**Andrew Huberman** (0:00)
Welcome to the Huberman Lab Podcast, where we discuss science and science-based tools for everyday life. I'm Andrew Huberman, and I'm a professor of neurobiology and ophthalmology at Stanford School of Medicine. Today, I have the pleasure of introducing Dr. Robert Sapolsky. Thank you so much, Robert, for joining us today.
**Robert Sapolsky** (0:21)
Why, it's glad to be here.
**Andrew Huberman** (0:22)
I want to return to a topic that is near and dear to your heart, which is stress.
What is the difference between short and long-term stress in terms of their benefits and their drawback? How should we conceptualize stress?
**Robert Sapolsky** (0:38)
Basically, there are two graphs that one would draw. The first one is just all sorts of beneficial effects of stress short-term. And then once we get into the chronicity, it's just downhill from there. The sorts of chronic stressors that most people deal with are just undeniably in the chronic range, like having spent the last 20 years, daily traffic jams or abusive boss or some such thing. The other curve that's sort of perpendicular to this is dealing with the fact that sometimes stress is a great thing. Like our goal is not to cure people of stress because if it's the right kind, we love it.
We pay good money to be stressed that way, like a scary movie or roller coaster ride. What you wind up seeing is when it's the right amount of stress, it's what we call stimulation.
**Andrew Huberman** (1:37)
One thing that's really striking to me is how that physiologically, the stress response looks so much like the excitement response to a positive event. But is there anything else that we know about the biology that reveals to us what really creates this thing we call valence, that an experience can be terrible or feel awful or it can feel wonderful, depending on this somewhat subjective feature we call valence.
**Robert Sapolsky** (2:08)
On a really mechanical level, if you're in a circumstance that is requiring that your heart races and your breathing is fast and you're using your muscles and some such thing, you're going to be having roughly the same brain activation profile, whether this is for something wonderful or something terrible, with the one exception being that if the amygdala is part of the activation, this is something that's going to be counting as adverse. The amygdala in some ways is kind of the checkpoint as to whether we're talking about excitement or terror.
**Andrew Huberman** (2:47)
Let's use the amygdala as a transition point to another topic that you've spent many years working on and thinking about, which is testosterone and other sex steroid hormones. How should we think about the role of testosterone in the amygdala, given that the engagement of the amygdala is fundamental in this transition point between an exhilarating positive response and a negative stressful response? Or maybe just broadly, how should we think about testosterone and its effects on the brain?
**Robert Sapolsky** (3:20)
Basically, almost everybody out there has completely wrong ideas to what testosterone does, which is testosterone makes you aggressive because males, virtually every species out there have more testosterone and are more aggressive. And the reality is, testosterone doesn't do such a thing. It doesn't cause aggression. And you can see this both behaviorally and in the amygdala, it lowers the threshold for the sort of things that would normally provoke you into being aggressive so that it happens more easily. It makes systems that are already turned on, turn on louder, rather than turning on aggressive music or some such thing. It's not creating aggression, it's just upping the volume of whatever aggression is already there.
**Andrew Huberman** (4:07)
Yeah. And in terms of status and the relationship between individuals, either non-human primates or humans, can we say that relative levels of testosterone between individuals is correlated to status within the hierarchy?
**Robert Sapolsky** (4:22)
Yes. Like you go back whatever number of decades, the endocrinology texts and there were two totally reliable findings in there, which is higher levels of testosterone, predict higher levels of aggression in peonies and other animals, higher levels of testosterone predict higher levels of sexual activity. And the correlation is there. And when you look closely, we've got cause and effect stuff. Sexual behavior raises testosterone levels, aggression raises testosterone levels. Your levels beforehand are barely predictive of what's going to happen. So it's a response rather than a cause. Just a great footnote. If you have the right type of willing to die in the trenches devotion sort of thing, watching your favorite team play a sport will raise your testosterone levels as you sit there with the potato chips in your armchair. So it's not the physicality of aggression. It's the psychological framing of it. So yeah, testosterone is not causing that. And the great way to appreciate that is you do a subtraction study, you remove the testes, and as I said before, levels of sexual behavior goes down. Good. We've just shown that testosterone is somehow causative. Critically, they go down, but not down to zero. Whether you are a rat or a monkey or a human, whatever. And what predicts how much residual sexual behavior is there? How much sexual behavior there was before castration?
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