Dr. Matthew Hill

But it really was one of the first demonstrations that adding in a terpene could actually influence a component of the intoxicated state in a blinded manner, I think is interesting. And Ziva Cooper, who's here at UCLA, is doing some work with beta-caryophyllene, which is probably... probably the second most abundant terpene, I think, from Nick Chikomas' work.

I think myrcene may have been the highest prevalent terpene across all types of cannabis. Beta-caryophyllene is probably the second, and limonene, I think, is probably the third. And So I think they, I mean, and so they're looking at, I think Ziva's work is in the context of pain.

I think myrcene may have been the highest prevalent terpene across all types of cannabis. Beta-caryophyllene is probably the second, and limonene, I think, is probably the third. And So I think they, I mean, and so they're looking at, I think Ziva's work is in the context of pain.

I think myrcene may have been the highest prevalent terpene across all types of cannabis. Beta-caryophyllene is probably the second, and limonene, I think, is probably the third. And So I think they, I mean, and so they're looking at, I think Ziva's work is in the context of pain.

So they're trying to look at if a fixed dose of THC, if you add in varying levels of beta-caryophyllene, does this influence this? So, because again, you do see this in patient communities where they say, well, this strain helps my pain better than that strain. And so it's like, okay, is there actual legitimacy to this?

So they're trying to look at if a fixed dose of THC, if you add in varying levels of beta-caryophyllene, does this influence this? So, because again, you do see this in patient communities where they say, well, this strain helps my pain better than that strain. And so it's like, okay, is there actual legitimacy to this?

So they're trying to look at if a fixed dose of THC, if you add in varying levels of beta-caryophyllene, does this influence this? So, because again, you do see this in patient communities where they say, well, this strain helps my pain better than that strain. And so it's like, okay, is there actual legitimacy to this?

Or again, is this just an expectancy bias because someone who sold this to you told you that this strain is better for pain? And the problem is these are all subjective endpoints. I mean, this is, Like pain, sleep, anxiety, these are all how someone personally experiences it.

Or again, is this just an expectancy bias because someone who sold this to you told you that this strain is better for pain? And the problem is these are all subjective endpoints. I mean, this is, Like pain, sleep, anxiety, these are all how someone personally experiences it.

Or again, is this just an expectancy bias because someone who sold this to you told you that this strain is better for pain? And the problem is these are all subjective endpoints. I mean, this is, Like pain, sleep, anxiety, these are all how someone personally experiences it.

And we know from all the clinical trials that study pain, sleep, and anxiety, there's massive placebo effects that happen in all these conditions. And so it's very difficult to actually make any kind of sound statements about this in the absence of there being kind of clinical trials that have clearly started to do this. But it's like, as you can imagine, when you start doing the math,

And we know from all the clinical trials that study pain, sleep, and anxiety, there's massive placebo effects that happen in all these conditions. And so it's very difficult to actually make any kind of sound statements about this in the absence of there being kind of clinical trials that have clearly started to do this. But it's like, as you can imagine, when you start doing the math,

And we know from all the clinical trials that study pain, sleep, and anxiety, there's massive placebo effects that happen in all these conditions. And so it's very difficult to actually make any kind of sound statements about this in the absence of there being kind of clinical trials that have clearly started to do this. But it's like, as you can imagine, when you start doing the math,

given the amount of terpenes and the amount of combinations at different levels, how overwhelming this could become. Because maybe, you know, there's a few that you need in there that interact with THC, not just one. There is like a lot of work that's happened in the last few years that has really started to try and look at if these terpenes or minor cannabinoids act at the cannabinoid receptor.

given the amount of terpenes and the amount of combinations at different levels, how overwhelming this could become. Because maybe, you know, there's a few that you need in there that interact with THC, not just one. There is like a lot of work that's happened in the last few years that has really started to try and look at if these terpenes or minor cannabinoids act at the cannabinoid receptor.

given the amount of terpenes and the amount of combinations at different levels, how overwhelming this could become. Because maybe, you know, there's a few that you need in there that interact with THC, not just one. There is like a lot of work that's happened in the last few years that has really started to try and look at if these terpenes or minor cannabinoids act at the cannabinoid receptor.

which none of them seem to. So this isn't like you've got things that modulate how THC is binding to CB1. If they're doing something else, it's probably through an interaction with another neurochemical system that's influencing what THC is doing. So I'm not against the idea that different chemovars or what people call strains of cannabis could do different things subjectively.

which none of them seem to. So this isn't like you've got things that modulate how THC is binding to CB1. If they're doing something else, it's probably through an interaction with another neurochemical system that's influencing what THC is doing. So I'm not against the idea that different chemovars or what people call strains of cannabis could do different things subjectively.

which none of them seem to. So this isn't like you've got things that modulate how THC is binding to CB1. If they're doing something else, it's probably through an interaction with another neurochemical system that's influencing what THC is doing. So I'm not against the idea that different chemovars or what people call strains of cannabis could do different things subjectively.

I just am remiss to believe this until I see some blinded data because I think outside of that, we know how powerful an expectancy bias is. So it makes it very, very challenging to make any kind of firm statements. And so kind of in the context of like how you introduced this, that was – again, I think like one of the issues that I took with the other podcast was because –