NAD+: A Coenzyme at the Center of Cellular Energy and Aging Research

This article is for informational purposes only and does not constitute medical advice. Superpower Health facilitates access to NAD+ through licensed providers and compounding pharmacy partners. Always consult a qualified healthcare provider before starting any prescription compound.

Every cell in your body runs on NAD+. Without it, the enzymes that generate ATP, repair DNA, and regulate gene expression cannot function. Yet NAD+ levels in human tissue fall measurably and consistently across the lifespan, beginning in early adulthood. The question researchers have been asking for the past decade is whether replacing what is lost can change the trajectory of aging-associated biology.

NAD+ (nicotinamide adenine dinucleotide) is a coenzyme, not a peptide. It is present in every living cell and sits at the intersection of metabolism, genomic stability, and mitochondrial function. Here is how it works, what the clinical evidence supports across delivery methods, and which biomarkers matter before you begin.

Key Takeaways

• Regulatory Status: Not FDA-approved for any specific indication. Available as a compounded prescription (intranasal) through licensed providers and licensed compounding pharmacies. Oral precursors (NMN, NR) are available as dietary supplements and do not require a prescription.
• Research Stage: Clinically studied across multiple delivery forms; human RCT evidence is growing but remains early-stage for most anti-aging claims
• Availability: Prescription intranasal form through Superpower's licensed provider network and compounding pharmacy partners; oral precursors available OTC
• Prescribing information: View compound reference data on PubChem (CID 5893)
• How it works: Serves as an electron carrier in redox reactions and a substrate for sirtuins, PARPs, and CD38 that regulate DNA repair, gene expression, and metabolic homeostasis.
• What the research shows: Supplementation with NAD+ precursors consistently raises blood NAD+ levels; clinical effectiveness for anti-aging outcomes remains under active investigation.

What Is NAD+?

NAD+ (nicotinamide adenine dinucleotide) is a dinucleotide coenzyme synthesized from precursors including tryptophan, nicotinamide, nicotinamide riboside (NR), and nicotinamide mononucleotide (NMN). It cycles between its oxidized form (NAD+) and reduced form (NADH), transferring electrons between metabolic reactions. Beyond this redox role, NAD+ is a consumed substrate for three enzyme families that regulate genomic integrity and cellular stress responses: sirtuins (SIRT1-7), poly(ADP-ribose) polymerases (PARPs), and cyclic ADP-ribose synthases (CD38/BST1). Plasma NAD+ concentrations are measurably lower in older adults compared to younger controls, a finding documented across multiple tissue types. Superpower Health facilitates access to intranasal NAD+ through its licensed provider network.

How NAD+ Works in the Body

Cellular Energy Production and Mitochondrial Function

NAD+ is the primary electron acceptor in glycolysis and the citric acid cycle. In each pathway, metabolic intermediates donate electrons to NAD+, converting it to NADH. NADH then delivers those electrons to the mitochondrial electron transport chain, where they drive ATP synthesis. A 2020 review by Covarrubias and Perrone in Nature Reviews Molecular Cell Biology documents that declining mitochondrial NAD+ availability is mechanistically associated with reduced ATP output, impaired fatty acid oxidation, and features of metabolic dysfunction in aging tissue. The relationship between NAD+ and mitochondrial function is bidirectional: impaired mitochondria deplete NAD+ faster, accelerating the cycle. This makes NAD+ availability a rate-limiting factor for cellular energy production rather than a simple downstream marker of metabolic health.

Sirtuin Activation and Gene Regulation

Sirtuins are a family of seven NAD+-dependent deacylases that regulate gene expression, DNA repair, and metabolic adaptation. SIRT1 and SIRT3 are the most studied in the context of aging. They require NAD+ as a consumed substrate, not a cofactor: each catalytic cycle depletes one molecule of NAD+. A 2020 review by Katsyuba and Romani in Nature Metabolism describes how declining NAD+ availability reduces sirtuin activity, impairing the transcriptional programs that govern mitochondrial biogenesis, inflammation control, and stress resistance. This pathway is one of the primary rationales for NAD+ supplementation in longevity research. Caloric restriction, which reliably extends lifespan in animal models, elevates NAD+ and activates sirtuins, establishing a plausible mechanistic link.

DNA Repair via PARP Enzymes

PARP1 and PARP2 are nuclear enzymes that detect single-strand DNA breaks and coordinate repair. Each activation event consumes multiple molecules of NAD+. In scenarios of high DNA damage, such as oxidative stress, radiation exposure, or aging, PARP activation can deplete cellular NAD+ substantially. A 2023 study by Munk and Merchut-Maya in Nature Cell Biology tested exogenous NAD+ across multiple human and mouse cell lines (including MRC5, BJ, HeLa, and T98G) at concentrations ranging from 0.64 µM to 2 mM and found that short-term incubation boosted pyrimidine biosynthesis and mitochondrial electron transport, while extended 24-hour exposure at 2 mM depleted pyrimidines, caused purine accumulation, activated the replication stress response, and triggered cell cycle arrest — underscoring that dose and duration matter. Separately, a 2025 review by Bohr in Aging Cell synthesized clinical evidence across rare premature aging syndromes with defective DNA repair: in Werner syndrome (N=9), 1,000 mg/day NR for 52 weeks raised plasma NAD+ by approximately 140% versus a 4% decrease on placebo and improved arterial stiffness and skin ulcer size; in ataxia telangiectasia (N=24), 25 mg/kg/day NR for 4 months improved ataxia scores, with effects reversing after withdrawal — offering proof-of-concept that PARP-mediated NAD+ depletion is clinically relevant beyond animal models.

Neuronal Resilience and Brain Aging

Neurons have high energy demands and limited regenerative capacity, making NAD+ availability particularly consequential in the central nervous system. A 2019 review by Lautrup and Sinclair in Cell Metabolism described NAD+ as playing a key role in neuronal resilience to metabolic and oxidative stressors, with declining levels associated with vulnerability patterns seen in neurodegenerative disease. The NR-SAFE randomized trial, published in Nature Communications by Berven and Kverneng in 2023, enrolled 20 Parkinson's disease patients (10 NR, 10 placebo) and administered 3,000 mg/day NR for 4 weeks. The NR group showed a mean MDS-UPDRS total score decrease of 10.7 points versus no change in the placebo group (between-group p = 0.024), with blood NAD+ rising approximately 3.7-fold; all 42 reported adverse events across both groups were graded mild, though the small sample size and single-center design limit generalizability. This is among the few controlled human trials of NAD+ precursors in a neurological population.

Redox Balance and Inflammatory Regulation

The NAD+/NADH ratio is a direct read of redox state in the cell. When NAD+ falls relative to NADH, the cell shifts toward a more reduced redox environment. This shift activates pro-inflammatory pathways and impairs the oxidative stress response. A 2019 comprehensive review by Braidy and Berg in Antioxidants and Redox Signaling documented the biochemical links between NAD+ redox balance, NF-kB inflammatory signaling, and reactive oxygen species accumulation across multiple tissue types. CD38, an NAD+-consuming enzyme that rises with age and in inflammatory states, is a significant driver of age-related NAD+ decline independent of biosynthesis capacity. Elevated inflammatory markers are associated with accelerated NAD+ depletion, creating a feedback loop relevant for individuals with chronic low-grade inflammation.

What the Research Shows About Effectiveness

NMN Supplementation: Dose-Dependent Blood NAD+ Elevation

The strongest human trial evidence for NAD+ precursors comes from NMN studies. A 2022 multicenter RCT by Yi and Maier in GeroScience enrolled 80 healthy middle-aged adults (mean age 47) and randomized them to NMN at 300 mg/day, 600 mg/day, 900 mg/day, or placebo for 60 days. All NMN-treated groups showed statistically significant increases in blood NAD+ concentrations at day 30 and day 60 versus both placebo and baseline (all p ≤ 0.001), with the 600 mg group rising from approximately 8 nM at baseline to 39 nM at day 30 and 45 nM at day 60 — roughly a 5-fold increase — and the 600 mg and 900 mg groups significantly outperforming 300 mg, suggesting peak efficacy at 600 mg/day. No serious adverse events were reported at any dose. A separate 2022 RCT by Okabe and Yaku in Frontiers in Nutrition randomized 30 healthy adults to 250 mg/day NMN or placebo for 12 weeks and found that NMN approximately doubled whole-blood NAD+ levels versus placebo at 4 weeks (p < 0.001), with the elevation sustained through 12 weeks and no abnormalities in laboratory safety tests or adverse effects. A 2022 study by Pencina and Lavu in the Journal of Gerontology Series A randomized 32 middle-aged and older adults to MIB-626 (microcrystalline NMN) at 1,000 mg once daily, 1,000 mg twice daily, or placebo for 14 days and found dose-dependent blood NMN increases of 1.7-fold and 3.7-fold above baseline in the once-daily and twice-daily groups respectively, with corresponding NAD+ increases of approximately 2-fold (once daily) and 3-fold (twice daily) above baseline, and no significant difference in adverse events versus placebo. Across these trials, raising blood NAD+ is reproducible. What these studies did not establish is whether raising blood NAD+ translates to the anti-aging clinical outcomes observed in animal models.

NR Supplementation: Safety and Cardiovascular Signals

Nicotinamide riboside (NR) has a similar evidence profile to NMN. A 2018 crossover RCT by Martens and Denman in Nature Communications enrolled 24 healthy middle-aged and older adults on 1,000 mg/day NR or placebo for two 6-week periods and found NR raised whole-blood NAD+ by approximately 60% versus placebo (p = 0.048), with an exploratory signal in participants with elevated baseline blood pressure showing systolic BP approximately 9 mmHg lower after NR versus placebo and a trend toward reduced carotid-femoral pulse wave velocity. The study was not powered to confirm cardiovascular outcomes. A 2018 review by Johnson and Imai in F1000Research concluded that NAD+ biosynthesis dysfunction contributes to age-associated diseases and that supplementing with NAD+ intermediates has potential as an anti-aging intervention, while acknowledging that human trial evidence remained limited at the time. A 2019 safety RCT by Conze and Brenner in Scientific Reports randomized 140 healthy overweight adults to NR at 100, 300, or 1,000 mg/day or placebo for 8 weeks and found dose-dependent whole-blood NAD+ increases of 22%, 51%, and 142% respectively, with no reports of flushing, no significant difference in adverse event rates between NR and placebo groups, and no elevation in LDL cholesterol or disruption of one-carbon metabolism.

Overall Evidence Assessment

A 2026 PRISMA systematic review by Gallagher and Emmanuel in Ageing Research Reviews screened the literature from 2010 to 2025 and included 113 eligible studies — 33 human intervention trials (28 randomized, 5 nonrandomized) and 80 rodent studies — across all NAD+ precursor forms. The review found clear biological activity: supplementation consistently and dose-dependently raises blood NAD+ across study populations. However, clinical effectiveness for anti-aging outcomes, including improvements in physical function, cognitive performance, or metabolic endpoints, remained inconclusive based on the available evidence, with human results described as heterogeneous and often null or endpoint-specific. No pooled quantitative synthesis was performed because of heterogeneity across study designs. The authors noted that most positive signals come from animal models or from human studies that measured surrogate endpoints (blood NAD+) rather than clinical outcomes. This is the most current and balanced summary of the field.

NAD+ vs. NMN: Key Differences

NAD+ and NMN target the same cellular systems but differ fundamentally in how they enter cells, their bioavailability by delivery route, and their regulatory classification.

NMN is a direct biosynthetic precursor to NAD+, one step upstream in the salvage pathway. It is absorbed intact and converted intracellularly to NAD+ via the enzyme NMNAT. NMN can be taken orally as a dietary supplement; it does not require a prescription. IV and intranasal delivery of NMN have also been studied in real-world settings, as documented in a 2026 retrospective comparison by Reyna and Heinzen in Frontiers in Aging, which administered 500 mg IV NAD+ (n=6) or 500 mg IV NR (n=8) over four consecutive days and found that 100% of NAD+ recipients experienced moderate-to-severe gastrointestinal distress, chest pressure, and elevated heart rate, while 62.5% of NR recipients reported only mild tingling and minor cramping, with all symptoms in both groups resolving upon infusion completion over a 30-day follow-up.

Direct NAD+ administration, particularly by IV or intranasal routes, bypasses precursor conversion entirely and raises plasma NAD+ faster than oral precursors. A 2019 pilot study by Grant and Berg in Frontiers in Aging Neuroscience infused 750 mg NAD+ intravenously over 6 hours in 8 healthy males (with 3 saline controls) and found plasma NAD+ rose 398% above baseline by the end of infusion, with parallel increases in nicotinamide (409%), ADPR (393%), and methylnicotinamide (350%), though no metabolite changes appeared until after the 2-hour mark and levels began declining within approximately 2 hours post-infusion. Intranasal delivery represents a more practical prescription route for outpatient use: it avoids the time and cost of IV infusion while potentially offering higher CNS bioavailability than oral routes, though human nasal-to-brain pharmacokinetic data remains limited to animal studies. Preclinical reviews cover the pharmacokinetic rationale for intranasal delivery in neurological applications, but direct human evidence for nasal-to-brain NAD+ transport has not yet been published.

The practical distinction: oral NMN and NR are accessible, studied in humans, and carry a well-characterized safety profile for raising blood NAD+. Prescription intranasal NAD+ represents a higher-bioavailability alternative for individuals working with a licensed provider on a specific clinical rationale. IV NAD+ offers the fastest and most complete systemic elevation but requires clinical administration.

NAD+ Delivery Forms

NAD+ and its precursors are available through several routes, each with different bioavailability, onset of action, and access requirements.

Intranasal NAD+ is the prescription form Superpower facilitates through its licensed provider network. It is administered via a compounded nasal spray, typically containing NAD+ in a buffered vehicle. Intranasal delivery offers rapid absorption through the nasal mucosa, potential direct access to cerebrospinal fluid via olfactory pathways (demonstrated preclinically in rat models with analogous compounds), and avoidance of first-pass hepatic metabolism that limits oral bioavailability of direct NAD+. Dose and frequency are determined by the prescribing provider.

IV NAD+ produces the most rapid and complete elevation of plasma NAD+ but requires clinical administration, takes several hours per session, and is associated with transient infusion reactions at higher doses. It is not available through Superpower's current offering.

Oral NMN and NR are dietary supplements available without a prescription. They consistently raise blood NAD+ in controlled trials at doses studied (300-600 mg/day for NMN; 1,000 mg/day for NR in the NADPARK trial and up to 3,000 mg/day in the NR-SAFE trial). Sublingual and liposomal formulations of NMN/NR are marketed with claims of higher bioavailability, but controlled comparisons against standard oral forms in human pharmacokinetic studies are limited.

Oral direct NAD+ has poor bioavailability due to hydrolysis in the gastrointestinal tract; most oral NAD+ is broken down to nicotinamide before absorption. For practical purposes, oral precursors (NMN or NR) are more effective than oral NAD+ itself.

Side Effects and What to Expect

The safety profile of NAD+ supplementation has been characterized across multiple formulations and doses. Most reported adverse effects are mild and dose-related, with IV forms carrying a distinct tolerability profile from oral or intranasal routes.

Common side effects across formulations:

• Nausea or gastrointestinal discomfort (primarily with oral NMN/NR at higher doses; typically dose-dependent and self-limited)
• Flushing or warmth (more common with higher doses; less frequent with NR than niacin-form precursors)
• Transient headache (reported across routes; typically resolves with dose adjustment)
• Nasal irritation or mild congestion (intranasal form; typically transient)

IV-specific reactions (less common but reported):

• Chest tightness, anxiety, or palpitations during infusion (common at faster infusion rates; managed by slowing rate; discontinue and contact provider if persistent)
• Muscle cramping or jaw tightness during infusion (infusion-rate dependent; resolves after infusion)
• Nausea or lightheadedness during or after infusion, as documented in a 2026 retrospective by Reyna and Heinzen in Frontiers in Aging

The NR-SAFE trial administered 3,000 mg/day NR to 10 Parkinson's disease patients (with 10 on placebo) for 4 weeks; all 42 reported adverse events across both groups were graded mild, with no significant difference in frequency between NR and placebo arms. Long-term safety data beyond 8-16 weeks remains limited for most formulations. Providers assess individual risk factors before prescribing any route.

Who Is NAD+ Typically Prescribed For?

Adults with Documented NAD+ Decline or Related Metabolic Concerns

Providers typically evaluate candidates for prescription NAD+ based on clinical presentation and relevant biomarker findings. NAD+ decline is not currently measurable by a standard clinical blood test, but associated markers such as elevated inflammatory burden, HbA1c trends toward the upper range, and declining cellular energy markers provide relevant context. Adults in their forties and older with fatigue, metabolic concerns, or interest in longevity medicine may be evaluated. NAD+ is not FDA-approved for any indication. No other uses have been approved by the FDA. The safety and efficacy of NAD+ for any use have not been established through adequate and well-controlled clinical trials reviewed by the FDA. Any prescribing represents the independent clinical judgment of the licensed provider.

Individuals With Specific Neurological or Metabolic Contexts

The most robust human evidence for benefit from NAD+ precursors is in populations with documented deficiencies in NAD+ biosynthesis pathways, such as rare premature aging syndromes with DNA repair defects. Evidence from the NR-SAFE trial supports tolerability in Parkinson's disease, though effectiveness for this indication remains under investigation. Providers working in metabolic health, functional medicine, or longevity medicine may also evaluate NAD+ in the context of insulin resistance, cellular aging biomarker profiles, and mitochondrial function concerns. Candidacy is assessed individually based on clinical history and baseline testing.

Who Should Not Use NAD+

A licensed provider will evaluate individual risk factors before prescribing. The following are generally considered contraindications or conditions warranting additional clinical scrutiny:

• Active malignancy: NAD+ supports cellular energy and DNA repair mechanisms broadly; potential effects on tumor cell metabolism have not been studied adequately in oncology populations, and providers typically do not prescribe NAD+ to individuals with active cancer without specialist input
• Pregnancy and breastfeeding: Safety has not been established in these populations; avoid
• Severe renal or hepatic impairment: NAD+ metabolism involves hepatic processing; impaired clearance may alter the safety profile; eGFR and liver function should be assessed at baseline
• Known hypersensitivity to nicotinamide, niacin, or related compounds: cross-reactivity has been reported; inform your provider of any prior reactions
• Concurrent use of PARP inhibitors: NAD+ is the substrate consumed by PARP enzymes; pharmacological PARP inhibition combined with NAD+ supplementation has not been studied in humans and may produce unpredictable interactions

This is not an exhaustive list. A licensed provider will review current medications, medical history, and individual risk factors before prescribing NAD+ in any form.

What to Test Before Starting NAD+

No single biomarker measures tissue NAD+ levels directly in a standard clinical context. Baseline testing establishes a reference for the metabolic and physiological systems NAD+ most directly influences, and provides the safety data required before a provider initiates any prescription compound.

• Fasting glucose and HbA1c: NAD+ plays a central role in glucose metabolism and insulin signaling pathways. Elevated fasting glucose or HbA1c may reflect the metabolic dysfunction most associated with NAD+ decline in aging. These markers establish a metabolic baseline that makes changes during use interpretable.
• Fasting insulin: Insulin sensitivity is closely tied to NAD+ and sirtuin signaling. Baseline fasting insulin provides a more sensitive window into early insulin resistance than glucose or HbA1c alone, particularly in individuals without established diabetes.
• hs-CRP: Chronic low-grade inflammation drives CD38 activation, which consumes NAD+ and accelerates its depletion. Elevated hs-CRP identifies individuals most likely to have higher baseline NAD+ deficits due to inflammatory depletion. It also provides a reference point for tracking any anti-inflammatory response during supplementation.
• Complete metabolic panel (CMP): Covers liver function markers (ALT, AST, bilirubin) and kidney function markers (creatinine, eGFR, BUN) relevant to any prescription compound. NAD+ precursor metabolism involves hepatic processing; liver enzyme elevation or renal impairment affects prescribing decisions and dose selection.
• Vitamin B12: B12 is required for one-carbon metabolism and methylation reactions central to overall metabolic health. While the B vitamins most directly involved in tryptophan-kynurenine NAD+ biosynthesis are B2 and B6 (which serve as essential cofactors for kynurenine pathway enzymes), B12 status affects methylation capacity broadly and is a standard baseline marker for any metabolic intervention. Baseline B12 is particularly relevant in older adults and those with dietary restrictions.
• CBC (complete blood count): Provides a baseline for hematologic health before initiating any prescription compound. NAD+ influences erythrocyte metabolism; this is a standard safety reference rather than a primary monitoring target.
• Lipid panel: Niacin-pathway metabolism (which overlaps with NAD+ precursor pathways) can affect lipid profiles. Baseline lipids establish a reference that may be relevant depending on the precursor form and dose used.

What Your Bloodwork May Show While on NAD+

Blood NAD+ levels are not a standard clinical laboratory test, but several downstream markers provide indirect evidence of metabolic response. Providers who monitor patients on NAD+ supplementation typically track fasting glucose and insulin for directional changes in metabolic efficiency, HbA1c at 3-month intervals, and hs-CRP as an indicator of inflammatory burden. In the human RCT literature, blood NAD+ levels (measured in whole blood or PBMCs) are the most consistent biomarker of supplementation response, rising dose-dependently within 2-4 weeks of initiating NMN or NR. Functional clinical endpoints such as fatigue, exercise capacity, and cognitive performance have been reported as patient-reported outcomes in some trials, but objective biomarker correlates for these changes in humans are not yet established. Comparing any marker movement to your pre-therapy baseline is what makes the data clinically useful, rather than comparing to population reference ranges alone.

That principle is central to Superpower's approach to preventive health: objective biomarker data should precede every clinical decision and continue through every intervention. Your baseline is not paperwork. It is the reference that makes your data interpretable.

Frequently Asked Questions

What is the difference between NAD+ and NMN?

NMN (nicotinamide mononucleotide) is a direct biosynthetic precursor to NAD+, one enzymatic step upstream in the salvage pathway. When you take NMN orally, it is absorbed and converted intracellularly to NAD+ via the enzyme NMNAT. Direct NAD+ administration (IV or intranasal) delivers the coenzyme itself, bypassing precursor conversion and raising plasma NAD+ faster and to higher levels than oral precursors. The clinical significance of this speed and peak difference in humans is still under investigation. Oral NMN is a dietary supplement; prescription intranasal NAD+ is compounded and requires a licensed provider.

Is NAD+ IV better than oral supplements?

IV NAD+ produces the fastest and highest plasma NAD+ elevation of any delivery route — a 2019 pilot by Grant and Berg found a 398% increase in plasma NAD+ after a 750 mg, 6-hour infusion in 8 healthy males. Oral NMN and NR consistently raise blood NAD+ in controlled trials but more slowly and at lower peaks. Whether the higher peak achieved by IV translates to better clinical outcomes than oral precursors has not been established in head-to-head trials. IV infusions are also associated with transient side effects during administration that oral forms do not produce. The appropriate route depends on clinical context and is determined by the prescribing provider.

How often do you need NAD+ infusions or intranasal doses?

There is no established standard protocol based on randomized evidence. IV NAD+ infusion frequency in clinical practice varies widely, from single sessions to weekly or monthly schedules, based on provider judgment and patient response. Intranasal NAD+ dosing protocols for compounded formulations are similarly provider-determined. Oral NMN and NR in the human RCT literature have been studied at daily oral dosing for 60 days to 12 weeks. A provider will determine the appropriate dose and frequency based on clinical presentation and baseline testing.

Is NAD+ FDA-approved?

NAD+ is not FDA-approved for any specific indication. It is a naturally occurring coenzyme present in all human cells. Prescription-grade compounded intranasal NAD+ is available through licensed providers and licensed 503A compounding pharmacies. Oral NMN and NR are classified as dietary supplements and are available without a prescription, though they are not FDA-approved drugs and their efficacy claims have not undergone FDA review. A licensed provider can prescribe compounded NAD+ for a patient-specific clinical need under compounding law, which is distinct from FDA approval.

What are the side effects of NAD+?

Side effects vary by delivery route. Oral NMN and NR are generally well-tolerated; the most common reports are gastrointestinal discomfort, flushing, and transient headache at higher doses. The NR-SAFE trial found no serious adverse events at 3,000 mg/day of NR over 4 weeks. IV NAD+ carries a distinct tolerability profile: chest tightness, palpitations, nausea, and muscle cramping are reported during infusion and are managed by reducing infusion rate. Intranasal NAD+ may cause transient nasal irritation. Systematic long-term safety data beyond 12-16 weeks is limited for all formulations.

Can NAD+ improve energy and fatigue?

NAD+ is mechanistically central to mitochondrial ATP production, and fatigue is among the most commonly reported subjective improvements in observational reports and some trials. However, the current human RCT evidence primarily establishes that supplementation raises blood NAD+ rather than demonstrating objective improvements in energy output or fatigue as a clinical endpoint. The distinction matters: a surrogate biomarker rising does not confirm the clinical outcome. Studies measuring patient-reported fatigue have shown mixed results. Individuals with documented metabolic dysfunction, mitochondrial concerns, or chronic fatigue biomarker patterns may be the most appropriate candidates for evaluation by a provider.

What blood tests should I get before starting NAD+?

The most relevant baseline markers are fasting glucose, HbA1c, fasting insulin, hs-CRP, a complete metabolic panel (covering liver and kidney function), vitamin B12, and a CBC. These reflect the metabolic and inflammatory systems most influenced by NAD+ availability. They also establish the safety baseline a provider needs before prescribing any compounded compound. The guide to energy biomarkers provides additional context for understanding cellular energy-related testing.

This article is for informational purposes only and does not constitute medical advice. Superpower Health facilitates access to NAD+ through licensed providers and compounding pharmacy partners. Always consult a qualified healthcare provider before starting any prescription compound.