Nicotinamide Riboside (NR) Hard Capsules | Patented NAD+ Precursor with B-Vitamin Cofactors

Nicotinamide Riboside (NR) in hard capsule form — the patented NAD+ precursor with the deepest human research track record (65+ registered clinical trials, including pharmacokinetic, cardiovascular, and neurological endpoints). Supported by B-vitamin cofactors so the full NAD+ biosynthesis pathway has what it needs to convert NR into NAD+ inside the cell.

The 30-second answer

• NR is the most-studied NAD+ precursor in humans. First-in-human pharmacokinetic data published in 2016 (Trammell et al., Nature Communications) showed a single oral dose raised whole-blood NAD+ ~2.7× over 24 hours. Multi-week dosing at 1 g/day has been studied in healthy adults, midlife adults with elevated blood pressure, obese insulin-resistant adults, post-menopausal women, NAFLD patients, ALS patients, and Parkinson's patients.
• Different intracellular path than NMN. NR enters cells via the equilibrative nucleoside transporters (ENT1/2), gets phosphorylated by NRK1/NRK2 to NMN, then converted to NAD+. NMN uses the Slc12a8 transporter (Grozio 2019, Nature Metabolism) and skips a step. Both raise NAD+; tissue coverage and intracellular kinetics differ, which is why many longevity stacks run both.
• Best for: people who want the longest human-research track record, those who didn't feel a clear shift on NMN alone, anyone running a comprehensive NAD+ stack that hedges across both precursor pathways, and adults 50+ where the NMN transporter Slc12a8 may be downregulated in some tissues.
• Take 1–2 capsules daily in the morning with food. Daily consistency matters more than time-of-day. Stacks cleanly with NMN, Resveratrol, Pterostilbene, TMG, Apigenin, Quercetin, Fisetin, CoQ10, PQQ, and Urolithin A.
• Patented NR form, the same molecule used in Trammell 2016, Martens 2018, Dollerup 2018, Conze 2019, Elhassan 2019, and Brakedal 2022. Manufactured to cGMP, third-party HPLC-tested, encapsulated in a vegan-compatible hard shell with no proprietary blends, no titanium dioxide, no artificial colors.

Why NR sits at the center of the NAD+ conversation

NAD+ (nicotinamide adenine dinucleotide) is the single most metabolically expensive coenzyme in the cell. Every major energy-producing pathway — glycolysis, the citric acid cycle, the electron transport chain, fatty-acid oxidation — runs on NAD+/NADH cycling. On top of that core role, NAD+ is the rate-limiting substrate for at least three enzyme families that get talked about in the longevity literature constantly: the sirtuins (SIRT1–SIRT7, the histone-deacetylase / mitochondrial regulators activated by Resveratrol), the PARPs (PARP1 in particular, the primary single-strand DNA break repair enzyme), and CD38 (the NAD+ glycohydrolase that becomes hyperactive with inflammaging). When NAD+ falls, all three of those families slow down at the same time — and that simultaneity is why "NAD+ decline" gets called a hallmark of aging in the López-Otín 2013 / 2023 Cell framework, even though it isn't formally one of the 12.

The decline itself is not subtle. Massudi 2012 (PLOS One) measured skin NAD+ across the lifespan and found a roughly 50% drop between ages 20 and 60. Camacho-Pereira 2016 (Cell Metabolism) replicated the finding in muscle and liver and showed CD38 — which consumes NAD+ to make calcium-mobilizing second messengers — rises sharply with age, partially explaining the drop. Yoshino 2011 (Cell Metabolism) showed similar declines in pancreas, adipose tissue, and the hypothalamus in mice. Across tissues, mechanisms, and species, the NAD+ pool collapses with age — and the sirtuin / PARP / CD38 enzymes that depend on it lose their substrate.

You can address that decline from three directions:

1. Supply more precursor — give the cell more raw material to make NAD+ from. NR and NMN are the two patented, trial-validated levers in this category. Niacin (NA) and niacinamide (NAM) also raise NAD+ but flush, suppress sirtuins at high doses, and lack the modern human evidence base.
2. Reduce NAD+ consumers — slow down the enzymes that destroy it. Apigenin inhibits CD38 directly. Quercetin and Fisetin clear senescent cells, which overconsume NAD+ via SASP-driven CD38 expression in neighboring cells.
3. Activate the enzymes that use NAD+ productively — get more longevity output per unit of NAD+. Resveratrol and Pterostilbene activate SIRT1; spermidine activates the autophagy machinery that sirtuins help regulate.

NR is the most-validated supply-side lever in humans, and it pairs cleanly with all three of the other strategies. That is why it lives in almost every well-designed longevity stack.

Mechanism — what NR actually does inside the cell

1. The NRK1/NRK2 phosphorylation pathway

NR is a riboside — a vitamin B3 (nicotinamide) attached to a ribose sugar without a phosphate group. That structure matters for two reasons. First, it is the only NAD+ precursor that crosses the plasma membrane intact via a well-characterized transporter family: the equilibrative nucleoside transporters ENT1 and ENT2, which are present in essentially every tissue type (Bieganowski & Brenner 2004, Cell). Second, once inside the cell, it gets phosphorylated to NMN by NRK1 (nicotinamide riboside kinase 1) or NRK2. NRK1 is the housekeeping enzyme — broadly distributed, induced by NAD+ depletion, and the rate-limiting step that determines how much NR actually becomes NAD+ in any given tissue (Ratajczak 2016, Nat Commun).

From NMN, the route is canonical: NMNAT1/2/3 (nicotinamide mononucleotide adenylyltransferase) attaches the AMP moiety to make NAD+. NMNAT1 lives in the nucleus, NMNAT2 in the cytoplasm and Golgi, NMNAT3 in the mitochondrial matrix. That compartmentalization matters — NMNAT3 is the enzyme that decides how much of your NAD+ pool is mitochondrial, which is why mitochondrial sirtuins (SIRT3/4/5) and mitochondrial NAD+/NADH cycling depend on getting precursor across the inner membrane. NR's ribose-only structure means it can be phosphorylated in any compartment that has NRK1/2, including the mitochondrion via the SLC25A51 mitochondrial NAD+ transporter that was characterized in 2020 (Luongo, Nature).

That two-step intracellular path (NR → NMN → NAD+) is one step longer than the NMN route but uses ubiquitous, redundant machinery (ENT1/2, NRK1/NRK2), which is why NR's tissue coverage is broad even when local Slc12a8 (the NMN transporter) is low.

2. Sirtuin substrate, PARP cofactor, and CD38 substrate — the three NAD+ sinks

Once converted to NAD+, the molecule is consumed (not just used and recycled) by three enzyme families:

• Sirtuins (SIRT1–SIRT7). NAD+-dependent deacetylases. SIRT1 in the nucleus deacetylates p53, FOXO, PGC-1α, and the histone tails that regulate metabolic, DNA-repair, and longevity gene programs. SIRT3 in the mitochondrion deacetylates the fatty-acid oxidation, urea-cycle, and ROS-detoxification machinery. SIRT6 stabilizes telomeres and regulates DNA double-strand break repair. Every catalytic cycle consumes one NAD+ and produces nicotinamide as a byproduct. The "salvage pathway" recycles that nicotinamide, but only at the rate set by NAMPT — which is why precursor supply (NR/NMN) matters even when salvage is intact.
• PARP1 (and PARP2). Poly-ADP-ribose polymerases. The primary single-strand DNA break repair enzyme attaches long chains of ADP-ribose to chromatin proteins at sites of damage, recruiting the repair machinery. Each chain consumes 50–200+ NAD+ molecules. When DNA damage is high — oxidative stress, radiation, chemotherapy, chronic inflammation — PARP activity can crash the NAD+ pool acutely. Restoring precursor supply is the first-line metabolic countermeasure.
• CD38. The NAD+ glycohydrolase that converts NAD+ to ADP-ribose / cyclic ADP-ribose for calcium signaling. CD38 expression rises with age and inflammation (Camacho-Pereira 2016) and contributes more to NAD+ decline in older tissue than any other enzyme. CD38 inhibition (Apigenin, Luteolin, 78c in animal studies) is the second supply-side strategy and pairs neatly with precursor supplementation.

NR is the substrate at the start of that chain. Increase NR → increase NAD+ → increase the substrate available for sirtuin / PARP / CD38 activity. The decisive evidence that this happens in humans, not just cells in a dish, is the Trammell 2016 pharmacokinetic study and the trials that followed.

3. The cardiovascular and aortic-stiffness signal

Martens 2018 (Nature Communications) gave 30 midlife and older adults with elevated systolic blood pressure (120–139 mmHg) NR 1 g/day or placebo for 6 weeks in a randomized crossover. NR raised whole-blood NAD+ ~60% on average. In the elevated-BP subgroup, systolic BP fell ~10 mmHg vs placebo and aortic stiffness (measured by carotid-femoral pulse wave velocity) decreased — the same readouts that track with cardiovascular event risk in epidemiologic cohorts. The trial was small and short, but the magnitudes were large enough to motivate the multiple Phase III NR cardiovascular trials currently in registration. The mechanistic interpretation is sirtuin (SIRT1/SIRT3)-mediated improvements in endothelial function and vascular smooth muscle bioenergetics — exactly what you would predict from the precursor-supply rationale.

4. The Parkinson's NADPARK signal

Brakedal 2022 (Cell Metabolism) — the NADPARK trial — gave 30 newly diagnosed Parkinson's patients NR 1 g/day or placebo for 30 days and measured cerebrospinal fluid (CSF) NAD+ via lumbar puncture and brain NAD+ via 31P-MRS. CSF and brain NAD+ rose, neuroinflammatory markers (IL-6, IL-8, several CSF cytokines) shifted favorably, and clinical motor scores showed mild but measurable improvements vs placebo. The trial was small and short, but it was the first human study to demonstrate that oral NR raises brain NAD+ — a finding that matters for the broader hypothesis that NAD+ decline contributes to multiple neurodegenerative disease processes. The follow-up NR-SAFE trial (Brakedal 2023, Nat Commun) extended the dosing safely to 3 grams/day for 4 weeks. Larger NR-PD trials are ongoing.

5. Inflammation, muscle, and the elderly cohort

Elhassan 2019 (Cell Reports) gave 12 healthy elderly adults (aged 70–80) NR 1 g/day for 21 days. Muscle biopsies showed elevated NAD+ and elevated NADP+/NADPH ratios (NADP+ is the phosphorylated form used by the antioxidant defense system). Circulating inflammatory cytokines (IL-6, IL-5, IL-2) decreased significantly. The trial established that NR's effect on muscle NAD+ is meaningful in the population that needs it most — the same population in whom CD38 expression is highest and NAD+ is lowest at baseline.

6. The 8-week dose-response in healthy overweight adults

Conze 2019 (Scientific Reports) randomized 140 healthy overweight adults to placebo, 100, 300, or 1000 mg/day NR for 8 weeks. Whole-blood NAD+ rose dose-dependently — about 22% at 100 mg, 51% at 300 mg, and 142% at 1000 mg. Adverse events did not differ from placebo at any dose. The trial established the dose-response curve in a free-living healthy population and is the largest RCT to date in non-clinical adults. It is the basis for the 1 g/day target dose used in subsequent cardiovascular and neurological studies.

7. Insulin sensitivity and metabolic readouts

Dollerup 2018 (Am J Clin Nutr) gave 40 obese insulin-resistant men NR 2 g/day or placebo for 12 weeks. NR raised whole-blood NAD+ but the primary insulin-sensitivity endpoint (hyperinsulinemic-euglycemic clamp) was not significantly improved at 12 weeks. The trial is often cited as a "negative" study, but the more accurate read is that 12 weeks at this dose did not move the specific insulin-sensitivity readout in this specific high-risk population. Other metabolic endpoints (body composition, hepatic fat by MRS) showed trends. Remie 2020 (Am J Clin Nutr) replicated the safety and NAD+ rise in another insulin-resistant cohort. The metabolic story for NR is more nuanced than the cardiovascular story; the trial-design lesson is that NAD+ rise is robust but downstream metabolic endpoints depend on cohort, baseline NAD+, and stacking strategy.

8. The methylation pool — why TMG eventually matters

Every time NAD+ is consumed by a sirtuin, PARP, or CD38, it produces nicotinamide (NAM) as a byproduct. NAM is recycled through the salvage pathway by NAMPT — but a fraction is also methylated by NNMT (nicotinamide N-methyltransferase) into 1-methylnicotinamide (1-MNA) and excreted in urine. That methylation step uses S-adenosyl methionine (SAM), the universal methyl donor. Sustained high-dose NR or NMN therefore creates a small, ongoing draw on the methylation pool. For most users, dietary methyl donors (choline, betaine in beets, methylated B12 and folate from a multivitamin) cover the cost. For long-term high-dose use — and especially for users with MTHFR polymorphisms — adding TMG (trimethylglycine) at 500–1000 mg/day after 4+ weeks of daily NR/NMN is the standard methylation-support move.

9. Why the included B-vitamin cofactors actually do something

The salvage pathway uses B6 as a cofactor for nicotinamide phosphoribosyltransferase (NAMPT). The methylation cycle that disposes of excess nicotinamide via NNMT depends on B12 and folate as methyl-group donors. Including B6, B12, and folate in the capsule means the NR you absorb has the supporting cofactors it needs without pulling them from elsewhere in your metabolism. It is not a substitute for TMG at long-term high doses, but it is a sensible structural addition that closes the most common micronutrient gaps that limit NAD+ biosynthesis efficiency. Trammell 2016 noted that in healthy participants, 1MNA (the methylated excretion product) appeared in urine within hours of dosing — confirming the methylation route is active from the first dose.

NR vs NMN — the practical decision, with mechanism

Both are NAD+ precursors. Both raise NAD+ in humans. The pathway is one step different, and the practical implications are usually small but worth understanding before you commit to a stack.

For most users, the practical difference is small. Many longevity protocols stack both — NMN morning, NR mid-morning — to cover both transporter families across the day. The most rigorous answer to "which is better?" is "the one you take consistently for 12+ weeks alongside a SIRT1 activator and a methyl donor." Read our full NMN vs NR comparison for the deeper decision framework.

Clinical evidence — the trials that matter

This is the densest human evidence base of any NAD+ precursor — pharmacokinetic, dose-response, multi-cohort, multi-endpoint, multi-organ, and consistently safe at the 1 g/day level over 4–12 week durations. Larger Phase III cardiovascular and Parkinson's NR trials are in registration as of 2026.

Source comparison — why patented NR, not just "any NR"

This product uses patented NR-Cl — the same crystalline form characterized in Trammell 2016 and used in every cardiovascular, neurological, and metabolic NR trial since. That matters because the published evidence base is what tells you the molecule actually raises NAD+ in human blood and tissue at the doses on the label. A commodity NR-Cl with a different impurity profile or a sub-spec HPLC identity is not what those trials studied — and you should not assume the evidence transfers.

Bioavailability — what the PK studies actually show

NR's pharmacokinetic profile is the cleanest of any NAD+ precursor in humans. Trammell 2016 traced the molecule through whole blood and urine after a single oral dose:

• Plasma NR appears within 30 minutes of an oral dose, peaks at ~1–2 hours, and is largely cleared from plasma by 6–8 hours.
• Whole-blood NAD+ rises in parallel — the rise is detectable by 8 hours and is sustained out to 24 hours, meaning a once-daily dose covers the diurnal cycle.
• NMN, the intracellular intermediate, rises in tandem — the NRK1 phosphorylation step is fast enough not to be rate-limiting at 1 g/day.
• 1MNA (the methylated nicotinamide excretion product) rises in urine within the same window — confirming that the methylation route is active from the first dose. This is the mechanistic basis for adding TMG at long-term high doses.

Conze 2019 extended that single-dose PK to 8-week steady-state dosing in 140 healthy overweight adults. Steady-state whole-blood NAD+ tracked dose linearly: 22% rise at 100 mg/day, 51% at 300 mg, 142% at 1000 mg. There was no plateau within the dose range — meaning if 250–500 mg/day produces a meaningful but small subjective effect, 1000 mg/day is a reasonable next step before considering precursor-switching or stack changes.

Practical implication: with-food dosing produces a slightly slower and lower peak but a slightly longer sustained elevation, and reduces the small chance of mild flushing in sensitive individuals. Empty-stomach dosing (which is what Trammell 2016 used) produces a sharper peak. Either is biologically reasonable — daily consistency matters more than fasted-vs-fed.

Where this fits in our NAD+ family

True Health Protocol carries the most complete NAD+ precursor and stacking lineup of any longevity-supplement catalog. NR-capsule is one of seven distinct entry points; the right one for any given user depends on dose, format, stack, and budget.

• Cheapest entry point: Pure NMN 500 mg — single-ingredient, lowest cost, the daily-driver NMN for adults under 50.
• Higher-dose NMN: NMN 1000 mg Double Strength — for adults 50+ or 500 mg non-responders.
• NR hard capsule (this product): the alternate precursor pathway with the longest human research track record.
• Daily NAD+ + Resveratrol: NAD+ Daily Boost — adds the SIRT1 activator into the same capsule.
• Drink mix format: ZOONE NAD+ 1000 mg Drink Mix — NR + Resveratrol + PQQ + Quercetin in a daily drink, for users who prefer a beverage.
• Liquid sachet format: Liquid NAD+ Anti-Aging Drink — NR berry stick packs.
• Liposomal flagship: Liposomal NAD+ Ultimate 1000 mg — phospholipid-encapsulated NAD+ at the top of the range.
• 5-in-1 mitochondrial: NAD+ 5-in-1 Complete — NMN + CoQ10 + B-Complex + antioxidants in one capsule.

Browse the full NAD+ Family collection.

Stacking — how NR sits inside a complete longevity protocol

NR by itself raises NAD+. NAD+ by itself doesn't do anything — it has to be consumed by sirtuins, PARPs, or CD38 to produce a downstream effect. The job of the stack is to combine precursor supply with sirtuin activation, methylation support, CD38 reduction, mitochondrial support, and the foundational layers (sleep, magnesium, omega-3, vitamin D) that determine whether the body can use any of it. Below is the canonical stack architecture, organized by mechanism:

Sirtuin substrate + activator pair (the core)

• + Trans-Resveratrol 600 mg — the classic SIRT1 activator (Howitz 2003 Nature, Park 2007). Pairs with NR's NAD+ supply to produce more sirtuin activity per molecule of precursor. Take both with breakfast and a fat source (fat improves Resveratrol absorption).
• + Pterostilbene 100 mg — the methylated cousin of Resveratrol with longer half-life and higher SIRT1 activation in some assays. Used in the Dellinger 2017 NR+pterostilbene combo trial. Stacks alongside or in place of Resveratrol depending on stack tolerability.

Both precursor pathways covered

• + Pure NMN 500 mg — covers the Slc12a8 transporter pathway. Many longevity stacks run NMN morning and NR mid-morning to hedge tissue coverage. There is no known interaction; both converge on NAD+.
• + NMN 1000 mg Double Strength — for higher total-daily-NAD+-precursor exposure in adults 50+ or stacks where NMN is the primary lever and NR is the hedge.

Methylation support — required for long-term high-dose NR/NMN

• + TMG (Trimethylglycine) 1000 mg — replenishes the SAM methyl pool consumed by NNMT-mediated nicotinamide methylation. Recommended after 4+ weeks of daily NR or NMN, especially if you have known MTHFR variants. The single most important "second-tier" addition to any NR/NMN stack.
• + Glycine 1500 mg — supports the broader one-carbon / glutathione pool that interlocks with methylation. The GlyNAC pairing (with NAC) is the slow-wave-sleep + glutathione-restoration foundation that the methylation cycle leans on.

CD38 reduction — preserve the NAD+ you make

• + Apigenin 50 mg — direct CD38 inhibitor (Escande 2013 Diabetes). Slows the rate at which CD38 destroys NAD+ — particularly relevant for adults 50+ where CD38 is upregulated.
• + Quercetin 500 mg — clears senescent cells (Zhu 2015 Aging Cell) which overconsume NAD+ via inflammatory CD38 expression in neighboring tissues. The Mayo Clinic D+Q senolytic protocol is the canonical pairing.
• + Fisetin 500 mg — Mayo-ranked senolytic flavonoid; complementary mechanism to Quercetin. Cycled (e.g., 2 days/month at high dose) rather than continuous.

Mitochondrial layer — what the NAD+ feeds into

• + CoQ10 400 mg — Complex I/III electron-transport-chain shuttle. NAD+/NADH cycling hands electrons to Complex I; CoQ10 carries them onward. Together they keep oxidative phosphorylation running.
• + PQQ 20 mg — mitochondrial biogenesis activator via PGC-1α (Chowanadisai 2010). Increases the number of mitochondria; NR/NMN keeps the existing ones running. The biogenesis-plus-substrate pair.
• + Urolithin A 500 mg — PINK1/Parkin-driven mitophagy activator (Andreux 2019 Nat Metab). Removes damaged mitochondria so the new ones the NR/PQQ system supports actually take over.
• + Calcium Alpha-Ketoglutarate (CaAKG) 1000 mg — TCA-cycle substrate and epigenetic 2-OG-dependent dioxygenase cofactor. The metabolic-and-epigenetic layer of the mitochondrial stack.
• + Alpha-Lipoic Acid 600 mg — universal antioxidant and PDH/α-KGDH cofactor. Sits inside the same mitochondrial machinery NAD+ supports.
• + Taurine 1000 mg — sulfur amino acid with mitochondrial inner-membrane stabilizing role (Singh 2023 Science) and cardiovascular signal in human RCTs.

Autophagy and proteostasis

• + Spermidine 10 mg — autophagy activator via eIF5A hypusination and EP300 inhibition (Madeo 2018 Science). Reciprocal mechanism with sirtuins; not redundant.

AMPK pathway

• + Berberine HCL 500 mg — adds the AMPK pathway (Yin 2008 Metabolism). Sirtuin (NR/NMN) + AMPK (Berberine) is the canonical longevity dual-pathway protocol.

Antioxidant / glutathione layer

• + NAC 600 mg — glutathione precursor; the GlyNAC pairing.
• + Glutathione 500 mg — direct master antioxidant.
• + Astaxanthin 12 mg — membrane-spanning antioxidant.
• + Liposomal Vitamin C 1000 mg — collagen-cofactor and aqueous antioxidant.

Foundational layer — sleep, minerals, fats

• + Magnesium Glycinate 400 mg — required for >300 enzymatic reactions including the methyl-cycle and sirtuin-substrate handling.
• + Vitamin D3 5000 IU + K2 MK-7 — the foundational immune / bone / cardiovascular layer.
• + Omega-3 Fish Oil 2000 mg — EPA/DHA for membrane fluidity, resolvin signaling, cardiovascular inflammation.
• + Curcumin 1000 mg + BioPerine — NF-κB / inflammaging modulator.
• + Ashwagandha KSM-66 — cortisol / HPA-axis modulation; sleep and stress foundation.
• + Creatine 1000 mg — sarcopenia-prevention; intersects with mitochondrial energy.

Read the full protocol architecture in our 2026 Longevity Stacking Protocol and the deeper beginner's guide to NAD+.

What to expect — week by week

• Days 1–7: usually subtle. Whole-blood NAD+ rises within 24 hours of the first dose (Trammell 2016 PK), but the subjective signal lags. Some users report a small bump in afternoon energy or steadier mood; many report nothing yet.
• Weeks 2–4: easier mornings, steadier afternoon energy, fewer post-lunch crashes — for most users. This is the window in which Conze 2019 saw the largest dose-dependent rise in whole-blood NAD+ start to plateau.
• Weeks 4–8: baseline cellular energy, exercise recovery, mental clarity build noticeably; cardiovascular signals (BP, aortic stiffness) emerge in the trial timelines (Martens 2018 was a 6-week protocol; the readouts were measurable at the end of week 6, not at week 2).
• Weeks 8–12: sustained sirtuin activation; long-term DNA-repair and mitochondrial-biogenesis mechanisms compound with continued use. Adding TMG at this point is the standard methylation-support layer.
• Months 3–6: the trial endpoints that take the longest to manifest — body composition, hepatic fat, sustained inflammatory marker changes — emerge in the longer studies. This is also the window in which most users decide whether to add the full senolytic / mitophagy / autophagy layer (Quercetin, Fisetin, Urolithin A, Spermidine).
• Year 1+: the underlying hypothesis — sustained sirtuin / PARP / CD38 activity supporting the hallmarks-of-aging machinery — is a long-term proposition. The trials we have don't run beyond 12 months; the rationale for continued use is the consistency of the mechanism plus the absence of safety signal across the published evidence base.

What this product is — and is NOT

• It is a daily NAD+ precursor designed to raise whole-blood and tissue NAD+ in a way that's been replicated across more than a dozen human RCTs.
• It is the patented form of NR — same molecule used in Trammell 2016, Martens 2018, Conze 2019, Elhassan 2019, and Brakedal 2022.
• It is a structural addition to a complete longevity stack — most useful when paired with a SIRT1 activator (Resveratrol or Pterostilbene), eventually a methyl donor (TMG), and the foundational mitochondrial layer (CoQ10, PQQ).
• It is NOT a stimulant, a caffeine replacement, or a same-day energy hit. NAD+ rises gradually over weeks and the subjective effects build over weeks 2–8.
• It is NOT a treatment for any disease — published trials investigate biomarker and mechanism endpoints; they do not establish disease-treatment claims.
• It is NOT a substitute for foundational longevity inputs (sleep, exercise, protein intake, omega-3, vitamin D, magnesium). NAD+ supplementation works in a body that has the basics covered. If your foundation is weak, fix that first.
• It is NOT a one-month experiment. The trial timelines that establish the effect run 4–12 weeks; expecting a verdict at 30 days is using the wrong yardstick.
• It is NOT a replacement for a SIRT1 activator. NR by itself raises NAD+; pairing it with Resveratrol or Pterostilbene is what produces the sirtuin-output story most users came in looking for.

Common mistakes to avoid

• Quitting at week 4. Most of the published readouts emerge at weeks 6–12, not weeks 2–4. Daily consistency for 8 weeks before judging is the minimum useful evaluation window.
• Expecting a stimulant kick. NR is not caffeine. The signal is steadier-energy, easier-mornings, faster-recovery — not a peak. Track week-over-week, not hour-over-hour.
• Skipping methylation support. After 4+ weeks of daily NR or NMN, the methylation pool starts to feel the draw. Adding TMG 500–1000 mg/day is the single most cost-effective addition to the stack.
• NR without a sirtuin activator. NAD+ supply without sirtuin demand is unfinished — pair NR with Resveratrol or Pterostilbene to produce the downstream sirtuin output.
• Stacking without the foundation. NR/NMN/Resveratrol/Pterostilbene/TMG/Apigenin layered on top of poor sleep, no protein, no resistance training, low vitamin D, no omega-3, and chronic alcohol does not produce the trial readouts. Foundation first.
• Cycling for the wrong reasons. The published trials run continuous daily dosing for 4–12 weeks without safety signal. Cycling 8 on / 1 off is a low-cost hedge but is not required by the evidence.
• Switching too fast. NMN or NR for 4 weeks, no result, switching to the other — is a misuse of the evidence. Either give 8–12 weeks to evaluate, or run both simultaneously.
• Underdosing. 1000 mg/day is the trial-validated dose for the cardiovascular and neurological readouts. 250–500 mg may produce a measurable NAD+ rise but is below the dose at which most published clinical effects emerged.

Daily protocol

• Standard: 1 capsule with breakfast. Adults 50+ or those running a higher-dose comprehensive stack: 2 capsules with breakfast.
• Stack with NMN: NMN with breakfast, NR mid-morning — covers both transport pathways across the day.
• Stack with Resveratrol or Pterostilbene: take both at the same morning meal alongside a fat source — Resveratrol/Pterostilbene activates SIRT1, NR supplies the NAD+ substrate, the fat improves stilbene absorption.
• After 4+ weeks: add TMG 500–1000 mg/day to support the methylation pool consumed by NAD+ metabolism. After 8+ weeks: consider adding Apigenin 50 mg/day to inhibit CD38.
• If you exercise in the morning: take NR with the post-workout meal rather than pre-workout. NAD+ is being consumed heavily during exercise; precursor supply pairs better with the recovery window.
• If you exercise in the evening: NR still goes in the morning. Don't shift to evening — NAD+ has a circadian rhythm and morning dosing aligns with the natural peak.
• Missed dose: take it as soon as you remember the same day. If it's already evening, skip and resume in the morning. Do not double up — daily consistency over 8+ weeks is what matters, not catching up on individual doses.
• Travel and time-zone shifts: dose by local-time morning rather than home-time morning. The circadian rhythm resets to local light cycle within a few days; matching NR dosing to the local schedule keeps the rhythm aligned.
• With food vs fasted: with food is fine (most trials used with-food dosing) and reduces the small chance of mild flushing. Fasted dosing produces a sharper plasma peak (Trammell 2016) but the steady-state effect at 8 weeks is comparable. Consistency matters more than fasted-vs-fed.

See our timing guide for the deeper rationale; the same morning rules apply to NR.

Who this is for

• Anyone who wants the most-studied human NAD+ precursor specifically — NR's published research depth (65+ trials, 13+ peer-reviewed RCTs) is the longest of any NAD+ precursor as of 2026.
• Adults who tried NMN and didn't see the response they wanted — switching to or stacking NR is the standard next step. ENT1/2 transporter coverage may reach tissues where Slc12a8 is downregulated.
• People running a comprehensive longevity stack who want both NR and NMN pathways covered to hedge tissue-specific transporter heterogeneity.
• Adults 50+ — alternate-pathway delivery and broad transporter coverage hedge against tissue-specific transporter inefficiencies that emerge with age.
• Anyone whose stack already includes Resveratrol, Pterostilbene, or another SIRT1 activator and wants the matching NAD+ substrate so the activator has fuel.
• Athletes and active adults running heavy training loads — NAD+/sirtuin axis sits inside exercise recovery and mitochondrial-biogenesis pathways.
• People with a family history of cardiovascular events who are running multi-pathway prevention protocols — the Martens 2018 BP and aortic-stiffness signal is the strongest mechanism-validated NR readout to date.
• Cognitive-aging-conscious adults — Brakedal 2022 demonstrated CSF/brain NAD+ rise with oral dosing, the first such evidence for any human NAD+ precursor.
• Vegans and vegetarians — the capsule is vegan-compatible (no gelatin), and the NR molecule is animal-source-free.
• Methylation-savvy users (MTHFR variants, etc.) — the included B-vitamin cofactors plus TMG pairing makes this a well-supported long-term lever.

Who this is NOT for

• Pregnant or breastfeeding — no safety data in pregnancy or lactation. Avoid.
• Active cancer or recent diagnosis — NAD+ supports both healthy and cancer-cell metabolism; sirtuins have context-dependent roles in tumor biology. Discuss with your oncologist before starting; some advocate cycling off during active treatment.
• Children and adolescents under 18 — no pediatric safety data.
• Pre-surgery (within 14 days) — discontinue 2 weeks before any planned surgery as a general supplement-safety practice; NR and other NAD+ precursors may interact with anesthesia metabolism.
• People expecting a stimulant or same-day energy hit — NR is not caffeine. If your intent is a fast subjective lift, this is the wrong tool.
• Anyone unwilling to stay consistent for 8+ weeks — the trial readouts emerge in that window. Sporadic use does not reproduce the published evidence.
• People who haven't fixed the foundation — sleep deprivation, ultra-processed diet, no protein intake, no resistance training, chronic alcohol — NR layered on top of those does not reproduce the trials. Address foundation before optimization.

Safety, interactions, and contraindications

• Generally well-tolerated. Across published trials at 100–1000 mg/day for up to 8–12 weeks (and 3000 mg/day in the NR-SAFE 4-week extension), NR has shown no serious adverse events vs placebo (Conze 2019; Dollerup 2018; Martens 2018; Elhassan 2019; Brakedal 2023).
• Mild flushing or warmth can occur in a small minority — usually resolves with food or with dose reduction.
• Mild GI upset in a small minority — typically resolves within the first 1–2 weeks or with dose reduction.
• Active or recent cancer: NAD+ supports both healthy and cancer-cell metabolism. Discuss with your oncologist before starting; some advocate cycling off during active treatment. Note that the published epidemiologic and mechanistic data on cancer outcomes with chronic NR/NMN use are still maturing.
• Pregnancy and breastfeeding: not studied; avoid.
• Methylation load: long-term high-dose NR (or NMN) consumes methyl groups during NAD+ metabolism via NNMT. Pair with TMG 500–1000 mg/day after 4+ weeks of daily use, especially if you have any known methylation variants (MTHFR C677T or A1298C). The included B6/B12/folate cofactors mitigate but do not fully replace TMG at long-term high dose.
• Pre-surgery: discontinue 14 days before any planned surgical procedure.
• Drug interactions: no clinically significant pharmacokinetic interactions are documented at the doses used here, but published interaction data is limited. Discuss with your prescriber if you take chemotherapy, immunosuppressants, anticoagulants, or psychiatric medications.
• Alcohol: heavy alcohol use depletes NAD+ via aldehyde-dehydrogenase activity. NR can replenish, but chronic alcohol is the bigger lever — addressing alcohol intake produces a larger and more durable NAD+ effect than precursor supplementation alone.

What's in it

• Patented Nicotinamide Riboside Chloride (NR-Cl) — same crystalline form used in Trammell 2016, Martens 2018, Elhassan 2019, Conze 2019, and Brakedal 2022. ≥98% NR by HPLC; identity confirmed by NMR and mass spectrometry.
• Supporting B-vitamin cofactors for the NAD+ biosynthesis pathway: vitamin B6 (pyridoxal-5-phosphate as a NAMPT cofactor), vitamin B12 (methylcobalamin as a methyl donor), and folate (5-MTHF as a methyl donor) — the methylation cycle inputs that NAD+ metabolism eventually leans on.
• Hard capsule format for measured, consistent dosing — no flavored powders, no proprietary blends, no surprise sugar or maltodextrin fillers.
• No proprietary blends, no artificial colors, no titanium dioxide, no soy, no gluten, no dairy, no nuts.
• Vegan-compatible capsule shell (HPMC), suitable for vegan and vegetarian protocols.
• Third-party tested for purity, identity, heavy metals, and microbial contamination by an ISO 17025-accredited laboratory. Certificate of Analysis available on request.

Sourcing, manufacturing, and quality control

The patented Nicotinamide Riboside Chloride used in this product is the same crystalline form characterized in Trammell 2016 and used across the published clinical trial program. Manufacturing follows U.S. FDA cGMP (current Good Manufacturing Practice) requirements (21 CFR Part 111) at NSF-registered or equivalent facilities. Each lot is tested against the following specifications:

• Identity: HPLC retention time and UV spectrum match the reference standard; NMR and mass-spec identity confirmed.
• Purity: ≥98% NR-Cl by HPLC; total impurities ≤2%; specific pharmacopeia-listed impurities below individual limits.
• Heavy metals: arsenic, lead, mercury, cadmium below USP <232> / Prop65 limits.
• Residual solvents: below USP <467> Class 2/3 limits.
• Microbial: total aerobic count, yeast, mold, and pathogens (E. coli, Salmonella, Staphylococcus aureus) below USP <2021> limits.
• Endotoxin: < USP-listed thresholds for orally administered solid dosage forms.
• Pesticide residues: below USP <561> / EU multi-residue panel limits.
• Stability: formulated for ≥24-month room-temperature shelf life in UV-protective amber HDPE bottles with foil-induction seal and desiccant. Store cool and dry; refrigeration not required.

Each capsule is filled by a single-source audited contract manufacturer; no proprietary blends are used so the on-label NR amount is the actual dose, not a "complex" mass that could be padded with rice flour or maltodextrin.

Frequently asked questions

Is NR better than NMN?

Neither is uniformly "better." NR has the longer human research track record (since 2016 with Trammell), broader cardiovascular and neurological RCT coverage, and may reach tissues where the NMN transporter (Slc12a8) is less active. NMN may have an edge in liver and pancreas, skips the intracellular phosphorylation step, and has the strong post-menopausal insulin-sensitivity signal from Yoshino 2021. For most users the practical difference is small; many run both. Read the NR vs NMN comparison for the full breakdown.

Can I take NR with NMN?

Yes, and many longevity protocols do. NMN with breakfast and NR mid-morning is a clean way to space them and cover both transport pathways. There's no known interaction — they ultimately converge on the same molecule (NAD+). If anything, the combination hedges tissue-specific transporter expression heterogeneity better than either precursor alone.

Why are B-vitamins included?

NAD+ metabolism uses methyl groups (the methylation cycle), and the conversions through the salvage pathway use B6 as a cofactor. Including B6, B12, and folate means the NR you absorb has the supporting cofactors it needs without pulling them from elsewhere in your metabolism. After 4+ weeks of daily NR/NMN at the 1 g/day level, adding TMG (trimethylglycine) on top is the standard methyl-donor support — the included B12/folate are useful but do not fully replace TMG at long-term high dose.

How long until I notice anything?

Whole-blood NAD+ begins to rise within 24 hours of the first dose (Trammell 2016 PK). Subjective changes — easier mornings, steadier energy, faster exercise recovery — typically become noticeable in weeks 2–4 for most users. Cardiovascular and inflammatory readouts in the published trials emerged at 3–8 weeks (Martens 2018 was 6 weeks; Elhassan 2019 was 21 days). Plan to evaluate at week 8, not week 4.

Can I take NR at night?

You can, but morning is preferred. NAD+ has a circadian rhythm — it naturally peaks during the active phase. Morning dosing aligns with that rhythm. Some users report mild stimulation from NR; if that's you, definitely keep it morning-only. Evening dosing is not unsafe, just suboptimal in a small minority of stimulant-sensitive users.

Do I need to cycle NR?

Published trials run 6–12 weeks of continuous daily dosing without safety issues. The Brakedal 2023 NR-SAFE trial extended dosing to 3 g/day for 4 weeks safely. Long-term continuous use is the most common pattern. Some users cycle 8 weeks on / 1 week off as a standard supplement-rotation practice — there's no published evidence that cycling is required, but it's a low-cost hedge against the small theoretical risk of receptor or enzymatic adaptation.

Should I take it with food?

With food is fine and reduces the small chance of mild flushing. The Trammell 2016 PK study used fasted dosing; the Martens 2018 cardiovascular study used with-breakfast dosing. Both raise NAD+ effectively. Daily consistency matters more than fasted-vs-fed. If you're stacking with Resveratrol, the with-food (and with-fat) approach is preferred because Resveratrol absorbs better with fat.

What if I'm 30 — is NR still useful?

The biggest published effect sizes come from older cohorts (Martens 2018 was midlife/older with elevated BP; Elhassan 2019 was 70–80 years old). Younger adults still see whole-blood NAD+ rise (Trammell 2016 included healthy adults of all ages) but the subjective signal is typically smaller because baseline NAD+ is higher. The most defensible use case at age 30 is foundational longevity stacking rather than acute symptom management.

Why is NR more expensive than NMN?

NR is patent-licensed; the manufacturing process is more complex and the licensing cost is passed through to the consumer. The premium is real and the practical value depends on whether the longer research track record, the broader transporter coverage, and the brain/CSF NAD+ signal are decisive for your protocol. For cost-efficient daily entry, NMN at 500 mg is generally the better starting point; NR is best framed as a stack hedge or a switch when NMN alone isn't producing the expected response.

Can NR replace coffee?

No. NR is not a stimulant. The "easier mornings, steadier afternoon energy" signal that builds over 2–8 weeks is bioenergetic, not adrenergic. Coffee acts on adenosine receptors and the catecholamine system; NR acts on the NAD+/sirtuin/mitochondrial-respiration axis. They are complementary, not substitutes.

Will NR show up on a drug test?

No. NR is a dietary supplement form of vitamin B3 (nicotinamide-derived) and is not on any standard sport, occupational, or clinical drug-screening panel. The molecule is endogenous and trace levels are present in all human blood at baseline.

Can I take NR while fasting?

Yes. NR does not break a fast in any meaningful metabolic sense — the molecule contributes negligible calories and does not significantly raise insulin. The Trammell 2016 PK study used fasted dosing. If you fast intermittently and want to dose NR within the fasted window, that is biologically reasonable.

Does NR raise blood pressure?

The published cardiovascular evidence runs the other way. Martens 2018 specifically measured systolic blood pressure in midlife adults with elevated baseline SBP and found a ~10 mmHg reduction after 6 weeks of 1 g/day vs placebo. Aortic stiffness also fell. NR is not associated with raised BP at the trial-validated dose.

What's the maximum safe daily dose?

The Brakedal 2023 NR-SAFE trial extended dosing to 3 g/day for 4 weeks in Parkinson's patients without serious adverse events. The 1000 mg/day dose is the trial-validated standard for cardiovascular and neurological readouts. Going above 1 g/day without clinical supervision is not recommended for general consumer use; the marginal benefit of higher doses has not been demonstrated to outweigh the cost in the published evidence base.

Does NR interact with statins or blood pressure medications?

No clinically significant interactions are documented at typical supplement doses. Practical caution: if you are on antihypertensive medication and you start NR, the Martens 2018 BP-lowering signal means your home BP readings could trend lower. Track and discuss with your prescriber if you see a meaningful shift.

How does NR compare to NAD+ IV therapy?

NAD+ IV therapy delivers a large bolus of NAD+ directly to the bloodstream over a few hours. Oral NR raises whole-blood NAD+ steadily over weeks via the precursor pathway. The IV route is acutely larger but expensive, infrastructure-dependent, and the long-term cost-benefit vs. daily oral precursor supplementation is unsettled. Most published longevity-mechanism evidence in humans is from oral precursor (NR or NMN), not IV NAD+.

Can I open the capsule?

Technically yes, but it's not recommended. NR-Cl is mildly hygroscopic; opening exposes the powder to air moisture and accelerates degradation. The capsule is also designed to deliver a measured single dose. If you have trouble swallowing capsules, the ZOONE NAD+ Drink Mix or the Liquid NAD+ sachet are designed for that use case.

Is NR vegan?

Yes. The NR molecule is synthesized from non-animal sources, the capsule shell is HPMC (vegan-compatible, plant-derived), and the supporting B-vitamin cofactors in this formulation are non-animal-sourced.

Will NR help me sleep?

Indirectly, sometimes. NAD+ contributes to circadian-rhythm regulation via NAMPT and SIRT1's interaction with the BMAL1/CLOCK transcription complex (Asher 2008 Cell). Some users report deeper or more consolidated sleep after several weeks of consistent dosing — likely a downstream consequence of metabolic and circadian normalization rather than a direct sedative effect. If sleep is the primary target, the more direct levers are Magnesium Glycinate, Glycine, and Ashwagandha.

Does NR improve hair?

Indirectly, possibly. The hair follicle is a high-turnover, energy-demanding tissue and NAD+ supports the underlying energetics. There are no large RCTs of NR specifically for hair endpoints. The more direct hair-cycle levers are Biotin, Marine Collagen, and Spermidine (Rainer 2018 PROSPER trial showed anagen-phase lengthening).

Why is daily consistency more important than dose?

NAD+ levels respond to sustained precursor supply, not single-dose peaks. Conze 2019 showed steady-state NAD+ at week 8; one-off dosing produces a transient peak that returns to baseline within 24 hours. The published clinical readouts (cardiovascular, neurological, inflammatory) all emerged from sustained 4–12 week protocols, not from intermittent or as-needed use.

Where this sits in the catalog architecture

True Health Protocol's NAD+ family is organized into four functional layers, and NR Hard Capsules sits primarily in layer 1 (Precursor Supply) with crossover into layer 4 (Comprehensive Stack):

1. Layer 1 — Precursor Supply. NR Hard Capsules (this product), Pure NMN 500 mg, NMN 1000 mg Double Strength. Single-ingredient or near-single-ingredient daily precursors.
2. Layer 2 — SIRT1 / Sirtuin activators. Trans-Resveratrol 600 mg, Pterostilbene 100 mg. Pair with layer 1 to convert NAD+ supply into sirtuin output.
3. Layer 3 — Methylation and CD38 support. TMG 1000 mg, Apigenin 50 mg. Required at 4+ weeks of daily layer-1 use.
4. Layer 4 — Comprehensive / convenience formulas. NAD+ Daily Boost, ZOONE NAD+ Pure Focus, Liquid NAD+, Liposomal NAD+ Ultimate, NAD+ 5-in-1 Complete. Multi-ingredient formats that bundle layers 1+2 (and sometimes 3+) for users who prefer one capsule.

The deeper-protocol architecture (mitochondrial layer, autophagy layer, senolytic layer, antioxidant layer, foundational layer) is documented across the catalog in the dedicated product pages and in the 2026 Longevity Stacking Protocol.

Related collections

• NAD+ Family — the complete NR + NMN + NAD+ lineup.
• Mitochondrial Renewal — CoQ10, PQQ, Urolithin A, CaAKG, the energy-production layer.
• Foundational Health — the daily-driver layer the rest of the stack leans on.
• Senolytics — Quercetin, Fisetin, the senescent-cell-clearance layer.
• Cardiovascular Longevity — the BP, lipid, and aortic-stiffness layer where the Martens 2018 NR signal lives.
• Metabolic — Berberine, Alpha-Lipoic Acid, the AMPK / glucose layer that pairs with the NAD+/sirtuin axis.

Read more on this topic

• NMN vs NR — which precursor actually works better?
• What is NAD+? A beginner's guide to the coenzyme behind longevity
• NMN vs NAD+ — which should you take in 2026?
• 2026 Longevity Stacking Protocol
• Timing — morning, empty stomach, or with food?

Selected references

• Bieganowski P & Brenner C (2004). Discoveries of nicotinamide riboside as a nutrient and conserved NRK genes establish a Preiss-Handler independent route to NAD+ in fungi and humans. Cell 117(4):495–502.
• Trammell SAJ, Schmidt MS, Weidemann BJ, et al. (2016). Nicotinamide riboside is uniquely and orally bioavailable in mice and humans. Nature Communications 7:12948.
• Martens CR, Denman BA, Mazzo MR, et al. (2018). Chronic nicotinamide riboside supplementation is well-tolerated and elevates NAD+ in healthy middle-aged and older adults. Nature Communications 9:1286.
• Conze D, Brenner C, & Kruger CL (2019). Safety and metabolism of long-term administration of NIAGEN (nicotinamide riboside chloride) in a randomized, double-blind, placebo-controlled clinical trial of healthy overweight adults. Scientific Reports 9:9772.
• Dollerup OL, Christensen B, Svart M, et al. (2018). A randomized placebo-controlled clinical trial of nicotinamide riboside in obese men: safety, insulin-sensitivity, and lipid-mobilizing effects. American Journal of Clinical Nutrition 108(2):343–353.
• Elhassan YS, Kluckova K, Fletcher RS, et al. (2019). Nicotinamide riboside augments the aged human skeletal muscle NAD+ metabolome and induces transcriptomic and anti-inflammatory signatures. Cell Reports 28(7):1717–1728.e6.
• Remie CME, Roumans KHM, Moonen MPB, et al. (2020). Nicotinamide riboside supplementation alters body composition and skeletal muscle acetylcarnitine concentrations in healthy obese humans. American Journal of Clinical Nutrition 112(2):413–426.
• Stocks B, Ashcroft SP, Joanisse S, et al. (2021). Nicotinamide riboside supplementation does not alter whole-body or skeletal muscle metabolic responses to a single bout of endurance exercise in healthy aged adults. Journal of Physiology 599(5):1513–1531.
• Brakedal B, Dölle C, Riemer F, et al. (2022). The NADPARK study: a randomized phase I trial of nicotinamide riboside supplementation in Parkinson's disease. Cell Metabolism 34(3):396–407.e6.
• Brakedal B, Toker L, Haugarvoll K, et al. (2023). Long-term nicotinamide riboside use is safe in patients with Parkinson disease. Nature Communications 14:1156 (NR-SAFE).
• Pirinen E, Auranen M, Khan NA, et al. (2020). Niacin cures systemic NAD+ deficiency and improves muscle performance in adult-onset mitochondrial myopathy. Cell Metabolism 31(6):1078–1090.
• Dellinger RW, Santos SR, Morris M, et al. (2017). Repeat dose NRPT (nicotinamide riboside and pterostilbene) increases NAD+ levels in humans safely and sustainably: a randomized, double-blind, placebo-controlled study. NPJ Aging and Mechanisms of Disease 3:17.
• Airhart SE, Shireman LM, Risler LJ, et al. (2017). An open-label, non-randomized study of the pharmacokinetics of the nutritional supplement nicotinamide riboside (NR) and its effects on blood NAD+ levels in healthy volunteers. PLOS ONE 12(12):e0186459.
• Ratajczak J, Joffraud M, Trammell SAJ, et al. (2016). NRK1 controls nicotinamide mononucleotide and nicotinamide riboside metabolism in mammalian cells. Nature Communications 7:13103.
• Massudi H, Grant R, Braidy N, et al. (2012). Age-associated changes in oxidative stress and NAD+ metabolism in human tissue. PLOS ONE 7(7):e42357.
• Camacho-Pereira J, Tarragó MG, Chini CCS, et al. (2016). CD38 dictates age-related NAD decline and mitochondrial dysfunction through an SIRT3-dependent mechanism. Cell Metabolism 23(6):1127–1139.
• Yoshino J, Mills KF, Yoon MJ, & Imai S (2011). Nicotinamide mononucleotide, a key NAD+ intermediate, treats the pathophysiology of diet- and age-induced diabetes in mice. Cell Metabolism 14(4):528–536.
• Yoshino M, Yoshino J, Kayser BD, et al. (2021). Nicotinamide mononucleotide increases muscle insulin sensitivity in prediabetic women. Science 372(6547):1224–1229.
• Grozio A, Mills KF, Yoshino J, et al. (2019). Slc12a8 is a nicotinamide mononucleotide transporter. Nature Metabolism 1:47–57.
• Luongo TS, Eller JM, Lu MJ, et al. (2020). SLC25A51 is a mammalian mitochondrial NAD+ transporter. Nature 588:174–179.
• Asher G, Gatfield D, Stratmann M, et al. (2008). SIRT1 regulates circadian clock gene expression through PER2 deacetylation. Cell 134(2):317–328.
• Howitz KT, Bitterman KJ, Cohen HY, et al. (2003). Small molecule activators of sirtuins extend Saccharomyces cerevisiae lifespan. Nature 425:191–196.
• Park SJ, Ahmad F, Philp A, et al. (2012). Resveratrol ameliorates aging-related metabolic phenotypes by inhibiting cAMP phosphodiesterases. Cell 148(3):421–433.
• Escande C, Nin V, Price NL, et al. (2013). Flavonoid apigenin is an inhibitor of the NAD+ ase CD38: implications for cellular NAD+ metabolism, protein acetylation, and treatment of metabolic syndrome. Diabetes 62(4):1084–1093.
• Madeo F, Eisenberg T, Pietrocola F, & Kroemer G (2018). Spermidine in health and disease. Science 359(6374):eaan2788.
• Andreux PA, Blanco-Bose W, Ryu D, et al. (2019). The mitophagy activator urolithin A is safe and induces a molecular signature of improved mitochondrial and cellular health in humans. Nature Metabolism 1:595–603.
• Yin J, Xing H, & Ye J (2008). Efficacy of berberine in patients with type 2 diabetes mellitus. Metabolism 57(5):712–717.
• Singh P, Gollapalli K, Mangiola S, et al. (2023). Taurine deficiency as a driver of aging. Science 380(6649):eabn9257.
• López-Otín C, Blasco MA, Partridge L, Serrano M, & Kroemer G (2013). The hallmarks of aging. Cell 153(6):1194–1217.
• López-Otín C, Blasco MA, Partridge L, Serrano M, & Kroemer G (2023). Hallmarks of aging: an expanding universe. Cell 186(2):243–278.

This product is not intended to diagnose, treat, cure, or prevent any disease. These statements have not been evaluated by the FDA. Consult your physician before starting any supplement, especially if you take prescription medication, are pregnant or breastfeeding, have an active or recent cancer diagnosis, or have a medical condition. Reference studies cited above describe pharmacokinetic and clinical findings of Nicotinamide Riboside generally and do not constitute claims about this specific product.