Anandamide (AEA) Research Dashboard
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CannaKeys has 548 studies associated with Anandamide (AEA).
Here is a small sampling of Anandamide (AEA) studies by title:
- Protective actions of vitamin D, anandamide and melatonin during vascular inflammation: Epigenetic mechanisms involved
- Inhibition of anandamide hydrolysis does not rescue respiratory abnormalities observed in an animal model of Parkinson's disease
- Cannabinoids for the treatment of cannabis use disorder: New avenues for reaching and helping youth?
- The Role of the Possible Receptors and Intracellular Pathways in Protective Effect of Exogenous Anandamide in Kindling Model of Epilepsy
- Endocannabinoid System in Polycystic Kidney Disease
Components of the Anandamide (AEA) Research Dashboard
- Top medical conditions associated with Anandamide (AEA)
- Proven effects in clinical trials for Anandamide (AEA)
- Receptors associated with Anandamide (AEA)
- Individual study details for Anandamide (AEA)
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Overview - Anandamide (AEA)
Description of Anandamide (AEA)
Anandamide was the first endogenous (naturally occurring inside the human body) cannabinoid to be discovered in 1992 by R. Mechoulam, L. Hanus et al. The team named the compound combining the Sanskrit word for bliss, "ananda," and the word "amide" describing an organic chemical compound to arrive at the name anandamide. The naturally occurring enzyme fatty acid amide hydrolase (FAAH) breaks down AEA.
Other Names:
Anandamide (N-arachidonyl ethanolamide)Anandamide, Arachidonylethanolamide, Arachidonoyl ethanolamide, N-Arachidonoylethanolamine
IUPAC Name: (5Z,8Z,11Z,14Z)-N-(2-hydroxyethyl)icosa-5,8,11,14-tetraenamide
Molecular Formula: C22H37NO2
Source–PubChem
Anandamide (AEA) Properties and Effects
Anandamide (AEA):
- AEA induces significant airway relaxation (A. Simon et al., 2022)
- CB1 and CB2 receptor activation by AEA play a therapeutic role in mitigating pain, improving mood and cognition, and reducing inflammation and oxidative stress, for instance.
- TRPV1 activation by AEA have relevance to immune and cardiovascular functions (vasodilation), inflammation, and pain.
- AEA-base modulation of 5-HT receptors (serotonin) improve mood, reducing stress, fear, anxiety, depression, and pain for instance with potential relevance to the treatment of diverse psychiatric disorders characterized by impairments in social behavior, such as autism or schizophrenia.
- AEA induces anti-inflammatory via PPAR-Gamma.
- In the presence of the corticosteroids (steroidal hormones involved in a number of functions such as stress responses), the body increases its production of AEA, which may account for the way in which the endocannabinoid boosts the antidepressant effects of exercise.
- AEA enhances the experience of pleasure derived from food.
- AEA is capable of destroying numerous types of cancers in the laboratory.
- Oxytocin, a naturally occurring hormone—associated with trust, intimacy, and close and meaningful relationships—increases the production of AEA.
- CBD inhibits the enzyme that breaks down AEA (i.e., FAAH) and as such may increase its presence (or bioavailability of AEA) and with it all the effects it engenders.
- Chronic stress reduces AEA levels whereas relaxation or meditation practices may increase AEA levels naturally
- Electro acupuncture has been shown to increase levels of AEA.
- Osteopathic manipulations have been shown to increase levels of AEA.
Anandamide (AEA) Receptor Binding
Endocannabinoid System (ECS) and AEA:
- CB1 weak agonist with a mean ~239±62 (using human tissue data from 16 trials) (J. McPartland et al., 2007)
- CB2 weak agonist with a mean ~440±96 (using human tissue data from 22 trials) (J. McPartland et al., 2007)
Endocannabinoidome (eCBome) and AEA:
- TRPV1
- PPAR-α
- PPAR-y
- 5-HT/serotonin allosteric modulation (indirect)
Ki legend:
- Full/strong agonist Ki ~1-9nM
- Moderate agonist Ki ~10-99nM
- Weak agonist Ki ~100-999nM
- Very weak agonist Ki ~1,000-up nM
(The reader is reminded that a smaller Ki is associated with the strongest effects.)
Disclaimers: Information on this site is provided for informational purposes only and is not meant to substitute for the advice provided by your own physician or other medical professional. You should not use the information contained herein for diagnosing a health problem or disease. If using a product, you should read carefully all product packaging. If you have or suspect that you have a medical problem, promptly contact your health care provider.
Information on this site is based on scientific studies (human, animal, or in vitro), clinical experience, or traditional usage as cited in each article. The results reported may not necessarily occur in all individuals. For many of the conditions discussed, treatment with prescription or over-the-counter medication is also available. Consult your physician, nutritionally oriented health care practitioner, and/or pharmacist for any health problem and before using any supplements or before making any changes in prescribed medications.
