Study: Fat People Cheaper To Treat (‘Why?’)

From the Netherlands, a study showing that fat people (and smokers!) spend less on health care, and cost less to treat, even for systems with socialized medicine.

And can you guess why?

Oh, it’s because they die way sooner. Those pesky thin non-smokers just live and live; they’re very annoying.

The researchers found that from age 20 to 56, obese people racked up the most expensive health costs. But because both the smokers and the obese people died sooner than the healthy group, it cost less to treat them in the long run.

On average, healthy people lived 84 years. Smokers lived about 77 years, and obese people lived about 80 years.

The point of the study being to debunk the myth that reducing obesity will reduce national health care costs: “We are not recommending that governments stop trying to prevent obesity, but they should do it for the right reasons.”

Read an article about the study, from the Associated Press.
“Fat people cheaper to treat, study says”

Read the study itself, in the Public Library of Science.
“Lifetime Medical Costs of Obesity: Prevention No Cure for Increasing Health Expenditure”

“They’re cheaper! Isn’t that splendid? I think that’s splendid!”

Part 9:  …Especially Fructose

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One piece of advice that you wouldn’t imagine to be controversial, at least, is to minimize your intake of sugar. But even here, the mainstream voice can surprise: the American Diabetes Association still to this day says that for diabetics, “Sucrose-containing foods can be substituted for other carbohydrates in the meal plan or, if added to the meal plan, covered with insulin or other glucose-lowering medications.” And since the ADA wants everyone, even diabetics, to get at least 130g of carbohydrates (about 520 calories) every day, why, hell, go ahead and have a soda!

Why would they feed extra sugar to someone whose body has impaired blood sugar control? It seems ludicrous, and in fact, I think it’s terrible advice. But to understand, at least in part, how this situation arose, we have to talk about fructose and the glycemic index.

The glycemic index is a measure of the effect a food has on blood glucose levels. The scale is defined such that a solution of glucose itself (which, as you can imagine, raises blood glucose levels substantially) is assigned a value of 100. A food that only raises blood glucose levels half as much would have a value of 50, and so on. Dieters are often advised to avoid foods with a glycemic index higher than 55.

Here’s a short table listing the glycemic index of a few foods, just to illustrate the idea. Lower is better. You can take these values as ‘very approximate’, since I pulled them from a random web site.

glucose                100
baked potato            95
refined white flour     85
table sugar (sucrose)   70
banana (ripe)           60
banana (unripe)         45
carrot juice            40
carrot (raw)            30
fructose                20
asparagus               15
beef                     0

Americans eat a lot of sugar, and about 1/2 of it is fructose (a kind of sugar found in fruit), either as table sugar (sucrose, which is 50% fructose, 50% glucose), or as high-fructose corn syrup, (HFCS, or HFCS-55, which is 55% fructose, 45% glucose).

Hey, and fructose was in the table above, nestled snugly down there with the vegetables. It has almost no effect (at least in the short term) on blood glucose or insulin levels. This led, in the 1980’s, to its promotion as a ‘healthy’ sugar, and table sugar, being half fructose, looked pretty attractive (for a sugar), especially compared to baked potatoes and bread made from refined white flour. In The New England Journal of Medicine, diabetologist John Bantle wrote, “We see no reason for diabetics to be denied foods containing sucrose.”

Sounds great! But mark the sequel:

Unlike glucose (70% of which is taken up by the body’s cells before ever encountering the liver), fructose is not immediately usable by the body; it must be metabolized in the liver, which converts it to triglycerides (“fructose-induced lipogenesis”). Now, this is bad enough — high triglyceride levels are a far better predictor of cardiovascular disease than total cholesterol — but it gets worse:

…fructose apparently blocks both the metabolism of glucose in the liver and the synthesis of glucose into glycogen, the form in which the liver stores glucose locally for later use. As a result, the pancreas secretes more insulin to overcome this glucose traffic-jam at the liver, and this in turn induces the muscles to compensate by becoming more insulin resistant. The research on this fructose-induced insulin resistance was done on laboratory animals, but it confirmed what Reiser at the USDA had observed in humans and published in 1981: given sufficient time, high-fructose diets can induce high insulin levels, high blood sugar, and insulin resistance, even though in the short term fructose has little effect on either blood sugar or insulin and so a very low glycemic index. It has also been known since the 1960s that fructose elevates blood pressure more than an equivalent amount of glucose does, a phenomenon called fructose-induced hypertension.

Because sucrose and high-fructose corn syrup (HFCS-55) are both effectively half glucose and half fructose, they offer the worst of both sugars. The fructose will stimulate the liver to produce triglycerides, while the glucose will stimulate insulin secretion. And the glucose-induced insulin response in turn will prompt the liver to secrete even more triglycerides than it would from the fructose alone, while the insulin will also elevate blood pressure apart from the effect of fructose…

The effect of fructose on the formation of advanced glycation end-products — AGEs, the haphazard glomming together of proteins in cells and tissues — is worrisome as well. Most of the research on AGE accumulation in humans has focused on the influence of glucose, because it is the dominant sugar in the blood. Glucose, however, is the least reactive of all sugars, the one least likely to attach itself without an enzyme to a nearby protein, which is the first step in the formation of AGEs. As it turns out, however, fructose is significantly more reactive in the bloodstream than glucose, and perhaps ten times more effective than glucose at inducing the cross-linking of proteins that leads to the cellular junk of advanced glycation end-products. Fructose also leads to the formation of AGEs and cross-linked proteins that seem more resistant to the body’s disposal mechanisms than those created by glucose. It also increases markedly the oxidation of LDL particles, which appears to be a necessary step in atherosclerosis.

…from Good Calories, Bad Calories (Knopf, 2007), by Gary Taubes, p. 200-201

The above is especially alarming considering that our national per-capita consumption of sugars has increased from a stable historical mean of 110-120 pounds per year from the 1920’s (or even the 1950’s) up to almost 150 pounds per year (almost half a pound a day!), with virtually all of the increase due to high-fructose corn syrup (e.g. soda pop, Snapple, ice cream, candy, low-fat yogurt, salad dressings, you name it).

As for me, I’ve cut back my consumption of all kinds of sugars…especially on added fructose.

To be continued…

Part 8: Insulin, High Blood Sugar, and Dementia

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By the 1990’s, researchers started reporting that heart disease and Alzheimer’s seemed to share risk factors: hypertension, atherosclerosis, and smoking were all associated with an increased risk of Alzheimer’s disease.

The connection with insulin and high blood sugar is concrete: “Type 2 diabetics have roughly twice as much risk of contracting Alzheimer’s disease as nondiabetics. Diabetics on insulin therapy…[have] a fourfold increase in risk. Hyperinsulinemia and metabolic syndrome are also associated with an increased risk of Alzheimer’s disease.”

In part, this is due to vascular damage, which is more common in diabetics — and vascular damage in the brain is a well-known cause of dementia.

But vascular dementia aside, there are two other lines of evidence linking high blood sugar and/or high insulin levels to Alzheimer’s disease proper:

  1. When blood sugar levels are high, the excess sugars are more likely to semi-randomly bind with proteins — the sugar molecules are sticky, in a chemical way, to protein molecules. In fact, they’re so sticky that a protein might end up folded over and attached in more than one place to a sugar molecule, or multiple proteins may glom together with one or more sugar molecules into a big untidy mess.

    These glycated (“sugar-frosted”) proteins can end up as twisted, gnarled Advanced Glycation End-products (“AGEs”), which can overwhelm and confound our bodies’ clean-up crews. Plus, they’re a source of oxidative stress, generating free radicals. Bad news all around.

    Now, organic chemicals depend on their shape as much as their chemical formula for their actions: Our bodies, for example, can only use so-called right-handed sugar; the chemically-identical, but physically mirror-imaged left-handed sugar is indigestible. As another example, Mad Cow disease is caused by a perfectly-normal protein being folded into an abnormal shape, which “infects” other proteins by encouraging them to take on this same dysfunctional and highly-stable shape. Not only are the proteins wrong, they like being wrong, and are good at persuading other proteins to join their evil gang.

    But I digress. The main point here is that your body’s workhorse chemicals can get an unwelcome sugar coating that is difficult to remove. In fact, one of the better tests for diabetes and insulin resistance is the A1c, which measures the percentage of your hemoglobin that has become sugar-frosted. Mine is 5.2%. We like it to be below 6.0%. Diabetics are happy to get it down to 7.0%. Unlike the fasting blood glucose test, which measures blood sugar levels due to what you’ve been doing in the last few hours, the A1c measures your average blood sugar level over the last two to three months. And the reason it can do that is because once your hemoglobin has been glycated, it tends to stay that way.

    When this process happens to brain proteins, the results aren’t pretty:

  2. Investigators studying AGEs have proposed that Alzheimer’s starts with glycation — the haphazard binding of reactive blood sugars to…brain proteins. Because the sugars stick randomly to the fine filaments of the proteins, this in turn causes the proteins to stick to themselves and to other proteins. This impairs their function and, at least occasionally, leaves them impervious to the usual disposal mechanisms, causing them to accumulate in the spaces between neurons. There they cross-link with other nearby proteins, and eventually become advanced glycation end-products. All of this would then be exacerbated by the fact that the glycation process itself generates more and more toxic reactive oxygen species (free radicals), which in turn causes even more damage to the neurons. In theory, this is what causes the amyloid plaques and leads to the degeneration of neurons, the cell loss, and the dementia of Alzheimer’s. The theory is controversial, but the identification of AGEs in the plaques and tangles of Alzheimer’s is not.

    …from Good Calories, Bad Calories (Knopf, 2007), by Gary Taubes, p. 206

  3. And what about high insulin levels? Sure, they’re implicated as well. Imagine, for a moment, that you’re a pancreas. Your host eats a sugary meal, extremely delicious, but blood glucose levels are rising, and must be suppressed. Quick, a shot of insulin! Perfect, the glucose levels go down (or don’t, depending on how insulin-resistant the host is).

    But consider: we need some mechanism to bring insulin levels back down to normal after the pancreas stops spewing it out into the bloodstream. And it turns out that there’s an enzyme, IDE (insulin degrading enzyme) that really likes to tear down insulin.

    Seems like a good system, but IDE has a second job, a side job, that it agreed to do in its spare time if there wasn’t much super-important insulin to tear down. Wanna guess? Yes, that’s right: tearing down the amyloid plaques that clutter the brains of Alheimer’s patients:

  4. The more insulin available in the brain, by this scenario, the less IDE is available to clean up amyloid, which then accumulates excessively and clumps into plaques. In animal experiments, the less IDE available, the greater the concentration of amyloid in the brain. Mice that lack the gene to produce IDE develop versions of both Alzheimer’s disease and Type 2 diabetes…

    In 2003, [Suzanne Craft, a neuropsychiatrist at the University of Washington], reported that when insulin was infused into the veins of elderly volunteers, the amount of amyloid in their cerebral spinal fluid increased proportionately. This implied that the level of amyloid protein in their brain had increased as well. The older the patient, the greater the increase in amyloid protein. As Craft sees it, if insulin levels are chronically elevated (hyperinsulinemia), then brain neurons will be excessively stimulated to produce amyloid proteins, and IDE will be preoccupied with removing the insulin, so that less will be available to clean up the amyloid…

    This isn’t to say that eating carbohydrate foods to excess is a [proven] cause of Alzheimer’s, only that mechanisms have now been identified to make the hypothesis plausible.

    …from Good Calories, Bad Calories (Knopf, 2007), by Gary Taubes, p. 208

Continued in Part Nine

Part 7: Safety Second — Deficiency

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Will a low-carb diet lead to diseases of deficiency? It shouldn’t, because we don’t actually restrict the bulk of fruits and vegetables. Only refined sugar, flour, bread, potatoes, rice, beer, and those foods composed chiefly of these need be restricted.

This leaves a rather large remainder for our nutrition: this week, for example, I’ve had an apple, asparagus, broccoli, carrots, garlic, mushrooms, onions, tomatoes, yellow squash, and zucchini in mass quantities, in addition to copious amounts of delicious meat and cheese.

But what if we did eat only meat? Again, the experiment has already been done, and a long time ago:

In the early 1920s, a Harvard anthropologist-turned-Arctic-explorer named Vilhjalmur Stefansson publicized the idea of a carbohydrate-restricted diet based on fatty meat.

What follows is quite a long quote, but stick with it: I, at least, found it absolutely fascinating.

[Stefansson] was concerned with the overall healthfulness of the diet, rather than its potential for weight loss. [He] had spent a decade eating nothing but meat among the Inuit of northern Canada and Alaska. The Inuit, he insisted, as well as the visiting explorers and traders who lived on this diet, were among the healthiest if not the most vigorous populations imaginable.

…The ability to thrive on such a vegetable- and fruit-free diet was also noted by the lawyer and abolitionist Richard Henry Dana, Jr., in his 1840 memoirs of life on a sailing ship, Two Years Before the Mast. For sixteen months, Dana wrote, “we lived upon almost nothing but fresh beef; fried beefsteaks, three times a day…[in] perfect health, and without ailings and failings.”

…None of Stefansson’s findings would have been controversial had not the conventional wisdom been — as it still is — that a varied diet is essential for good health.

…This philosophy, however, was based almost exclusively on studies of deficiency diseases, all of which were induced by diets high in refined carbohydrates and low in meat, fish, eggs, and diary products. When the Scottish naval surgeon James Lind demonstrated in 1753 that scurvy could be prevented and cured by the consumption of citrus juice, for example, he did so with British sailors who had been eating the typical naval fare “of water gruel sweetened with sugar in the morning, fresh mutton broth, light puddings, boiled biscuit with sugar, barley and raisins, rice and currants.” Pellagra was associated almost exclusively with corn-rich diets, and beriberi with the eating of white rice rather than brown.

…What nutritionists of the 1920s and 1930s didn’t then know is that animal foods contain all of the essential amino acids (the basic structural building blocks of proteins), and they do so in the ratios that maximize their utility to humans. They also contain twelve of the thirteen essential vitamins in large quantities.

…The thirteenth vitamin, vitamin C, ascorbic acid, has long been the point of contention. It is contained in animal foods in such small quantities that nutritionists have considered it insufficient and the question is whether this quantity is indeed sufficient for good health.

…the dangers of an all-meat diet were considered sufficiently likely that even Francis Benedict, as Stefansson told it, claimed that it was “easier to believe” that Stefansson and all the various members of his expeditions “were lying, than to concede that [they] had remained in good health for several years on an exclusive meat regimen.”

In the winter of 1928, Stefansson and Karsten Anderson, a thirty-eight-year-old Danish explorer, became the subjects in a yearlong experiment that was intended to settle the meat-diet controversy. The experiment was planned and supervised by a committee of a dozen respected nutritionists, anthropologists, and physicians. Eugene Du Bois and ten of his colleagues from Cornell and the Russell Sage Institute of Pathology would oversee the day-to-day details of the experiment.

For three weeks, Stefansson and Anderson were fed a typical mixed diet of fruits, cereals, vegetables, and meat while being subjected to a battery of tests and examinations. Then they began living exclusively on meat, at which point they moved into Bellevue Hospital in New York and were put under twenty-four-hour observation. Stefansson remained at Bellevue for three weeks, Anderson for thirteen weeks. After they were released, they continued to eat only meat for the remainder of one year. If they cheated on the diet, according to Du Bois, the experimenters would know it from regular examinations of Stefansson’s and Anderson’s urine. “In every individual specimen of urine which was tested during the intervals when they were living at home,” Du Bois wrote, “acetone [ketone] bodies were present in amounts so constant that fluctuations in the carbohydrate intake were practically ruled out.”

The experimental diet included many types of meat… Stefansson and Anderson each consumed an average of almost two pounds of meat per day, or 2,600 calories: 79 percent from fat, 19 percent protein, and roughly 2 percent from carbohydrates (a maximum of 50 calories a day), which came from glycogen contained in the muscle meat…

“The only dramatic part of the study was the surprisingly undramatic nature of the findings,” wrote Du Bois, when he later summarized the results. “Both men were in good physical condition at the end of the observation,” he reported in 1930, in one of the nine article he and his colleagues published on the study. “there was no subjective or objective evidence of any loss of physical or mental vigor.” Stefansson lost six pounds over the course of the year, and Anderson three, even though “the men led somewhat sedentary lives.” Anderson’s blood pressure dropped from 140/80 to 120/80; Stefansson’s remained low (105/70) throughout. The researchers detected no evidence of kidney damage or diminished function, and “vitamin deficiencies did not appear.” Nor did mineral deficiencies, although the diet contained only a quarter of the calcium usually found in mixed diets, and the acidic nature of a meat-rich diet was supposed to increase calcium excretion and so deplete the body of calcium. Among the minor health issues reported by Du Bois and his colleagues was the observation that Stefansson began the experiment with mild gingivitis (inflammation of the gums), but this “cleared up entirely, after the meat diet was taken.”

…Nutritionists would establish by the late 1930s that B vitamins are depleted from the body by the ocnsumption of carbohydrates. “There is an increased need for these virtamins when more carbohyrdrate in the diet is consumed,” as Theodore Van Itallie of Columbia University testified t the McGovern’s Select Committee in 1973. A similar argument can now be made for vitamin C. Type 2 diabetics have roughly 30 percent lower levels of vitamin C in their circulation than do nondiabetics. Metabolic syndrome is also associated with “significantly” reduced levels of circulating vitamin C, which suggests that vitamin-C deficiency might be another disorder of civilization. One explanation for these observations — described in 1997 by the nutritionists Julie Will and Tim Byers, of the Centers for Disease Control and the University of Colorado respectively, as both “biologically plausible and empirically evident’ — is that high blood sugar and/or high levels of insulin work to increase the body’s requirements for vitamin C.

The vitamin-C molecule is similar in configuration to glucose and other sugars in the body. It is shuttled from the bloodstream into the cells by the same insulin-dependent transport system used by glucose. Glucose and vitamin C compete in the cellular-update process, like strangers trying to flag down the same taxicab simultaneously. Because glucose is greatly favored in the contest, the uptake of vitamin C by cells is “globally inhibited” when blood-sugar levels are elevated. In effect, glucose regulates how much vitamin C is taken up by the cells…if we increase blood-sugar levels, the cellular uptake of vitamin C will drop accordingly. Glucose also impairs the reabsorption of vitamin C by the kidney, and so, the higher the blood sugar, the more vitamin C will be lost in the urine. Infusing insulin into experimental subjects has been shown to cause a “marked fall” in vitamin-C levels in the circulation.

In other words, there is significant reason to believe that the key factor determining the level of vitamin C in our cells and tissues in not how much or little we happen to be consuming in our diet, but whether the starches and refined carbohydrates in our diet serve to flush vitamin C out of our system, while simultaneously inhibiting the use of what vitamin C we do have.

…from Good Calories, Bad Calories (Knopf, 2007), by Gary Taubes, p. 320-326

Continued in Part Eight

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