Home » Fat Chance: Fructose 2.0 by Dr. Robert Lustig (Transcript)

Fat Chance: Fructose 2.0 by Dr. Robert Lustig (Transcript)

Most clearly, mother’s diet but you want to blame the newborn for that problem? Is that their problem? Is that their fault?

So you want to blame the pregnant mother? Well you know… then, just go backwards like that, so basically blame everybody, or blame nobody. I blame nobody. Actually I do blame somebody but you’re going to get there at the end.

So we are talking about behavior, right? Behavior, so this is the definition of behavior, this is all from the original video. A stereotyped motor response to a physiological stimulus, so let’s take that apart.

Stereotyped, same every time, so, yes, eating is a behavior; motor, muscles have to move, a thought is not a behavior, and finally, physiological, and that’s where I come in.

What’s the physiology behind the obesity epidemic?

Why do you eat too much and exercise too little?

Because all behaviors have a biochemical basis. Now sometimes we are smart enough to know what it is and sometimes we are not smart enough to know what it is. Give you an example: schizophrenia.

For 100 years schizophrenia was behavioral disorder. Now we know it’s a defect in dopamine neuro transmission, and probably actually a defect in glucose transport across the brain. These are biochemical problems, that ultimately manifest themselves as a behavioral disorder, this is no different.

So what are the biochemical underpinnings behind gluttony and sloth? That’s the question, and that’s what we’re going to try to answer now.

So in order to answer that we have to know some science, and I’m going to make this very brief and very quick.

We’re going to talk about these two hormones right over here, called leptin and insulin. So leptin is a hormone that comes from your fat cell, goes to your brain and tells your brain, you have enough energy on board, to engage in normal, expensive metabolic processes. You can burn energy at a normal rate and feel good doing it. And tells your brain, you’ve got enough energy on board, if your leptin goes down, or if your brain doesn’t see your leptin, then your brain sees that as starvation.

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Everybody got that?

Insulin is equally interesting, because insulin tells your fat cell one thing, it says, store energy and it tells your brain something else, it tells your brain: stop. I’m in the middle of metabolizing a meal, I don’t need any more, let me deal with what I’ve got, and so it’s part of the satiety signal.

So it tells your fat cell, get bigger and it tells your brain, stop feeding your fat cell. So it’s got a dichotomist role, and it’s that dichotomist role that is the linchpin in terms of understanding the physiology of obesity. And we’re going to go there.

So here’s how it works, we have to explain a paradox. Here’s the paradox. Who has children? Enough of you. What happens if you give a 5 year old kid a cookie? Yeah, they eat it, yeah, I know they eat it, what happens after that? They bounce of walls, is what they do, ask any kindergarten teacher what happens when the cupcakes roll out for the birthday party.

That’s the end of the lesson. They are bouncing off walls, is known as the sugar high. So what’s going on, the fat cell gets filled, because of the cookie, the leptin goes up, tells the brain “hey, I’ve got extra energy on board”, it tells the sympathetic nervous system, the fighter/flight part of the nervous system that innervates your muscles, and innervates your fat cells, “hey, I got too much energy”, so what happens? You burn it off, so the sympathetic nervous system tone to the muscles give you the fidgeting and the sympathetic nervous system tone to the fat cells releases the extra fat, and that gets used for energy later, and so this is a nice negative feedback pathway that keeps you in energy balance as long as your brain can see its leptin. So far so good.

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So here’s the paradox? What happens if you give an obese 5 year old kid a cookie instead? They are in the pantry looking for more cookies. Anybody ever see a sugar high in an obese kid? Doesn’t exist, doesn’t exist. And that’s why they are obese, it’s because they don’t get the sugar high, because they can’t see their leptin because if they could see their leptin they’d have a sugar high. But they don’t, that’s the point.

So something is blocking that leptin signal, that’s the paradox, the question is, what is it?

So we learned about leptin from this patient over here. This is the obi obi mouse, the leptin deficient mouse, who has a gene defect in the leptin gene, so this animal’s leptin is zero. So his brain thinks he’s starving all the time, so he’ll eat anything in sight, not only will he eat anything in sight, but this animal is the ultimate couch potato, because his brain can’t see his leptin, so he thinks he’s starving, so he doesn’t want to burn energy, he wants to store it.

So the only reason this animal ever gets off his hind is if you put the food on the other side of the cage, and they’ll waddle over to that sit down, eat it there, and stay there instead. Everybody got it?

Now, the reason? Because leptin tells the hypothalamus that you’ve got the energy to burn. So if the hypothalamus sees the leptin signal, then this diamond over here gets activated, anorexigenesis, that is, I’m not hungry, I don’t need any more, and I can burn energy effectively. And so it tells the sympathetic nervous system turn on to fidget and to release fat from the fat cell and it tells the vagus nerve, the energy storage nerve, “hey, I’m not hungry, appetite down, and stop releasing insulin”. Everybody with me?

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