Dr. Matthew Walker
π€ SpeakerAppearances Over Time
Podcast Appearances
The worry is the same with your pineal gland, which is going to release melatonin, that if you keep exogenously giving your brain vast amounts, it says, well, you're giving it to me, so I don't need to produce it anymore. And once it stops, does it ever restart? There are some data where they looked at an individual who was blind.
And the reason that they were looking at this individual is because when you're blind and depending on the level of blindness, if it's at, let's say, the level of the retina or the optic nerve, you don't receive light signals. So you don't get the light to reset your circadian rhythm. So you're bouncing with your sleep all over the place. It's very difficult for these patients.
And the reason that they were looking at this individual is because when you're blind and depending on the level of blindness, if it's at, let's say, the level of the retina or the optic nerve, you don't receive light signals. So you don't get the light to reset your circadian rhythm. So you're bouncing with your sleep all over the place. It's very difficult for these patients.
And the reason that they were looking at this individual is because when you're blind and depending on the level of blindness, if it's at, let's say, the level of the retina or the optic nerve, you don't receive light signals. So you don't get the light to reset your circadian rhythm. So you're bouncing with your sleep all over the place. It's very difficult for these patients.
So what we typically do is we give them exogenous melatonin to at least feed them the signal of melatonin darkness at night to try to regulate their sleep. And they did a study where they were tracking the melatonin of this individual and they were giving exogenous melatonin. And then they stopped and then looked to see, did that individual stop producing their own natural melatonin?
So what we typically do is we give them exogenous melatonin to at least feed them the signal of melatonin darkness at night to try to regulate their sleep. And they did a study where they were tracking the melatonin of this individual and they were giving exogenous melatonin. And then they stopped and then looked to see, did that individual stop producing their own natural melatonin?
So what we typically do is we give them exogenous melatonin to at least feed them the signal of melatonin darkness at night to try to regulate their sleep. And they did a study where they were tracking the melatonin of this individual and they were giving exogenous melatonin. And then they stopped and then looked to see, did that individual stop producing their own natural melatonin?
And the answer was no. So people say, well, that's a good thing. And it was about a 30-day experiment. Other people, I think, have looked across about six weeks of dosing. And when they stop, the people keep producing it. And some people have argued that's the evidence then that we don't have to worry about that. The problem is most people don't use melatonin like that.
And the answer was no. So people say, well, that's a good thing. And it was about a 30-day experiment. Other people, I think, have looked across about six weeks of dosing. And when they stop, the people keep producing it. And some people have argued that's the evidence then that we don't have to worry about that. The problem is most people don't use melatonin like that.
And the answer was no. So people say, well, that's a good thing. And it was about a 30-day experiment. Other people, I think, have looked across about six weeks of dosing. And when they stop, the people keep producing it. And some people have argued that's the evidence then that we don't have to worry about that. The problem is most people don't use melatonin like that.
They've been using it for three or four years. So we don't know. And it could be perfectly harmless. The second concern about melatonin is that it's a hormone that regulates the timing signal for when you should sleep. It doesn't participate in the generation of sleep itself. So melatonin is like the starting official at the 100-meter race.
They've been using it for three or four years. So we don't know. And it could be perfectly harmless. The second concern about melatonin is that it's a hormone that regulates the timing signal for when you should sleep. It doesn't participate in the generation of sleep itself. So melatonin is like the starting official at the 100-meter race.
They've been using it for three or four years. So we don't know. And it could be perfectly harmless. The second concern about melatonin is that it's a hormone that regulates the timing signal for when you should sleep. It doesn't participate in the generation of sleep itself. So melatonin is like the starting official at the 100-meter race.
It brings all of the sleep races to the line and begins the great sleep race, but it doesn't participate in the sleep race itself. That's a different set of chemicals and compounds.
It brings all of the sleep races to the line and begins the great sleep race, but it doesn't participate in the sleep race itself. That's a different set of chemicals and compounds.
It brings all of the sleep races to the line and begins the great sleep race, but it doesn't participate in the sleep race itself. That's a different set of chemicals and compounds.
So that's why when people have done what we call meta-analyses, where you get all of the individual studies looking at melatonin in sleep, and you put them all together in the same big statistical bucket, and you ask, what's the overall effect? Melatonin only improved the speed with which you fell asleep by about 3.9 minutes, which is not that much more relative to placebo.
So that's why when people have done what we call meta-analyses, where you get all of the individual studies looking at melatonin in sleep, and you put them all together in the same big statistical bucket, and you ask, what's the overall effect? Melatonin only improved the speed with which you fell asleep by about 3.9 minutes, which is not that much more relative to placebo.
So that's why when people have done what we call meta-analyses, where you get all of the individual studies looking at melatonin in sleep, and you put them all together in the same big statistical bucket, and you ask, what's the overall effect? Melatonin only improved the speed with which you fell asleep by about 3.9 minutes, which is not that much more relative to placebo.
And it only improved your sleep efficiency by about 2.2%. So again, largely trivial. Now, I think, however, despite touting those statistics, I think there is a subset of people for whom melatonin is sleep generating. And therefore, melatonin is not just the starting official. It's also one of the racers. And we don't yet understand why.