Benefits
Traditional calming and digestive herbal tea
Catnip has a folk history as a medicinal herb. A review lists it among herbs discussed for sleep, and researchers describe its traditional use for stomach and breathing complaints, a use shared by other Nepeta plants. No controlled trial has tested oral catnip in people for any of these uses, so they rest on tradition and on the animal and lab findings below.
Relaxes gut and airway muscle in lab tissue studies
In isolated rabbit intestine and guinea pig windpipe tissue, catnip essential oil relaxed muscle contractions in a way consistent with calcium channel blocking and phosphodiesterase inhibition. The authors suggest this may explain the traditional use for gut cramping and cough. This was lab tissue exposed to oil, not people drinking the tea.
Nervous system effects in animal studies
Animal results point in opposite directions. An ethanol extract made more young chicks fall asleep at low and moderate doses but fewer at high doses, and catnip oil lengthened drug-induced sleep in mice. Yet mice fed the herb became more active, slept less after a sedative and were more prone to drug-induced seizures. None of this has been tested in people.
Liver markers in rodent toxin studies
In mice given a liver-damaging overdose of acetaminophen, catnip essential oil by mouth lowered markers of liver injury and shifted liver enzymes toward safer breakdown of the drug. In rats, oral catnip extracts given before a liver toxin improved liver enzyme and DNA damage measures. These are animal toxin models only; no human data exist.
Mechanism of action
Nepetalactone, the compound cats respond to
Nepetalactone is a volatile iridoid that attracts cats and repels insects; its biosynthesis, including a metabolic gene cluster, re-evolved in the Nepeta lineage after iridoid production was lost in its ancestors. Catnip oil is not uniform: one commercial oil was about 40% nepetalactone and 43% nepetalic acid, while another oil's main components were 1,8-cineole (about 21%), alpha-humulene and alpha-pinene.
Calcium channel and phosphodiesterase effects on smooth muscle (lab)
In isolated tissue, catnip oil shifted calcium responses and enhanced the relaxing effect of isoprenaline, pointing to dual calcium channel blocking and phosphodiesterase inhibition, much like the reference drug papaverine. At 25 to 80 times higher concentrations it also depressed isolated heart tissue.
Targets an insect irritant receptor, not the human one
In lab tests, catnip extract and nepetalactone directly activated the TRPA1 irritant receptor of flies and mosquitoes (some but not all of the TRPA1 variants tested), and flies and mosquitoes lacking TRPA1 were no longer repelled by catnip. Catnip did not activate human TRPA1. This concerns catnip as an insect repellent and says nothing about drinking catnip tea.
Opioid-linked nepetalactone effects in a related Nepeta species (animals)
The essential oil of a related species, Nepeta caesarea, which is 92 to 95% one nepetalactone isomer, eased pain responses and caused marked sedation in animal tests, and both effects were blocked by naloxone, pointing to opioid receptor involvement. These results have not been shown for catnip, and whether catnip tea delivers enough nepetalactone to have any such effect in people is unknown.
Clinical trials
Single case report with a review of published reports on whether catnip affects human consciousness (Osterhoudt et al. 1997, Vet Hum Toxicol)
One toddler who consumed a large quantity of catnip.
The child showed central nervous system depression and was obtunded (hard to rouse), and the authors found no other cause. It is a single case, so it cannot show how common such reactions are or at what amount they occur, but it is the main human safety signal for eating catnip.
Animal study in which mice were fed catnip as 10% of their diet for 2 hours a day for 1 or 7 days, followed by behavioral and drug-challenge tests (Massoco et al. 1995, Vet Hum Toxicol)
Mice; no human participants.
Both single and repeated feeding increased rearing and movement. A single exposure increased stereotyped behavior and seizure susceptibility and shortened pentobarbital sleeping time; after 7 days, tolerance developed and susceptibility to picrotoxin and strychnine seizures rose. The authors suggested an amphetamine-like action, the opposite of a sedative.
Chemical analysis plus toxicity and behavior tests of catnip oil, a nepetalactone-enriched fraction and nepetalic acid in rodents (Harney et al. 1978, Lloydia)
Mice and rats; no human participants.
The commercial oil was about 40% nepetalactone and 43% nepetalic acid. The dose lethal to half of mice was 1,300 mg/kg for catnip oil, 1,550 mg/kg for the nepetalactone fraction and 1,050 mg/kg for nepetalic acid. Catnip oil (500 mg/kg) and nepetalic acid (62.5 mg/kg) lengthened hexobarbital sleep in mice, and injections impaired trained avoidance performance in rats.
Animal dose-response study of an ethanol extract of catnip on behavior in young chicks (Sherry et al. 1979, Experientia)
Young chicks; no human participants.
At low and moderate doses (25 to 1,800 mg/kg), increasing numbers of chicks fell asleep; above about 2 g/kg, fewer chicks slept. The result suggests a sedative-like effect that reverses at high doses in this species.
Chemical analysis and isolated-tissue pharmacology of catnip essential oil, compared with papaverine and verapamil (Gilani et al. 2009, J Ethnopharmacol)
Isolated rabbit jejunum and guinea pig trachea and atria; no human participants.
The oil's main components were 1,8-cineole (21%), alpha-humulene, alpha-pinene and geranyl acetate. It inhibited gut and airway contractions through apparent calcium channel blocking and phosphodiesterase inhibition, and depressed heart tissue at 25 to 80 times higher concentrations.
Controlled animal study of catnip essential oil, obtained by supercritical fluid extraction and given by mouth after an injected acetaminophen overdose (Tan et al. 2019, Biosci Rep)
50 mice in five groups of ten.
The oil significantly reduced acetaminophen-induced liver damage. It raised expression of phase II detoxifying enzymes (glucuronosyltransferases and sulfotransferases) and inhibited CYP2E1, the enzyme that forms the toxic acetaminophen byproduct, with Nrf2 activation proposed as part of the mechanism.