Dr. Matthew Hill

So again, same situation, you can get the animal stoned and it will re-engage in eating that food that it had devalued through being paired with a nauseant. So through either satiety or making it kind of a negative associated flavor because the animal got nauseous before. you can kind of override these effects by giving THC.

So again, same situation, you can get the animal stoned and it will re-engage in eating that food that it had devalued through being paired with a nauseant. So through either satiety or making it kind of a negative associated flavor because the animal got nauseous before. you can kind of override these effects by giving THC.

So again, same situation, you can get the animal stoned and it will re-engage in eating that food that it had devalued through being paired with a nauseant. So through either satiety or making it kind of a negative associated flavor because the animal got nauseous before. you can kind of override these effects by giving THC.

And so that could be a complex process that either involves changes in the reward circuitry. This could be something that's like from the orbit of frontal cortex, which is a very important part of the brain that scales reward and kind of assesses how much someone wants to work or an organism wants to work to achieve a reward at the end.

And so that could be a complex process that either involves changes in the reward circuitry. This could be something that's like from the orbit of frontal cortex, which is a very important part of the brain that scales reward and kind of assesses how much someone wants to work or an organism wants to work to achieve a reward at the end.

And so that could be a complex process that either involves changes in the reward circuitry. This could be something that's like from the orbit of frontal cortex, which is a very important part of the brain that scales reward and kind of assesses how much someone wants to work or an organism wants to work to achieve a reward at the end.

So we haven't figured out the circuitry of this and where exactly it's acting. But I would say a lot of the stuff that, you know, we and others have done kind of supports this idea that a lot of what the munchies is, is this ability to kind of almost lock in the reward value of food so that it doesn't decay.

So we haven't figured out the circuitry of this and where exactly it's acting. But I would say a lot of the stuff that, you know, we and others have done kind of supports this idea that a lot of what the munchies is, is this ability to kind of almost lock in the reward value of food so that it doesn't decay.

So we haven't figured out the circuitry of this and where exactly it's acting. But I would say a lot of the stuff that, you know, we and others have done kind of supports this idea that a lot of what the munchies is, is this ability to kind of almost lock in the reward value of food so that it doesn't decay.

Despite satiety, despite eating over time, it just keeps it highly salient so that they want to work for it still. And then similarly, we and others have also done work to show it can block satiety signals. So we know endocannabinoids, at least, are capable of overriding leptin.

Despite satiety, despite eating over time, it just keeps it highly salient so that they want to work for it still. And then similarly, we and others have also done work to show it can block satiety signals. So we know endocannabinoids, at least, are capable of overriding leptin.

Despite satiety, despite eating over time, it just keeps it highly salient so that they want to work for it still. And then similarly, we and others have also done work to show it can block satiety signals. So we know endocannabinoids, at least, are capable of overriding leptin.

So leptin is an anorectic molecule, comes out from the fat, and usually we release it when we've eaten a lot, and it's one of these things that tells our brain, stop eating. It works through, again, populations in the arcuate nucleus and changes the way those neurons function to drive food-seeking behavior.

So leptin is an anorectic molecule, comes out from the fat, and usually we release it when we've eaten a lot, and it's one of these things that tells our brain, stop eating. It works through, again, populations in the arcuate nucleus and changes the way those neurons function to drive food-seeking behavior.

So leptin is an anorectic molecule, comes out from the fat, and usually we release it when we've eaten a lot, and it's one of these things that tells our brain, stop eating. It works through, again, populations in the arcuate nucleus and changes the way those neurons function to drive food-seeking behavior.

And we and others have shown previously that, you know, if you elevate endocannabinoids, you can override that. And actually one of the mechanisms by which leptin seems to suppress feeding is actually by turning on the metabolism of endocannabinoids so that their levels decline. And so as you lose that endocannabinoid function, the animal is less interested in eating.

And we and others have shown previously that, you know, if you elevate endocannabinoids, you can override that. And actually one of the mechanisms by which leptin seems to suppress feeding is actually by turning on the metabolism of endocannabinoids so that their levels decline. And so as you lose that endocannabinoid function, the animal is less interested in eating.

And we and others have shown previously that, you know, if you elevate endocannabinoids, you can override that. And actually one of the mechanisms by which leptin seems to suppress feeding is actually by turning on the metabolism of endocannabinoids so that their levels decline. And so as you lose that endocannabinoid function, the animal is less interested in eating.

And so you can prevent these anorectic effects of leptin by like goosing up endocannabinoid activity. Yeah.

And so you can prevent these anorectic effects of leptin by like goosing up endocannabinoid activity. Yeah.