M
mlenny
I was told that lateral root is heady and stump is heavy. Would you agree with this?
No, lateral roots are more potent while the stump has a smaller concentration of kavalactones.
Headiness and heaviness are determined by the different concentrations of the varying individual kavalactones. (we look at the major 6)
When we examine the effects of these six kavalactones, we can get a better understanding how each play off each other but more importantly the order will dictate the effect profile of the kava. Some kavas are notoriously headier, less heavy with more sociable effects, such as Tongans, Lewenas from Fiji usually fit this category as well (these are kavas with a higher concentration of the stump part of the plant, but it does not mean it is headier because of that).
Here are the major 6 kavalactones we have the most studies on, and with this information, we get a better idea of effects in each kava. Bare in mind some strains will have identical chemotype profiles with varying effects. This is largely due to the strain of the kava and the growing region/conditions of these plants. i.e., soil type, amount of sunlight, age of the plants, and so on. There are major outside factors to consider that will determine a kavas end effects.
1. Desmethoxyyangonin (DMY) - Generally the scarcest of the 6 kavalactones in most kava root and not much is known about its effects or pharmacology. Induces CYP2A23 activity. Potent inhibitor of CYP1A2, and CYP2C19. May play a role in the increasing and decreasing rate of metabolism of some specific compounds. Has shown in invitro studies to increase dopamine levels.
2. Dihydrokavain (DHK) - "heavy" kavalactone. Found highest concentrations in the leaves of the plant, but also readily found in the roots. Effects include sedation, muscle relaxation; moderately long-lasting. Plays major role in anxiety reduction. No significant changes in dopamine levels are reported with this kavalactone.
3. Yangonin (Y) - This is the only kavalactone known to drastically decrease dopamine in research. Known to be a ligand at the CB1 cannabinoid receptor, but whether this plays a role in subjective effects is unknown. Clearly inhibits CYP1A2, and CYP2C19 isoforms, but had no effect on CYP2D6 or CYP2E1. Also shown to have the most potent MAOI activity of the 6 kavalactones. Also plays a role as an anti-oxidant. Protective effect on cholestasis or when the flow of bile from the liver is blocked or reduced. Decreases synthesis of bile acids. Induces autophagy and sensitizes bladders cancers cells to FKA. Shown to protect against non-alcoholic fatty liver disease. May play a significant part in dopamine modulation. Several studies have shown a sharp decrease in dopamine levels followed by a steady return to baseline. Generally accounts for 10%-20% of total kavalactones, and only found in significant concentrations in the roots
4. Kavain (K) - the main heady kavalactone. Kicks in quickly and for a short duration, effects are mental relaxation, euphoria, feelings of well-being. Shown to enhance ligand binding in GABA receptors but at an atypical site (not the GABA nor benzodiazepine binding site). Known to block voltage-gated fast-acting sodium and calcium channels. Anti-inflammatory effects, cancer reduction, and neuroprotection. Shown to reduce glutamate release. Has shown to increase levels of dopamine in the brain. Increases sleep time and decrease sleep latency. Shown in studies to markedly increase delta brainwave activity in sleep disturbed rats.
5. Dihydromethysticin (DHM) - Found concentrated highest in kava leaves. very sedating and long-lasting, can cause nausea. The likely culprit behind the next-day sluggishness after a large kava session. DHM is generally pretty low in noble kavas since it's generally the most undesirable kavalactone and has been selected against over the hundreds (or thousands) of years of kava domestication. Along with methysticin, this KL has been seen to induce CYP1A1 enzymes. Likely the KL that causes the analgesic (pain relief) effect. Affects cyclooxygenase enzymes and has been found that 120mg/kg DHM were equal to 200mg/kg pain relief actions of aspirin. Can block the effects of strychnine poisoning. Also may block some carcinogenesis (cancer formation) by reducing DNA damage in tobacco consumers. Also may work together with methysticin to exhibit neuroprotective effects in strokes.
6. Methysticin (M) - Known to act a sodium channel blocker/antagonist (along with kavain). Known as a potent CYP1A1 inducer at the gene expression level, protein expression level, and enzymatic activity. Potent inhibitor of CYP2C19 and CYP3A4. Shows moderate inhibition at CYP1A2, CYP2C9 and CYP2E1. Shows anti-oxidant activity. Anti-convulsant and neuroprotective properties have been shown. This KL blocks all forms of induced epilepsy. Protects against oxidative stress, and inflammation. Also improved long term memory models in mice with induced Alzheimer's disease.
Original Source (with LINKED studies) and credit to Kapmcrunk.