Insomnia is a common sleep disorder, affecting approximately 30% of the global population to varying degrees. Today, we explore the mechanisms of action through which NMN (nicotinamide mononucleotide) improves sleep quality.
01 Regulating the Circadian Rhythm
The human circadian rhythm is crucial for regulating the sleep-wake cycle. NMN can increase NAD+ (nicotinamide adenine dinucleotide) levels in the body, thereby influencing the expression and regulation of circadian rhythm genes.
NAD+ participates in various intracellular metabolic processes and serves as a key coenzyme for deacetylases such as SIRT1.
SIRT1 can perform deacetylation modification on circadian rhythm proteins, regulating the regularity of the circadian rhythm to make it more stable and consistent. This in turn helps adjust the sleep-wake cycle, aligning the times of falling asleep and waking up with the natural physiological rhythm.
02 Promoting Neurotransmitter Balance
Neurotransmitters such as gamma-aminobutyric acid (GABA) and serotonin play a key role in regulating sleep.
By improving cellular metabolism and energy levels, NMN supports the normal function of nerve cells, which helps maintain the balance of neurotransmitter synthesis, release, and metabolism.
Mechanism of Action
For example, NMN may promote the synthesis of GABA or enhance the function of its receptors. As an inhibitory neurotransmitter, GABA calms the nervous system, reduces the excitability of neural activity, and thus induces a relaxed state in the body—facilitating falling asleep and maintaining sleep.
(Note on related molecules: Vigabatrin (VGB); Glutamate; GABA; GAD (glutamate decarboxylase); GABA-T (GABA transaminase); SSADH (succinic semialdehyde dehydrogenase); Succinic semialdehyde; Alpha-ketoglutarate)
03 Reducing Oxidative Stress and Inflammation
Oxidative stress and inflammatory responses are closely associated with decreased sleep quality. NMN exhibits antioxidant effects, which can lower intracellular oxidative stress levels, reduce the production of free radicals, and minimize cell damage.
At the same time, it can inhibit inflammatory signaling pathways and decrease the expression and release of inflammatory factors.
(Note on related molecules: ROS (reactive oxygen species); Transferrin; Transferrin receptor; IREG1 (iron-regulated protein 1); Fenton reaction; Ferritin; MT-III (metallothionein-III); Labile Iron Pool; IRP-1 (iron regulatory protein 1); DMT1 (divalent metal transporter 1); SOD (superoxide dismutase); Lysosome; Endosome; Carbon nanotubes coated vesicle; Nucleus; Mitochondrion)
When the body is in a state of low oxidative stress and low inflammation, the nervous system and various organs can rest and recover better—leading to improved sleep quality, characterized by fewer nighttime awakenings and deeper sleep.
04 Improving Mitochondrial Function
During sleep, the body’s cells rely on healthy mitochondrial function to carry out activities such as energy storage and metabolic waste clearance.
NMN can increase intracellular NAD+ levels, activate genes and signaling pathways related to mitochondrial function, promote mitochondrial biogenesis and functional repair, and improve the efficiency of cellular energy production.
Sufficient energy supply helps maintain the normal physiological functions of the body during sleep, ensuring the depth and quality of sleep—leaving people feeling more energetic upon waking.
(Note on related pathways: Angiogenesis; OXPHOS (oxidative phosphorylation); TCA cycle (tricarboxylic acid cycle); VEGF pathway (vascular endothelial growth factor pathway); HIF-1α (hypoxia-inducible factor 1α); TIMP-2 (tissue inhibitor of metalloproteinases-2); PGM (phosphoglucomutase); PFK (phosphofructokinase); P53 (tumor protein P53); LDHA (lactate dehydrogenase A); GLY (glycolysis); PDH (pyruvate dehydrogenase); Bax/Bcl-2/Bcl-xL (apoptosis-related proteins); ATP (adenosine triphosphate); Apoptosis; LKB1 (liver kinase B1); ATM (ataxia-telangiectasia mutated); Chk1 (checkpoint kinase 1); CDK (cyclin-dependent kinase); CDC25A (cell division cycle 25A); S phase; Apaf (apoptotic protease activating factor); Cyto C (cytochrome C); CASP (caspase); Derlin; IRE1 (inositol-requiring enzyme 1); ASK1 (apoptosis signal-regulating kinase 1); MKK7 (mitogen-activated protein kinase kinase 7); JNK (c-Jun N-terminal kinase); SREBP1C (sterol regulatory element-binding protein 1C); ACC2 (acetyl-CoA carboxylase 2); CPT1 (carnitine palmitoyltransferase 1); FFA (free fatty acid); FAS (fatty acid synthase); ER stress (endoplasmic reticulum stress); Misfolded protein accumulation; TRAF2 (TNF receptor-associated factor 2))