Dr. Mark Hyman

And so it's not that we've depressed them, it's that we've turned them over more rapidly because we're not sustaining their functional ability.

And so it's not that we've depressed them, it's that we've turned them over more rapidly because we're not sustaining their functional ability.

And so it's not that we've depressed them, it's that we've turned them over more rapidly because we're not sustaining their functional ability.

Did I get that right? I mean, yes, you did phenomenologically. I think, yes, you did. But I think mechanistically, I think there's maybe a little bit more to the story. It has to do with the turnover and life cycle of these different cells within our immune system. So as we've said earlier in this discussion, immune cells kind of sacrifice themselves often for their defense.

Did I get that right? I mean, yes, you did phenomenologically. I think, yes, you did. But I think mechanistically, I think there's maybe a little bit more to the story. It has to do with the turnover and life cycle of these different cells within our immune system. So as we've said earlier in this discussion, immune cells kind of sacrifice themselves often for their defense.

Did I get that right? I mean, yes, you did phenomenologically. I think, yes, you did. But I think mechanistically, I think there's maybe a little bit more to the story. It has to do with the turnover and life cycle of these different cells within our immune system. So as we've said earlier in this discussion, immune cells kind of sacrifice themselves often for their defense.

They will undergo cell suicide as a consequence of when they are overly called on. And so maybe what we're talking about as an immune system that looks like it's underactive with these natural killer cells, it's actually just that the system is so turned on that they're not able to replicate and keep their function. And so what we need to do is lower the burden to allow them to catch up.

They will undergo cell suicide as a consequence of when they are overly called on. And so maybe what we're talking about as an immune system that looks like it's underactive with these natural killer cells, it's actually just that the system is so turned on that they're not able to replicate and keep their function. And so what we need to do is lower the burden to allow them to catch up.

They will undergo cell suicide as a consequence of when they are overly called on. And so maybe what we're talking about as an immune system that looks like it's underactive with these natural killer cells, it's actually just that the system is so turned on that they're not able to replicate and keep their function. And so what we need to do is lower the burden to allow them to catch up.

That's right. So rather than give more natural killer cells, what we need to do is find the mechanism that's causing the eradication or the overactivity of those cells. They're short in lifetime. and reduce the senescence of the cells.

That's right. So rather than give more natural killer cells, what we need to do is find the mechanism that's causing the eradication or the overactivity of those cells. They're short in lifetime. and reduce the senescence of the cells.

That's right. So rather than give more natural killer cells, what we need to do is find the mechanism that's causing the eradication or the overactivity of those cells. They're short in lifetime. and reduce the senescence of the cells.

As I said earlier, one of the most important lessons for me in all my years of studying cell biology and health is that every process that I can think of in the body that I've come in contact with has a destructive or a breakdown phase and a buildup phase. So think of this as a highway with two lanes. One lane is the area of breaking down

As I said earlier, one of the most important lessons for me in all my years of studying cell biology and health is that every process that I can think of in the body that I've come in contact with has a destructive or a breakdown phase and a buildup phase. So think of this as a highway with two lanes. One lane is the area of breaking down

As I said earlier, one of the most important lessons for me in all my years of studying cell biology and health is that every process that I can think of in the body that I've come in contact with has a destructive or a breakdown phase and a buildup phase. So think of this as a highway with two lanes. One lane is the area of breaking down

On the other side of the highway is a lane that's building back up. Now, in terms of metabolism, we call that catabolism and anabolism. We say catabolism is you break down macronutrients, protein, carbohydrate, and fat into calories of energy. And then you use those calories of energy to build back up tissues like muscle and other tissues that are needed.

On the other side of the highway is a lane that's building back up. Now, in terms of metabolism, we call that catabolism and anabolism. We say catabolism is you break down macronutrients, protein, carbohydrate, and fat into calories of energy. And then you use those calories of energy to build back up tissues like muscle and other tissues that are needed.

On the other side of the highway is a lane that's building back up. Now, in terms of metabolism, we call that catabolism and anabolism. We say catabolism is you break down macronutrients, protein, carbohydrate, and fat into calories of energy. And then you use those calories of energy to build back up tissues like muscle and other tissues that are needed.

So catabolism and anabolism, we'd like to be balanced. But that can occur, that same model can go right down to every cell type. So let's talk about molecules that we want to put a label on. Let's talk about prostaglandin E2, which we call an inflammatory molecule. So we say, oh, gee, we see a high level of that molecule in the blood if a person has a lot of inflammation.

So catabolism and anabolism, we'd like to be balanced. But that can occur, that same model can go right down to every cell type. So let's talk about molecules that we want to put a label on. Let's talk about prostaglandin E2, which we call an inflammatory molecule. So we say, oh, gee, we see a high level of that molecule in the blood if a person has a lot of inflammation.