Lyophilized NAD+ 98.7% potency ► 250mg

The microscopic city: understanding what NAD+ is

Imagine your body as a vast city made up of trillions of microscopic inhabitants called cells. Each of these cells is like a tiny factory working tirelessly, producing energy, manufacturing new materials, repairing damage, and communicating with its neighbors. Now, for all this activity to function, cells need something very special: a currency that allows them to perform all these tasks. That currency is called ATP, and it is literally the energy that keeps everything moving. But here's the fascinating part: to manufacture this energy currency, cells need an indispensable helper, a facilitator that makes it possible for energy to flow correctly. That facilitator is NAD+, a coenzyme molecule that acts as the essential messenger and transporter in hundreds of vital processes. Without NAD+, the cellular factory simply cannot function, because it is the bridge that connects the nutrients we eat with the energy we use to live.

The energy journey: how NAD+ turns your food into fuel

Every time you eat, your body receives nutrients: carbohydrates, fats, and proteins. But these nutrients can't be used directly for energy, just as a tree can't power a car simply because it's potential fuel. They must first be transformed, and this is where NAD+ comes into play in a spectacular way. Think of NAD+ as a very special mail carrier that collects tiny packets of energy (in the form of electrons) from food molecules and transports them to the mitochondria, those tiny power plants that live inside every cell. In the mitochondria, something like an ultra-fast assembly line takes place: NAD+ delivers its packets of electrons, they pass through a series of stations called the respiratory chain, and at the end of the process, ATP, the energy currency we mentioned earlier, is produced. What's amazing is that NAD+ isn't used up in this process; after delivering its cargo, it's recycled and starts all over again, participating hundreds of times a day in this vital cycle that keeps your heart beating, your brain thinking, and your muscles moving.

The Nighttime Repair Team: NAD+ and DNA Maintenance

Now imagine that your DNA is like the original blueprint for the entire cellular city, the master guide containing all the instructions for every cell to know what to do and how to do it. But this blueprint isn't locked away in a perfectly protected vault; it's constantly exposed to tiny accidents. Solar radiation touching your skin, normal breathing processes that produce reactive molecules, even the simple fact that the cell divides—all of these cause thousands of tiny damages to the DNA every day. If these damages weren't repaired, they would accumulate like cracks in a building, eventually compromising the entire structure. This is where a specialized repair team called PARP enzymes comes in, and these enzymes have one absolute requirement to function: they need NAD+ as their primary tool. NAD+ is literally consumed by these enzymes as they work, detecting every break in the DNA and repairing it with molecular precision. It's as if NAD+ is the cement the repair team uses to mend every crack in the master blueprint, maintaining the integrity of the genetic information cell after cell, day after day.

The guardians of time: sirtuinas and the clock of aging

Within each cell are extraordinary proteins called sirtuins, and if we could describe them with a metaphor, they would be like the conductors of a cellular orchestra, coordinating multiple aspects of aging and long-term health. But here's the crucial detail: these sirtuins are completely useless without their partner, NAD+. Imagine an orchestra conductor without a baton; technically, they're still a conductor, but they can't do their job. Sirtuins depend on NAD+ to activate and function, and when they do, they begin to regulate fascinating processes: they decide which genes should be active or silenced according to the needs of the moment, they monitor the health of the mitochondria, they coordinate how the cell responds to stress, and they even influence how the cell manages its metabolism. Scientists have discovered that these proteins are deeply connected to the processes of cellular longevity, and that in many organisms studied, from yeast to mammals, the proper activation of sirtuins is associated with a longer and healthier cellular lifespan. By providing sufficient NAD+, we give these sirtuins the tool they need to perform their function as guardians of cellular time.

The city's electrical system: NAD+ in the brain

Your brain is probably the most energy-hungry organ in your entire body. Although it makes up only about two percent of your body weight, it consumes roughly one-fifth of all the energy you produce. That's because every thought, every memory, every emotion, and every command you send to your body requires trillions of neurons to communicate with each other using electrical and chemical signals—and all of that is a voracious energy eater. Think of your brain as the control center of the cellular city, with communication cables (nerves) extending to every corner, constantly transmitting information. To keep this network running, neurons need massive amounts of ATP, and therefore, massive amounts of NAD+ to produce that ATP. But NAD+ does more than just provide energy to the brain; it also participates in the synthesis of neurotransmitters—those chemical messengers neurons use to talk to each other—and contributes to the protective mechanisms that keep neurons healthy against natural wear and tear. When NAD+ levels drop, it's as if the city lights begin to dim; Communication becomes less efficient and cognitive processes may be affected.

The dilemma of aging: when money becomes scarce

Here we arrive at one of the most important discoveries in modern aging research: NAD+ levels in our bodies don't remain constant throughout life. Imagine that when we're born, our cellular city has an abundant reserve of this essential currency; the banks are full, and every cellular factory has all the NAD+ it needs to operate at peak capacity. But as the years go by, something begins to change. NAD+ production declines, demand remains high or even increases due to accumulated wear and tear, and gradually the currency becomes scarcer. By the time a person reaches 50 or 60, their NAD+ levels may have dropped to about half of what they were in their youth. This scarcity doesn't happen all at once, but gradually, like a tap slowly turning off. The consequences are subtle but cumulative: mitochondria produce energy less efficiently, sirtuins can't fully activate, DNA repair mechanisms work more slowly, and all those cellular processes that depended on abundant NAD+ begin to function under limitations. It's as if the city began to experience intermittent blackouts, not severe enough to stop everything, but enough to make things not work as well as before.

The replenishment strategy: how supplementation works

A logical question then arises: if NAD+ levels decline with age, can we simply replenish this molecule from external sources? The answer is fascinating and more complex than it seems. The body has multiple ways of making NAD+, much like a city with several supply routes for a critical resource. It can manufacture it from scratch using an amino acid called tryptophan, or it can recycle it from simpler precursor molecules through what are known as "salvage pathways." When we supplement with NAD+ directly, especially in its high-potency freeze-dried form, we are providing the complete, ready-to-use molecule. The freeze-dried form is particularly interesting because the freeze-drying process removes water through sublimation, protecting the molecule's delicate structure from degradation—as if you were perfectly freezing and preserving a valuable resource so that it arrives intact at its destination. Once the supplemented NAD+ reaches the cells, it can be used immediately or stored briefly, joining endogenous reserves and increasing the overall availability of this coenzyme in the tissues. Scientific studies have shown that different tissues respond to supplementation at different rates and magnitudes, some being more receptive than others, but in general an increase in cellular levels of NAD+ is observed, which can translate into better functioning of all processes that depend on this molecule.

The domino effect: when each cell has what it needs

What's truly fascinating about NAD+ is that it's not a specialist doing just one thing; it's a master generalist involved in hundreds of different processes simultaneously. When NAD+ levels are adequate, a positive ripple effect is triggered throughout the entire cellular system. Mitochondria produce energy more efficiently, meaning every cell has more ATP available to do its job. With more energy available, muscle cells can contract more effectively, neurons can fire signals more clearly, and the heart can beat more efficiently. Simultaneously, sirtuins are properly activated, regulating genes that influence metabolism, stress response, and cellular maintenance. DNA repair teams have the fuel they need to work continuously, maintaining genetic integrity. Antioxidant systems can regenerate more effectively, protecting cells from oxidative damage. It's as if the entire system shifts from operating in a mode of austerity and scarcity to a mode of abundance and efficiency, where every department, every factory, every communication system has the resources it needs to function optimally. This is the fundamental principle behind why NAD+ has garnered so much attention in scientific research on health, metabolism, and aging: because supporting the levels of this single molecule can have cascading positive effects that extend across virtually every aspect of cellular physiology.

The whole story in one picture

To summarize this fascinating story, imagine your body as a bright city at night, with thousands of lights alight, traffic flowing smoothly, and all systems functioning in harmony. Each light represents a cell performing its task, and the electricity that keeps them lit is produced by microscopic power plants called mitochondria. NAD+ is like the electrical transmission system that connects fuel sources to the power plants, ensuring a constant flow of energy. But it's also the maintenance crew that repairs damaged wires, the communication system that coordinates different neighborhoods of the city, and the master regulator that decides when to turn certain systems on or off based on current needs. Over time, this transmission system can deteriorate; the lights begin to dim slightly, and maintenance processes slow down. NAD+ supplementation is like bringing in reinforcement equipment and new materials to restore the infrastructure, allowing the cellular city to regain its brightness and efficiency, keeping all vital functions operating at the level they were designed to.

Participation in the mitochondrial electron transport chain

NAD+ plays a central role in aerobic cellular respiration as an electron acceptor in multiple redox reactions that occur during nutrient catabolism. In the context of cytosolic glycolysis, NAD+ accepts electrons from glyceraldehyde-3-phosphate to form NADH, while in the mitochondrial Krebs cycle it acts as a cofactor in reactions catalyzed by isocitrate dehydrogenase, α-ketoglutarate dehydrogenase, and malate dehydrogenase. The resulting NADH transfers its electrons to Complex I of the mitochondrial electron transport chain, initiating a cascade of redox reactions that culminates in the reduction of molecular oxygen to water and the pumping of protons across the inner mitochondrial membrane. This electrochemical proton gradient drives ATP synthesis by ATP synthase via oxidative phosphorylation. The NAD+/NADH ratio functions as an indicator of cellular redox status and an allosteric regulator of multiple metabolic enzymes, influencing the flow through glycolytic, lipid, and protein pathways according to cellular energy demands.

Activation of poly ADP-ribose polymerase enzymes in DNA repair

The PARP family of enzymes, particularly PARP-1 and PARP-2, use NAD+ as a substrate to catalyze the poly-ADP-ribosylation of nuclear proteins involved in the DNA damage response. When single- or double-strand breaks are detected in DNA, PARPs rapidly bind to these injury sites and consume NAD+ to synthesize poly-ADP-ribose chains that attach to acceptor proteins, including histones, transcription factors, and PARPs themselves. This post-translational modification serves as a recruitment signal for DNA repair proteins, facilitates chromatin remodeling to allow access for the repair machinery, and regulates the activity of factors involved in the decision between cellular repair and apoptosis. The massive consumption of NAD+ by PARPs in response to extensive DNA damage can temporarily deplete cellular stores of this coenzyme, creating competition with other NAD-dependent processes and establishing a balance between repair capacity and the maintenance of normal metabolic function.

Regulation of sirtuins and protein deacetylation

Sirtuins are a family of seven proteins (SIRT1-7) that catalyze the NAD+-dependent removal of acetyl groups from lysine residues in target proteins, generating nicotinamide, 2'-O-acetyl-ADP-ribose, and the deacetylated protein. This deacetylase activity directly links cellular energy status, reflected in NAD+ levels, with epigenetic regulation and post-translational modification of key proteins. SIRT1, located primarily in the nucleus, deacetylates histones, altering chromatin structure and gene expression, as well as transcription factors including PGC-1α (peroxisome proliferator-activated receptor γ coactivator 1-α), FOXO (forkhead box O proteins), and p53, thereby modulating mitochondrial biogenesis, oxidative stress resistance, carbohydrate and lipid metabolism, and responses to cellular damage. The mitochondrial sirtuins SIRT3, SIRT4, and SIRT5 regulate mitochondrial energy metabolism by deacetylating components of the respiratory chain, enzymes of the Krebs cycle, and proteins involved in fatty acid oxidation. The stoichiometric dependence of sirtuins on NAD+ makes them metabolic sensors that translate the availability of this coenzyme into changes in protein activity and gene expression.

Modulation of fatty acid metabolism by beta-oxidation

NAD+ acts as an essential cofactor in the beta-oxidation of fatty acids, the catabolic process by which lipids are sequentially broken down into acetyl-CoA units for subsequent oxidation in the Krebs cycle. The enzyme 3-hydroxyacyl-CoA dehydrogenase, which catalyzes the conversion of 3-hydroxyacyl-CoA to 3-ketoacyl-CoA in the third step of each beta-oxidation cycle, requires NAD+ as an electron acceptor, generating NADH in the process. This mitochondrial NADH then fuels the electron transport chain for ATP production, establishing a direct link between lipid oxidation and energy generation. The availability of NAD+ influences the rate of beta-oxidation and, by extension, the balance between carbohydrate and lipid utilization as energy substrates. Furthermore, through the activation of SIRT1 and the subsequent deacetylation of PGC-1α, NAD+ promotes the expression of genes involved in fatty acid oxidation and mitochondrial biogenesis, creating a positive feedback loop that enhances cellular oxidative capacity in response to increased energy demands or caloric restriction.

Influence on mitochondrial biogenesis and function

NAD+ exerts regulatory control over mitochondrial biogenesis, the process by which cells generate new mitochondria in response to increased energy demands or metabolic stress signals. This control is primarily exerted through the activation of SIRT1, which deacetylates and activates PGC-1α, the master regulator of mitochondrial biogenesis. Active PGC-1α stimulates the transcription of nuclear genes encoding mitochondrial proteins and promotes mitochondrial DNA replication by activating mitochondrial transcription factor A. Simultaneously, SIRT3 in the mitochondrial matrix deacetylates and activates multiple enzymes of oxidative metabolism, including components of Complexes I, II, and III of the respiratory chain, as well as manganese-dependent superoxide dismutase 2, enhancing both ATP production efficiency and mitochondrial antioxidant capacity. This coordination between NAD+/SIRT1-mediated nuclear signaling and SIRT3-mediated mitochondrial functional optimization establishes an integrated mechanism by which NAD+ availability can influence both the quantity and quality of the cellular mitochondrial population.

Participation in neurotransmitter synthesis and neuronal function

In the central nervous system, NAD+ contributes to the synthesis of monoaminergic neurotransmitters through its participation in biosynthetic pathways that require redox reactions. The conversion of tryptophan to serotonin involves tryptophan hydroxylase, an enzyme that, although primarily using tetrahydrobiopterin as a cofactor, indirectly depends on regenerative systems that require NADPH, which is closely related to the NAD+ pool. Beyond neurotransmitter biosynthesis, NAD+ is critical for maintaining neuronal energy homeostasis, given that neurons are highly differentiated post-mitotic cells with exceptionally high metabolic demands to sustain resting membrane potential, synaptic transmission, and axonal transport. NAD+-dependent sirtuin-mediated signaling in neurons influences synaptic plasticity, neuronal survival in the face of metabolic stress, and the expression of neurotrophic factors such as brain-derived neurotrophic factor. Additionally, the role of NAD+ in modulating neuroinflammation processes has been investigated through its influence on the activation of microglial cells and the production of cytokines.

Regulation of the molecular circadian clock

NAD+ participates in the regulation of the circadian clock system, the molecular mechanism that generates approximately 24-hour biological rhythms in most cells of the body. Cellular NAD+ levels exhibit robust circadian oscillations, with peaks during active phases of the cycle and nadirs during resting phases. These oscillations are controlled by the circadian clock itself through the transcriptional regulation of the rate-limiting enzyme in NAD+ biosynthesis, nicotinamide phosphoribosyltransferase. Conversely, NAD+ influences the circadian clock by activating SIRT1, which deacetylates core components of the clock machinery, including BMAL1 and PER2, modulating the amplitude and phase of circadian oscillations. This bidirectional feedback between NAD+ and the circadian clock creates an integrated system that coordinates metabolic rhythms with environmental time cycles. Disturbances in this relationship, such as those that occur with age-related NAD+ decline or external circadian desynchronizers, can result in decoupling between the molecular clock and metabolic processes, with implications for energy homeostasis, lipid and glucose metabolism, and sleep-wake patterns.

Modulation of inflammatory responses and innate immunity

NAD+ influences multiple aspects of immune function, particularly the regulation of inflammatory responses through sirtuin-dependent mechanisms. SIRT1 and SIRT6 modulate the activity of nuclear factor kappa B, a master regulator of pro-inflammatory gene transcription, by deacetylating the RelA/p65 subunit, thereby altering the magnitude and duration of inflammatory responses. In macrophages, NAD+ availability influences the polarization between M1 (pro-inflammatory) and M2 (anti-inflammatory) phenotypes, partly through effects on cellular metabolism and sirtuin-mediated signaling. Activated immune cells undergo dramatic metabolic changes, including the transition to aerobic glycolysis even in the presence of oxygen, a phenomenon that alters NAD+ requirements and utilization. Additionally, extracellular NAD+ and its metabolites can act as signaling molecules by activating purinergic receptors, influencing chemotaxis, activation, and apoptosis of leukocytes. Research has investigated how modulating NAD+ levels can influence the balance between appropriate immune responses and low-grade chronic inflammation.

Contribution to endogenous antioxidant systems

NAD+ contributes indirectly to cellular antioxidant defense through multiple interconnected mechanisms. NADPH, generated from NADH by mitochondrial nicotinamide nucleotide transhydrogenase or via the pentose phosphate pathway in the cytosol, is the essential reducing cofactor for the regeneration of reduced glutathione from oxidized glutathione, catalyzed by glutathione reductase. Reduced glutathione is one of the most abundant low-molecular-weight antioxidants in cells and is critical for the detoxification of hydrogen and lipid peroxides. Simultaneously, mitochondrial SIRT3 deacetylates and activates superoxide dismutase 2, the main enzyme that dismutates the superoxide anion in mitochondria, thereby reducing mitochondrial oxidative stress. SIRT1 also influences the antioxidant response by deacetylating and activating FOXO3a, a transcription factor that promotes the expression of antioxidant enzymes, including catalase and superoxide dismutase. NAD+ availability can thus influence multiple layers of the cellular antioxidant system, from the regeneration of low-molecular-weight antioxidants to the activation of antioxidant enzymes and the transcriptional regulation of oxidative stress response programs.

Regulation of carbohydrate metabolism and insulin sensitivity

NAD+ influences carbohydrate metabolism through its direct participation as a cofactor in glycolytic and gluconeogenic reactions, as well as through sirtuin-mediated regulatory effects on gene expression and post-translational modification of metabolic enzymes. SIRT1 deacetylates and modulates the activity of FOXO1, a transcription factor that regulates the expression of hepatic gluconeogenic enzymes such as phosphoenolpyruvate carboxykinase and glucose-6-phosphatase, thereby influencing hepatic glucose production. In skeletal muscle and adipose tissue, NAD+- and sirtuin-mediated signaling influences glucose transport and glucose oxidation by affecting the expression and translocation of the glucose transporter GLUT4. SIRT6 regulates glycolysis by repressing glycolytic genes, while mitochondrial SIRT3 activates pyruvate dehydrogenase through deacetylation, facilitating the entry of glycolytic pyruvate into the Krebs cycle. Research has focused on how modulating NAD+ levels and sirtuin activity can influence metabolic flexibility—the ability of cells to efficiently switch between carbohydrate and lipid oxidation based on substrate availability and energy demands.

Influence on endothelial function and vascular homeostasis

NAD+ contributes to endothelial function, the set of processes by which the cells lining the inside of blood vessels regulate vascular tone, permeability, hemostasis, and inflammatory responses. SIRT1 in endothelial cells deacetylates and activates endothelial nitric oxide synthase, the enzyme that produces nitric oxide, a critical vasodilator and modulator of multiple vascular functions, including the inhibition of platelet aggregation and leukocyte adhesion. NAD+ availability also influences endothelial energy metabolism, which relies predominantly on glycolysis even in the presence of oxygen—a metabolic pattern that requires the continuous recycling of NAD+. Research has investigated how the decline in NAD+ associated with age or adverse metabolic conditions can compromise endothelial function by reducing nitric oxide bioavailability, increasing endothelial oxidative stress, and activating proinflammatory pathways. Additionally, sirtuins modulate angiogenesis, the process of forming new blood vessels, through effects on pro-angiogenic factors and the endothelial response to hypoxic signals.

Participation in autophagy processes and protein quality control

NAD+ influences autophagy, the catabolic process by which cells degrade and recycle damaged or superfluous cellular components, including misfolded proteins, protein aggregates, and dysfunctional organelles. SIRT1 promotes autophagy by deacetylating components of the autophagic machinery, including ATG (autophagy-related) proteins and factors that regulate autophagosome initiation and elongation. AMPK activation, which can be indirectly influenced by changes in the NAD+/NADH ratio, also promotes autophagy while simultaneously inhibiting mTOR-mediated protein synthesis, thus coordinating anabolic and catabolic processes according to the cell's energy status. In the mitochondrial context, a specialized autophagic process called mitophagy selectively eliminates damaged or senescent mitochondria, and this process is influenced by NAD+-dependent mitochondrial sirtuins. Autophagy plays critical roles in maintaining protein homeostasis, adapting to metabolic stress, and preventing the accumulation of potentially toxic cellular materials, and the modulation of this pathway by NAD+ represents a mechanism by which the availability of this coenzyme can influence cellular quality control and longevity.

Energy metabolism and mitochondrial function

• CoQ10 + PQQ: Coenzyme Q10 (ubiquinol) works in direct synergy with NAD+ in the mitochondrial electron transport chain, as both molecules act as electron carriers in different complexes of the respiratory chain. While NAD+ donates electrons to Complex I (NADH dehydrogenase), CoQ10 receives these electrons and transfers them to Complex III, creating a sequential flow essential for ATP production. Pyrroloquinoline quinone (PQQ) complements this synergy by promoting mitochondrial biogenesis and activating signaling pathways that increase the number and efficiency of mitochondria, thus multiplying the impact of NAD+ on total cellular energy capacity. Studies have shown that the combination of NAD+ with CoQ10 significantly reduces fatigue and improves mitochondrial function more effectively than either compound alone.

• Eight Magnesiums: Magnesium is absolutely critical for NAD+ function and ATP synthesis, since biologically active ATP exists predominantly as the ATP-Mg complex, and magnesium participates directly in the formation of the transition state where ATP synthase catalyzes ATP synthesis. Additionally, magnesium stabilizes the structure of NAD+ and facilitates its interaction with dehydrogenase enzymes, acts as a cofactor in more than 300 enzymatic reactions that use NAD+ as a coenzyme, and regulates adenylate homeostasis in the mitochondrial intermembrane space through adenylate kinase balance. Adequate magnesium availability is essential for maintaining the NAD+/NADH balance, optimizing the mitochondrial proton gradient that drives ATP synthesis, and supporting the function of NADPH transhydrogenase, which regenerates NADPH from NADH in the mitochondrial matrix.

• B-Active: Activated B Vitamin Complex: B vitamins, particularly riboflavin (B2) and niacin (B3), are direct precursors of the NAD+ pool and work synergistically with supplemented NAD+ to maintain optimal levels of this coenzyme. Riboflavin is necessary for the endogenous synthesis of NAD+ from tryptophan via the de novo pathway, as the enzymes that convert tryptophan to quinolinate require flavin adenine dinucleotide (FAD), a riboflavin derivative. Additionally, vitamin B6 (pyridoxine) and folic acid are essential cofactors in multiple steps of NAD+ biosynthesis, while vitamin B12 (as methylcobalamin) supports methylation processes that are critical for NAD+ metabolism and recycling, preventing the depletion of methyl donors that can occur with long-term NAD+ supplementation.

Activation of sirtuins and cellular longevity

• Resveratrol or Pterostilbene: These stilbenes act as direct activators of sirtuins, particularly SIRT1 and SIRT3, and exhibit a powerful synergy with NAD+ because sirtuins require NAD+ as an essential substrate for their deacetylase activity. Pterostilbene has approximately 80% bioavailability compared to 20% for resveratrol, making it more potent at equivalent doses. The combination of NAD+ with these polyphenols creates a multiplier effect: NAD+ provides the substrate that sirtuins need to function, while resveratrol or pterostilbene increases the expression and sensitivity of sirtuins to available NAD+, thus amplifying the effects on mitochondrial biogenesis, metabolic regulation, the oxidative stress response, and processes associated with cellular longevity.

• Quercetin: This flavonoid exhibits a unique synergy with NAD+ by acting as an inhibitor of the CD38 enzyme, one of the main consumers of NAD+ in the body, which degrades NAD+ into nicotinamide and cyclic ADP-ribose. By inhibiting CD38, quercetin preserves endogenous NAD+ levels and prolongs the half-life of supplemented NAD+, allowing more NAD+ to be available for sirtuins, PARP, and other NAD-dependent enzymes. Additionally, quercetin possesses antioxidant properties that reduce mitochondrial oxidative stress, thus decreasing the demand for PARP-mediated DNA repair, which consumes massive amounts of NAD+. This combination of NAD+ preservation and inhibition of its degradation makes quercetin one of the most strategic cofactors for maximizing the impact of NAD+ supplementation.

Antioxidant protection and mitochondrial function

• Alpha-lipoic acid: Alpha-lipoic acid (ALA) is a mitochondrial cofactor that complements NAD+ through multiple synergistic mechanisms related to energy metabolism and antioxidant protection. ALA acts as an essential cofactor in mitochondrial enzyme complexes that require NAD+, specifically the pyruvate dehydrogenase complex and the alpha-ketoglutarate dehydrogenase complex of the Krebs cycle, optimizing the efficiency with which these enzymes use NAD+ for substrate oxidation. Additionally, ALA regenerates other antioxidants such as vitamin C, vitamin E, and glutathione, indirectly reducing the oxidative burden that consumes NAD+ through the activation of PARP for DNA repair. ALA also improves mitochondrial sensitivity to NAD+ by promoting electron transport function and maintaining the structural integrity of mitochondrial membranes.

• Vitamin C Complex with Camu Camu: Vitamin C contributes synergistically to the effect of NAD+ primarily through its role in regenerating the cellular antioxidant pool and its participation in redox reactions that protect NAD+ from oxidation. Vitamin C regenerates oxidized glutathione back to its reduced form, thus supporting the NADPH-dependent glutathione reductase system (closely related to the NAD+ pool). Furthermore, vitamin C protects mitochondrial structures from oxidative damage, reducing the need for massive PARP activation that would rapidly deplete NAD+ reserves. Camu camu provides not only vitamin C but also additional polyphenols that can offer synergistic effects on mitochondrial function and nutrient bioavailability.

Support for methylation processes

• Betaine (Trimethylglycine): Betaine functions as a critical methyl donor, preventing the depletion of methyl groups that can occur during NAD+ metabolism and recycling. When NAD+ is degraded by sirtuins, PARP, or CD38, nicotinamide is produced, which must be methylated by the enzyme NNMT (nicotinamide N-methyltransferase) for excretion—a process that consumes S-adenosylmethionine (SAM), the body's universal methyl donor. Betaine supplementation provides additional methyl groups that can regenerate SAM through the conversion of homocysteine ​​to methionine, thus preserving the pool of methyl donors needed to sustain continuous NAD+ recycling without compromising other critical methylation processes such as neurotransmitter synthesis, epigenetic regulation of DNA, and phospholipid metabolism.

• Methylfolate: Methylfolate (5-MTHF) is the active form of folic acid that participates directly in the methylation cycle by donating methyl groups for the conversion of homocysteine ​​to methionine, thus regenerating the SAM pool, which is essential for NAD+ metabolism. This methylation cycle is particularly important when NAD+ is supplemented long-term, as the constant metabolism of nicotinamide derived from NAD+ degradation can place significant stress on methylation systems. Methylfolate also supports the synthesis of purines and pyrimidines necessary for ATP production and DNA repair, processes that work in conjunction with the functions of NAD+ in maintaining genomic integrity and cellular energy production.

Bioavailability and absorption

• Piperine: Piperine, the active alkaloid in black pepper, may increase the bioavailability of various nutraceuticals, including NAD+, by modulating multiple absorption pathways and first-pass metabolism. This compound inhibits phase II conjugation enzymes such as glucuronosyltransferases and sulfotransferases in the liver and intestine, reducing the premature metabolism of bioactive compounds before they reach systemic circulation. Additionally, piperine increases gastrointestinal thermogenesis and improves intestinal mucosal blood flow, thus facilitating nutrient transport across the epithelial barrier. For these reasons, piperine is frequently used as a cross-enhancing cofactor that can significantly improve the absorption and utilization of NAD+ and other synergistic cofactors mentioned in this section, maximizing the impact of comprehensive supplementation.

How long does it take to notice any effects after starting to take NAD+?

The perceived effects vary considerably among individuals depending on factors such as age, basal metabolic rate, level of physical activity, and the specific goals of supplementation. Some people report subtle changes in energy levels and mental clarity within the first 48 to 72 hours of starting supplementation, particularly those who maintain an active lifestyle and a balanced diet. However, for most users, the most consistent and noticeable effects tend to appear after 2 to 4 weeks of continuous use, a period during which cellular NAD+ levels gradually accumulate in different tissues. Effects related to energy metabolism and overall vitality are usually the first to be noticed, while changes associated with cognitive function, physical recovery, and general well-being may require 4 to 8 weeks of consistent supplementation to become apparent. It is important to maintain realistic expectations and understand that NAD+ supports fundamental cellular processes whose effects are cumulative and build over time, rather than producing immediate dramatic changes.

Is it better to take NAD+ on an empty stomach or with food?

NAD+ can be taken on an empty stomach or with food, and the optimal choice depends on individual goals and digestive tolerance. Taking it on an empty stomach may promote faster and more direct absorption, as it doesn't compete with other nutrients for intestinal transport mechanisms. This may be preferable for people seeking a more immediate effect on energy levels or taking the supplement specifically before activities requiring high physical or mental performance. On the other hand, taking NAD+ with a light meal, particularly one containing a small amount of healthy fats or protein, may improve gastrointestinal tolerance in sensitive individuals and provide a more gradual and sustained release. If you experience any mild digestive discomfort when taking the supplement on an empty stomach, taking it with food usually resolves this issue without significantly compromising effectiveness. There's no need to take NAD+ with very large meals, as this could unnecessarily delay absorption without providing any additional benefit.

Can I open the capsules and mix the contents with liquids or food?

Although the 250 mg capsules are designed to be swallowed whole with water, you can open the capsules and mix the contents with liquids or soft foods if you have difficulty swallowing capsules. Lyophilized NAD+ is relatively stable at room temperature for short periods, so it can be mixed with room temperature water, natural juices, protein shakes, or foods such as yogurt or fruit puree. It is recommended to consume the mixture immediately after preparation to minimize any potential degradation of the compound, and to avoid mixing the powder with very hot liquids, which could affect the molecular stability of the NAD+. The taste of pure NAD+ can be slightly bitter or acidic, so many people prefer to mix it with foods or beverages with stronger flavors to mask the taste. If you choose this method of administration, it is important to ensure you consume the entire mixture to receive the full dose, as some of the powder may adhere to the walls of the container.

What should I do if I forget to take a dose?

If you forget to take a dose of NAD+, simply continue with your next scheduled dose at the usual time without doubling the amount. Taking a double dose to make up for the missed dose is neither necessary nor recommended, as this will not provide any additional benefits and could unnecessarily increase the metabolic load on your NAD+ processing systems. NAD+ supplementation works by gradually building up and maintaining elevated cellular levels over time, so an occasional missed dose will not significantly compromise the long-term effects, especially if you have been taking the supplement consistently for several weeks. If you find yourself frequently forgetting doses, it can be helpful to establish a routine by linking taking the supplement to a specific daily activity such as breakfast, brushing your teeth, or starting your workday, or by setting reminders on your mobile phone. Consistency in supplementation is more important than absolute timing.

Can I take NAD+ continuously without taking breaks?

Although NAD+ can be taken continuously for extended periods, many supplementation protocols suggest incorporating periodic breaks to allow the body's endogenous NAD+ synthesis mechanisms to remain active and responsive. A common pattern is to follow 12- to 16-week cycles of continuous supplementation followed by 1 to 2 weeks of rest, which may help prevent the body's adaptation and maintain the sensitivity of the receptors and enzymes that utilize NAD+. Alternatively, some people implement a pattern of 5 days of supplementation followed by 2 days of rest each week, allowing for virtually continuous supplementation while providing brief windows for the body to rely on its own production. For long-term healthy aging support, continuous supplementation for many months may be appropriate, especially in individuals over 40 years of age, where endogenous NAD+ production is naturally declining. The decision about whether and how often to take breaks should be based on individual goals, perceived response to the supplement, and general recommendations from long-term supplement use protocols.

Is it normal to experience more energy at first and then notice that the effect diminishes?

It is relatively common for some people to experience a more pronounced energy boost during the first few weeks of NAD+ supplementation, which then stabilizes at a more moderate but sustained level. This pattern does not necessarily indicate a loss of effectiveness, but rather a normalization of cellular NAD+ levels and the body's adaptation to the increased availability of this coenzyme. In the initial stages, when NAD+ levels may be significantly depleted, supplementation can produce a noticeable contrast in energy levels that is quite perceptible. Over time, as cellular reserves are optimized and metabolic processes stabilize, the effect becomes more subtle but equally important at the cellular level. If a marked decrease in the effects is observed after several weeks, a short break of 1 to 2 weeks could be considered to allow the body to "reset" its sensitivity, or it could be assessed whether external factors such as stress, sleep quality, diet, or exercise intensity have changed and are affecting the perceived energy levels. It may also be helpful to review whether the current dose is still optimal for individual needs and consider adjustments based on the observed response.

Can I combine NAD+ with caffeine or energy drinks?

NAD+ can be combined with caffeine and other stimulants without known negative interactions, although it's advisable to be aware of individual responses and adjust amounts accordingly. Since NAD+ supports natural energy production at the cellular level by optimizing mitochondrial metabolism, some people find they need less caffeine than usual when supplementing with NAD+ regularly. Combining the two can provide a synergistic effect, with NAD+ offering sustained, deep energy at the cellular level while caffeine provides the more immediate and noticeable stimulant effect. However, if you are particularly sensitive to stimulants or experience nervousness, a rapid heart rate, or difficulty sleeping when combining NAD+ with caffeine, it would be wise to reduce caffeine intake or temporarily separate their consumption, taking NAD+ in the morning and limiting caffeine to the early hours of the day. It's important to remember that the goal of NAD+ supplementation is to support healthy metabolic function over the long term, not to replace adequate rest or compensate for sleep deprivation through the use of stimulants.

Does NAD+ affect sleep quality if I take it in the afternoon or at night?

Although NAD+ is not a stimulant in the traditional sense like caffeine, its role in supporting cellular energy production means that some people may experience increased alertness or vitality, which could interfere with falling asleep if taken too close to bedtime. Sensitivity to this effect varies considerably among individuals, with some reporting that they can take NAD+ even at night without problems, while others find that taking it after 3:00-4:00 PM impairs their ability to relax properly at night. As a general rule, it is recommended to take NAD+ in the morning or early afternoon, especially during the first few weeks of supplementation while assessing individual response. If your protocol requires two daily doses, the second dose should ideally be taken before noon or in the early afternoon. Paradoxically, although NAD+ taken too late may initially disrupt sleep in sensitive individuals, regular and well-timed supplementation can help support healthy circadian rhythms in the long term and promote more consistent sleep patterns by influencing the molecular biological clock.

Can I drink alcohol while supplementing with NAD+?

Alcohol consumption can be counterproductive when supplementing with NAD+, as alcohol metabolism consumes large amounts of NAD+ in the liver through the enzyme alcohol dehydrogenase, which converts alcohol into acetaldehyde. This process directly depletes the NAD+ reserves that supplementation is intended to optimize, potentially reducing the supplement's effectiveness and perceived benefits. Additionally, alcohol can negatively affect mitochondrial function, increase oxidative stress, and compromise multiple metabolic processes that NAD+ is meant to support. If you consume alcohol occasionally, it is advisable to keep the amounts moderate and consider that NAD+ levels may be temporarily reduced on days of alcohol consumption. To maximize the benefits of NAD+ supplementation, especially if the goals include metabolic optimization, liver function support, or improved body composition, limiting or eliminating alcohol consumption would be most beneficial. If alcohol is consumed, ensuring adequate hydration and maintaining consistency in NAD+ supplementation in the following days can help restore optimal levels more quickly.

Do I need to take NAD+ every day or can I take it only when I need it?

For the most complete and consistent benefits, NAD+ works best when taken regularly and continuously rather than sporadically based on perceived need. This is because the effects of NAD+ are primarily cumulative and depend on the sustained elevation of cellular levels of this coenzyme over time. The processes that NAD+ supports, such as mitochondrial function, sirtuin activation, DNA repair, and metabolic maintenance, are continuous and benefit from a steady rather than fluctuating supply. Taking NAD+ only occasionally when experiencing fatigue or before specific events might provide some short-term benefit, but it wouldn't allow for the full optimization of cellular systems that rely on this coenzyme. The nature of NAD+ supplementation is preventative and maintenance-oriented rather than corrective and immediate. For people seeking occasional energy support, other supplements with more acute effects might be more appropriate, while NAD+ is ideal for those seeking sustained metabolic optimization, support for healthy aging, and long-term improvement of cellular function through a consistent usage protocol.

What happens if I stop taking NAD+ after several months?

When NAD+ supplementation is discontinued after prolonged use, cellular levels of this coenzyme will gradually decline and return to baseline levels determined by age, diet, lifestyle, and the body's endogenous synthesis capacity. This process is not abrupt, nor does it produce a negative "rebound" effect; it simply represents a return to the metabolic state prior to supplementation. The rate at which NAD+ levels decline after discontinuing supplementation varies between tissues, with some organs, such as the liver, showing a relatively rapid reduction (days to weeks), while other tissues may maintain elevated levels for somewhat longer periods. Individuals may gradually notice a return of the lower energy levels, reduced mental clarity, or subtle changes in physical recovery they experienced before starting supplementation, although this depends heavily on how deficient the initial levels were and the lifestyle changes implemented during the supplementation period. There is no risk of dependence or adverse effects from discontinuing NAD+, and supplementation can be restarted at any time if the benefits are desired. Some users choose to cycle supplementation with active and rest periods as part of their long-term strategy.

Is it safe to take higher doses than recommended to get faster effects?

Increasing the dose beyond the recommendations established in usage protocols does not necessarily accelerate or intensify the benefits and could unnecessarily increase the metabolic load without providing additional advantages. NAD+ and its effects on cellular function do not follow a simple linear relationship where more always equals better results. Instead, there is an optimal range where supplementation effectively supports cellular processes without overloading utilization pathways. Excessively high doses can saturate cellular transport mechanisms and the enzymes that metabolize NAD+, which could result in inefficient utilization and an increase in the production of metabolites that must be processed and excreted. Additionally, very high doses can place excessive pressure on the body's methylation systems, as the processing and elimination of excess nicotinamide derived from NAD+ metabolism consumes methyl groups that are necessary for many other vital functions. The most effective strategy is to start with moderate doses following the suggested protocols, evaluate the individual response over several weeks, and only then consider gradual adjustments if necessary, always within well-established safety ranges for NAD+ supplementation.

Can I take NAD+ along with other supplements or multivitamins?

NAD+ can be safely combined with most common supplements and multivitamins, and in fact, certain combinations can be synergistic and mutually beneficial. Supplements such as B complex, magnesium, CoQ10, resveratrol, quercetin, alpha-lipoic acid, and antioxidants in general can complement and enhance the effects of NAD+ through various mechanisms that support mitochondrial function, antioxidant protection, and energy metabolism. It is advisable to space out the intake of different supplements throughout the day when possible, not for reasons of incompatibility, but to optimize the absorption of each compound and avoid competition for intestinal transport mechanisms. If you are taking a comprehensive multivitamin, there is generally no problem combining it with NAD+, although you might consider taking the multivitamin with a meal and the NAD+ at a different time of day to maximize the bioavailability of both. The only important consideration is to avoid megadoses of niacin (vitamin B3) taken simultaneously with NAD+, as both contribute to the same cellular NAD+ pool, and very high doses of niacin can interfere with methylation metabolism. For specific combinations with specialized supplements or medicinal herbs, it is wise to research potential interactions or consult specialized supplementation resources.

Does NAD+ lose effectiveness if I take it with fiber supplements or probiotics?

Fiber supplements can potentially interfere with NAD+ absorption if taken concurrently, as fiber can physically bind to various compounds in the digestive tract and reduce their bioavailability. To optimize NAD+ absorption, it is recommended to space the intake of fiber supplements (such as psyllium, glucomannan, or mixed fiber supplements) at least 1 to 2 hours before or after taking NAD+. This allows NAD+ to be absorbed efficiently without the physical interference of fiber in the gut. Regarding probiotics, the relationship is more complex and interesting, as there is evidence that the gut microbiota can metabolize NAD+ precursors such as NR and NMN through deamination processes, converting them into nicotinic acid, which is then absorbed and reincorporated into NAD+ synthesis pathways. This suggests that a healthy gut microbiota could even facilitate the utilization of supplemented NAD+. There's no reason to avoid taking probiotics when supplementing with NAD+, and in fact, maintaining a healthy gut microbiota could indirectly support the overall effectiveness of the supplementation protocol. If you're taking both fiber and NAD+, the optimal strategy is to take the NAD+ on an empty stomach in the morning and the fiber with your first meal or in the evening.

How do I properly store NAD+ capsules to maintain their potency?

Freeze-dried NAD+ is relatively stable when stored properly, but certain precautions are necessary to maintain its maximum potency over time. The capsules should be stored in a cool, dry place away from direct sunlight, heat, and humidity. While refrigeration isn't strictly necessary for high-quality freeze-dried NAD+, keeping the bottle in a cool environment can extend its shelf life, especially in warm or humid climates. It's crucial to keep the container tightly sealed when not in use, as exposure to air and ambient humidity can gradually degrade the compound. Avoid storing the capsules in the bathroom, kitchen, or near heat sources such as radiators or appliances, as these environments tend to have temperature and humidity fluctuations that can compromise stability. If you live in a particularly warm or humid climate, consider storing the bottle in the refrigerator inside an additional airtight container to prevent condensation, and allow the bottle to reach room temperature before opening it to prevent moisture from forming inside. Never transfer the capsules to any container other than the original, as it is specifically designed to protect the product. With proper storage, freeze-dried NAD+ capsules can maintain their potency for many months.

Can I take NAD+ if I'm following a special diet like ketogenic, vegan, or intermittent fasting?

NAD+ is compatible with virtually all special diets and can even complement certain nutritional approaches particularly well. For people following a ketogenic diet, NAD+ can support the efficiency of fatty acid metabolism and mitochondrial function, which are central to the success of this dietary approach, as lipid beta-oxidation requires NAD+ as an essential cofactor. People on vegan diets can especially benefit from NAD+ supplementation, as some of the richest natural dietary sources of NAD+ precursors come from animal products, and supplementation can help ensure optimal levels regardless of dietary restrictions. NAD+ is fully compatible with vegan and vegetarian diets. For those practicing intermittent fasting, NAD+ can be taken during the eating window or even during the fasting period, as the capsules contain a minimal amount of calories that would not significantly disrupt the fasting metabolic state. In fact, some protocols suggest that taking NAD+ during fasting could be particularly synergistic, as both practices support sirtuin activation, autophagy, and metabolic optimization. NAD+ supplementation may be a valuable tool to support metabolic adaptation and cellular function during any significant dietary transition.

Is it normal to notice changes in urine after starting to take NAD+?

Some people may notice their urine becoming a brighter or more intense yellow after starting NAD+ supplementation, which is a completely normal and expected effect that does not indicate any problem. This color change is due to the excretion of vitamin B metabolites, particularly riboflavin, and NAD+ metabolism products such as N-methylnicotinamide and its pyridone derivatives. When the body receives more NAD+ than it immediately needs for cellular functions, the excess is metabolized, and the byproducts are eliminated through urine, which can impart this characteristic color. The intensity of the color may vary depending on hydration level, being more noticeable when dehydrated and diluted with adequate fluid intake. This phenomenon is similar to what occurs when taking high-potency B-complex supplements and does not represent a loss of effectiveness or waste of the supplement, but simply the normal functioning of the body's regulatory systems that maintain optimal levels and eliminate excess. There is no need to adjust the dose due to this effect, although maintaining adequate hydration is always recommended to support all metabolic processes and healthy kidney function.

Should I have blood tests done before or during NAD+ supplementation?

Blood tests are not strictly necessary before starting NAD+ supplementation for most healthy individuals using it as part of a general metabolic optimization and wellness protocol. NAD+ is an endogenous molecule that the body produces naturally, and supplementation simply supports the maintenance of optimal levels of this coenzyme. However, some people choose to have baseline and follow-up blood tests for several valid reasons. Measuring NAD+ levels directly in blood can be technically complex and is not routinely available in most standard clinical laboratories, but there are indirect markers that can provide insights into overall metabolic status and the effectiveness of supplementation. Parameters such as liver enzyme levels, homocysteine, oxidative stress markers, mitochondrial function, and overall metabolic profile can offer useful contextual information. If you have very specific health goals, are monitoring particular markers of aging or metabolism, or simply want a more quantitative approach to evaluating your supplementation protocol, conducting periodic tests every 3 to 6 months could provide valuable data. For most users, however, subjective assessments of energy, recovery, mental clarity, and overall well-being are sufficient to determine the effectiveness of supplementation.

Can I use NAD+ to support recovery after intense exercise?

NAD+ can be a valuable tool for supporting recovery processes after intense exercise through multiple mechanisms related to energy metabolism, mitochondrial function, and the cellular stress response. During intense exercise, NAD+ stores can be depleted due to high energy demands, and supplementation can help restore these levels more quickly, potentially shortening recovery time between training sessions. Additionally, NAD+ supports the function of sirtuins, which are involved in the adaptive response to exercise, including mitochondrial biogenesis and enhanced muscle oxidative capacity—key components of training adaptations. To optimize NAD+ utilization in the context of athletic performance, many individuals take a dose before training to support energy production during the session and another dose after exercise or with a post-workout meal to support recovery and repair processes. Combining NAD+ with other recovery-supporting nutrients, such as high-quality protein, carbohydrates (depending on the type of training), electrolytes, and antioxidants, can create a comprehensive athletic performance support protocol. It is important to remember that NAD+ supports the underlying metabolic function but does not replace the essential foundations of recovery, which include adequate rest, proper nutrition, and intelligent training periodization.

Are there people who don't respond well or don't notice any effects with NAD+?

Individual responses to NAD+ supplementation can vary considerably, and a small percentage of people report no significant effects even after several weeks of consistent use. This variability in response may be due to multiple factors, including genetic differences in the enzymes that metabolize and utilize NAD+, baseline NAD+ levels before starting supplementation, age, overall metabolic status, the composition of the gut microbiota (which can influence the absorption and metabolism of NAD+ precursors), and individual expectations about what changes should be noticeable. Younger individuals with still-robust endogenous NAD+ levels may experience more subtle effects than older individuals with significant depletion. Additionally, lifestyle factors such as chronic stress, lack of sleep, a diet poor in essential nutrients, alcohol or tobacco use, and lack of physical activity can compromise the body's ability to efficiently utilize supplemented NAD+ and translate it into noticeable benefits. If no effects are experienced after 6 to 8 weeks of consistent use, it may be helpful to evaluate these contextual factors, consider adjusting the dosage, review the quality and purity of the product used, or explore the addition of synergistic cofactors that could improve NAD+ utilization. It is also important to recognize that some of the most significant benefits of NAD+ occur at the cellular level and may not be immediately perceptible subjectively, even though they are supporting fundamental long-term health processes.

What is the difference between taking NAD+ and other precursors such as NR or NMN?

Although NAD+, NR (nicotinamide riboside), and NMN (nicotinamide mononucleotide) are all related and contribute to the same cellular pool of NAD+, differences in their molecular structures, absorption pathways, and metabolism can influence their relative effectiveness. NAD+ is the complete, active molecule that cells use directly, while NR and NMN are precursors that must be converted to NAD+ once inside the cells. Traditionally, NAD+ was thought to be incapable of being absorbed intact due to its molecular size, but recent research has identified specific transporters that can enable direct NAD+ absorption in certain tissues, and the lyophilized form may offer advantages in terms of stability and bioavailability. NR and NMN follow different metabolic pathways once ingested: NR is phosphorylated by NRK enzymes to form NMN, which is then converted to NAD+ by NMNAT enzymes, while NMN can be converted directly to NAD+ or first dephosphorylated to NR, depending on the tissue and conditions. Recent studies have also shown that both NR and NMN can be metabolized by the gut microbiota via deamination to nicotinic acid before being reabsorbed and incorporated into NAD+ synthesis pathways. In practical terms, the choice between NAD+, NR, or NMN may depend on factors such as individual bioavailability, cost, personal response, and specific goals, and some protocols even rotate between different precursors to take advantage of their unique characteristics.

Is it safe to take NAD+ during pregnancy or breastfeeding?

Due to the lack of specific studies on the safety of NAD+ supplementation during pregnancy and lactation, and following the precautionary principle applicable to all supplements during these special periods, it is generally recommended that pregnant or breastfeeding women avoid NAD+ supplementation unless there is a specific and well-founded reason for its use. Although NAD+ is an endogenous molecule that the body produces naturally and that is essential for fetal development and normal cell function, external supplementation with concentrated doses has not been systematically evaluated in these populations. Pregnancy and breastfeeding are periods of extraordinary metabolic demands where nutritional requirements increase significantly. Although NAD+ plays important roles in energy metabolism and cell development, the safest way to support NAD+ levels during these periods is through a balanced diet rich in NAD+ precursors, such as high-quality proteins containing tryptophan, and foods rich in niacin and other B vitamins. Women in these stages who are considering any form of supplementation should do so only under appropriate supervision and guidance, always prioritizing the safety of both mother and baby.

Can NAD+ interact with prescription medications?

Although NAD+ is an endogenous molecule and is generally considered safe, there is potential for interactions with certain medications due to its influence on cellular metabolism and liver enzymes. The most relevant interactions to consider include medications that affect hepatic metabolism, particularly those metabolized by cytochrome P450 enzymes, since NAD+ is a cofactor in multiple phase I reactions of hepatic detoxification and could theoretically influence the rate of metabolism of certain drugs. Cardiovascular medications, particularly those that affect blood pressure or heart rate, may require monitoring if NAD+ supplementation is initiated, given its role in endothelial function and cardiac energy metabolism. Immunosuppressant medications may have potential interactions considering the role of NAD+ in immune function. Glucose-control medications also warrant attention, as NAD+ influences carbohydrate metabolism and cellular sensitivity. It is particularly important to consider interactions if medications with a narrow therapeutic window are being taken, where small changes in absorption or metabolism could have significant consequences. If you are taking any prescription medication, especially for chronic conditions, it is wise to inform us about any new supplementation you plan to start, including NAD+, to allow for proper assessment of potential interactions and necessary adjustments to monitoring or dosages.

Recommendations

• Store the product in a cool, dry place away from direct sunlight, heat, and humidity. Keep the container tightly closed when not in use to preserve the product's quality and potency.
• Start with the lowest recommended dose for the first 5 days to allow the body to gradually adapt to the supplementation, especially if it is the first time using this type of product.
• It is best taken during the first hours of the day to optimize synchronization with the body's natural metabolic rhythms and avoid possible interference with natural nighttime rest patterns.
• Maintain adequate hydration while using the product, consuming enough water throughout the day to support natural metabolic processes and kidney function.
• To optimize results, combine supplementation with a balanced diet rich in essential nutrients, regular physical activity, proper stress management, and consistent sleep patterns.
• If you are taking multiple supplements simultaneously, consider spacing out your administration throughout the day to optimize the absorption of each compound and avoid competition for transport mechanisms.
• Maintain consistency in supplementation by following the chosen protocol for at least 4 to 8 weeks before fully evaluating the individual response to the product.
• If you experience any mild digestive discomfort when taking the product on an empty stomach, consider taking it with a light meal to improve tolerance without significantly compromising effectiveness.
• Periodically review individual response to the product and adjust dosage or protocol as needed, always keeping amounts within the ranges suggested for safe supplementation.

Warnings

• This product is a food supplement intended to complement the diet and should not be used as a substitute for a varied and balanced diet or a healthy lifestyle.
• Do not exceed the recommended dose. Consuming amounts higher than suggested will not provide additional benefits and could unnecessarily increase the metabolic burden on the body's processing systems.
• Do not use if the safety seal is broken or missing. Check the product's integrity before first use and discard if there are any signs of tampering or damage to the packaging.
• Keep out of reach of unauthorized persons. Store in a secure location where it cannot be inadvertently accessed.
• People with pre-existing health conditions, those taking medication regularly, or those with specific concerns about supplementation should carefully consider their individual situation before using this or any supplement.
• Pregnant or breastfeeding women should avoid this product due to the lack of specific studies on its safety during these special periods.
• Discontinue use and assess the situation if unexpected or unwanted effects are experienced after starting supplementation.
• This product may interact with certain medications, particularly those that affect liver metabolism, cardiovascular function, the immune system, or glucose control. People taking prescription medications should consider informing their doctor about any new supplements.
• Do not use as a treatment, prevention, or cure for any health condition. This product supports natural metabolic processes as part of an overall wellness approach.
• Alcohol consumption can significantly reduce the effectiveness of this product by depleting the cellular reserves that are being optimized through supplementation.
• The changes you'll see with this product are generally gradual and cumulative. Don't expect immediate or dramatic effects, as the product supports fundamental cellular processes that optimize over time.
• This product has not been evaluated by health authorities to diagnose, treat, cure, or prevent any health condition.
• Do not use after the expiration date printed on the packaging. The potency and safety of the product cannot be guaranteed beyond this date.
• Individual response to supplementation can vary considerably depending on factors such as age, basal metabolic status, lifestyle, individual genetics, and other aspects of personal health.
• If you are using fiber supplements, space your intake at least 1 to 2 hours before or after this product to avoid interference with absorption.
• The effects perceived may vary between individuals; this product complements the diet within a balanced lifestyle.

• Use during pregnancy and lactation is not recommended due to the lack of clinical studies evaluating the safety of NAD+ supplementation in these populations. Although NAD+ is an essential endogenous molecule, supplementation with concentrated doses has not been sufficiently investigated during these special physiological periods.
• Avoid concomitant use with immunosuppressant drugs, as NAD+ is involved in the regulation of immune responses and could potentially interfere with the therapeutic effects of these drugs by modulating the function of immune cells and inflammatory signaling pathways.
• Simultaneous use with anticoagulants and antiplatelet agents without appropriate supervision is discouraged, because NAD+ can influence endothelial function and nitric oxide production, which could theoretically affect hemostasis and potentiate the effects of these medications.
• Do not combine with high pharmacological doses of niacin (nicotinic acid) used for lipid modification, as both compounds contribute to the same cellular NAD+ pool and the combination could put excessive pressure on the body's methylation systems, increasing the production of methylated metabolites that must be processed and excreted.
• Avoid use in people with known hypersensitivity to compounds derived from vitamin B3 or with a history of adverse reactions to NAD+ precursors such as nicotinamide riboside or nicotinamide mononucleotide, due to the structural and metabolic relationship between these compounds.
• Concomitant use with hypoglycemic medications or insulin without adequate monitoring is not recommended, as NAD+ is involved in the regulation of carbohydrate metabolism and could influence cellular sensitivity to insulin and glucose transport, which could require adjustments in the doses of these medications.
• Avoid use in people with severely compromised liver function, considering that the liver is the main site of NAD+ metabolism and recycling, and the reduced capacity to process this coenzyme and its metabolites could result in accumulation or inefficient utilization.
• Do not combine with monoamine oxidase inhibitors (MAOIs) without appropriate consideration, as NAD+ is involved in metabolic pathways related to the synthesis and metabolism of monoaminergic neurotransmitters, and there could be a potential for interaction that affects the levels of these compounds.
• Use is not recommended in people with known disorders of methionine metabolism or with genetic variants that significantly affect methylation pathways, since the processing of NAD+ requires methyl donors and could aggravate pre-existing imbalances in these systems.
• Avoid concomitant use with chemotherapeutic agents without appropriate oncological supervision, as NAD+ is involved in DNA repair and cellular metabolism processes that could theoretically interfere with the mechanisms of action of certain antineoplastic agents that depend on DNA damage or metabolic stress for their effectiveness.