Viral TikTok sensation Kava explained!
If you are like me, someone who spends time on social media and watches countless reels and TikToks, you’ve likely come across this ‘new’ wonder ethnobotanical Kava-Kava.
Every time an ethnobotanical compound becomes viral on social media, I can’t help but think about the future repercussions this will have in the psychedelic community. Not for the fact that these compounds don’t work but for the fact that we’ll likely have people who have zero understanding of the pharmacodynamics and potential threats advertising such compounds to everyone might have.
I don’t want to believe that some people do this with evil intent but to express their love for the effects of a compound, just like what is currently happening in the craze over Ayahuasca or Sapo (5-MeO-DMT). We have celebrities broadly advertising for effects that may not be the same as theirs, may not benefit everyone, and can even be harmful.
Picture this. You are a social media influencer with no knowledge about the compound. You hear that it does wonders, and a brand reaches out to you to promote it. So, you do the best thing you can. You binge-watch a few TikToks or regurgitate what the brand told you to say. And someone who is an avid follower of yours and has a family history of schizophrenia or heart disease hears your Instagram story saying that 5-MeO-DMT is the next best thing that can happen in your life, you will have an experience of rebirth, and all of your problems will disappear.
They decide to try it, have an unpleasant experience that triggers their schizophrenia that will haunt them for life, or die while having a heart attack.
Unfortunately, such scenarios can happen. All for the sake of a compound going viral on social media, and companies reaching out to influencers who may or may not have the knowledge about the science of these compounds and are now advertising the compound broadly without any knowledge of potential health repercussions based on what they have experienced or what a brand has told them.
This case is no different! As always, we considered discussing what Kava is and whether it’s suitable for you or not!
Kava Kava (or Kava for short) is a drink made from the ground roots of Piper methysticum, a plant originally found in the Pacific Islands.
What brought so much attention to this brew was the same hype that we witnessed a few years ago with high doses of Kratom.
Influencers are advertising the brew as an alternative to pharmaceutical analgesics and anxiety medication.
Considering Kava is a depressant drug, some go even as far as saying it can be an alternative to alcohol.
The dense array of Kavalactones present in the chemical constitution of the plant is responsible for such effects between them:
- Kavain
- Dihydrokavain
- Methysticin
- Dihydromethysticin
- Yangonin,
- Desmethoxyyangonin
Such compounds are said to be responsible for Kava’s major pharmacological activity. But how do these compounds work?
Kava’s effects are caused by facilitating GABA transmission, inhibiting voltage-gated ion channels, blocking the reuptake of noradrenaline, and inhibiting cyclooxygenase by suppressing the synthesis of thromboxane A2).
Talking more about specifics, the Kavalactones Methysticin, Kavain, Dihydromethysticin, and Dihydrokavain enhance the binding of ligands to the GABAA receptor, like other depressant compounds such as benzodiazepines, for example. However, Kavalactones act on a different side of GABAA to facilitate the binding of GABA and increase Cl– flow.
The whole experience, like any botanical entheogen, has various molecules working together in a synergy.
Kavain has a specific inhibitory action on sodium channels and other constituents, while other Kava constituents have varying inhibitory activity on the sodium ion channels. Kavain inhibits L-type Ca2+ channels, subsequently releasing glutamate.
Contrary to news shared in the media, Kavalactones do not directly alter serotonin, dopamine, or their metabolite concentration. They inhibit MAOB to change the concentration of monoamines.
Kavain has a biphasic effect on dopamine, decreasing its concentration at a low dose and increasing it or not altering it at a high dose.
Desmethyoxyyangonin increases dopamine levels in the nucleus accumbens, while Yangonin decreases dopamine concentration in some regions of the brain. Some kavalactones do not affect brain dopamine levels.
Kavain reduces serotonin levels, inhibits cyclooxygenase, and lowers thromboxane A2 concentrations, which enhances GABA function in the brain.
In summary, Kava’s analgesic action is not mediated through opioid receptors like typical analgesics. Instead, its analgesic effects are believed to result from interactions with GABAergic and monoamine neurotransmitters.
Kava also has promising neuroprotective and anxiolytic effects due to its blocking action on voltage-gated Na+ and Ca2+ channels.
Synchronized sleep, sedative, and antiseizure effects are also caused by its inhibitory effects on voltage-gated ion channels and facilitating effect on GABA.
Although Kava has many benefits and could eventually replace medication, the plant, and its compounds are depressants and don’t fall too far from the typical issues other depressant compounds may cause us.
Like long-term use of alcohol, Kava may cause Major liver issues, leading to the ban in many countries.
Alongside, there are other reported side effects associated with Kava consumption, including:
- Dermatological reactions
- Impaired motor function
- Visual impairment
- Urinary retention
- Exacerbation of Parkinson’s disease
- Extrapyramidal effects
- Myoglobinuria
- Severe rhabdomyolysis
- GI discomfort
- Euphoria,
- Tremors
- Ataxia.
For this reason, Kava should be used cautiously in patients with renal or liver disease, blood disorders, Parkinson’s disease, or depression and completely avoided by children and pregnant or breastfeeding women. Regular liver function tests may be warranted.
We hope this detailed article has helped clarify any questions about Kava. If you have more questions, feel free to email us!
Stay safe!
