Part 6: Safety First — Excess

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Is a low-carb diet safe? A diet that is lower in carbohydrates is by necessity higher in protein and fat. And everybody knows that’s supposed to be trouble, right? After all, researchers have been focusing on dietary fat and cholesterol for a long, long time as a potential source of cardiovascular disease. But in part, it was because a simple test had been discovered to measure serum cholesterol, and, like the drunk in the old joke, the researchers were looking for their car keys over near the streetlight, where the light was better.

In fact, there wasn’t even a good association between total dietary fat or total serum cholesterol and total mortality. The picture got a little clearer when LDL was considered separately from HDL, but it also made all the old recommendations nonsensical:

The observation that monounsaturated fats both lower LDL [‘bad’] cholesterol and raise HDL [‘good’ cholesterol] also came with an ironic twist: the principal fat in red meat, eggs, and bacon is not saturated fat, but the very same monounsaturated fat as in [‘heart-healthy’] olive oil. The implications are almost impossible to believe after three decades of public-health recommendations suggesting that any red meat consumed should at least be lean, with any excess fat removed.

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 [the same fat that comprises olive oil]. 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.

…from Good Calories, Bad Calories (Knopf, 2007), by Gary Taubes, p. 168-169

Continued in Part Seven

Part 5: Prescription

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Well, it’s pretty obvious what this has been leading up to, isn’t it?

The only thing that can cause fat loss is a low insulin level, and to do that, you have to restrict carbohydrates. You can either do that by restricting total calories, or by restricting carbohydrates specifically, but you’ll be a lot happier if you focus on the carbohydrates.

Remember our fellow omnivores, the rats? They have an uncanny ability to eat what they need. If given a choice between sugar and diet sweetener, they’ll eat about 50/50 at first, but by the third day, they’ll have dropped the diet sweetener for the sugar. Furthermore…

…rats whose adrenal glands are removed cannot retain salt, and will die within two weeks on their usual diet, from the consequences of salt depletion. If given a supply of salt in their cages, however, or given the choice of drinking salt water or pure water, they will choose either to eat or drink the salt and, by doing so, keep themselves alive indefinitely. These rats will develop a “taste” for salt that did not exist prior to the removal of their adrenal glands. Rats that have had their parathyroid glands removed will die within days of tetany, a disorder of calcium deficiency. If given the opportunity, however, they will drink a solution of calcium lactate rather than water — not the case with healthy rats — and will stay alive because of that choice. They will appear to like calcium lactate more than water. And rats rendered diabetic voluntarily choose diets devoid of carbohydrates, consuming only protein and fat. “As a result,” Richter said, “they lost their symptoms of diabetes, i.e. their blood sugar fell to its normal level, they gained weight [as opposed to being emaciated], ate less food and drank only normal amounts of water.”

…from Good Calories, Bad Calories (Knopf, 2007), by Gary Taubes, p. 430

How low-carb do you have to go? That pretty much depends on you, and how insulin-resistant you are.

For my own part, I’d have to admit that ever since trying the (low-carb) Zone diet in 1997, and seeing the miraculous weight loss, without hunger, I have always restricted my carbohydrates when trying to lose weight, even if I wasn’t on an official diet — it was always there, in the background, guiding my food choices, and producing positive results.

And, given what we’ve been discussing, it’s easy to understand why it works: with few carbohydrates to provoke an insulin response, there’s nothing to prevent the fat cells from releasing their energy stores. Add to that a sufficient quantity of protein and fat being ingested, and there is plenty of fuel available for the other non-fat tissues. So, no hunger, a revved-up metabolism, and plenty of weight loss.

But, is a low-carb diet safe, or sustainable? Well, let’s start out by saying this: the fewer carbohydrates you eat, the leaner you will be. Now, whatever level you can sustain, that’s your own business. It’s not even controversial anymore to advise a dieter to stay away from the ‘white’ foods: sugar, flour, bread, potatoes, rice, pasta, and beer (it’s…white-ish). Eat as little of those as you can, and your hunger will be lower, and you’ll lose weight faster.

As for the safety, we’ll have a look at that next time.

Continued in Part Six

Part 4: Insulin, Hunger and Satiety

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Suppose you have some lab rats. If offered rat chow, they’ll eat until they’re satisfied, and then stop. But what, exactly, triggers that satisfied feeling? What makes a rat happy? What makes a rat hungry?

Proponents of high-fiber diets claim that adding fiber to meals helps promote a feeling of fullness, without adding a lot of calories. Similar reasons are given for the often-heard advice to drink 8 cups of water every day — if you’re full on fiber and water, you won’t be hungry for bagels.


The seminal experiments on this question were done by the University of Rochester physiologist Edward Adolph back in the 1940s. Adolph diluted the diets of his rats with water, fiber, and even clay, and noted that the rats would continue to eat these adulterated diets until they consumed the same amount of calories they had been eating when he had fed them unadulterated rat chow. The more Adolph diluted the chow with water, the more the rats consumed — until the meals were more than 97 percent water. At these very low dilutions, the rats apparently expended so much energy drinking that they couldn’t consume enough calories to balance the expenditure. When Adolph put 90 percent of their daily calories directly into their stomachs, “other food was practically refused for the remainder of the twenty-four hour period.” Putting water into their stomachs had no such effect.

…from Good Calories, Bad Calories (Knopf, 2007), by Gary Taubes, p. 309

Hunger was being driven, not by the stomach being full, but by the immediate needs of the body’s cells being satisfied, regardless of the size of the fat stores that might be available elsewhere for long-term use, and our old friend insulin turns out to be a key player here, as well.

Even miniscule amounts of insulin cause fat cells to stop releasing free fatty acids into the bloodstream, and to start taking up glucose and free fatty acids and storing them as triglycerides. Fuel is swept out of the bloodstream and back in the fat cells, reducing the fuel available to the rest of the body’s cells, which the brain registers as hunger.

Anorexics, for example, if given a shot of insulin, will eat, and put on weight. And this is no placebo effect; it can also be seen in our friends, the rats. Infuse insulin into a rat, even a sleeping rat, and it will immediately awaken and begin eating, and will continue to eat as long as the insulin infusion continues.

What’s been clear for almost forty years is that the levels of circulating insulin in animals and humans will be proportional to body fat. “The leaner an individual, the lower his basal insulin, and vice versa,” as Stephen Woods, now director of the Obesity Research Center at the University of Cincinnati, and his colleague Dan Porte observed in 1976. “This relationship has also been shown to occur in every commonly used model of altered body weight, including…genetically obese rodents and overfed humans. In fact, the relationship is sufficiently robust that it exists in the presence of widespread metabolic disorder, such as diabetes mellitus, i.e. obese diabetics have elevated basal insulin levels in proportion to their body weight.” Woods and Porte also noted that when they fattened rats to “different proportions of their normal weights,” this same relationship between insulin and weight held true. “There are no known major exceptions to this correlation,” they concluded. Even the seasonal weight fluctuations in hibernators agree with the correlation; the evidence suggests that annual fluctuations in insulin secretion drive the yearly cycle of weight and eating behavior, although this has never been established with certainty.

…from Good Calories, Bad Calories (Knopf, 2007), by Gary Taubes, p. 439

Note, too, that someone who is insulin-resistant doesn’t have to wait for his blood sugar levels to fall to become hungry from higher insulin levels. His non-fat cells cannot easily use glucose, and with insulin levels high, his fat cells aren’t releasing the free fatty acids that his non-fat cells are capable of using well. Despite high blood glucose levels, the insulin-resistant person’s non-fat cells are starved, and he’s hungry. If he’s trying to diet by one of the low-calorie, high-carbohydrate diets such as Pritikin, he’s ravenous.

All right, we’ve got to get insulin levels down, but how? Tune in next time, when once again the rats will show the way.

Continued in Part Five

Gary Taubes Interview on Quirks and Quarks

Alert Reader and Industry Figure Stephen Newell sends a note about a nice interview with Gary Taubes, author of Good Calories, Bad Calories (Knopf, 2007), on the CBC’s Quirks and Quarks radio program.

The show’s web page about the the interview is here, and has some helpful links,
and the interview itself is available as MP3 here.

Quirks and Quarks
November 17, 2007

Part 3: Insulin and Diabetes

(Back to Parts One or Two)

Well, we could keep dancing around the subject, but we’re going to have to talk about insulin sooner or later. But we’ll need a good segue. We can’t just rush into it cold.

Hmm. So…ah!

“Speaking of metabolic disorders…”, there’s the metabolic disorder, Syndome X, the Metabolic Syndrome. What about that?

Well, two chief symptoms of the Metabolic Syndrome are overweight and insulin resistance. Hey, we’ve already been talking about overweight, that’s interesting! So, what does this insulin do, when it’s working properly?

All right, most people know that insulin lowers blood sugar, and that diabetics have some sort of problem with high blood sugar. We’re going to have to know a little more, though.

Let’s start with this: insulin is how your body signals its cells that you’re well-fed, particularly with sugars and other carbohydrates. “There’s plenty of food available, everybody dig in!” In response, muscle cells and liver cells take up glucose and store fuel as glycogen. Fat cells take up glucose and free fatty acids and store fuel as triglycerides. Protein degradation is suppressed. It’s a free feed.

When insulin levels drop, the liver tears down glycogen and releases it as glucose into the bloodstream, fat cells tear down triglycerides and release them as free fatty acids into the bloodstream, and the muscle cells…just hang on to their glycogen, if they can. It’s theirs. But if push comes to shove, and no food shows up, muscle protein will be torn down to make fuel for everyone else.

This is a simplification, of course, but the effect of insulin is enormous, and the simplification is useful. In particular, this point can’t be over-emphasized: if you want your fat cells to get smaller, you’ve got to lower your insulin levels, so that energy flows out of the fat cells, rather than into them.

Okay. Next up — diabetes! There are (at least) two types:

Type 1 (‘juvenile’ diabetes): Type 1 diabetics basically don’t make enough insulin, due to an auto-immune destruction of the insulin-producing beta cells in their pancreas. If untreated, they’re hungry (and especially thirsty) all the time, and no matter what they eat, they don’t put on weight.

Type 2 (‘adult-onset’ diabetes): Type 2 diabetics are typically overweight, at least, at first. Their pancreas still makes enough insulin, or what would be enough insulin in a normal person. But their body cells have become resistant to the insulin signal, and the blood sugar level remains stubbornly high. The pancreas responds with even more insulin. Ultimately, if untreated, their body cells become so resistant to insulin, and their pancreatic beta cells so exhausted, that they can’t put on weight, and end up as emaciated as untreated Type 1 diabetics. Also, like Type 1 diabetics, Type 2 diabetics are characteristically hungry, and thirsty, as their blood sugar spills over into their kidneys and is excreted in urine.

Okay, well, that’s really, uh, fascinating, but what does that have to do with me and my weight problem?

Ah! Step with me into the Wayback Machine, Sherman. We’re going all the way back to 1905 (“Wow, that’s over 100 years ago, Mr. Peabody!” “Quiet, you.”), when Carl von Noorden fomulated the third of his speculative hypotheses of obesity:

…what he called diabetogenous obesity. His ideas were remarkably prescient. They received little attention because insulin had not yet been discovered, let alone the technology to measure it.

Von Noorden suggested that obesity and diabetes are different consequences of the same underlying defects in the mechanisms that regulate carbohydrate and fat metabolism. In severe diabetes (Type 1), he noted, the patients are unable either to utilize blood sugar as a source of energy or to convert it to fat and store it. This is why the body allows the blood sugar to overflow into the urine, which is a last resort since it wastes potentially valuable fuel. The result is glycosuria, the primary symptom of diabetes. The diabetics must be incapable of storing or maintaining fat, von Noorden noted, because they eventually become emaciated and waste away. In obese patients, on the other hand, the ability to utilize blood sugar is impaired, but not the ability of the body to convert blood sugar into the fat and store it. “Obese individuals of this type have already an altered metabolisms for sugar,” von Noorden wrote, “but instead of excreting the sugar in the urine, they transfer it to the fat-producing parts of the body, whose tissues are still well prepared to receive it.” As the ability to burn blood sugar for energy further deteriorates and “the storage of the carbohydrates in the fat masses [also suffers] a moderate and gradually progressing impairment,” sugar appears in the urine, and the patient becomes noticeably diabetic. Using the modern terminology, this is the route from obesity to Type 2 diabetes. “The connection between diabetes and obesity,” as von Noorden put it, “ceases in the light of my theory to be any longer an enigmatical relation, and becomes a necessary consequence of the relationship discovered in the last few years between carbohydrate transformation and formation of fat.”

…from Good Calories, Bad Calories (Knopf, 2007), by Gary Taubes, p. 377

Now, this theory fits insulin resistance and the metabolic syndrome rather nicely, and no one has ever disproven it: suppose that the body’s non-fat cells become relatively more resistant to insulin than its fat cells (which have been described, by the way, as being exquisitely sensitive to insulin)? You’d have the very scenario described in part 1, with the top hats. The fat cells, fattening. The other body cells, basically starving, in the middle of an ocean of fat.

Okay, that sounds bad, but what do to? We’re going to have to deal with this problem head-on.

Continued in Part Four

Obesity as a Metabolic Disorder, Part 2

(Back to Part One)

Well, this business of genetically-obese mice, that’s not so convincing, is it? I mean, they’re mice, not humans, and specially-fat mice, not normal humans, and they get fat on most any diet, not just on certain diets. Doesn’t seem too compelling.

No, that was irony, just now. I’ve got all kinds of evidence against the calorie theory of weight gain and loss.

For example, if you put people on a diet of 800 calories per day, split up as 400 calories of fat, and 400 calories of protein, they’ll be perfectly content, and lose tons of weight.

The number of calories isn’t even all that important. There have been studies on people feeding them 2,700-2,800 calories per day of fat and protein — their metabolism revved up, and they still lost weight. Needless to say, they were also perfectly well-satisfied.

But suppose, instead of an 800 calorie diet, as 400 calories protein, 400 calories fat, you served up a 1,570 calorie diet — almost twice as much as 800, or about half as much as 2,800 — arranged as 400 calories a day of protein, 270 calories a day of fat, and 900 calories a day of carbohydrates?

Well, we don’t have to imagine the results, because the experiment has been done, in 1944, by Ancel Keys, on 32 young male conscientious objectors:

More than fifty pages of the two-volume final report by Keys and his collegues, The Biology of Human Starvation, document the “behavior and complaints” included by the constant and ravenous hunger that obsessed the subjects. Food quickly became the subject of conversations and daydreams. The men compulsively collected recipes and studied cookbooks. They chewed gum and drank coffee and water to excess; they watered down their soups to make them last. The anticipation of being fed made the hunger worse. The subjects came to dread waiting in line for their meals and threw tantrums when the cafeteria staff seemed slow. Two months into the semi-starvation period, a buddy system was initiated, because the subjects could no longer be trusted to leave the laboratory without breaking their diets.

Eveantually five of the subjects succumbed to what Keys and his collegues called “character neuroses,” to be distinguished from the “semi-starvaiton neurosis” that all the subjects experienced; in two cases, it “bordered on a psychosis.” One subject failed to lose weight at the expected rate, and by week three was suspected of cheating on the diet. In week eight, he binged on sundaes, milk shakes, and penny candies, broke down “weeping, [with] talk of suicide and threats of violence,” and was committed to the psychiatric ward at the University Hospital. Another subject lasted until week seven, when “he suffered a sudden ‘complete loss of willpower’ and ate several cookies, a bag of popcorn, and two overripe bananas before he could ‘regain control’ of himself.” A third subject took to chewing forty packs of gum a day. Since his weight failed to drop significantly “in spite of drastic cuts in his diet,” he was dropped from the study. For months afterward, “his neurotic manifestations continued in full force.” A fifth subject also failed to lose weight, was suspected of cheating, and was dropped from the study.

…from Good Calories, Bad Calories (Knopf, 2007), by Gary Taubes

So, 800 calories per day, or even 2,800 calories per day, of fat and protein, happy campers, losing tons of weight. But 1,570 calories per day, (about half the calories the men were previously eating in their normal lives), where 57% is carbohydrates, and you’ve got insufficient weight loss and neurosis, even psychosis. Excellent!

More to the point: it doesn’t seem as if just doing the math of calories in and calories out is an adequate model for human weight gain and loss.

Continued in Part Three

Obesity as a Metabolic Disorder, Part 1

Back when I posted the rule-of-thumb about the relationship between a 10-calorie-a-day change and overweight (+10 calories a day from eating or sloth equals +1 pound a year, -10 calories a day from diet or exercise equals -1 pound a year), my old friend Jeff Lorenzini e-mailed me to say that this was complete nonsense. He had been on a raw vegan diet for years, and…

…when I was doing 100% raw, I was shocked when we sat down and added up my calories every day, almost 3,000, which is a shitload, and yet I was losing weight like crazy and eventually plateau’d at less than 130 pounds, which was pretty skinny. Then, I slowly built the weight back up, which is what every raw fooder that I’ve talked to reports happening to them as well. So, it’s more than just saying 10 extra calories a day, your body has all kinds of ways to regulate metabolism.

And the thing is, I knew he was right. When I had been on extremely-low-carb diets in the past, I too could eat 3,000 calories a day, and still lose weight, without doing more than walking 30 minutes a day and riding my bike for less than an hour, a few times a week. I typically ate less than that, but regardless, I wasn’t hungry, and in 2004, I went from 252 pounds to 223 pounds, and dropped 5 inches off my waistline, in 19 weeks, before falling afoul of Halloween and falling off the wagon. And I was losing body fat faster on that diet than my current “eat a little less, exercise a lot more” regimen.

So, what gives? It’s going to take more than a single post to answer — let’s take our time and enjoy it!

Think of the cells in your body as semi-independent individuals. Suppose that there were some way, or ways, that the fat cells could be become deranged, or at least out-of-balance compared to the rest of the body.

Fat cells, after all, can choose either to get fatter, sucking lipids from the bloodstream and storing them as triglycerides, or they can reverse the process and shrink, releasing nourishment as free fatty acids into the bloodstream. Suppose that the fat cells were a little more prone to suck nourishment from the blood, compared to the other tissues? Well, you’d get fatter.

And what if you tried to lose the extra fat by eating quite a bit less, without doing anything to address the core problem? The fat cells would still be very enthusiastic about their blood-sucking, and since you weren’t eating very much to begin with, the rest of the body would be left with even less nourishment, while the fat cells (who are on the side of the fat cells) padded their coffers, probably wearing top hats.

So, in the presence of this metabolic derangement, low-calorie diets make you feel listless and ravenous, because your non-fat tissues are semi-starving in the midst of plenty — if the fat cells are in the “suck in nourishment” mode, they’re not spewing as much of it out to the bloodstream. Even though you’ve got ample reserves stored as fat, it’s mostly locked away in the vault, unavailable for use.

But, is there a shred of evidence for this view? Oh, yes. Let’s start with genetically obese mice, as described on page 368 of Gary Taubes’s Good Calories, Bad Calories (Knopf, 2007):

…it is invariably the case, as Jean Mayer discovered in the early 1950s, that these animals will fatten excessively regardless of how much they eat. Their obesity is not dependent on the excessive calories they consume, although allowing them to consume excessive calories may speed up the fattening process. “These mice will make fat out of their food under the most unlikely circumstances, even when half starved,” Mayer had reported. And if starved sufficiently, these animals can be reduced to the same weight as lean mice, but they’ll still be fatter. They will consume the protein in their muscles and organs rather than surrender the fat in their adipose tissue. Indeed, when these fat mice are starved, they do not become lean mice; rather, as William Sheldon might have put it, they become emaciated versions of fat mice. Francis Benedict reported this in 1936, when he fasted a strain of obese mice. They lost 60 percent of their body fat before they died of starvation, but still had five times as much body fat as lean mice that were allowed to eat as much as they desired.

Continued in Part Two