High Fat Diets: The Sweet Deception

Robert Lustig was recently interviewed by KQED and had this to say:

How do you get diet induced obesity in a rat? People say put them on a high fat diet. Garbage.

You can't get a rat to eat a high fat diet...unless you add 20% sucrose to the diet. Basically you're giving them cookie dough.

But if you give them lard they won't eat it. They actually lose weight on that because that's the Atkins diet for them. It's not palatable. They don't like it and they actually lose weight and their metabolic parameters improve.

The only way to get an animal; a rat, monkey, or any other animal, for that matter, to eat a high fat diet is to lace the fat with sucrose.

So the question is: which is doing the damage, the fat or the sucrose in that case? And the answer is both.

In a recent post entitled Diabetic nephropathy and the lost Swede at Hyperlipid, Peter links to a recent paper in PLoS which demonstrated a partial reversal of diabetic nephropathy in mouse models.

“These studies demonstrate that diabetic nephropathy can be reversed by a relatively simple dietary intervention,” conclude the authors of the paper.

Peter goes on to cite a Swedish paper - that the recent paper above did not cite - which demonstrated a reversal of renal failure by a low-carbohydrate diet.

While the PLoS study neglected to mention the Swedish paper, they referenced a 2007 paper entitled A high-fat, ketogenic diet induces a unique metabolic state in mice.

Bottom line for these researchers? “These data indicate that KD [Ketogenic Diet] induces a unique metabolic state congruous with weight loss.”



The diets were:

1) Control, or, Chow (16.7% fat, 26.8% protein, 56.4% carbohydrate (6.5% sucrose))
2) High Fat (45% fat, 24% protein, 35% carbohydrate (17% sucrose))
3) Ketogenic Diet (95% fat, 5% protein, 0% carbohydrate)

Wait, so which one is the “high-fat” diet, again? “High-fat” is 45% fat, while KD is 95% fat. It has been mentioned before at this blog, and warrants mentioning again: in science, you need well-defined variables.

When researchers compare a low-carbohydrate diet to a low-fat diet, what constitutes “low” depends on which team of researchers you ask. There is no well-defined number or percentage. Also, invariably, when the diets are compared, the low-carbohydrate diet is ad libitum, which is a fancy way of saying “all-you-can-eat.” The low-fat diet is restricted in calories, but more often than not, the researchers do not make this distinction throughout their articles. These are just a couple of examples to the limitations of the current definitions, and there are more, to be sure.

With a “high-fat” diet which happens to contain 162% more sucrose as a percentage of carbohydrates compared to the chow, perhaps the researchers and the people reporting the results should mention something about this? Considering when the researchers remove the sucrose and add fat (i.e., the ketogenic diet), the problems magically disappear, it just might warrant mentioning, and might bring into question the quite liberal use of the term "high-fat" in this context.

While Dr. Lustig and I can agree that we think it’s garbage to claim that we induce obesity by feeding mice, or humans for that matter, a “high-fat diet,” it seems we part ways regarding why the mice eat less on a ketogenic diet (i.e., a  high-fat, little-to-no-carbohydrate diet) and also regarding what is doing the damage. Lustig thinks its sucrose and fat? A little bit odd coming from the guy who said “It ain't the fat, people.” Perhaps I'm picking nits, but doesn’t this imply that you need to feed a human both sucrose and fat to induce damage? (I would also like to address the idea that the KD is not “palatable” and the absurd implication that dieters eat less out of boredom that many researchers, academicians, journalists, physicians, and authors alike invoke, but will save it for another post. To keep you “satiated” in the interim, here is a great post by Dr. Eades on the subject.)

In other words, if we had two arms of a randomized controlled trial (RCT):

1. 2500 kcal: 90% Fat; 10% Protein; 0-1% CHO
2. 2500 kcal 0-1% Fat; 10% Protein; 90% Sucrose;

Would both of these groups lose weight and improve their metabolic parameters? Let’s say prior to baseline they have an average BMI of 32, and they have been relatively weight stable in the past 6 months eating:

2500 kcal: 30% Fat; 10% Protein; 60% CHO (about 20% sucrose)

As Lustig has said, a calorie is not a calorie, and calories can be isocaloric, but not isometabolic.

In other words, the second arm of the RCT is taking in 90%, or about 2250 calories of sugar, and 1125 calories of fructose. This amounts to about 281 grams. Lustig has said to shoot for less than 50 gm.

Why would the fructose be particularly damaging? After all we’re talking about “fruit” sugar. How can something in fruit be bad for us? Sugar is natural. Have we just refuted the idea that sugar is toxic, poison, and evil?

As Gary Taubes pointed out in a recent interview on NPR, and Paracelsus (not sure if it was on NPR as well) in the early 16th century, the effective dose makes the poison.

One of the points biochemists will make is you can’t just say that something is natural.

A metaphor is I could lean on you and apply a gentle pressure for 10, 20 minutes, an hour, it’s not going to do you any harm. But if I take that same amount of pressure and condense it into a split-second, then I’m hitting you in the arm pretty hard, and it hurts, and I’m going to cause swelling and pain, etc.

And that’s what we’re doing when we consume these sugars in this quantity and especially in liquid-form, it’s like we’re hitting the liver with them, and the liver responds by going “ouch,” and turns it into fat and becomes a little insulin resistant, and then the rest of the body becomes insulin resistant, and over the course of months or years, you end up quite likely with this problem called metabolic syndrome, and all of these chronic diseases stem from there.

As Dr. Lustig pointed out in an interview with Jimmy Moore:

Basically, if you look at the stereoscopic model of fructose, you can’t even imagine how it can stay together as a ring. It’s going to fly apart almost on contact and that means that that reactive ketone group that’s in the fructose is going to react with just about any protein around and it’s going to contribute reactive oxygen species, which ultimately cause vascular damage. That’s basically you down the road to cardiovascular disease. If you’ve let that fructose get past your liver, you’re screwed.

We shouldn’t let researchers, or journalists, or professors, or anyone for that matter, off the hook when they implicate a “high-fat” diet in causing, or even curing, an ailment, without them making the distinction that a “high-fat” diet is a “high-fat-high-sugar” diet in this context.

It could be likely that the increase in sugar is the driver of disease, while the “high-fat” content is along for the ride. The results of the 90% fat ketogenic diets certainly seem to make a case for it.

The Russian Literature Paradox

And in knowing, that you know nothing, makes you the smartest of all. - Socrates

When I was attending Gary Taubes’s lecture at Tufts University, there was a fair amount of “audience participation.” I mean this somewhat facetiously because I was practically the only individual taking part.

Taubes would present a slide and a quote by someone in the field of nutrition and he would ask the audience of predominately nutritional science students and professors to raise their hands if anyone had heard of the quoted person.

“Who here has heard of Louis Newburgh?” Crickets. I would sheepishly raise my hand.

A few slides would go by. “Anyone familiar with Carl von Noorden?” Hay bale drifts through the room. My hand goes up. "You don't count; you read my book," quipped Taubes. Fair enough.

But I think there’s an important lesson in this.

I have been taking a distance (read: online) clinical nutrition course in which there is a great deal of discussion on the message boards. Each week, a group of two or three students post a question related to the week’s course topic. Gestational diabetes, carbohydrates and diabetes, metabolic syndrome, childhood obesity, bariatric surgery, saturated fats, and so on. And virtually every week, my opinion runs counter to at least 90% of the students.

Seemingly, it should be relatively easy to dismiss the lunatic with the tinfoil hat (it's comfortable, okay?) as a charlatan, but something odd happens en route. I’m the one presenting the science, the history of nutrition, and the observations that refute the claims of the vast majority. This goes off like a fart in church. Everything popular is wrong? Maybe.

Some people in the class are somewhat supportive, but most, at best, are condescendingly back-patting and thanking me, in their best Dr. Oz impression, for “kicking the tires.” This is what Oz said to Taubes during his appearance. In hindsight, Taubes said that he should have responded: ‘well, Dr. Oz, I'm not sure kicking the tires makes a damn bit of difference after you've totaled the car,’ (his other shelved rebuttal allegedly was ‘the jerk store called, and they’re running out of you’) though he also conceded that this would have been edited out, along with his explanation of the complications of cholesterol, and why he declined having a cholesterol test if they weren’t going to do a comprehensive panel, like the one he ended up getting.)

Others in the class claim that I’m introducing “a totally new science” to health and nutrition and that I should start my own special field. Go home and get your shinebox, Bob.

But here’s the rub: I am introducing science - not a ‘totally new science’ - science, into a field that seems to be actively avoiding it. I'm also just bringing up historical information regarding nutrition and it feels like many people think I'm coming out of left field.

I'm seen as a crackpot by the class when I bring up names like Louis Newburgh, Carl Von Noorden, Hugo Rony, Jean Mayer, Julius Bauer, Ancel Keys, John Yudkin, George Mann, George Bray, George Cahill, Eugene Du Bois, Francis Benedict, et al.

If this were a graduate level physics course (and this is something Taubes illuminated in his lecture), if I brought up names like Plank, Einstein, Tesla, Faraday, Heisenberg, Bohr, Curie, Feynman, Volta, Hubble, Fermi, et al., everyone would know who I was talking about, what they accomplished, and their contributions to the field.

In physics, if you didn't recognize these names, you would be laughed out of the field. In public health, you're mocked if you do.

If I polled the class on the recognition of the twelve names in nutrition and weight regulation I mentioned, how many of these people would they recognize? These people are pioneers in the field, yet we’re not taught very much, if at all, about them. I think it would be helpful.

I happen to know the names of guys like Rony and Bauer and their contributions to the field. For the most part, I know them because Taubes knows the names, too, and included them in articles like The Soft Science of Dietary Fat, What if It’s All Been a Big Fat Lie, The (Political) Science of Salt, and wrote books such as Good Calories, Bad Calories and Why We Get Fat.

It doesn’t make me smarter than anyone that I’m the only one in the lecture hall of 200 people to pass the Taubes test, but I would argue it makes me more informed. And one of the limitations to nutrition as I see it, is that if you really want to have a full understanding of obesity, for example, you need to be familiar with endocrinology, metabolism, weight regulation in animals, anatomy, clinical treatment and trials of obesity in humans, anthropology, exercise physiology, reproduction, cell biology, and have a familiarity with the relevant research, epidemiology, and clinical trials, and the list goes on. It might take a few lifetimes to achieve this.

But it doesn’t absolve the field from trying to learn the basic sciences and have at the very least a cursory understanding of the aforementioned topics. Instead, when I invoke biochemistry and endocrinology in the regulation of adipose tissue in my class, or when I tell them that the brain can run predominately on ketone bodies, they respond that I have “interesting opinions.” It’s the science! I’m not making it up!

This brings me to the latest podcast (episode 76) by Robb Wolf and Greg Everett at The Paleo Solution.

Robb was wonderfully agitated by the following question:

6. Brain Function without Dietary Carbohydrate

Craig Says: My girlfriend is a very recent graduate of nursing school and has been very helpful in my transition from a fellow vegetarian to a “things-with-a-face eater.” But she is very hesitant about my adoption of the Paleo diet mostly based on her contention that the brain cannot function properly without complex carbohydrates such as pastas and rice.  I’ve been 98% paleo for the last two months with a few slips into ice cream hell.  Can you give me a medical explanation that will help me in this battle?  She will not join the meat-eating bandwagon but has definitely reaped the benefits of switching our diet to entirely whole foods.  She is complete agreement with this aspect of Paleo nutrition but can’t understand the low-carb effect on the brain and other important bodily function.  Thanks for being such an accessible and reliable scientific resource.

So Robb dusts off his 4th edition of Stryer’s Biochemistry (I happen to have a copy myself so I think that makes us beaker-brothers or something nerdy - or perhaps we’re just both interested in science - which seems to be such a rarity in the field of nutrition, that it appears peculiar that we would have science textbooks?) and goes to town: the human brain can run predominately on ketone bodies during relative caloric, or carbohydrate, unavailability.

But it, too, brought up a larger point, which is very much related to the previous one about nutritionists having no understanding of the history of the field; they have virtually no understanding of the science behind nutrition as well.

It is valid to point out that physicians receive little to no nutrition training. Chris Kresser was just pointing this out in a podcast with Jimmy Moore. Why listen to your doctor when they have so little training in nutrition? Good question.

But what of the registered dietitians? What are they learning? I happen to be completing my didactic program requirement in dietetics, and feel free to have a look for yourself of the course requirements. There are science courses, to be sure, but it doesn’t seem to explain my experience with dietitians and dietetic students. It is safe to say that most of them don’t understand the biochemistry, endocrinology, biology, physiology, and organic chemistry, for example, at a level where they can explain relatively pedestrian mechanisms of action. To be fair, I was recently trying to work out a problem related to organic chemistry, and turned to an expert in the field, who subsequently asked if I had indeed passed organic chemistry in college. Passed? Yes. Grasped? No. But I’m trying and will continue to do so until I can at least speak the language.

I try to make it a point to surround myself with people who are smarter than me; people who often will tell me that I’m wrong more often than I’m right. Criticism is far more useful than praise. This is how you grow. To remain stagnant is to ignore the voices questioning your methods and results and never seeking alternative explanations or questioning your own ideas. The public health authorities are phenomenal at this.

I don’t think most dietetics students make this kind of effort. What Richard Feynman called “a specific, extra type of integrity that is not lying, but bending over backwards to show how you are maybe wrong, that you ought to have when acting as a scientist.” And “this is the responsibility of scientists,” (perhaps dietitians and public health authorities are immune), “certainly to other scientists, and I think to laymen.”

In fact, most people I know don’t seem to be making the effort, or claim that they just don’t have the time. That’s why I think people like Lalonde, Kresser, Taubes, Lustig, Wolf, et al. are so invaluable, and unfortunately, so rare.

Wolf, later in his diatribe, posited a couple of questions: Why aren’t the nursing and medical students reading the textbooks and scientific literature and questioning the conventional wisdom? And why is the convention wisdom what it is when it seems to run counter to science?

I think it’s because the foundation and core principles of public health operate as a political institution. It may be fair to say that the opposite of science is politics, i.e., politics is anti-science. And this is coming from a blogger who studied political science (an oxymoron, perhaps?) as an undergrad.

Robb also mentioned that he was “mean” to his conference attendees - at a hospital, addressing the medical staff - during a recent presentation and asked them basic biochemistry and metabolism questions; and they could not answer them correctly. And maybe half the people were present to tell Robb what he was saying is wrong.

Sounds a lot like Taubes, his lectures, and his point about the dearth of understanding of one’s own field. Yet these same people in the audience of a Taubes or Wolf lecture are the ones discrediting the lecturer and dispensing the dietary advice; while Gary and Robb are relegated to “kicking the tires.”

Another point that Robb illuminated was The Russian Literature Paradox.

If you run into a PhD in Russian Literature and tell them you read Crime and Punishment, and get into a discussion about Russian lit, and the PhD rattles off names like Alexander Blok, Sergei Yesenin, Anna Achmatova, Marina Tsvetaeva, Osip Mandelstam, Boris Pasternak, Joseph Brodsky, Vladimir Mayakovsky, Ivan Bunin, Vladimir Nabokov, Mikhail Sholokhov, Mikhail Bulgakov, Andrey Platonov, Vassily Grossman and Aleksandr Solzhenitsyn, (I had to look up just a few of these names!) perhaps you should defer to this man’s opinion. It doesn’t mean that his convictions are necessarily true, but it most likely means that he is more informed and has a better grasp on the subject. And perhaps you should educate yourself on the subject before you join the discussion.

With nutrition, everyone eats, therefore everyone is apparently an expert in nutrition. Everyone has an opinion, and anyone who has lost more than three pounds in their life (about 99% of the population), feels that they can instill their wisdom upon the masses to great fanfare.

Problem is, even the supposed experts in nutrition can't tell you who the nutritional European and American equivalents to Nabokov, Dostoyevsky, Gogol, and Chekhov are, but boy are they are willing to commentate and pontificate with great resolve.

With Russian Literature, most people are wise enough to heed the advice of Mark Twain: “It is better to keep your mouth closed and let people think you are a fool than to open it and remove all doubt.”

With nutrition, every Tom, Dick, and Harry - and seemingly every public health authority - has no problem opening their mouths and removing all doubt.

In other words, the "experts" in the field of nutrition do not understand nutrition. Therefore, anyone who can rub two brain cells together can contribute to the field.

Meanwhile guys like Gary Taubes, Robb Wolf, Chris Kresser, Chris Masterjohn, Kurt Harris, Stephan Guyenet, Petro Dobromylskyj, Michael Eades, Robert Lustig, Eugene Fine, Eric Westman, Steve Phinney, Jeff Volek, et al., are having collective aneurysms on a daily basis and at some point, I believe, we are all going to realize that engaging the "experts" in a dialogue is like playing handball against the drapes.

I feel like I speak for the bloggers, physicians, and researchers above in a collective message to the public health authorities, channeling my inner-Will-Hunting: “I’m sorry you can’t do this, I really am, because I wouldn’t have to fuckin’ sit here and watch you fumble around and fuck it up.”

I try - and I think this is a common thread among the aforementioned bloggers, writers, researchers, and physicians above - to treat the field of nutrition like a science, because that’s what it presumably is. And I think a significant part of the reason for the massive health problem we have is that it’s not treated as such.

Low-Carbohydrate Diets and LOSING Weight while Pregnant

Since my wife is pregnant, I have been thinking more about maternal and fetal issues and how they relate to nutrition, fuel partitioning, and weight management. She is thrilled for me.

One question I had while going for a walk was: Is it dangerous for a woman to lose weight during pregnancy? Dr. James Carlson has reported that he probably worked with thousands of mothers who lost weight during pregnancy on a low-carbohydrate diet and developed healthy babies while dropping as much as 50-60 pounds in the process.

The conventional wisdom holds that a mom shouldn't be losing weight while pregnant because there is an implicit assumption that the mother would be restricting calories; she would be semi-starving herself, therefore she would be starving the fetus, which would obviously be a problem, for both mother and fetus.

However, when you view it from the carbohydrate-hypothesis paradigm, low carbohydrate diets do not restrict calories, they do not restrict essential nutrients, and they generally improve the relative health of the mother, and therefore the baby as well.

When a mother is losing weight on a low-carbohydrate diet, while pregnant or not, she is not losing weight because she is eating less, she is eating less because she is losing weight.

For a non-pregnant woman, more fatty acids are liberated from adipose tissue and she literally has more energy circulating to provide endogenous fuel to her cells and, if she 'overeats,' for increased expenditure through both exercise (“activity thermogenesis”) and non-exercise activity thermogenesis (NEAT). She doesn't eat as much energy because her body is now providing more energy from her fat stores.

If higher levels of insulin drive more fat accumulation, lower levels of insulin help drive fat utilization. (It is worth noting that there is physiological insulin resistance that occurs during pregnancy. This will be covered in a subsequent post.)

For a pregnant woman losing weight on a low-carbohydrate diet, the same holds true as above, but in addition, she is also supplying energy to the baby. She eats less because she is losing weight through lipolysis, and now some of that fuel gets partitioned to the fetus as well. So long as she has ample fat tissue and is providing adequate energy and nutrients for her own needs, as well as her fetus, who cares how many calories she is eating?

A low-calorie, low-fat, low-cholesterol diet flies in the face of reason while pregnant. Keep in mind that this very same argument for pregnant women holds true for the population at large.

The fetus needs adequate energy, fat, and cholesterol for proper and healthy development.

All human beings require the same. To restrict calories, fat, or cholesterol is to restrict the organism from its physiologic needs. If one of these essential nutrients is being restricted, why wouldn’t we feel less than adequate?

For a woman with adequate adipose tissue, losing weight while pregnant is not dangerous, so long as the "weight", i.e., the energy, is being supplied to the fetus.

We're not violating the laws if thermodynamics here, we're transferring our energy to the fetus, and the result is that one system gets relatively smaller (the mother's fat tissue) and another system gets bigger (the fetus).

And for a non-pregnant woman on a low-carbohydrate diet, one fuel supply gets smaller (exogenous calories, i.e., food, i.e., "calories-in") while another fuel supply gets larger (endogenous calories, i.e., body fat, i.e, "calories-out").

We lose weight on a low-carbohydrate diet while we are in "energy balance" as the conventional wisdom portrays it. The conventional wisdom doesn't account for "calories-out" provided by our own energy stores in this context. But this is the fundamental driver of obesity and leanness. Expenditure is exceeding intake at the level of the fat tissue. Isn't that what we care about if we don’t want to be obese?

And for the fetus, does it grow because it takes in more energy or does it take in more energy because it’s growing? So long as we are supplying a metabolically healthy fetus with adequate nutrients, it will take what it needs for normal development. The fetus "eats more" because the fetus is developing and requires more energy.

We haven’t even begun to discuss the importance of breast milk, which also requires fuel to produce (breast milk is fuel, after all); and the rationale is for pregnant women to gain 10 pounds to provide a reserve to be utilized for breast milk. But if the pregnant mother is obese, for example, doesn’t she already have the maternal reserve?  

And what does "calories-in/calories-out" have to do with this fuel partitioning as well? Are we that naive to think there has to be a conscious, or behavioral, manipulation of caloric intake in order for us to gain the appropriate weight for breastfeeding as well as embryological and fetal development? 

Why are we this naive when it comes to obesity and leanness?

Sugar --> Diabetes, Cancer, Obesity, Metabolic Syndrome?

In this Sunday's New York Times Magazine, Gary Taubes writes about Sugar and whether it has unique metabolic effects apart from "empty calories" (as we're often told by public health authorities).

The article is now available online. Must read.

In a related topic, which I think ties in nicely with the article above: I had a message board assignment this week on carbohydrates and diabetes. I thought I would share the commentary, questions, and my responses, below:

From the Moderator:

Carbohydrates sure do get a bad rap. We hear it all the time, “don’t eat “carbs” because you will gain weight.” The Atkins diet is a famous low carb diet that has gained attention from mass amounts of people. Often times, when one food group is severely limited, people consume other food groups in excess. For example, cutting out carbs may cause a person to consume more fat which can be just as harmful. Many people talk about the wonders of low carb diets and how they trick your body into extreme weight loss. While cutting out carbs will likely result in weight loss, it can send the body into a state of ketosis. People are confused when it comes to the topic of carbohydrates, and the truth is, they are an important part of a balanced diet--especially for diabetics. Carbohydrates are the body’s primary source of energy, and as health professionals, it is crucial to emphasize the healthy sources of carbohydrates. Diabetes is growing in epidemic proportions, and patients should be educated to distinguish between a “good” carb and a “bad” carb. According to the article we need to get away from the terms of what is “good” and “bad” and educate people on what is healthy. It is important that diabetic patients understand the glycemic index and how foods affect the body’s glucose levels.

Click on the following link to read the article:
http://www.buffalonews.com/life/health-parenting/health/article384918.ece

1. What is the effect of a low carbohydrate diet on the body, and why do people rely on it for weight loss? Is this a harmful approach for diabetics, Why or Why not?

2. Distinguish the difference between a complex carb and a simple carb.

3. Are potatoes that bad for us? The article insinuates that baked potatoes are not the best choice, would you agree with this statement?

4. Define the terms: glycemic index and glycemic load and explain how we can use these terms to help diabetic patients improve their diets.

5. Evaluate this statement to be true or false and justify your answer: Eating too much sugar causes diabetes.

My Response:

First, I want to address the commentary that preceded the article link and questions.

“Often times, when one food group is severely limited, people consume other food groups in excess.”

Agree. Dietary trade-offs are an inescapable reality.

“For example, cutting out carbs may cause a person to consume more fat which can be just as harmful.”

I feel like this needs to be substantiated with evidence. For example, much of the research conducted in the last ten years in randomized-controlled trials of low-carbohydrate (ad libitum) diets compared to low-fat (calorie-restricted) diets have observed beneficial effects in terms of both weight loss, lipids, and other risk factors for the subjects adhering to the low-carbohydrate diet. Further, most studies show that when people replace saturated fats with carbohydrates, their health prospects worsen.

“Many people talk about the wonders of low carb diets and how they trick your body into extreme weight loss.”

I guess this is true, but for the people that claim that a low-carbohydrate diet “tricks” your body into weight loss, they’re missing the point. For many people going on a low-carbohydrate diet, they shift toward oxidizing relatively more fat for fuel than they have been accustomed to on a high-carbohydrate diet (which can elevate insulin, which promotes fat storage and inhibits fat mobilization). I would argue that when these people lose weight, they’re shedding the excess fat accumulation that has occurred in large part to the quality of their diet. They’re not losing fat because they’re losing weight; they’re losing weight because they’re losing fat.

“While cutting out carbs will likely result in weight loss, it can send the body into a state of ketosis.”

Ketosis is a natural physiological state in the body. In fact, most of us are technically in ketosis overnight (when we sleep) and our brains are primarily using ketones for fuel. The ketone level in our bodies upon waking will be around 5 mg/dl - and on an severely restricted carbohydrate diet (i.e., Atkins induction) the level is around 5 to 20 mg/dl. While you are reading this, it is likely you are in ‘ketosis,’ which is another way of saying you’re burning fat for fuel.

The ketone level in diabetic ketoacidosis typically exceeds 200 mg/dl.

Many diets that are low-carbohydrate are going to be more ketogenic in nature which is not a bad thing and is quite normal from an evolutionary standpoint. It's basically being more 'fat adapted' and using more of your body fat for fuel rather than glucose derived from dietary carbohydrates, which is "the body's preferred fuel" because it wants to get rid of it, i.e, bring blood glucose back to stable levels.

“Carbohydrates are the body’s primary source of energy, and as health professionals, it is crucial to emphasize the healthy sources of carbohydrates.”

This is false. The primary source of energy in the body is derived from fatty acids. You could argue that the body needs glucose to survive, and is vitally important, however there is no dietary need for carbohydrates. They are a nonessential exogenous nutrient.

As health professionals, we should emphasize healthy sources of carbohydrates, over what? Unhealthy sources of carbohydrates? Or emphasize them over all other foods in general? How would you define healthy sources of carbohydrates?

“Diabetes is growing in epidemic proportions, and patients should be educated to distinguish between a “good” carb and a “bad” carb.”

Agree, and at its core, I would say that diabetes is a disorder of carbohydrate metabolism. Even if you’re trapped in the diet-heart paradigm, restricting or virtually eliminating carbohydrates in a diabetic patient has a greater benefit-to-risk ratio.

Again, I would appreciate a definition of what a good carb is and a bad carb is going forward.

1. What is the effect of a low carbohydrate diet on the body, and why do people rely on it for weight loss? Is this a harmful approach for diabetics, Why or Why not?

I would say that most people rely on a low-carbohydrate diet for weight loss because it gets them the results they want. When they stay on a low-carbohydrate diet, they maintain their weight loss from the low-carbohydrate diet, and when they stray from it, i.e., increase their carbohydrate consumption, they gain the weight they lost back, so in that sense, they rely on a low-carbohydrate diet because it’s what makes them lose weight and what keeps it off.

The effect of a low-carbohydrate diet on the body, while this depends on the level of carbohydrate restriction, especially on people who are overweight and obese, generally speaking, is that insulin levels are lowered. Elevated insulin, when working properly, is a signal that there are elevated levels of glucose in the body. Insulin drives nutrients into their tissues, including adipocytes. Insulin also inhibits lipolysis, or the breakdown of triglycerides to be used for fuel. Carbohydrates, especially the most refined and easily digestible, drive insulin secretion. When carbohydrates are removed, insulin levels are lowered and the opposite effect occurs; less nutrients are being partitioned to the fat cells and we observe an increase in lipolysis.

A low-carbohydrate diet is generally not harmful for diabetics, however, since low-carbohydrate diets actually correct some of the abnormalities in diabetic patients (i.e., a low-carbohydrate diet is healthful for diabetics), one of the problems is a reason for contraindicating medications such as insulin and high blood pressure medications because a low-carbohydrate diet has an anti-hypertensive effect and creates a reduced requirement for insulin.

Also, I wanted to add here a quote from the article and my response:

“Everyone agrees that replacing saturated fats with unsaturated fats is good, but citing numerous studies that show an elevated risk of heart disease when carbohydrates replace saturated fats, scientists have been rethinking the role of carbs in cardiovascular disease.”

Everyone does not agree. There are people who believe that saturated fats from animal sources are just as good, if not more beneficial, than unsaturated fats.

Also, it’s not as clear-cut as replacing one type of fat for another. For example, lard, yes, lard, is mostly monounsaturated fat. And the saturated fat in lard has qualities that raise HDL and have no effect on LDL.

Gary Taubes wrote about this in Good Calories, Bad Calories:

"Consider a porterhouse steak with a quarter-inch layer of fat.  After broiling, this steak will reduce to almost equal parts fat and protein.  Fifty-one percent of the fat is monounsaturated, of which 90 percent is oleic acid.  Saturated fat constitutes 45 percent of the total fat, but a third of that is stearic acid, which will increase HDL cholesterol while having no effect on LDL.  (Stearic acid is metabolized in the body to oleic acid, according to Grundy’s research.)  The remaining 4 percent of the fat is polyunsaturated, which lowers LDL cholesterol but has no meaningful effect on HDL.  In sum, perhaps as much as 70 percent of the fat content of a porterhouse steak will improve the relative levels of LDL and HDL cholesterol, compared with what they would be if carbohydrates such as bread, potatoes, or pasta were consumed.  The remaining 30 percent will raise LDL cholesterol but will also raise HDL cholesterol and will have an insignificant effect, if any, on the ratio of total cholesterol to HDL.  All of this suggests that eating a porterhouse steak in lieu of bread or potatoes would actually reduce heart-disease risk, although virtually no nutritional authority will say so publicly.  The same is true for lard and bacon."

And how about human fat? What are we made of?

Ren et al. (2008): Human adipose tissue is composed largely of triglycerides. Seven fatty acids predominate as follows (number of carbons:number of double bonds, typical abundance): myristic (14:0, 3%), palmitic (16:0, 19–24%), palmitoleic (16:1, 6–7%), stearic (18:0, 3–6%), oleic (18:1, 45–50%), linoleic (18:2, 13–15%), and linolenic (18:3, 1–2%) ( 22, 23). These fatty acids account for well over 90% of the fatty acids in human adipose tissue. Odd-carbon fatty acids, longer chain fatty acids, and shorter chain fatty acids account for the remainder. Each of these less-abundant fats individually contributes much less than 1% ( 22).

So our adipose tissue is comprised of the same composition of the foods the public health authorities tell us to avoid. Interesting?

2. Distinguish the difference between a complex carb and a simple carb.

Complex carbohydrates are generally a polymer, containing multiple mono-saccharides linked together. Simple sugars generally refer to the mono-saccharides occurring in foods individually, i.e., no polymer.

Generally, simple and complex carbohydrates refer to sugars and starches, respectively.

Complex carbohydrates, in and of themselves, do not significantly affect the absorption rate of carbohydrates in the body.

3. Are potatoes that bad for us? The article insinuates that baked potatoes are not the best choice, would you agree with this statement?

I feel a little like Bill Clinton here, but, define “us”?

For a metabolically sound, lean individual, a potato may not be particularly deleterious.

If you were to tell the Kitavans that eating tubers were going to compromise their metabolic systems, they would probably argue otherwise and have reportedly lived on a diet high in tubers and starches:

From WholeHealthSource.com:

There's a lot to be learned from the Kitava study. Kitavans eat a diet of root vegetables, coconut, fruit, vegetables and fish and have undetectable levels of cardiovascular disease (CVD), stroke and overweight. Despite smoking like chimneys. 69% of their calories come from carbohydrate, 21% from fat and 10% from protein. This is essentially a carbohydrate-heavy version of what our paleolithic ancestors ate. They also get lots of sunshine and have a moderately high activity level.

Eating potatoes is eating akin to eating glucose. Yams and sweet potatoes, for instance, contain very little amounts of fructose, which may be the necessary agent - in excessive amounts - in causing metabolic disease in otherwise healthy individuals and further exacerbating it in the rest of the population.

For a diabetic, who by definition, has a disorder of carbohydrate metabolism, a potato may not be a good choice at all. Diabetics have a hard time clearing glucose, so it would probably be wise not to challenge the system with a bolus of carbohydrate in any form.

For a diabetic, I would agree that a baked potato is a bad choice of food to eat. For otherwise healthy, lean individuals, I would certainly still argue that potatoes are not “the best choice,” but I also believe that these people can consume this food without inducing damage (but would have to be taken in the context of the exclusion of excess fructose; sugar and HFCS among the major culprits).

4. Define the terms: glycemic index and glycemic load and explain how we can use these terms to help diabetic patients improve their diets.

From The Glycemic Index website (www.glycemicindex.com):

The glycemic index or GI describes this difference by ranking carbohydrates according to their effect on our blood glucose levels... The glycemic index (GI) is a ranking of carbohydrates on a scale from 0 to 100 according to the extent to which they raise blood sugar levels after eating. Foods with a high GI are those which are rapidly digested and absorbed and result in marked fluctuations in blood sugar levels. Low-GI foods, by virtue of their slow digestion and absorption, produce gradual rises in blood sugar and insulin levels, and have proven benefits for health.

Measuring the GI:

To determine a food's GI rating, measured portions of the food containing 10 - 50 grams of carbohydrate are fed to 10 healthy people after an overnight fast. (From wikipedia: The glycemic index of a food is defined as the area under the two hour blood glucose response curve (AUC) following the ingestion of a fixed portion of carbohydrate (usually 50 g).) Finger-prick blood samples are taken at 15-30 minute intervals over the next two hours. These blood samples are used to construct a blood sugar response curve for the two hour period. The area under the curve (AUC) is calculated to reflect the total rise in blood glucose levels after eating the test food. The GI rating (%) is calculated by dividing the AUC for the test food by the AUC for the reference food (same amount of glucose) and multiplying by 100 (see Figure 1). The use of a standard food is essential for reducing the confounding influence of differences in the physical characteristics of the subjects. The average of the GI ratings from all ten subjects is published as the GI of that food.

According to Wikipedia: 

The glycemic load (GL) is a ranking system for carbohydrate content in food portions based on their glycemic index (GI) and the portion size. Glycemic load or GL combines both the quality and quantity of carbohydrate in one ‘number’. It’s the best way to predict blood glucose values of different types and amounts of food. The formula is: GL = (GI x the amount of available carbohydrate) divided by 100.

In theory, glycemic index and glycemic load can help diabetics because they help determine what the impact of a particular food will be in the body, and for diabetics especially, they should want to avoid any food that is going to significantly elevate their blood glucose.

One of the severe limitations of glycemic index and glycemic load is that it doesn’t properly account for the amount of fructose consumed in the diet. For example, sucrose (glucose-fructose) has a lower GI than a potato, but I would rather have people eating potatoes than sucrose, if I had to make the choice.

From the subject article: “By contrast, fruit sugars are simple carbs, but they minimally impact blood sugar levels and insulin production.”

Again, we’re talking about fructose here, which many argue is a dose-dependent hepatotoxin. It minimally impacts blood sugar levels because fructose travels straight to the liver, and when consumed in excess, it can create the metabolic damage that is found in metabolic syndrome, insulin resistance, and diabetes.

5. Evaluate this statement to be true or false and justify your answer: Eating too much sugar causes diabetes.

I would say that eating too much sugar [sucrose/HFCS] is a cause of type 2 diabetes. Type 1 diabetes is less clear, but it is possible that excess sucrose can create, promote, or exacerbate an autoimmune disorder in the body.

To say that excess sugar is a cause of diabetes because anything in excess leads to weight gain, which leads to diabetes, wildly misses the point.

There are unique effects of fructose on human metabolism that implicate its consumption in the development of metabolic syndrome, which is virtually synonymous with insulin resistance, which is virtually synonymous with type 2 diabetes. The mechanisms of action are observable and have been shown to uniquely contribute to hepatic insulin resistance, leading to type 2 diabetes, among other issues.

And to come full-circle, this final question is comprehensively addressed in Gary Taubes's New York Times Magazine article (set to print: April 17, 2011) and Robert Lustig's Sugar: The Bitter Truth lecture.