Quick Comparison
| CDP-Choline | NMN (Nicotinamide Mononucleotide) | |
|---|---|---|
| Half-Life | 56-71 hours (long elimination half-life) | 2-3 minutes in blood (rapidly converted to NAD+). NAD+ half-life: 1-2 hours in tissue |
| Typical Dosage | Standard: 250-500 mg daily in 1-2 doses. Clinical (stroke/cognitive decline): 500-2000 mg daily. Most nootropic users find 250-500 mg sufficient. | Standard: 250-1000 mg daily. Sublingual may improve bioavailability by bypassing first-pass metabolism. Take in the morning — NAD+ follows circadian rhythm and morning supplementation aligns with natural peaks. Effects build over weeks. |
| Administration | Oral (capsules, tablets). Very well-absorbed with nearly 100% oral bioavailability. | Oral (capsules, powder, sublingual). Sublingual may improve bioavailability. Store in cool, dry place. |
| Research Papers | 10 papers | 10 papers |
| Categories |
Mechanism of Action
CDP-Choline
CDP-Choline is hydrolyzed by nucleotidases and phosphatases into choline and cytidine after oral ingestion. Choline enters the acetylcholine synthesis pathway via choline acetyltransferase. Cytidine is phosphorylated to CTP and converted to uridine monophosphate (UMP), which enters the Kennedy pathway and stimulates the synthesis of phosphatidylcholine via the enzyme CTP:phosphocholine cytidylyltransferase — phosphatidylcholine is a critical component of neuronal cell membranes and synaptic vesicles. This dual mechanism simultaneously boosts neurotransmitter production and repairs membrane damage from oxidative stress or ischemia. CDP-Choline also increases dopamine D2 receptor density in the striatum and enhances dopamine release. It may modulate glutamate excitotoxicity and support mitochondrial function.
NMN (Nicotinamide Mononucleotide)
NMN is transported into cells via the Slc12a8 transporter (highly expressed in the small intestine and brain) and converted to NAD+ by nicotinamide mononucleotide adenylyltransferases (NMNAT1 in the nucleus, NMNAT2 in axons/Golgi, NMNAT3 in mitochondria). Elevated NAD+ activates the sirtuin family of NAD+-dependent protein deacetylases: SIRT1 deacetylates PGC-1alpha to promote mitochondrial biogenesis, SIRT3 activates superoxide dismutase 2 (SOD2) and isocitrate dehydrogenase 2 (IDH2) for mitochondrial antioxidant defense, and SIRT6 promotes base excision repair of oxidative DNA damage. NAD+ is also consumed by poly(ADP-ribose) polymerases (PARP1/2) during DNA repair — age-related NAD+ depletion impairs PARP function, allowing DNA damage accumulation. In neurons, NAD+ is required for glycolysis (GAPDH cofactor), the TCA cycle, and Complex I of the electron transport chain, directly fueling the enormous ATP demands of synaptic transmission. NAD+ decline with aging (approximately 50% reduction between ages 40-60) reduces all of these processes simultaneously, creating a cascade of mitochondrial dysfunction, impaired DNA repair, and neuroinflammation that NMN supplementation aims to reverse.
Risks & Safety
CDP-Choline
Common
Headache, nausea, diarrhea, insomnia.
Serious
Very safe — extensive clinical safety data.
Rare
Blurred vision, chest pain, allergic reactions.
NMN (Nicotinamide Mononucleotide)
Common
Mild flushing, nausea, headache initially.
Serious
Long-term human safety data still limited (first human trials completed 2020-2023). Theoretical concern about promoting cancer growth in existing tumors (NAD+ fuels fast-growing cells).
Rare
Insomnia if taken late.
Full Profiles
CDP-Choline →
Also known as Citicoline, this is a naturally occurring compound that provides both choline and cytidine (which converts to uridine in the body). This dual action supports both acetylcholine synthesis and cell membrane repair, making it both a cognitive enhancer and a neuroprotectant. Prescribed in many countries for stroke recovery and cognitive decline.
NMN (Nicotinamide Mononucleotide) →
A direct precursor to NAD+ (nicotinamide adenine dinucleotide), a coenzyme essential for cellular energy production, DNA repair, and sirtuin activation. NAD+ levels decline 50% between ages 40 and 60, contributing to age-related cognitive decline and neurodegeneration. NMN supplementation restores NAD+ levels and improves mitochondrial function, memory, and neuroplasticity in animal models.