Thursday, May 5, 2011

The Robert Lustig Diet?



I get a number of inquiries, both through the search engines and in person, regarding Dr. Lustig, and what diet he recommends. The following is not the “Lustig Diet” per se, but it is what he and the University of California, San Francisco Center (UCSF) for Obesity Assessment, Study & Treatment (COAST) recommends.

From Sugar: The Bitter Truth:

We write this on the back of a matchbook. It’s just as simple as you can make it. We have four things we teach the kids to do, and the parents.

1. Get rid of every sugared liquid in the house. Bar none. Only water and milk. There is no such thing as a good sugar beverage. Period.

2. Eat your carbohydrate with fiber. Why? Because fiber is good. Fiber is supposed to be an essential nutrient and we can talk later if you want, after the cameras turn off, as to why fiber is not an essential nutrient – because the government doesn’t want it to be. Because then they couldn’t sell food abroad.

3. Wait 20 minutes for second portions, to get that satiety signal.

4. Finally, buy your screen time minute for minute with physical activity. That’s the hardest one to do. If you play for ½ hour, you can watch TV for ½ hour. You want to watch TV for an hour? Play for an hour. That one’s a hard one.

We follow our patients every three months. Here’s my question: does it work? What do you think? Yeah, it works.

In sum:

1. Eliminate sugar-sweetened beverages.
2. Eat carbohydrates with natural sources of fiber
3. Wait 20 minutes for second portions
4. Buy screen time with physical activity, minute for minute.

Monday, April 11, 2011

Gary Taubes: The Complications of Cholesterol


In 2005, my wife and I interviewed Gary Taubes at his apartment in New York City. We were planning on doing a documentary on diet and health, and during this time (January 2005-May 2005) I went on a fast food diet. I was basically doing Fat Head before (I think) Fat Head. (Tom Naughton did an incredible job.)

Whether the documentary will eventually see the light of day is unclear, but I wanted to share some clips on the blog that we produced along the way.

"In the case of diet and heart disease, Ancel Keys's hypothesis that cholesterol is the agent of atherosclerosis was considered the simplest possible hypothesis, because cholesterol is found in atherosclerotic plaques and because cholesterol was relatively easy to measure," writes Gary Taubes in Good Calories, Bad Calories (GCBC). "But as the measurement technology became increasingly more sophisticated, every one of the complications that arose has implicated carbohydrates rather than fat as the dietary agent of heart disease." In this 2005 interview, before the publication of GCBC, Taubes discusses the cholesterol story. A more comprehensive account can be found in Chapter 9 of GCBC: Triglycerides and the Complications of Cholesterol




Below is a transcription:

[00:02:30.06] It's so bizarre, that when you realize what's happening -- I'm going to try and tell it. See if I can get this straight. They come up, they have this guy John Gofman, Berkeley, has this device that can fractionate lipoproteins. Basically, it can take the lipoproteins, which are the carriers of the cholesterol, from your blood. Say you've got so much LDL, so much VLDL, very low density, so much IDL. 

[00:03:02.17] And look, VLDL seems to be as much of a risk factor if not more. If you believe his equations, it's a greater risk of heart disease than LDL. And VLDL carries the triglycerides. Then another group of scientists, Pete Ahrens and some other people, Margaret, whose name I'm going to forget at the moment, who really did great work and I shouldn't forget her name, and it's embarrassing.

[00:03:30.20] Margaret [Albrink] got marginalized. She was at Yale and she took a job at West Virginia and it was like 'poof' -- West Virginia, who cares? Her husband got a job there, we don't care what you have to say. Anyway, they pushed. They said triglycerides, they're as great a risk factor as cholesterol. The studies show it. So in '67, this guy Donald Fredrickson and Robert Levy and a guy named Lees, they're at NIH and they put this five part series in the New England Journal of Medicine on -- it's called lipoprotein disorders, basically, and they classify them as five different lipoprotein disorders.

[00:04:04.02] Some of them are low LDL and some of them are low VLDL or high VLDL or high triglycerides. And they want to know how these things, the portion in the population at large, because they've just been studying patients who were referred to them at NIH. Frederickson and Levy are big deals at NIH. Back then it was the National Heart Institute instead of NHLBI. 

[00:04:26.08] So they get funding to give money to Framingham and five other big population studies, to see how much LDL -- how these lipoprotein disorders appear in the population. For the first time ever, these studies are going to measure LDL and VLDL cholesterol, total cholesterol. Nobody's ever measured VLDL or triglycerides in large populations. It's never been done. Now for the first time ever these big studies like Framingham have the money to do it.

[00:05:01.23] Frederickson, Levy and Lees also give them a ... they come up with a technology that makes it relatively inexpensive to measure these things. You don't need this huge equipment that Gofman had at Berkeley. So they go off to do this study and the problem is you can't measure LDL directly. Don't know the details why, but it can't be done. What you have to do is measure total cholesterol, triglycerides, and HDL and you do this equation and you calculate LDL.

[00:05:31.28] So they have to measure HDL also. Now, since 1950 or '51, I forget which, people have been saying HDL is the single most important risk factor for heart disease, and it's been ignored because if HDL is high, that means it's good for you. It's part of total cholesterol and Ancel Keys has been saying that total cholesterol is bad for you and that has to be low. And how do you make sense of part of total cholesterol being good, when total cholesterol is bad. And this is very confusing.

[00:06:01.05] So HDL has been ignored. Now they have to measure HDL in order to come up with the number for LDL. The head of -- the guy who does the biostatistics for Framingham and NIH and all these studies [Tavia Gordon] decides he's got the HDL data, this is now mid-70s, let's look at it. So he looks to see what kind of risk factor HDL is and lo and behold, HDL is four times a better predictor of heart disease than LDL. Total cholesterol, he finds out, is meaningless. 

[00:06:30.23] Total cholesterol doesn't predict heart disease. This is what's being measured. It's meaningless. LDL is a "marginal predictor." This is the phrase they use. And HDL, four times better. Four times more accurate at predicting heart disease. If HDL is low, that's a powerful indicator that you're going to get heart disease. And on top of it, for women, HDL is the only number that matters. So in 1976 they publish these articles. Two articles in particular.

[00:07:01.23] One from Framingham alone. And one from Framingham and the other five groups together. Two different types of studies. Both of them say the same thing. Total cholesterol is meaningless. LDL is a marginal predictor of heart disease risk. HDL is the single best predictor. And triglycerides are also a good predictor. Now the problem is, you have a half billion dollars of studies dedicated to lowering total cholesterol, the LRC, Lipid Research Clinics trial, and MRFIT trial, are both aimed at lowering total cholesterol.

[00:07:36.22] So what they say, and you see this in the papers. They say total cholesterol is meaningless but LDL makes up the biggest part of total cholesterol and we know that LDL is a marginal predictor. So we're going to play up how good LDL is. And as you watch the papers the adjectives used to describe it as a risk factor get more and more ... zealous, as the time ... it goes from being marginal to robust, without the data ever changing.

[00:08:08.12] And we're going to say everything we had said about total cholesterol, all the studies from the 1950s and 1960s, the famous seven countries studies, had all measured total cholesterol. They say "everything we say about total cholesterol is now going to apply to LDL cholesterol. And the MRFIT?? study and the Lipid Research Clinic study we're going to say are aimed at lowering LDL cholesterol.

[00:08:29.23] That's what we're trying to do because LDL is a predictor." Now the problem is, that in the clinic, where doctors all around the world are measuring total cholesterol, they're measuring something that's meaningless. But you can't measure LDL cholesterol. They don't have a test for it. You've got to measure all these other things and calculate LDL cholesterol which is too difficult to do.

[00:08:56.20] And it's not the kind of thing that they can tell doctors to do, because they're going to have all kinds of problems with mistakes and errors, and all these things that have to be worked out that they can't do. Meanwhile they have the doctors measuring total cholesterol. They're doing it all over the world. They say, in the clinic -- and you read this in the articles, I'm not making this up -- in the clinic, total cholesterol is a good enough substitute for LDL cholesterol that people can keep measuring total cholesterol and use that as their guide. So the study says that total cholesterol is meaningless.

[00:09:29.27] In the scientific discussion we're going to replace LDL ... total cholesterol with LDL cholesterol, because that's a marginal predictor, and then in the clinic we're going to re-replace LDL cholesterol with total cholesterol going back to the meaningless predictor on the basis that it's a close enough substitute for LDL that it'll suffice. So within three years, they can say that doctors should continue measuring total cholesterol, even though they now know that total cholesterol is meaningless. Meanwhile HDL and triglycerides just still continue to get left out totally because what do you do about that?

[00:10:00.15] And it's four times the predictor. [interviewer] And the problem ... the interesting thing is ...

Monday, April 4, 2011

Robert Lustig: Do Low Insulin Levels Cause Low-Carbohydrate Diets?

In a January episode of The Livin’ La Vida Low Carb (LLVLC) Show (Episode 429) with Jimmy Moore, Robert Lustig was the featured guest on the pocast, and what transpired was particularly illuminating for several reasons. I want to share one of them below.

(Dr. Lustig’s Sugar: The Bitter Truth lecture is approaching 1,000,000 views on youtube, and justifiably so.)

During the podcast, Jimmy asked Dr. Lustig about a study he had mentioned on a prior podcast of LLVLC (Episode 378):

Lustig: That was a pilot study. Everyone got drugged. It was not controlled it was not blinded and we went on a fishing expedition in which we gave people a drug that blocked insulin release called Octreotide. Octreotide is usually used to treat acromegaly, which treats growth hormone (GH) excess because it blocks growth hormone release as well as insulin release and so people who have pituitary tumors and oversecrete GH are on this drug. We used [Octreotide] instead to block insulin release and what we found was there was a group, out of the 44 we treated, 8 of them responded amazingly well.
Lustig: Their appetites went away, they stopped snacking between meals, their carbohydrate intake went down like a stone from 900 calories a day from carbohydrate to 350. They felt better and they lost a lot of weight. 12.6 kg in 24 weeks. And we didn't tell them to change the composition of their diet or to lose weight, they just did it, all by themselves.
Lustig: This was kind of amazing. But it only happened in eight out of the 44 study participants. It was cause-and-effect in the eight, or 18% of the subjects, because we could look before and after the treatment, and it turned out that the 18% who responded, all had one thing in common: all hypersecreted insulin. Their insulin response to glucose were all the same as each other and very different from the 36 who did not.
Lustig: So what we end up doing in this study was finding a subset of people who hypersecrete insulin, who oversecrete insulin for the same amount of glucose. Now, those people are walking the streets, they don’t know who they are, they don’t know what they look like. The doctors taking care of them don’t know who they are either. But we’ve shown in a clinic, where we do OGTT, as routine in our clinic, because that’s how we sort patients.
Lustig: This is going back to the first point; not everybody’s the same. We are not the same. Obesity is not a disease, it is a phenotype of many different pathologies. What we did in the study was we found one pathology. We found one reason for obesity. And we found one treatment that worked for obesity.
Lustig: You might say that you found the data post hoc, it wasn’t randomized, it wasn’t controlled, it wasn’t blinded. To which I would say: We did it again. We did it again in a randomized, double-blind, placebo-controlled fashion in a clinical trial. … The same group of people responded; the same group of people who hypersecreted insulin to start with.

I think this is fascinating for many reasons, but something that should not be overlooked is the pattern, or arrow of causation, that appears to be occurring in the subjects who are responding to the Octreotide.

Normally, we, the proponents of the carbohydrate/insulin hypothesis, would say that a low-carbohydrate diet causes lower levels of insulin. However, what Lustig has really shown in the studies above is that the causality can be flipped: lower levels of insulin can cause a low-carbohydrate diet.

As Dr. Lustig said, “They had a change in macronutrient preference. They were carboholics. We blocked their insulin, and now, they couldn’t care less about carbohydrate. By getting their insulin down, we changed what foods they ate.”

Acutely, when we eat a meal rich in carbohydrates, our insulin goes up in response. For the uninitiated, elevated levels of insulin in the body used to be a strong clue that there are an abundance of carbohydrates in the bloodstream. Insulin tells the muscles to burn carbohydrate for fuel and for the adipocytes to store nutrients as fat and inhibit the release of fat into the bloodstream. Why waste any stored fat when we have an abundant supply of energy in the bloodstream? Also, we know that elevated blood sugar is not a state we want to be in for several acute and chronic reasons, so the priority becomes clearing carbohydrates.

I say “used to be a strong clue,” because more and more people are becoming chronically hyperinsulinemic, insulin resistant, and type-2 diabetic.


Acute 'hyperinsulinism' may be seen as something physiological and not necessarily pathological: we eat like the Kitavans for a meal, lots of carbohydrates from glucose sources, and our insulin goes up, we burn carbohydrates for fuel, we temporarily inhibit lipolysis and store fat, but over time (perhaps overnight) we are ultimately homeostatic: our weight may fluctuate, but not by much, and we remain relatively weight stable and relatively lean.

Chronic hyperinsulinemia is another, and pathological, story. If you have elevated insulin levels most of the time, our bodies don’t know the difference between our acute response to a carbohydrate-rich meal and the chronic condition of hyperinsulinemia, so the response in the body is relatively the same. Fuel is partitioning in the same manner where insulin is telling muscles to burn carbohydrate; and fat tissues to store fat and protein, and to hang on to it.

Carbohydrates become the body’s food of choice. A hyperinsulinemic state can sap glucose from the energy supply because it ‘thinks’ glucose is in high supply. But it’s not. You should be burning free fatty acids (FFAs) for fuel while glucose is in relatively short supply. Not so for people who are chronically hyperinsulinemic. They crave carbohydrates because that’s what they can utilize for fuel and it is also what happens to be in short supply because of the way their fuel is partitioned.

The obese, hyperinsulinemic, will eat; store a little more of it as fat, and their insulin remains relatively elevated for longer periods of time; and they eat a little more, and they store a little more and burn a little less than a healthy, lean individual who is relatively insulin sensitive, a ‘hypo-secreter’ of insulin, if you will. And so the fat begins to accumulate progressively on the fat person, while the lean person remains in "energy balance."

The fat person isn’t fat, and isn’t getting fatter because he’s eating more; the fat person was, and is, eating more because he’s fat, and getting fatter. (Thank you, Gary Taubes, who would like to thank George Wade, who should probably thank Hugo Rony back to 1940. This isn't a new observation, but most people, i.e. the conventional wisdom interpret it from the wrong side of the 'arrow' of causality, at least when it comes to us weak-willed humans.)

The healthy, lean individual isn’t lean because he’s eating less; he’s eating less because he’s lean. The healthy person will eat; store fat, and then burn fat, so that he is in “caloric balance,” but calories really don’t have anything to do with it.

As Lustig noted, essentially the fundamental way an obese, hyperinsulinemic individual gets fat out of the fat tissue is to lower insulin levels. Octreotide did the trick in his patients. 

Low-carbohydrate, slow-carbohydrate, and safe-carbohydrate (Lustig: “I'm for safe carb, rather than low-carb, as a generalization”) diets, for example, can do the trick as well.

And, just as Lustig pointed out that when he blocked insulin secretion in subjects who otherwise secreted too much insulin and they went from “carboholics” to ostensible Atkins-dieters; the logic would hold that if you took a healthy individual and gave them a drug (insulin is on the nose) that kept insulin elevated, we would see the opposite: we would induce “carboholism.”

We're not just playing with words when we observe that, people who go on low-carbohydrate diets have lower levels of insulin, and people on high-carbohydrate diets have higher levels of insulin, and we conclude:

Lower levels of insulin cause low-carbohydrate diets...

...and...

...Higher levels of insulin cause high-carbohydrate diets.

And both may be a "vicious" cycle where lower levels of insulin leads to a lower-carbohydrate diet, which lowers insulin levels, which leads to a lower-carbohydrate diet.

The same holds true inversely: higher levels of insulin leads to a higher-carbohydrate diet, which raises insulin levels, which leads to a higher-carbohydrate diet.