NAD+
NAD+Important information. The data compiled from scientific literature is provided for educational purposes. Dosage ranges reflect what is reported in studies and do not constitute a recommendation, prescription, or usage guidance. Health decisions should always be made with a qualified professional.
Peptide Interactions
Works exceptionally well with this peptide
NAD+ precursors increase intracellular NAD+ biosynthesis and can amplify the intended effect of exogenous NAD+ on cellular redox and sirtuin-dependent pathways.
Sirtuin activators act on NAD+-dependent deacetylases and may enhance downstream metabolic and mitochondrial benefits when NAD+ availability is increased.
CoQ10 supports mitochondrial electron transport and may synergize with NAD+-driven improvements in mitochondrial function and cellular energy metabolism.
Omega-3s support mitochondrial health and anti-inflammatory pathways and can complement NAD+-mediated metabolic and cell-survival effects.
All interaction categories
Synergistic (4)
- Nicotinamide riboside (NR) / Nicotinamide mononucleotide (NMN): NAD+ precursors increase intracellular NAD+ biosynthesis and can amplify the intended effect of exogenous NAD+ on cellular redox and sirtuin-dependent pathways.
- Sirtuin activators (e.g., resveratrol, pterostilbene): Sirtuin activators act on NAD+-dependent deacetylases and may enhance downstream metabolic and mitochondrial benefits when NAD+ availability is increased.
- Coenzyme Q10 (ubiquinone): CoQ10 supports mitochondrial electron transport and may synergize with NAD+-driven improvements in mitochondrial function and cellular energy metabolism.
- Omega-3 fatty acids (EPA/DHA): Omega-3s support mitochondrial health and anti-inflammatory pathways and can complement NAD+-mediated metabolic and cell-survival effects.
Compatible (4)
- Vitamin D: Vitamin D supplementation has a neutral co-administration profile with NAD+ and does not require specific adjustment or monitoring.
- Standard multivitamin (excluding high-dose niacin): Routine multivitamin formulations are generally compatible with NAD+ therapy provided they do not contain pharmacologically high doses of NAD+ precursors or niacin.
- Magnesium (oral or IV formulations): Magnesium is frequently co-administered for general metabolic support and poses no known direct interaction with NAD+ supplementation.
- Paracetamol (acetaminophen): Paracetamol has no established pharmacodynamic interaction with NAD+ at therapeutic doses and is compatible for symptomatic analgesia/antipyresis.
Monitor (4)
- PARP inhibitors (e.g., olaparib, niraparib): PARP enzymes consume NAD+ during DNA repair, so co-administration can alter NAD+ dynamics and may require monitoring of clinical efficacy and adverse effects.
- Metformin: Metformin modifies cellular NAD+/NADH ratios via AMPK and mitochondrial effects, so glycaemic control and tolerance should be monitored when combined with NAD+ therapy.
- Antidiabetic agents (insulin, sulfonylureas): Because NAD+ can influence insulin sensitivity and cellular metabolism, glucose levels and antidiabetic dosing should be monitored to avoid hypoglycaemia or dosing mismatch.
- CD38-targeting therapies (e.g., daratumumab): CD38 modulates NAD+ catabolism, so concurrent use with NAD+ supplementation may alter pharmacodynamics and warrants monitoring of therapeutic response and immune-related adverse events.
Avoid (4)
- High‑dose niacin (nicotinic acid): High-dose niacin increases NAD+ precursor load and carries hepatotoxicity and flushing risks, so clinicians should evaluate cumulative NAD+ precursor exposure and liver function before combining.
- Ethanol (alcohol): Chronic or heavy alcohol use disrupts NAD+/NADH balance and increases hepatic stress, so combining with NAD+ supplementation requires careful assessment of liver function and alcohol intake.
- Active chemotherapy (cytotoxic agents): Cytotoxic chemotherapy can perturb cellular NAD+ metabolism and organ function, so NAD+ use should be carefully evaluated for potential effects on treatment efficacy and toxicity.
- Severe hepatic impairment: Because NAD+ precursors and related metabolism involve hepatic processing, clinicians should exercise caution and consider dose modification or avoidance in patients with significant liver dysfunction.