Kava

Kava has been consumed in Pacific Island communities for over 3,000 years in both social and religious rituals, often as a drink. Kava's constituents have a sedative effect and act mainly on the GABA and dopamine receptors, as well as the sodium and calcium ion channels, but have also been found to have action upon the endocannabinoid system, specifically the CB₁ receptor sites.^[1] Kava has been likened to the effects of alcohol without the heavy mental effects. Kava is primarily used to relieve anxiety (anxiolytic), to relieve pain (analgesic), and to boost sociability.

Commonly, kava is drank throughout the day by Pacific Islanders such as those on Vanuatu or the Islands of Hawaii. This drink is popularly consumed before spiritual rituals and before social events due to its mild psychotropic effects and its more potent sociability inducing effects. Kava replaces alcohol in many Pacific communities.^{[citation needed]}

Entheogen

Kava cultures are the religious and cultural traditions of western Oceania which consume kava.

Kava is found to contain eighteen different chemicals called kavalactones. Kava's effects are believed to only relate to six psychoactive and medicinal kavalactones: methysticin, dihydromethysticin, kavain, dihydrokavain, yangonin, and desmethoxyyangonin.

Pharmacologically, kava's effects stem from 18 different chemicals found within the plant called kavalactones, six of which have been found to be directly psychoactive in the body. The first of these are methysticin, dihydromethysticin, dihydrokavain, all of which act on the GABA_A receptor and behave as an agonist, creating the well-known anxiolytic effects. Dihydromethysticin is also a reversible selective Monoamine Oxidase Inhibitor, specifically acting upon the MAO-B enzyme. Next is yangonin, which is unique in its ability to activate the CB₁ receptor in the endocannabinoid system. Desmethoxyyangonin is also an MAO-B inhibitor and is able to increase dopamine levels in the Nucleus Accumbens. This, along with the potential increases of serotonin and other catecholamine concentrations, may be responsible for the purported attention-promoting effects of kava. Lastly is kavain. Kavain has shown evidence to be a serotonin-norepinephrine reuptake inhibitor (SNRI). It also shows evidence of being an activator of NMDA receptors. Kavain has also been proven to be an effective GABA_A receptor agonist and a positive allosteric modulator of GABA efficacy. Kavain is also weak anti-epileptic due to its sodium ion (Na⁺) channel antagonism. It is also an effective mood stabilizer, working as an antagonist on Ca₂⁺ (calcium ion) channels and as a positive modulator on K⁺ channels (potassium ion). Its effects on calcium ion channels also make it an effective anticonvulsant and, in synergy with yangonin, makes an effective analgesic (Pain reliever) working with both calcium ion channels and the endocannabinoid system.

Experience reports

There are currently no anecdotal reports which describe the effects of this compound within our experience index. Additional experience reports can be found here:

• Erowid Experience Vaults: Kava

Studies have shown that kava can and will induce a low level of hepatic apoptosis similar to how paracetamol affects the liver and also can affect hepatic enzymes. Because of this, certain medications can make kava unsuitable and even dangerous for some users. Noble kava root alone can not, without consuming very large amounts of the substance, induce toxic levels and no overdose has ever been recorded. The consumption of 'noble' kava root has very low toxicity, however consumption 'tudei' kava and the stems and leaves of kava plants may increase the risk of liver damage.

Lethal dosage

Some research has been done into finding the LD₅₀ of kavalactones with results stating that around 300-400 Mg/Kg daily would be the likely lethal dose based on animal studies. [1]

Tolerance and addiction potential

Kava is known to produce a "reverse tolerance" in many users, in a similar fashion to substances like kanna. This means that continued use is required in order to experience full effects. Some users do not experience this.

Kava is traditionally regarded as non-addictive especially in comparison to other chemically related drugs such as benzodiazepines. In some Pacific Island communities, there is some record of people who have a psychological addiction to kava and drink it like an alcoholic drinks alcohol.

Dangerous interactions

• Depressants (1,4-Butanediol, 2M2B, alcohol, benzodiazepines, barbiturates, GHB/GBL, methaqualone, opioids) - This combination potentiates the muscle relaxation, amnesia, sedation, and respiratory depression caused by one another. At higher doses, it can lead to a sudden, unexpected loss of consciousness along with a dangerous amount of depressed respiration. There is also an increased risk of suffocating on one's vomit while unconscious. If nausea or vomiting occurs before a loss of consciousness, users should attempt to fall asleep in the recovery position or have a friend move them into it.
• Dissociatives - This combination can unpredictably potentiate the amnesia, sedation, motor control loss and delusions that can be caused by each other. It may also result in a sudden loss of consciousness accompanied by a dangerous degree of respiratory depression. If nausea or vomiting occurs before consciousness is lost, users should attempt to fall asleep in the recovery position or have a friend move them into it.
• Stimulants - Stimulants mask the sedative effect of depressants, which is the main factor most people use to gauge their level of intoxication. Once the stimulant effects wear off, the effects of the depressant will significantly increase, leading to intensified disinhibition, motor control loss, and dangerous black-out states. This combination can also potentially result in severe dehydration if one's fluid intake is not closely monitored. If choosing to combine these substances, one should strictly limit themselves to a pre-set schedule of dosing only a certain amount per hour until a maximum threshold has been reached.
• Hepatic Route drugs - Kava inhibits several liver enzymes in the CYP family. Consequentially, combining kava with drugs metabolized via CYP pathways, such as paracetamol, may cause adverse effects. For a list of medications click here A 2010 review concluded that it's possible that ethanol combined with kava may be the cause of kava hepatotoxicity.^[2]
• Anticoagulants - Kava may increase the risk of bleeding if taken with anticoagulants. Specifically the kavalactone kavain.^[3] A list of anticoagulants can be found here
• Antiplatelet - Kava may increase the risk of bleeding if taken with antiplatelet agents. Specifically the kavalactone kavain.^[4] A list of antiplatelet agents can be found here

In some countries, kava has been banned but in most, it is simply regulated.

• Australia - Kava is regulated by the National Code of Kava Management. Only 18 year olds may have it and can only possess 2 Kg in their baggage.
• United Kingdom - In the UK it is illegal to sell, supply or import any medicinal product containing kava for human consumption. It is legal to possess kava for personal use, or to import it for purposes other than human consumption (e.g. for animals).
• United States - In the U.S., kava was once noted as a potential "Liver Damaging substance" but this remark has since been archived by the FDA and kava is legal for sale, trade, possession, use, and all other uses.
• Canada - While Health Canada has similar remarks to the U.S. regarding kava, there is no ban on the substance.

• Benzodiazepines

• Kava (Wikipedia)
• Kava (Erowid Vault)

 1. http://www.ncbi.nlm.nih.gov/pubmed/16011454
 2. https://www.erowid.org/plants/kava/