A Diet Manifesto: Drop the Apple and Walk Away

NY Times ^ | December 27, 2010 | ABIGAIL ZUGER, M.D.

[Dr. Scarpetta]

Thank you

[neverdem]

Besides, there is very little de novo lipogenesis in the human body.

This paper argues otherwise. Do you have any more up to date references than this?

Fructose, insulin resistance, and metabolic dyslipidemia

A high flux of fructose to the liver, the main organ capable of metabolizing this simple carbohydrate, perturbs glucose metabolism and glucose uptake pathways, and leads to a significantly enhanced rate of de novo lipogenesis and triglyceride (TG) synthesis, driven by the high flux of glycerol and acyl portions of TG molecules from fructose catabolism.

[aruanan]

Besides, there is very little de novo lipogenesis in the human body.

This paper argues otherwise. Do you have any more up to date references than this?

Fructose, insulin resistance, and metabolic dyslipidemia

A high flux of fructose to the liver, the main organ capable of metabolizing this simple carbohydrate, perturbs glucose metabolism and glucose uptake pathways, and leads to a significantly enhanced rate of de novo lipogenesis and triglyceride (TG) synthesis, driven by the high flux of glycerol and acyl portions of TG molecules from fructose catabolism.

The paper is a 2005 review paper. The study they cite for enhanced de novo lipogenesis is a 1993 paper (Am J Clin Nutr November 1993 vol. 58 no. 5 754S-765S). Not exactly recent.

At any rate, the amount of de novo lipogenesis in humans is very small. You could significantly enhance it and still have a relatively small contribution to total body fat. And all this would still be in the context of total kilocalorie intake. If your intake does not exceed your output, it wouldn't make any difference at all if some fructose led to de novo lipogenesis. You cannot store more energy than you take in. It would only make a difference if intake exceeded output. And you'd still wind up with the same problem. Your fat increase will be to the degree that your energy intake exceeds your energy output. Regardless of where the fat comes from (dietary intake versus de novo lipogenesis--which requires energy), it will not increase your body weight unless your energy expenditure falls below your energy intake.

Think of the de novo lipogenesis as an additional step that energy intake has to go through on its way to storage. That costs energy. So, in the end, if excess energy in the form of dietary fat goes directly to fat stores while carbohydrates are preferentially oxidized or if some of those carbohydrates trigger the genesis of new fat, the total amount of energy available for fat deposition can never be more than the amount energy intake in excess of energy expenditure. One could argue that an additional energy-intensive process, fat synthesis, or an increase in this process, would, for the same amount of excess energy intake, result in decreased fat deposition due to the higher energy costs in maintaining the synthesis.

[A Navy Vet]

Okay, sorta got it. I was using the old fallacy that skeletal muscles were consider as "stores". Plus, I confused the discussion with the mention of ATP.

What I still don't understand is at what point does the body start the cannibalization of skeletal muscle. Is that what body-building "over-training" is about - simple lack of protein vs exercise? Using the amino acids in other muscle groups to repair the damage of the muscles just exhausted? Sort of a self-defeating Peter paying Paul cycle? So more protein will correct this cycle? Right? At what point with additional protein are you adding fat plus muscle? That's the tough one for us amateur weight lifters.

I also don't get why nutritionists suggested 5 or more small meals (Weight Watchers) rather than 2 or 3 meals of comparable calories and macro-nutrient ratios. Although with your burn formula, I do now better understand why Atkins works so well. Thanks for the feedback. What a complex system our bodies are and no wonder there has always been so much contradicting info out there to us laymen.

[aruanan]

What I still don't understand is at what point does the body start the cannibalization of skeletal muscle. Is that what body-building "over-training" is about - simple lack of protein vs exercise? Using the amino acids in other muscle groups to repair the damage of the muscles just exhausted? Sort of a self-defeating Peter paying Paul cycle? So more protein will correct this cycle? Right? At what point with additional protein are you adding fat plus muscle? That's the tough one for us amateur weight lifters.

If you've radically increased your lean body mass in the form of skeletal muscles, you'll increase the required energy intake to fuel that muscle and stay at an energy balance where you won't gain fat. If you decrease your energy intake and maintain the same level of energy expenditure (not only resting metabolic rate, but large muscle activity), you'll make up the difference required from stored body fat. After that, the energy deficit will have to be made up from skeletal muscle. Also, if you've built up your muscles and increased muscle tone to a high degree and just stop the physical activities that led to that state, you'll lose both muscle tone and muscle mass. I don't know what the signaling pathways are for that, but it's not desirable from a survival standpoint to continue to expend large amounts of energy to maintain a level of musculature that is not being used. If you continue energy intake at the level needed by that level of muscular development, then you're going to be in energy surplus and will 1. lose muscle mass and 2. gain fat mass. That's probably where the idea came from that not using your muscles leads them to turn into fat. It's known for certain that moderate physical activity, an hour or so several times a week, even as light as brisk walking, is very helpful in maintaining weight loss. As far as the supply of amino acids for muscle repair goes, with a typical American diet you'll almost never be at a loss for adequate amino acids for muscle building and repair. You have more proteins in your diet than you need for protein synthesis plus your body is continuously breaking down proteins of all kinds and providing a pool of amino acids for continuous protein synthesis. Look at an 80 lb 13-year-old growing to a heavily muscled 160 lb 17-year-old. In four years he doubles his body weight and it's just by what he's getting in his everyday diet. You, on the other hand, are not anywhere near those kinds of demands for energy and growth. Your main problem as an adult is avoiding eating too much and getting an increase in fat mass.

I also don't get why nutritionists suggested 5 or more small meals (Weight Watchers) rather than 2 or 3 meals of comparable calories and macro-nutrient ratios. Although with your burn formula, I do now better understand why Atkins works so well.

If the kilocalorie content is the same, you could eat 1 meal or 15 small meals over the course of a day and it won't make any difference at all. There will be no difference in weight gain or loss except to the extent you over or undersupply your energy requirements. The larger number of smaller meals has the benefit of assuaging your hunger. People who eat only a couple of meals a day or who go for a long time between meals are more likely to overeat because they get so hungry. Once you start eating something, it takes a while for satiety to kick in. It's very easy to exceed what you need just by eating a whole lot very quickly. But regardless, your body is so efficient that it will absorb almost the entire nutrient content of what you eat whether you need it or not (unless, of course, you've had part of your small intestine resected). I remember discovering this when I was a teenager in Brazil when I was invited to eat at a missionary's house. I was so nervous and ate so slowly (that is, at the rate the others were eating, not my typical teenage jet intake) that after about 20 or 25 minutes I was amazed that I was no longer hungry in spite of having eaten so little. I had eaten at a rate at which my satiety signals weren't outrun by my rate of eating. This also calls to mind my nephew who, when he was little, was pretty hefty. I asked him once, "How do you know when you've eaten enough?" He replied, "When it hurts."

Thanks for the feedback. What a complex system our bodies are and no wonder there has always been so much contradicting info out there to us laymen.

Sure! The body really is fearfully and wonderfully made.

[aruanan]

BTW, I should have used a plate of pasta as a contrast with saltine crackers for differences in glycemic index. A baked potato is about the same as a cracker, ~100.

[dsc]

“But wasn’t the eating constrained to mealtimes?”

When I was a young enlisted man, I ate only when the chow hall or mess decks were open. Got lots of exercise, too. Put on weight.

Heck, I put on fat in boot camp.

[dsc]

“How about it, dsc; would you lose weight at the Hanoi Hilton?”

Is it your assertion that a person should have to reduce intake to Hanoi Hilton levels to maintain a normal weight? Surely not.

I am not saying that a person cannot starve to death. I am saying that it is *not*normal* when a person must both reduce intake to a preposterous level *and* exercise like an elite athlete to avoid obesity.

I am saying that those conditions indicate that there are other factors at work.

[dsc]

“whatever you do, don’t put your money where your mouth is. You’ll lose whatever you have”

If I expected to live long enough to collect, I’d ask if *you* were open to a wager.

[dsc]

“If you want to stuff your face, sit on your butt and get fatter, it’s your own business.”

Arrrgh, the sumg...it’s choking me.

I used to be an elite athlete—if you call a silver medal at a US national championship elite—and an avid camper and backpacker.

In June of 1978 I walked out of the rockies at 160 pounds after two weeks without hearing another voice or a man-made sound.

I kept my weight at reasonable levels for as long as my health allowed me to exercise like an elite athlete. When I no long could do so, weight gain set in, despite extraordinary efforts to control my weight through diet. (Staying up until 2am preparing and freezing measured portions of low-glycemic-index foods, et cetera.)

My wife, at 5’5” and 120 lbs, ate more than I did. (I am—or was—right at 6’, with a large frame.)

You might want to read the post that immediately followed the one I am responding to. And another twenty or thirty articles on the latest research into the causes of fattitude.

Or continue to pat yourself on the back for accidents of birth and the vicissitudes of life.

[Grizzled Bear]

I am not saying that a person cannot starve to death. I am saying that it is *not*normal* when a person must both reduce intake to a preposterous level *and* exercise like an elite athlete to avoid obesity.

Yes, it is NOT NORMAL. Earlier, you claimed that MOST of obesity is not related to intake/output. The fact is, when you need to starve yourself to lose weight, something is wrong.

A few years ago, I managed a Group level Air Force Fitness program. The base exercise physiologist gave the program managers an excellent explanation concerning calorie intake. He asked us to consider the number of fat paraplegics vs the number of fat quadriplegics. He said you rarely see a fat quadriplegic because they can only eat their prescribed diet. A paraplegic can feed them self and overeat.

We, the Program Managers, learned a lot of interesting stuff. For instance, drinking a lot of orange juice is NOT good for weight loss. You're still taking in a lot of sugar. Your body will convert the sugar into fat and store it. It's the same with soda and sugary "juice boxes."

[dsc]

“But at adulthood, many people develop a condition called insulin resistance. This condition causes your body to turn the starchy stuff you eat into fat instead of into energy. In a large percentage of the population, insulin resistance leads to type 2 diabetes in later life.”

I am very grateful for that information.

I am furious, but not at you, because this is the first time I have encountered that information. I have to wonder why the legions of people who should have told me about that never did.

“Read Gary Taubes’ “Good Calories, Bad Calories for a more thorough explanation.”

What a coincidence! I was clicking around yesterday from one article on nutrition to another, and ran across references to that in several places. It seems he has another book out, “Why We Get Fat: And What to Do About It.”

Some people said it was a shorter, more accessible version of “Good Calories, Bad Calories,” but I don’t know, not having read either book.

I am definitely going to read “Good Calories, Bad Calories,” and soon.

Thank you for contributing to a discussion rather than exacerbating a quarrel.

[skookum55]

The only gratuitous insult I see is you labelling my response as a gratuitous insult. I can only assume you to be an illiterate jerk. If you were literate I’d suggest that you, too, read the article.

[Lady Jag]

I cut out meat for three days. On the third night I dreamed I was a big cat eating out the gut of a fresh killed water buffalo. Went out for steak ASAP.

[Lady Jag]

Don’t listen to strangers who get paid by the word.

Exercise more.

[Mase]

I can only assume you to be an illiterate jerk

That's quite a claim when the original post (The root cause of most obesity is an overabundance of food and lack of physical activity) reflects established scientific fact.

Some people work hard to complicate the issue to support a political agenda. Some are motivated by a desire to say Oh, it isn't my fault I'm fat -- my obesity is caused by genetics.. The former is understandable. There are people who stand to gain politically from such a misunderstanding. The latter is caused by illiteracy, plain and simple.

.

If you were literate I’d suggest that you, too, read the article.

I've read the article and you can choose to believe Taubes if you'd like. But Taubes is a fraud who learned how to sell books a long time ago. Taubes is a proponent of the Atkins diet – a dubious dietary strategy not based on scientific evidence, which seems to have been designed to sell diet books – by telling people that they can eat as much as they like of some foods and still go on a weight-loss diet.

Demonizing one macronutrient or another is a common trait of diet fads. We've learned from recent history that you can sell diet advice more easily if you claim that fats or carbs are the problem – while the (obvious) idea that calories are the problem seems to be something that few people are willing to pay for.

Equating long time FReepers with the Obamas, because they adhere to established science, is not a formula for winning friends on the forum. But, if Kamikaze is your style, then, by all means, carry on.

[Eagle Eye]

Your alternate reality is very entertaining.

Since I have personal memories of JFK’s funeral I am certainly qualified to stand by statements.

Shakey’s was a treat, as was Henry’s and McDonald’s.

People then didn’t spend the time in front of the tube like they do today, nor did they gorge on fast foods like today.

Supersized hadn’t been invented yet.

[Eagle Eye]

So I can compare you to Hillary or Michelle and you’ll enjoy the compliment?

And that laughter you hear...we’re not laughing *with* you.

[dsc]

“Since I have personal memories of JFK’s funeral I am certainly qualified to stand by statements.”

Oh, I don’t know. That was 1963. If you were, say, three at that time, you wouldn’t have become aware enough to develop useful opinions until about 1970. Since we’re talking about the ‘50s and ‘60s, that would pretty much time you out.

Doesn’t matter. Until something dissipates that cloud of smug, there’s no point in even trying to talk with you.

[neverdem]

The paper is a 2005 review paper. The study they cite for enhanced de novo lipogenesis is a 1993 paper (Am J Clin Nutr November 1993 vol. 58 no. 5 754S-765S). Not exactly recent.

It appears that you're refering to:

Intermediary metabolism of fructose.

Most of the metabolic effects of fructose are due to its rapid utilization by the liver and it by-passing the phosphofructokinase regulatory step in glycolysis, leading to far reaching consequences to carbohydrate and lipid metabolism. These consequences include immediate hepatic increases in pyruvate and lactate production, activation of pyruvate dehydrogenase, and a shift in balance from oxidation to esterification of nonesterified fatty acids, resulting in increased secretion of very-low-density-lipoprotein (VLDL). These effects are augmented by long-term absorption of fructose, which causes enzyme adaptations that increase lipogenesis and VLDL secretion, leading to triglyceridemia, decreased glucose tolerance, and hyperinsulinemia. Acute loading of the liver with fructose causes sequestration of inorganic phosphate in fructose-1-phosphate and diminished ATP synthesis. Consequently, the inhibition by ATP of the enzymes of adenine nucleotide degradation is removed and uric acid formation accelerates with consequent hyperuricemia. These effects are of particular significance to potentially hypertriglyceridemic or hyperuricemic individuals.

Do you have anything more recent that refutes it? I'd be happy to read it. Here a more recent citation:

Fructose induced lipogenesis: from sugar to fat to insulin resistance.

Abstract
Increasing consumption of sugars is one of the contributing factors to the obesity epidemic. Both cane sugar and high-fructose corn syrup(HFCS) contain glucose and fructose. Fructose, in contrast to glucose, is known to potently stimulate lipogenesis, but the mechanisms responsible are not yet fully known. This paper reviews several possible pathways that might be involved, such as activation of pyruvate dehydrogenase, and transcriptional activation of sterol regulatory element binding protein 1c by key regulators such as peroxisome proliferator activated receptor-γ co-activator 1β and the splice variant of X-box binding protein 1. Together, these pathways might establish a feed forward cycle that can rapidly increase hepatic lipogenesis. As a result, dietary fructose might promote the development of nonalcoholic fatty liver disease, which in and of itself, can result in hepatic insulin resistance, a key feature of type 2 diabetes mellitus.

I never heard of nonalcoholic fatty liver disease when I was in medical school two decades ago, but I can find stories about it in Family Practice News now. I used to think that a six carbon monosaccharide wouldn't have any different effects from another six carbon monosaccharide, but fructose makes me question that assumption. The HFCS used in soft drinks is 55 % fructose and 42 % glucose. Couldn't the excess fructose shift the equilibrium from oxidation to esterification of nonesterified fatty acids?

Using fructose and (nafld or nonalcoholic fatty liver disease or non-alcoholic fatty liver disease) at PubMed gets 40 citations.