NAD+ precursors
Nicotinamide riboside (NR) and nicotinamide mononucleotide (NMN)
Not peptides, but included because they are the most human-tested way to support the same mitochondrial pathway the peptides above target.
Last reviewed · 1 references
How it works
NAD+ is the electron carrier at the centre of energy metabolism and the required substrate for sirtuins and PARPs. Its levels decline substantially with age. Oral NR and NMN reliably raise blood NAD+ levels in humans — that part is settled. Whether raising the level produces a felt clinical benefit is the contested question.
Human trials. Tested in controlled human trials. Still read the sample sizes — many are small.
What the research reports
- Multiple human RCTs confirming increased blood NAD+ levels
- Good safety profile across trials at commonly used doses
- Some improvement in muscle mitochondrial markers in older adults
What it has not been shown to do
- Consistent improvement in energy, mood or cognition in healthy adults
- Anti-ageing claims are not supported by human outcome data
- Effect on depression is untested
Dosing reference
Human trials commonly use 250–1000 mg/day of NR or NMN orally.
Calculate my dose for NAD+ precursors- Routes studied
- Oral, Subcutaneous
- Half-life
- Oral dosing raises NAD+ over hours; tissue effects accumulate over weeks
- Cycle length in the literature
- Trials run continuously for 8–12 weeks or longer
Working out a draw volume from a vial? Use the free reconstitution calculator.
Side effects and contraindications
Reported side effects
- Nausea
- Flushing (more with high-dose niacin than with NR/NMN)
- Mild GI upset
Do not use if
- Pregnancy and breastfeeding
- Active cancer — NAD+ metabolism is relevant to tumour biology; discuss with an oncologist
The practice that shares the mechanism
Raising the substrate does nothing if the demand signal is absent. NAD+ is consumed by sirtuins during metabolic stress — exercise and fasting create the demand that makes the substrate useful.
What amplifies it
- Exercise creates the NAD+ demand
- Sleep — NAD+ metabolism is strongly circadian
- Alcohol depletes NAD+ directly
Mechanism hubs
Stacks that include it
- Cognitive clarityA plasticity-first approach to fog and flat focus: what the BDNF compounds do, what they cannot do alone, and the practice that fills the window.
- Mitochondrial resetFor flatness and fatigue that sleep does not fix: the three distinct mitochondrial mechanisms, and which compounds hit which.
- Mood & motivationFor anhedonia and flat drive: the inflammation and plasticity angles, and why the practice half carries most of the weight here.
- Recovery & nervous systemFor the flatness of early recovery: what the dopamine baseline is doing, the limited peptide research, and the practices that carry it.
Common questions
- Because it targets the same pathway with far better human evidence, and pretending otherwise would be dishonest. If the goal is mitochondrial support, NAD+ precursors are the boring, well-tested option that belongs in the conversation.
Sources & evidence notes
Tested in controlled human trials. Still read the sample sizes — many are small.
Confidence score 20/100
Preliminary
Mechanism only. Nothing here establishes that a person would feel anything.
- 1.
Nature Communications, 2018 · Source (opens in a new tab)
Human trialModerate gradeHuman data, but open-label, uncontrolled, or from a single group.