracted Doxo-induced changes in pathways related to mitochondrial integrity and stress responses. These findings underscore NMN's potential to protect against chemotherapy-induced cardiotoxicity and promote physical recovery.

Sepsis can lead to multi-organ failure, including significant cardiac dysfunction. Cao et al (2023) showed that NMN restored NAD+ levels in mice with sepsis, reducing oxidative stress, inflammation and apoptosis [32]. NMN improved cardiac function, protected the lungs and kidneys, and reduced mortality. By enhancing mitochondrial function and activating the NAD+/SIRT3 pathway, NMN also promoted immune cell activity, increasing bacterial clearance and reducing vascular leakage. These findings underscore the potential of NMN as a therapeutic agent for heart failure and sepsis-related multi-organ failure. Heart failure often results from mitochondrial dysfunction. Yagi et al (2023) showed that NMN reduces lysosomal damage, restores autophagy and prevents ferroptosis in a mouse model of mitochondrial dysfunction [33]. NMN prolonged the life of mice with dilated cardiomyopathy by targeting lysosomal health and reducing lipid peroxidation. These studies underscore the therapeutic value of NMN in preventing chronic heart failure associated with mitochondrial and lysosomal dysfunction. In addition, sepsis-related myocardial dysfunction contributes significantly to mortality. Ni et al (2024) showed that NMN alleviates mitochondrial dysfunction, oxidative stress and lysosomal dysfunction in septic hearts [34]. By restoring NAD+ levels, NMN deacetylates cyclophilin F (PPIF), reducing mitochondrial permeability transition pore (mPTP) sensitivity and preserving ATP production. These effects improved cardiac energy metabolism and prevented myocardial damage, highlighting the potential of NMN as a therapeutic agent for sepsis-related cardiac complications.

Moreover, Hosseini et al (2020) evaluated the combined effects of NMN and melatonin on ischemia/reperfusion (I/R) injury in aged rats [35]. Pre-conditioning with NMN and melatonin after conditioning reduced infarct size, oxidative stress and mitochondrial dysfunction. The combination therapy showed synergistic benefits, significantly increasing mitochondrial membrane potential and preserving hemodynamic function. These findings suggest a promising strategy to protect aging hearts from I/R damage by targeting mitochondrial health. Additionally, Mokhtari et al (2024) investigated the effects of NMN and ubiquinol on ischemia/reperfusion-induced ventricular arrhythmias [36]. Combination therapy reduced the severity of arrhythmias, improved myocardial function and increased antioxidant enzyme activity. NMN and ubiquinol synergistically increased nitric oxide (NO) production, contributing to cardioprotection. This dual-targeted approach shows promise in preventing reperfusion arrhythmias, especially in elderly patients.

NMN for brain health and cognitive function

Combining NMN with lycopene, a powerful antioxidant found in tomatoes, may improve brain health. Liu et al (2022) found that the combination improved memory and reduced brain inflammation in aging rats [37]. The treatment also activated protective pathways, helping cells fight oxidative stress and slowing aging. This suggests that NMN, especially when combined with other supplements, may help protect against age-related cognitive decline.

In addition, Tarantini et al (2019) examined the effects of NMN supplementation on age-related decline in neurovascular and cognitive function in 24-month-old mice [38]. A two-week NMN regimen restored neurovascular coupling responses by increasing nitric oxide-mediated endothelial vasodilation and reducing mitochondrial oxidative stress. Mice treated with NMN showed improved spatial working memory and gait coordination. The study also showed that NMN increases mitochondrial bioenergetics in cerebral vascular endothelial cells, offering sirtuin-dependent protection against age-related oxidative damage. These findings suggest that NMN is a therapeutic candidate for vascular cognitive impairment in aging populations.

In another study, Park et al (2016) examined the neuroprotective effects of NMN in mice subjected to transient forebrain ischemia [39]. A single dose of NMN (62.5 mg/kg) given during reperfusion or 30 minutes after ischemia significantly improved neurological outcomes and reduced neuronal death in the hippocampus. NMN preserved NAD+ levels, prevented bioenergetic failure and inhibited poly-ADP-ribosylation, a marker of cellular stress. Importantly, the protective effect of NMN was independent of reperfusion conditions. These results underscore the potential of NMN as a therapeutic intervention for ischemic brain injury.

Alzheimer's disease often includes lumps of β-amyloid proteins, twisted tau proteins, and problems with memory and thinking. Ma et al (2024) found that NMN helps reduce these deleterious changes by stimulating cell self-cleansing (autophagy) and lowering oxidative stress [40]. In both mouse models and β-amyloid-treated cells, NMN helped remove the harmful form of tau protein and turned on the Nrf2/Keap1/NQO1 antioxidant pathway. When the researchers blocked autophagy, the benefits of NMN disappeared, showing that this process is how NMN works. NMN also helped the mice perform better on memory tests and protected their nerve cells from damage. According to these findings, NMN may be able to slow or even halt the progression of Alzheimer's disease by combating its underlying problems. Moreover, Wang et al (2016) showed that NMN supplementation (500 mg/kg) alleviated cognitive deficits and neuronal damage in an Alzheimer's disease (AD) model induced by amyloid-β (Aβ) oligomers [41]. NMN improved cognitive performance, preserved long-term potentiation and reduced oxidative stress in the hippocampus. By restoring NAD + and ATP levels, NMN counteracted Aβ-induced energy deficits. Also, Long et al (2015) showed that NMN restored mitochondrial respiratory function in a mouse model of AD by modulating NAD+-dependent enzymes such as SIRT1 and CD38 [42]. NMN improved mitochondrial dynamics, favoring fusion over fission, and improved mitochondrial morphology. These changes were associated with improved energy metabolism and reduced oxidative stress, highlighting NMN's potential to counteract AD-related cognitive decline by targeting mitochondrial dysfunction.

Additionally, Lundt et al (2024) evaluated the effects of NMN in a mouse model of amyotrophic lateral sclerosis (ALS) [43]. NMN supplementation prolonged lifespan, delayed motor dysfunction and improved neuromuscular junction (NMJ) function. Improved mitochondrial health and reduced nervous system inflammation were observed, along with better NMJ morphology and synaptic responses. These findings suggest that NMN is a promising therapeutic agent for managing the progression of ALS . In addition, Jiang et al (2024) investigated the ability of NMN to counteract neuroinflammation caused by particulate matter (PM) exposure [44]. NMN supplementation increased brain NAD+ levels, reduced microglia activation and restored lipid metabolism in affected brain areas, including the hippocampus and hypothalamus. NMN reversed PM-induced changes in triglycerides and glycerophospholipids, promoting membrane stability and anti-inflammatory responses. These findings suggest that NMN is a potential intervention for PM-induced neurological damage.

Nonylphenol (NP) is an industrial chemical that can harm learning and memory by inducing stress in brain cells and disrupting key chemicals. Li et al (2023) showed that NMN helps NP-exposed nerve cells by restoring healthy levels of NAD+ and lowering oxidative stress, which in turn protects important thinking and memory pathways [45]. NMN also increased the activity of certain protective proteins, and if these proteins were blocked, NMN's benefits disappeared. This means that NMN can help reduce NP-related damage and can be used in foods that promote brain health. In a similar study, Huang et al (2023) found that NMN reverses the harmful effects of NP by increasing NAD+/SIRT1 activity and balancing chemical signals in the brain [46]. This restored normal NAD+ levels in the brain's memory center and improved memory through the SIRT1/MAO-A pathway. Overall, these results suggest that NMN may help defend against cognitive problems caused by environmental toxins such as NP.

Sepsis-associated encephalopathy (SAE) leads to cognitive impairment due to inflammation, oxidative stress and reduced levels of NAD+ in the brain. Li et al (2023) report that NMN improves cognitive function and reduces hippocampal damage in mice with sepsis [47]. NMN restored NAD+ and SIRT1 activity, reducing apoptosis and inflammation in the hippocampus. In cellular models, NMN attenuated inflammatory responses in microglia cells. The study underscores that the protective effect of NMN is dependent on the SIRT1 pathway, as SIRT1 inhibition nullified the benefits. These findings suggest that NMN is a promising therapeutic agent for sepsis-induced cognitive decline.

Moreover, intracerebral hemorrhage (ICH) often leads to severe brain damage due to high levels of oxidative stress and inflammation. Wei et al (2017) found that NMN helped reduce brain swelling, limit oxidative damage and reduce inflammatory responses in mice with ICH [48]. They found that NMN turned on the Nrf2/HO-1 pathway, which enhanced the protective systems of the cells and reduced both microglia activity and neutrophil influx to the site of injury. Although NMN did not reduce the actual bleeding area, it helped restore function and improved neurological performance, suggesting that it may be a useful therapy for ICH.

Moreover, severely low blood sugar can lead to oxidative stress, brain cell death, and problems with memory and thinking. Wang et al (2020) showed that administration of NMN (500 mg/kg) after an episode of hypoglycemia protected the hippocampus by reducing nerve cell damage and improving connections between brain cells [49]. NMN restored NAD+ and ATP levels, reduced harmful reactive oxygen species and prevented excessive PARP-1 activation. Through these mechanisms, it helped restore normal learning and memory in rats, indicating that NMN can protect the brain after severe low blood sugar events. In addition, chemotherapy often leads to cognitive impairment, which significantly affects the quality of life of survivors. Yoo et al (2021) showed that cisplatin reduces NAD+ levels in both mouse and human neuronal brains, impairing neurogenesis and dendrite structure [50]. NMN supplementation restored NAD+ levels, improved neuronal progenitor proliferation and preserved cognitive function without compromising the antitumor efficacy of cisplatin. Similarly, Rashid et al (2022) found that NMN preserved mitochondrial integrity, reduced oxidative stress and restored ATP production in cortical neurons treated with cisplatin [51]. NMN also alleviated structural and functional neurotoxicity without compromising the antitumor efficacy of cisplatin. These results suggest that NMN is a viable option for protection against CICI while maintaining the efficacy of chemotherapy.

Postoperative cognitive dysfunction (POCD) often occurs after surgery and anesthesia, mainly due to oxidative stress and reduced NAD+ pathways. Xu et al (2024) showed that prior administration of NMN helped mice with isoflurane anesthesia-induced POCD perform better on memory tasks [52]. NMN improved both contextual and spatial memory, lowered oxidative stress markers and restored NAD+ levels in the hippocampus. It also increased SIRT1 and NAMPT levels, and these benefits depended on the NAD+-SIRT1 signaling pathway. This implies that NMN may be useful in reducing POCD by protecting the brain from oxidative damage. In addition, vascular cognitive impairment (VCI) is another issue that mainly affects the elderly and is caused by continuous reduced blood flow in the brain. Yu et al (2022) tested NMN on rats with VCI caused by blockage of both carotid arteries. NMN improved memory, preserved white matter, and reduced activation of microglia cells, which can be harmful when overactive [53]. It shifted microglia to a more anti-inflammatory state and reduced harmful breakdown of myelin. NMN was as effective as metformin and rapamycin, suggesting that it may help combat VCI by reducing inflammation and protecting brain cells.

Diabetes often leads to cognitive deficits through NAD+ depletion and mitochondrial dysfunction. Chandrasekaran et al (2020) showed that NMN supplementation restored hippocampal NAD+ levels in diabetic rats, normalized key metabolites and prevented neuronal loss [54]. NMN improved mitochondrial function, increased oxidative phosphorylation and activated the SIRT1-PGC-1α pathway, resulting in better cognitive performance. These findings indicate the potential of NMN to prevent diabetes-related cognitive impairment by directly targeting brain metabolic dysfunction.

Traumatic brain injury (TBI) often leads to secondary brain injuries involving inflammation and neuronal damage. Zhu et al (2023) showed that NMN significantly reduces brain swelling, neuronal death and histological damage in a rat model of TBI [55]. NMN treatment suppressed nervous system inflammation by inhibiting astrocyte and microglia activation, reducing inflammatory factors such as IL-6 and TNF-α, and modulating pathways such as NF-κB and Jak-STAT. It also reversed 792 genes associated with inflammation. These findings underscore NMN's role in alleviating secondary injury and improving cognitive performance, supporting its potential as a therapeutic agent for TBI. Moreover, neonatal hypoxia-ischemia (HI) leads to cognitive and motor deficits. Kawamura et al (2023) found that NMN restored NAD + and SIRT6 levels in the hippocampus, reduced apoptosis and decreased neuroinflammatory mediators such as HMGB1 [56]. NMN treatment improved motor skills and memory in newborn mice. By enhancing hippocampal regeneration and alleviating long-term damage, NMN is emerging as a potential intervention for neonatal HI, offering both neuroprotection and developmental improvement.

NMN appears to support overall brain health in several ways. A study by Ramanathan et al. (2022) found that NMN rapidly raised NAD+ levels in the brains of mice within 45 minutes of oral ingestion [57]. This suggests that it may help maintain energy balance in nerve cells and slow age-related decline in mental performance. Meanwhile, researchers led by Wei et al. (2017) examined how NMN helps when tissue plasminogen activator (tPA) is used to treat ischemic strokes [58]. They found that NMN keeps the blood-brain barrier intact and reduces harmful inflammation, which in turn reduces the risk of bleeding after tPA treatment. Moreover, Deng et al (2024) found that NMN protects against stress-induced depression by increasing ATP levels in the prefrontal area of the brain [59]. This action helped maintain normal brain function under stressful conditions. In a related line of research, Su et al (2024) showed that NMN protects brain cells from inflammation and ferroptosis - a form of iron-dependent cell death - by increasing antioxidant activity and reducing harmful byproducts [60]. All of these findings indicate that NMN may be a promising approach to supporting brain health, whether the goal is to protect nerve cells, reduce stroke-related complications, or maintain normal mood and cognitive function under stress.

NMN for metabolic disorders

Maternal obesity and a high-fat diet after weaning can cause significant metabolic problems in the offspring. Uddin et al (2020) showed that NMN improves glucose tolerance and reduces liver fatness in male offspring of obese mothers [61]. Daily injections of NMN for three weeks improved glucose tolerance in just eight days. It reduced liver triglyceride levels by 50% in offspring fed a cow-fed diet and by 23% in offspring fed a high-fat diet. NMN also increased the expression of genes involved in fat metabolism while suppressing those associated with fat synthesis. These findings suggest that NMN is a promising treatment for metabolic disorders resulting from overnutrition in early life. Moreover, Morita et al (2022) evaluated the effects of 300 mg/day NMN supplementation for eight weeks on metabolic and aging-related biomarkers in 17 postmenopausal women [62]. The study reported significant increases in nicotinamide (NAM) (from 45.2 to 164.7, p < 0.001) and adiponectin (from 13.6 to 16.2, p = 0.004), biomarkers associated with metabolic health. Participants also reported subjective improvements in skin texture, sleep quality and reduced fatigue. Safety was confirmed in 16 of 17 participants, with no adverse effects observed, except for one case of mild persistent headache, which led to discontinuation of the drug. This study highlights NMN as a safe and effective nutritional intervention to improve metabolism, hormones and skin health in postmenopausal women. In another study, NMN and exercise improved metabolic health in the offspring of obese mothers. Uddin et al (2017) found that NMN (administered daily for 18 days) reduced fat accumulation and improved liver metabolism more effectively than treadmill exercise [63]. Both interventions slightly improved glucose tolerance, but NMN showed a stronger effect on reducing liver fat and increasing NAD+ levels. These findings point to NMN as a potential alternative or adjunct to exercise to reverse metabolic dysfunction caused by maternal obesity.

Seizures impair energy metabolism and mitochondrial function in neurons, leading to impaired cognitive and motor functions. Cheng et al (2024) found that NMN supplementation significantly reduced seizure severity in a mouse model induced by pentylenetetrazole (37 mg/kg daily for 30 days) [64]. NMN improved learning, memory and motor activity by increasing mitochondrial energy production and reducing oxidative stress. It also regulated mitochondrial dynamics by promoting fusion (up-regulation of Mfn1, Mfn2) and reducing fission (down-regulation of Drp1, Fis1) of proteins. These benefits were mediated by the SIRT1-PGC-1α pathway, as inhibitors of this pathway negated the effects of NMN. The study underscores the potential of NMN in alleviating seizure-induced mitochondrial dysfunction, oxidative damage and neuronal apoptosis, providing a new therapeutic approach to epilepsy-related cognitive and behavioral disorders. Obesity, characterized by excess fat and impaired metabolism, can be treated with NMN supplementation. Zhang et al (2023) found that NMN reduced fat mass, improved glucose metabolism and reduced inflammation in obese mice [65]. It acted through the NAD+/SIRT6/LKB1 pathway to promote fat breakdown and reduce fat accumulation in the liver. These findings suggest that NMN is a promising therapy for obesity, improving overall metabolic health and reducing obesity-related complications.

NMN for diabetes

NMN offers significant benefits in combating and controlling high blood glucose levels. In a study, Yoshino et al (2021) examined the effects of NMN in postmenopausal pre-diabetic women for 10 weeks [66]. NMN improved insulin-stimulated glucose disposal in skeletal muscle and enhanced insulin signaling by regulating pathways necessary for glucose transport and utilization. NMN also promoted muscle regeneration by increasing the expression of genes associated with muscle remodeling. These findings underscore the potential of NMN to address insulin resistance and metabolic dysfunction in aging and obesity.

Moreover, in animal studies, Liu et al (2022) showed that NMN supplementation restored NAD+ levels in pancreatic islets after severe burns [67]. This activation of the SIRT1 pathway reduced oxidative stress, improved mitochondrial function and reduced apoptosis in islet cells. NMN increased glucose-stimulated insulin secretion, highlighting its therapeutic potential in maintaining pancreatic health under stress-induced conditions. In addition, Yoshino et al (2011) reported that NMN supplementation replenished NAD + levels in mouse models of diet- and age-induced type 2 diabetes (T2D) [68]. NMN improved glucose metabolism, increased hepatic insulin sensitivity and reduced oxidative stress. By activating the SIRT1 pathway, NMN restored impaired metabolic processes, indicating its potential benefit in the treatment of T2D. In addition, Wang et al (2024) examined the effects of NMN on β-cells (insulin-producing cells) when they are damaged by high levels of free fatty acids [69]. The results showed that NMN turned on the NAD+/AMPK/SIRT1/HIF-1α pathway, which helped these cells continue to produce insulin and function normally even under low oxygen conditions. These findings suggest that NMN may be a useful way to maintain healthy β-cells in people with diabetes.

NMN for gut health

Intestinal health can deteriorate with inflammation, but NMN shows promise for restoring it. Huang et al (2022) showed that NMN improves intestinal barrier function and reduces inflammation in a mouse model of colitis [70]. NMN increased the levels of beneficial gut bacteria, such as Akkermansia i Lactobacillus, and increased the regulation of tight junction proteins, strengthening the intestinal lining. It also reduced inflammatory markers such as TNF-α. These findings suggest the potential of NMN in treating inflammatory bowel diseases such as colitis. Moreover, the gut-brain axis links gut health to cognitive function, and NMN appears to benefit both. Zhao et al (2023) found that NMN altered the composition of the gut microbiota, increasing beneficial bacteria such as Lactobacillus [71].. The changes reduced nervous system inflammation and improved cognitive function in mouse models of Alzheimer's disease. The study indicates a dual role for NMN in improving gut health and combating neurodegenerative conditions.

NMN for respiratory health

Exposure to particulate matter (PM) leads to chronic lung damage and inflammation. Zhang et al (2023) found that NMN supplementation (500 mg/kg in drinking water) significantly reduced lung damage in mice exposed to PM for 16 weeks [72]. NMN restored NAD + levels, reduced inflammation and decreased collagen accumulation in lung tissue. It also improved immune function by inhibiting the IL-17 signaling pathway and reducing profibrotic cytokines. Increased lipid metabolism in immune cells further alleviated pathological changes. These findings suggest that NMN is a potential strategy for protecting the lungs from PM-induced damage. Moreover, NMN shows promise in the treatment of allergic asthma. Liang et al (2024) showed that NMN reduces airway inflammation and restores epithelial barrier integrity in models of house dust mite-induced asthma [73]. These benefits were mediated by SIRT3, a mitochondrial regulator whose stability NMN improved by reversing HDM-induced SUMOylation. NMN reduced mucus production, inflammation and cellular damage. These findings point to NMN as a new therapeutic option for asthma, targeting mitochondrial dysfunction and improving epithelial immunity.

In addition, silicosis, caused by inhalation of silica particles, is characterized by oxidative stress and inflammation. Wang et al (2022) found that NMN supplementation reduced lung damage in mice exposed to silica. NMN reduced reactive oxygen species, increased glutathione levels and activated antioxidant pathways through Nrf2 signaling [74]. Treatment reduced inflammatory cell infiltration and fibrosis while increasing antioxidant gene expression. These findings suggest the potential of NMN to treat silicosis by alleviating oxidative stress and promoting lung tissue repair.

NMN for reproductive health

Studies on NMN have also shown its potential benefits in supporting reproductive health. Huang et al (2022) examined the long-term effects of NMN supplementation on ovarian aging in mice [75]. Female mice treated with NMN for 20 weeks showed improvements in ovarian reserve, including increases in primary, primordial, secondary and antral follicles, as well as corpus luteum. NMN also reduced expression of the aging marker P16, increased mitochondrial biogenesis and improved autophagy levels in granulosa cells. These findings underscore NMN's ability to counteract reduced ovarian reserve by restoring mitochondrial health and reducing aging markers. Moreover, Liang et al (2024) showed that NMN supplementation restored NAD + levels, improved oocyte quality and quantity, and increased ovarian follicle reserve in aging mice [76]. NMN also improved mitochondrial morphology, reduced inflammation and enhanced antioxidant factors in granulosa cells. By promoting mitochondrial metabolism and energy, NMN offers a promising non-invasive strategy for improving fertility outcomes in aging individuals. In addition, Jiang et al (2023) evaluated the protective effect of NMN on benzyl butyl phthalate (BBP)-induced reproductive toxicity in mice [77]. Exposure to BBP disrupted spindle organization and mitochondrial function in oocytes, impairing meiotic maturation and early embryonic development. NMN mitigated these effects by reducing oxidative stress, restoring mitochondrial health and improving oocyte maturation. This underscores NMN's ability to combat reproductive damage caused by environmental pollutants.

In addition, Wang et al (2022) demonstrated the efficacy of NMN in improving oocyte quality in obese mice [78]. NMN reduced ovarian inflammation, improved mitochondrial function and reduced oxidative stress, lipid accumulation and DNA damage in oocytes. The offspring of obese mice treated with NMN showed normalized body weight, suggesting that NMN's benefits extend to subsequent generations. These findings position NMN as a potential intervention for obesity-related infertility. In another study, Nong et al (2024) examined the effects of NMN on aluminum chloride-induced testicular damage in rats [79]. NMN improved sperm quality, reduced apoptosis and restored glycolytic metabolism necessary for spermatogenesis. By promoting the regeneration of spermatogenic cells and the function of Sertoli cells, NMN showed its potential in alleviating male reproductive damage caused by toxic exposure.

In the case of polycystic ovary syndrome, Zhang et al (2024) examined the effects of NMN on endometrial health in a rat model [80]. NMN improved insulin sensitivity, decreased fasting insulin levels and increased glycolysis in the endometrium. It also stabilized endometrial morphology and decreased apoptosis, promoting a healthier environment for embryo implantation. Activation of the PI3K/AKT pathway by MNM underscores its therapeutic potential in improving reproductive outcomes in polycystic ovary syndrome. In addition, Arslan et al (2024) studied the effects of NMN and nicotinamide riboside (NR) on aging-related ovarian dysfunction in rats [81]. Both NMN and NR improved ovarian reserve, balanced the LH/FSH ratio and reduced excessive mitochondrial fission while promoting mitochondrial fusion. By activating Sirt1, NMN and NR alleviated mitochondrial stress and promoted folliculogenesis, making them promising agents for reversing ovarian aging.

NMN for liver health

Various studies have also shown significant benefits of NMN supplementation for liver health. Luo et al (2022) examined the effects of NMN on aging-related oxidative stress and liver function [82]. NMN supplementation reduced markers of oxidative damage (malondialdehyde and protein carbonyl levels) and restored Nrf2-mediated adaptive homeostasis in aging livers. This increased resistance to acetaminophen-induced liver damage through a Sirt3-dependent mechanism that deacetylates key antioxidant enzymes. These findings demonstrate the ability of NMN to protect against oxidative stress-induced liver damage and maintain liver health during aging.

Moreover, Wang et al (2024) conducted a meta-analysis of nine randomized controlled trials (RCTs) involving 412 middle-aged and elderly subjects to evaluate the effects of nicotinamide mononucleotide (NMN) supplementation on muscle and liver function [83]. NMN significantly improved gait speed (SMD: 0.34 m/s, 95% CI [0.03, 0.66], p = 0.033) and reduced alanine aminotransferase (ALT) levels (SMD: -0.29 IU/L, 95% CI [-0.55, -0.03], p = 0.028). Subgroup analysis showed that lower doses of NMN were most effective in reducing insulin resistance as measured by the HOMA-IR index. These findings suggest the potential of NMN to improve metabolic and functional health in aging populations. In addition, Dong et al (2024) evaluated the effects of NAD+ precursors, including NMN, on hyperglycemia-induced liver damage in a fish model [84]. All precursors improved cell viability and NAD+ levels, significantly affecting glucose metabolism, resistance to oxidative stress and inhibition of inflammation. Both NR and NMN improved hepatic NAD+ levels and the NAD+/NADH ratio, suggesting that they may offer greater therapeutic potential for metabolic and hepatic health.

Safety and pharmacokinetics

A clinical study examining the safety and pharmacokinetic profile of NMN in 10 healthy men found that single oral doses of 100, 250 and 500 mg were well tolerated and safe [85]. The researchers observed no serious changes in vital signs, and laboratory tests remained within normal ranges, despite slight changes in bilirubin, creatinine, chloride and blood glucose levels. There were also no problems with eye health or sleep quality throughout the 5-hour observation period. Regarding pharmacokinetics, the study showed a dose-dependent increase in NMN metabolites such as N-methyl-2-pyridone-5-carboxamide and N-methyl-4-pyridone-5-carboxamide. These results suggest that NMN can be effectively metabolized at doses up to 500 mg in healthy individuals.

Where to buy NMN?

NMN is available through many online retailers, local health food stores and supplement suppliers, who often provide third-party testing to confirm product quality and purity. Since guidelines can vary depending on where you live, it is wise to verify any regional requirements and make sure the brand adheres to established standards.

Disclaimer

This article was written for educational purposes and is intended to raise awareness of the substance being discussed. It is important to note that the substance discussed is a substance, not a specific product. The information contained in the text is based on available scientific research and is not intended to serve as medical advice or promote self-medication. The reader should consult any health and treatment decisions with a qualified health professional.

 

 

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