by Anthony Roberts

When I first tried kratom, I was given a fairly substantial quantity of 30 gram packets, each identified vein (red, green, or white), and a location (indicating country/region of cultivation).



This is generally the accepted industry standard when it comes to selling kratom: the color of the vein running down the center of the leaf followed by the region it was cultivated in. Therefore if you’re buying Green Ma Daeng, it’s a green veined leaf grown in Haui Ma Daeng, Thailand. Or at least it’s supposed to be.

[Note: Some strains have been selectively bred for different properties, like Maeng Da kratom, which has a name that doesn’t follow the rest of the industry standard.]

As an inexperienced user, I can only detect minor differences in effect between, say, Green Thai and White Bali. To be honest, I’m not even sure what I’m looking for — I used the stuff on and off for about half a year, only trying two manufacturers. And like any natural product, there are inconsistencies from batch to batch and manufacturer to manufacturer.

But generally speaking, online accounts from various forums indicate that red vein kratom has a more pronounced sedative effect, while green and white display greater stimulant properties. There seems to be moderate disagreement over which strain is best for pain relief or assisting social anxiety, but common wisdom is to try several and figure out what works best on a case by case basis.

The pharmacological effect — or “feel” — of kratom is determined by the composition of the various alkaloids. Some of the alkaloids found in kratom affect the opioid receptors (more on this later), but many remain uncharacterized in terms of physiological effects.

The two most common alkaloids in kratom are mitragynine (MG) and 7-hydroxy mitragynine (7-OH MG). But the amount in one leaf or plant versus another can vary. In one study examining 13 commercial products, MG, 7-OH MG, and three other indole alkaloids were only detected in 11 of them. However, the relative concentrations of MG in these products ranged from 1.2% to 6.3%, and 7-OH MG ranged from 0.01% to 0.04%.

To put this in perspective, imagine drinking a few glasses of whisky & coke. But the ratio is of ingredients is totally different from one glass to the next, and sometimes the whisky is 80 proof and sometimes it’s 100 proof. This is exactly what we see happening with kratom, but it’s the ratio of alkaloids that can change, and therefore the overall potency and effect.

Ok, so let’s (arbitrarily) say there are 30 possible alkaloids in a given kratom leaf. This would be equivalent to a whisky bar with 30 different types of liquor on the shelves. You could be drinking rye, bourbon, or scotch and still be drinking whisky, all made from some type of grain. The same way you’ll find vastly different flavor, different alcohol content, etc… in a glass of Jack Daniels versus Macallan 21, you’ll find different effects from different types of kratom.

In both cases, the differences are (more or less) the same, and both the whisky and the kratom will be dependent on where the plant was grown, when it was harvested, and how it was processed.

Kratom grown in Malaysia has been found to contain between 12 and 25% mitragynine, while leaves from Thailand can go as high as 66%. Interestingly, there seems to be a fairly consistent level up to 2% of 7-OH MG.

And when we look at kratom grown in non-traditional areas (red vein was originally unique to Thailand, for example), sometimes mitragynine isn’t even the primary alkaloid. In kratom harvested too soon, we also find significantly lower concentrations of mitragynine.

And those are just a few of the factors that effect a single alkaloid in kratom. When you start to add up all of the possible variables, and multiply them by the total number of alkaloids (dozens, remember?), it becomes appreciable that different brands, strains, and veins, could have a considerably different chemical makeup.

Harvest your grain too early, and you don’t get the right alcohol content (or flavor) in your whisky. The same is true of kratom.

Process either of them badly, overheat, or don’t store properly, and you get a very different end product.

Do you toss & wash or make kratom tea? Does boiling water destroy some of the alkaloids? Does it enhance others? Even your method of consumption can change the overall physiological effect and the way kratom interacts with your opioid receptors.

There are three types of (classic) opioid receptors: mu, delta, and kappa (and a fourth non-classical one, called the Nociceptin receptor). Additionally, there are subtypes of each opioid receptor. Depending on how each receptor and each subtype is preferentially stimulated (agonized) or blocked (antagonized), we get a different physiological effect from various types of kratom (dependent on their alkaloid content and concentration).

Certain alkaloids can stimulate one receptor while not affecting another at all, or even stimulate all of them to varying degrees. Researchers at Columbia University have shown that Mitragynine and 7-OH Mitragynine, are partial agonists of the human mu-opioid receptor and competitive antagonists at the kappa- and delta-opioid receptors.

We see this in herbs other than Kratom as well…Black cohosh, for example, acts as a mixed competitor and partial agonist at the human mu opiate receptor.

This produces the wide variety of effects we see with kratom, and accounts for the fact that one type may be a stimulant and another a sedative, or why some have more pronounced analgesic effects (or why different effects may occur at lower versus higher doses). It further seems likely that a low dose is all that’s needed to produce a stimulant effect, as the alkaloid makeup is such that receptors are agonized at a lower dose; whereas higher doses are required to reach the same receptor threshold for a sedative effect.

Sound odd? It shouldn’t. A cup of regular tea (which has minimal caffeine) often produces a relaxing effect, while a cup of coffee (a much higher dose of caffeine) produces a stimulant effect. With caffeine, a low dose is sedating and a high dose is stimulating. Kratom seems to have the opposite dose-respondent effects.

There is also a reasonable amount of individual variance in how we each metabolize kratom, which can further account for people’s disparate experiences with it. This next table shows mean time points for kratom to reach maximum plasma concentration (about 50 minutes) and reach its terminal half life (about a day):

But that’s the mean, the central value of the these time points from a given set of kratom users. Take a look at what happens when we view their individual reactions:

One kratom user achieves a far higher plasma concentration and has a greater blood concentration than everyone else. Another user doesn’t quite peak as high, but also maintains a significantly greater kratom level in his blood. So while most people in this study experienced the same result in terms of plasma kratom levels, two (out of ten) were substantially different.

There is still a great deal to be explained regarding kratom, from specific the alkaloid contents of varying strains, to the unique enzymes and physiology that cause disparate effects in users.

Hopefully it’ll remain legal and in the hands of both scientists and the general public, and we’ll continue to fill in some of these gaps in our understanding of kratom.