DISCOVER

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At the heart of every cell lies NAD+: a tiny powerhouse built from nucleotides, serving so many vital functions in the body that without it we would not survive. NAD+ levels naturally decline with age, and replenishment is the key to anti-aging on a cellular level. Here's the breakthrough: NAD+ must turn into NADH (Nicotinamide Adenine Dinucleotide + Hydrogen) to directly fuel mitochondrial energy production. While NAD+ takes time to convert into energy, NADH, already bound to a hydride (a hydrogen atom carrying an electron), delivers instant energy straight to your mitochondria, the power plants of your cells. Our formula directly replenishes your cells’ energy source for optimal anti-aging benefits.

Our patented wellness supplement features 100 mg of 99.99% pure NADH and 0.1 mg of B12. Compounded in a U.S. pharmacy using GRAS-recognized ingredients, each batch meets rigorous FDA-registered facility standards, cGMP protocols, and undergoes third-party testing to ensure purity, potency, and compliance with state and federal regulations.

NAD+ precursors (NR, NMN) face FDA restrictions due to their status as potential drugs, especially in compounded or high-dose forms. NADH is the reduced, bioactive form of NAD+, not a precursor like NR or NMN. It doesn’t require metabolic conversion to be effective, which simplifies its regulatory profile. The FDA focuses more on precursors due to their novel status and drug-like claims, whereas NADH’s established role in metabolism reduces scrutiny. NADH bypasses precursor conversion, allowing it to remain accessible as a wellness supplement.

NAD+ is like raw material—your body must convert it into NADH, losing 80–90% along the way. Just 25mg of NADH outperforms 1,000mg of NAD+. Already active in the electron transport chain, NADH delivers instant cellular energy.

Research shows that low doses of NADH enhance cognitive function, stamina, and cellular repair faster than high-dose NAD+ drips, which hit a mitochondrial saturation limit. Our formula is designed for precision—delivering exactly what your cells need.

NADH drives ATP synthesis at the mitochondrial level and supports cellular repair through redox balance. Vitamin B12 complements this by promoting red blood cell function and oxygen transport, while also playing a key role in DNA synthesis and nerve regeneration. Together, they deliver more efficient, sustained cellular energy — combating fatigue and supporting overall vitality more effectively than either nutrient alone.

NADH enhances neurotransmitter synthesis (including dopamine and serotonin), while B12 preserves myelin integrity — a critical factor for healthy nerve signaling. This synergistic pairing supports both the chemical and structural foundations of brain health, promoting sharper focus, balanced mood, and lasting mental clarity.

Study: Forsyth et al. "Therapeutic effects of oral NADH on the symptoms of patients with chronic fatigue syndrome." Annals of Allergy, Asthma & Immunology, 82(2), 185–191.

Details: This clinical study administered 25mg of intravenous NADH daily for 10–14 days to patients with chronic fatigue syndrome. Results showed 61.7% of patients (21/34) experienced significant improvement in disability scores (>30%), including cognitive function and physical stamina, due to NADH’s role in enhancing ATP production via the electron transport chain.
Link: https://pubmed.ncbi.nlm.nih.gov/10071523/
Relevance: Supports the claim that low-dose NADH (25mg) enhances cognitive function and stamina efficiently.

Source: Xiao et al. "NAD(H) and NADP(H) Redox Couples and Cellular Energy Metabolism." Antioxidants & Redox Signaling, 28(3), 251–272.
Details: This review explains NADH’s direct role in ATP production via the electron transport chain (~2.5 ATP per NADH molecule) and its support for cellular repair processes like DNA repair and protein synthesis. It highlights NADH’s efficiency as the reduced, bioactive form compared to NAD+, which requires energy-intensive conversion.
Link: https://www.liebertpub.com/doi/10.1089/ars.2017.7216

Relevance: Underpins NADH’s role in cellular repair and its superior efficiency over NAD+ for immediate energy needs.

Source: Rajman et al. "Therapeutic Potential of NAD-Boosting Molecules: The In Vivo Evidence." Cell Metabolism, 27(3), 529–547.
Details: This review discusses NAD+ supplementation, including IV drips, and notes that mitochondrial NAD+ uptake is limited by transporter capacity, leading to saturation and breakdown into metabolites like nicotinamide. High doses (e.g., 500–1,000mg) show benefits over weeks but are less efficient due to metabolic losses.
Link: https://www.cell.com/cell-metabolism/fulltext/S1550-4131(18)30094-6
Relevance: Supports the claim that high-dose NAD+ drips face mitochondrial saturation, reducing efficiency compared to NADH.

Source: Ying, W. "NAD+/NADH and NADP+/NADPH in Cellular Functions and Cell Death: Regulation and Biological Consequences." Antioxidants & Redox Signaling, 10(2), 179–206.
Details: This study highlights NADH’s critical role in mitochondrial ATP production and redox balance, particularly under stress. Low doses of NADH enhance mitochondrial function and resilience, supporting stamina and cellular repair without overloading cellular pathways.
Link: https://www.liebertpub.com/doi/10.1089/ars.2007.1672
Relevance: Reinforces NADH’s rapid, direct impact on mitochondrial function, supporting the claim of faster efficacy.

Source: Belenky et al. "NAD+ Metabolism in Health and Disease." Trends in Biochemical Sciences, 32(1), 12–19.
Details: This review outlines NAD+’s conversion to NADH for ATP production, noting that 80–90% of NAD+ is lost due to inefficiencies in enzymatic processing and mitochondrial transport. NADH’s direct role in the electron transport chain makes it more effective for immediate energy needs, aligning with clinical findings on low-dose NADH’s rapid effects.
Link: https://www.sciencedirect.com/science/article/pii/S0968000406002517
Relevance: Supports the claim that NADH is more efficient than NAD+ due to its direct bioavailability, avoiding conversion losses.