"Life Without Bread"

‘Healthy’ cholesterol-reducing compounds found to be toxic to heart cells

http://www.drbriffa.com/2011/04/25/healthy-cholesterol-reducing-compounds-found-to-be-toxic-to-heart-cells/

‘Phytosterols’ are compounds that can impair the absorption of cholesterol from the gut. In this way, ‘sterols’ (as their name is often abbreviated to) can reduce cholesterol levels in the bloodstream, which conventional wisdom dictates is always a good thing. Sterols are added to ‘functional foods’ including special margarines that promise cholesterol-reducing and, therefore, health-enhancing properties.

However, the reality is that the impact a drug or foodstuff has on cholesterol levels is quite irrelevant – it’s its impact on health that is important. This distinction is critically important: Arsenic and cyanide might reduce cholesterol levels, but that does not make them healthy things to consume.

I was interested to read about a recent study in which the effect of sterols on rat heart cells was assessed [1]. The cells were exposed to levels of sterols commonly found in the bodies of individuals ingesting sterols. The cells ended up incorporating the sterols at the expense of cholesterol. However, at the same time, the metabolic activity of the heart cells decreased, as did their capacity for growth. In short, exposing heart cells to sterols appears to, err, poison them.

The authors point out, that the results of this study cannot necessarily be translated into conclusions about the effect of these compounds on heart health, but add that the findings “raises concerns about the safety of long-term exposure to physiologically relevant PS [phytosterol] concentrations.”

References:

1. Danesi F, et al. Phytosterol supplementation reduces metabolic activity and slows cell growth in cultured rat cardiomyocytes. British Journal of Nutrition 20 April 2011 [epub]

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Life Without Bread by Christian B. Allan said:

Chapter Five - Energy: Less is More

Energy is a topic that concerns us all, every day in every way. Whether you are trying to get the kids off to school or running a marathon, energy is the buzzword that all of us can relate to.

Most of us think of energy in terms of how we feel: "Am I tired?" "Do I have enough energy to finish mowing the lawn, or to make dinner?" Our overall well-being and ability to perform tasks is our individual measure of energy. But what is energy, and how is it created inside our body and in our cells?

These questions are so fundamentally important that we are devoting an entire chapter to discussing them. There are a great many myths surrounding energy production in the body and which foods supply energy. We hope to dispel some of the common themes that surround the dogma regarding carbohydrates and energy.

The most popular refrain for eating large amounts of carbohydrates is that people must consume them in their diet to get energy. Not only is this statement inaccurate, it also is misleading. The body has very specific mechanisms for generating energy. Using carbohydrates is only one such mechanism, and not necessarily the best one.

Furthermore, you do not need to eat carbohydrates to have them available for energy. Your body can make carbohydrates as needed, if the protein supply is adequate. Reducing your daily intake of carbohydrates to 72 grams or less-6 bread units—will result in more energy at your disposal, as long as you eat plenty of fat and protein. Don't just take our word for it: Try it for yourself! Only by direct experience will you appreciate the effects of low-carbohydrate nutrition on your own energy levels.

This chapter is one of the more technical chapters in this book. It may require reading more than once. Our purpose is to dispel some of the many inaccurate statements and old wives' tales that surround the physiology of energy production in people. Carbohydrates are not required to obtain energy. Fat supplies more energy than a comparable amount of carbohydrate, and low-carbohydrate diets tend to make your system of producing energy more efficient. Furthermore, many organs prefer fat for energy.

Here is a little tidbit that should shake you up. We have all been led to believe that low-fat diets are heart-healthy. But did you know that your heart primarily uses fat for energy? That's right. Carbohydrates contribute very little to the energy necessary to keep your heart beating, and the preferred fat is saturated fat. Thus, if you eat a high-carbohydrate diet, you are depriving your heart of exactly what it prefers to keep it beating.

If you are not interested in the specific biochemistry of energy production, then you could skip this chapter without losing the main point of the book. We will, however, use some of the principles from this chapter in chapter 10, so we recommend you at least glance through this material. But if you skip this chapter, you will need to accept our point that you do not need carbohydrates to get energy, even the much-touted fast energy.

ENERGY CYCLES

Energy production is a fundamental process required for life. It entails much more than simply having enough energy to walk up the stairs; without proper energy production, your cells cannot divide, all of the biochemical reactions that allow you to function will dissipate, and your body, as an organism, eventually will cease to function.

Energy can exist in many forms, such as heat, light, electrical, and chemical energy, but one of the basic laws of physics stipulates that energy cannot be created or destroyed. It can only he changed from one form to another, ands is how it works for life on Earth.

The overall energy cycle of life is derived from the sun. The sun supplies the initial energy from nuclear fusion reactions that make animal and plant life possible.

Sunlight, one form of energy, gets converted by plants, trees, and shrubs into carbohydrates and oxygen. This process is called photosynthesis. Besides sunlight, photosynthesis also requires carbon dioxide and water. Melvin Calvin and scientists who worked with him during the 1950s at the University of California at Berkeley deter¬mined the many chemical steps that were involved in photosynthesis. Calvin was awarded the Nobel Prize in chemistry in 1961 for his achievements in this area, and now photosynthesis is often called the Calvin cycle.

After making carbohydrates, animals consume the plants, and they use the breakdown of carbohydrates for energy. Carbohydrates also can be stored in animals as fat, which can be used by the other animals who eat them for energy. One by-product from the breakdown of carbohydrates is carbon dioxide, which the animals release into the environment, to be used by plants for photosynthesis. This, then, is the basic energy cycle.

In between the simple steps we just discussed there are many important steps that take place. In the course of this chapter, we want you to become familiar with how animals produce energy, as well as how animal energy production is different from primitive cell organisms. In turn, this information will help to dispel the myths surrounding carbohydrates and energy.

THE ENERGY OF LIFE

The energy used to support life is in the form of chemical energy that, as we have said, begins with the sun. This chemical energy arises from two basic processes. In one process energy, a molecule that supplies energy—food, for example—is oxidized to release energy. In another process, energy is obtained by rearrangement of molecules without oxidation.

Oxidation is a process that removes electrons (negatively charged subatomic particles) or adds oxygen to a molecule. The electrons that are removed from a food molecule are used by some cells to make energy. This process requires oxygen. In other types of cells, a process called fermentation takes place. Fermentation is a series of chemical steps that also yield energy, but this happens in the absence of oxygen, so no overall oxidation takes place.

In both of these processes, a molecule is generated called adenosine triphosphate, or ATP. This is the molecule that has the stored energy in the form of chemical bonds. Figure 5.1 shows the chemical structure of ATP. There are three phosphate groups (triphosphate) bound to an adenosine group. The important parts of this molecule are the phosphate groups because this is where the chemical energy is stored.

When cells need energy for their many different functions, the ATP molecule serves as the supplier by releasing the chemical energy stored within its chemical bonds. However, in order to release this energy for cells to use, the bonds must be broken. Two new molecules result from the bond breakage of ATP. These two new molecules are called adenosine diphosphate (ADP) and phosphate (P). By breaking one of the phosphate bonds, energy is released. This general process is summarized in Figure 5.2. In contrast, the stored energy in food is required to make ATP. This is another energy cycle of life.

The steps involved in making, storing, and using energy require an initial energy source. In the case of animals, this energy source is food. The food molecules get oxidized in the body's cells in order to release electrons from them. These electrons are used to make the ATP molecule, and in turn ATP is used by cells for energy. This is another of the many cycles that take place in life.

It is important to know:

• how different organisms obtain energy
• which food molecules are best for different organisms
• what the requirements are for different tissues and organs for the more complicated organisms

So many people believe, without scientific proof, that carbohydrates are what we need for energy, and that eating more carbohydrates will give us more energy. Yet, most of us have had experiences that suggest this isn't true. That sugary afternoon snack comes to mind—afterward you don't feel so great because energy levels usually decrease after the initial "rush." This is a direct result of low blood sugar from the overproduction of insulin.

So let's take a look at how different organisms create energy, and find out just how important carbohydrates are to humans.

CELLS: PAST AND PRESENT

The Earth is approximately four and a half billion years old. In all that time, only two different cell types have evolved: prokaryotes and eukaryotes. Bacteria were the first cells to live on this planet, and they are the prokaryotes. Higher life-forms marked the beginning of eukaryotic cell development, and eukaryotic cells make up the cells in all animals.

The main difference between these two cell types is that eukaryotes have cellular organelles, and prokaryotes don't. (You may recall the term organelle from biology class. Some representative organelles are the nucleus, ribosome, golgi apparatus, and mitochondria.) Organelles are specialized compartments within eukaryotic cells; they have specific functions and are surrounded by semipermeable membranes to isolate them from other parts of the cell.

Prokaryotes are much simpler than eukaryotes. In prokaryotic cells, there are no specialized organelles. All of the biochemical functions required to sustain life take place inside the cell in a kind of "cell soup," and there is no separation of different components.

The differences between these two types of cells are important because they give us clues about energy production in humans and how that differs from bacterial cell energy production. There also are some important differences in how these types of cells produce energy to sustain life.

ENERGY PRODUCTION IN PROKARYOTIC CELLS

We hope readers are still with us! This background information is essential for understanding the production of energy in human cells and because it relates to many aspects of cancer that will be pre¬sented in chapter 10. [See for instance "Can a high-fat diet beat cancer" to get an idea]

Since bacteria, or prokaryotes, appeared on Earth before oxygen was available, they had to produce energy in the absence of oxygen. This is the process of fermentation. Any process that takes place in the absence of oxygen is called an anaerobic process.

Bacteria mainly use glucose as their energy source. Glucose is a six-carbon molecule. The biochemical steps related to breaking down glucose to obtain energy are called glycolysis. The word glycolysis comes from the Greek roots glycos, meaning "sweet," and lysis, meaning "loosening," so glycolysis literally means "the loosening or splitting of something sweet."

The accepted view throughout the biochemical and biological scientific literature is that glycolysis is a primitive process, thought to have begun very early in biological history, before cells evolved to have specialized organelles. However, glycolysis remains a very im¬portant aspect of energy production in advanced life-forms, and oc¬curs in almost every living cell. Most of the decisive work in discovering the glycolytic pathways was done in the 1930s by the German biochemists G. Embden, 0. Meyerhof, and 0. Warburg.

Remember how energy production involves making ATP to be used throughout the cell? The basic steps in turning glucose into ATP involve the splitting, or breakdown, of the glucose molecule into two new molecules, each containing three carbons. One of the products of this breakdown is called glyceraldehyde-3-phosphate. Glyceraldehyde-3-phosphate is the only product from the glucose breakdown that can be oxidized; hence, its metabolism is the key to understanding how ATP is generated from glucose.

Here's how it works: After glyceraldehyde-3-phosphate is formed, a series of metabolic steps involving numerous enzymes convert it into phosphoenol pyruvate (PIT). The phosphate group is removed from PEP at this point to yield another very important molecule, called pyruvate. This is the exact step where ATP is gen¬erated from the original glycolysis of glucose. At this stage, two ATP molecules are generated for every one glucose molecule that was broken down because there are two PEP molecules for every glucose molecule. The ATP molecules can now be used for differ¬ent energy purposes inside the cells.

There are many more biochemical steps in glycolysis that are known to occur, but they are beyond the scope of this book. Still, it's important to at least have a feel for what takes place inside the cell.

Back to pyruvate. This three-carbon molecule has various fates, depending upon what type of cell it's from and what energy needs the cell has.

In one anaerobic reaction, pyruvate gets converted to the mole¬cule lactate. Lactate is an end product of the anaerobic oxidation of glucose. You may already have heard of lactic acid—it's a by-product that builds up in muscle tissue during strenuous exercise. This occurs because when depleted of oxygen, the cells in muscle tissue begin to make energy anaerobically, just like the cells of bacteria, and they produce lactic acid as the by-product.

The breakdown of glucose to lactate is only one type of fermentation, but it happens to be the simplest chemical fermentation that is known, which is consistent with its designation as a very primitive process.

Another type of fermentation is one that produces ethyl alcohol, otherwise known as the alcohol that you drink. In this process, the six-carbon glucose molecule is broken down to a two-carbon mole¬cule, ethyl alcohol, and a one-carbon molecule, carbon dioxide (CO2). Two ethyl alcohol and two carbon dioxide molecules are formed from every one-glucose molecule. Yeast are the organisms that are used to make the fermentation products that many of us enjoy from time to time. Yeast are among the simplest eukaryotic organisms, and are ac¬tually very interesting. One of the reasons yeast use fermentation is for survival. In an overripe piece of fruit, for example, yeast will ferment the sugar deep within the fruit where there is little oxygen, which will generate alcohol. The alcohol kills any bacteria that are present, but the yeast survive. Once the yeast are exposed to oxygen after the fruit decomposes, the yeast can switch and use the alcohol for energy. They're very clever little organisms!

ENERGY PRODUCTION IN EUKARYOTIC CELLS

As time progressed on Earth, plants eventually emerged and began to produce oxygen as a by-product of their metabolism. Other or¬ganisms then adapted to the presence of oxygen, and a major change was made in the way that energy was produced. Oxygen became the fuel that drives the generation of ATP. Respiration is the name given to the process of obtaining energy in the presence of oxygen.

Everyone knows that we need oxygen to live. This is because oxy¬gen is used by the body's cells to produce energy by aerobic oxidation. Eukaryotes produce energy in the cellular organelles called the mito¬chondria. The mitochondria are perhaps the most important organelles in our bodies because they generate almost all of the energy we need to survive. Without them, our cells could not support life.

The proper function of the mitochondria is critical to human health, and carbohydrates and fat play key roles in mitochondrial metabolism. Now we will reveal just how cells produce energy and why carbohydrates are not required as a specific dietary factor in en¬ergy production. We will also take a look at different organs and what their energy needs are. We hope you're beginning to see that there's much more to the story of energy in your body than simply the idea that you need plenty of carbohydrates for fuel.

RESPIRATION AND MITOCHONDRIA

The process of respiration, that is, using oxygen to generate energy, appeared on the Earth after oxygen became available. Oxygen has the chemical ability to remove electrons from other molecules.

After the atmosphere on Earth became concentrated with oxygen, cells evolved to use this as a source of oxidation instead of using the fermentation pathway. Eukaryotic cells, present in organisms more complex than bacteria, emerged from these changes. Along with the formation of eukaryotic cells came the evolutionary breakthrough known as the mitochondria.

Mitochondria are the power plants of the cell. Because they pro¬duce most of the energy in the body, the amount of energy available is based on how well the mitochondria are working. Whenever you think of energy, think of all those mitochondria churning out ATP to make the entire body function correctly. The amount of mitochon¬dria in each cell varies, but up to 50 percent of the total cell volume can be mitochondria. When you get tired, don't just assume you need more carbohydrates; instead, think in terms of how you can maxi¬mize your mitochondrial energy production through respiration.

INSIDE THE MITOCHONDRIA

If you could shrink to a small enough size to get inside the mito¬chondria, what would you discover? The first thing you'd learn is that the mitochondria are primarily designed to use fat for energy! This is a very important point that we need to examine further.

Mitochondria were specifically designed to use fat for energy.

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Exhibit 5.1
'The five major steps in producing ATP within the mitochondria
Step 1 Fuel source transported into mitochondria
Step 2 Fuel converted into acetyl-CoA
Step 3 Oxidation of acetyl-CoA to remove electrons
Step 4 Electrons transported through electron transport chain (or respiratory chain)
Step 5 Oxidative phosphorylation to produce ATP

ATP from the Mitochondria

The complete steps in making ATP within mitochondria are nu¬merous and very complicated, but a look at the five major parts of ATP production will be all that is needed for you to know how en¬ergy is created in our cells. These five steps are summarized in Exhibit 5.1. Each step is discussed in more detail below. Don't get bogged down with the scientific names. Just go with it for a while and you will see how it all fits together. Remember that these chem¬ical steps are taking place thousands of times per second all over your body.

Step 1: Transportation of a Fuel Source into the Mitochondria Since the process of making ATP actually takes place inside the mi-tochondria, the necessary fuel must first be transported there. The fuel is either derived from glucose or from fatty acids. Fatty acids are the chemical name for fat. They have a charged acidic group on the end of them, which is why they are called fatty acids. Fatty acids can be saturated or unsaturated.

Fatty acids are transported into the mitochondria completely intact. L-carnitine is the compound necessary to transport medium-and large-sized fatty acids inside the mitochondria from the cell soup (called cytosol). Think of L-carnitine as a subway train that brings people into the city from the suburbs; likewise, L-carnitine brings fats into the mitochondria. L-carnitine is chiefly found in animal products. (Its name is derived from the Greek word carnis, meaning "meat" or "flesh.") L-carnitine is one of many very important substances that are only found in appreciable quantities in animal foods, which is another reason to eat foods derived from animals. We will discuss more of these substances throughout the book, particularly in the chapter on vitamins and minerals.

Once inside our cells, glucose gets broken down by the process of glycolysis, just as in bacteria. This breakdown takes place outside the mitochondria. Two possibilities may now occur. The product from glycolysis (pyruvate) can either move into the mitochondria to be oxidized, or it can be broken down to lactate outside the mitochondria by a fermentative process similar to the one described for bacteria.

To summarize this step: Fat is transported into the mitochondria as a complete, intact molecule. Glucose gets broken down outside the mitochondria, and the product of this glycolysis (pyruvate) either gets transported into the mitochondria, or it is used anaerobically to produce energy and the by-product lactate.

Step 2: Fuel Is Converted into Acetyl-CoA

After the fatty acids are inside the mitochondria, they are oxidized by a process called beta-oxidation. Remember: Oxidation means that electrons are removed from a molecule. In the beta-oxidation process, fats are broken down into two carbon molecules. This process releases electrons to be used in step two. Acetyl-CoA is the direct product from beta-oxidation of fats inside the mitochondria . When pyruvate enters the mitochondria from glycolysis, it must be converted into acetyl-CoA by an enzyme reaction. Acetyl-CoA is the starting point for the next cycle in the production of ATP inside the mitochondria.

Step 3: Oxidation of Acetyl-CoA and the TCA Cycle

The cycle that oxidizes the acetyl-CoA is called the TCA (tricar-boxylic acid) cycle. Electrons are removed from acetyl-CoA, and carbon dioxide (CO2) is generated as a by-product. Carbon dioxide is the oxidized product of acetyl-CoA. Carbon dioxide is the byproduct of mitochondrial respiration, and is eliminated from our bodies through our breathing or through our skin.

Step 4: Electrons Are Transported Through the Respiratory Chain

'Ile electrons obtained from the oxidation of acetyl-CoA, which ultimately came from fats or sugar, are shuttled through many molecules as part of the electron transport chain inside the mitochondria. Some of the molecules are proteins, while others are small, non-protein cofactor molecules. One of these cofactor molecules is an¬other important substance that is mainly found in animal foods. It is called coenzyme Q-10. Without coenzyme Q-10, mitochondrial res¬piration would be unable to function, and energy production would he minimal.

Step four also is the step where oxygen comes into play. Oxygen accepts the electrons at this stage and is then chemically reduced to water.

Step 5: Oxidative Phosphorylation

As electrons travel down the electron transport chain, they cause electrical fluctuations between the inner and outer membrane in the mitochondria. These chemical gradients, as they are sometimes called, are the driving force that produces ATP in the process called oxidative phosphorylation. ATP is made from ADP and a phosphate molecule (the reverse of its breakdown for energy), just like in bac¬teria. The ATP is transported outside the mitochodria for the cell to use as energy for any of its thousands of biochemical reactions.

These five steps are summarized in Figure 5.3. [see attached image]

WHAT DOES IT ALL MEAN, ANYWAY?

During their evolution, cells developed an organelle that specifically uses fat for energy. This suggests that using fat metabolism for energy production is part of a higher form of life. If there were no mitochondria, then fat metabolism for energy would be limited and not very efficient. Bacteria are able to use some fat for energy, but they prefer glucose and other easily oxidized carbon sources.

[...][sorry, the scanned part of this chapter was unusable. It basically explains the amounts of energy produced from each energy source][...]

ENERGY CONSIDERATIONS IN DIFFERENT ORGANS

The Brain

Your brain uses between 150 and 200 grams of energy daily, mainly from glucose. Since we promote no more than 72 grams of utilizable carbohydrates per day, your body will need to make up the difference.

Fortunately, the body has many ways to do this. The first is a process called gluconeogenesis. This means "the new formation of glucose." The body can make glucose from amino acids obtained from proteins, or it can start with pyruvate. The signals to begin gluconeogenesis are sent out when glucose levels in the diet drop to low enough levels and the supply of glycogen in the liver is used up. Gluconeogenesis functions to bridge the gap until energy can be obtained from stored fat. With today's high-carbohydrate food intake, fat usage for energy is diminished. After reducing carbohy¬drates, it can take some time for the body to switch over to primar¬ily using fat for energy.

By reducing carbohydrate intake, the synthesis of glucose from protein is increased. The making of glucose is an anabolic process and requires energy to build up the glucose molecule from smaller pieces. We have already shown that, with adequate fat consump¬tion, large amounts of ATP will be generated in the mitochondria. This ATP can be used for gluconeogenesis.

This new pool of glucose can now be used for energy by the brain and other tissues. The beauty of this is that the glucose is made on an as-needed basis. This eliminates the excessive buildup of insulin and blood glucose levels that accompany excess carbohydrate consump¬tion. And, as we pointed out in chapters 3 and 4, excessive levels of insulin over a prolonged period of time can have dire consequences.

Many of our detractors have argued that the problem with this philosophy is that the body will use up too much protein, and muscle will wither away. This assertion is based on what is known about starvation. No one can argue against the fact that in times of starvation, the body will weaken and begin to wither away. But we're not talking about starvation. We're talking about a situation where there is plenty of protein available. After seeing the results of the low-carbohydrate diet on fat and muscle growth in thousands of people, we can confi¬dently assure our critics that no one has ever withered away. On the contrary, in the long run, people either lose fat or gain muscle—even very thin people.

Let's look at it another way. Would you rather have big muscles to supply protein for gluconeogenesis, or have big fat deposits from carbohydrates and use the stored fat for energy? Even if you choose the fat-deposit scenario, you'll have to reduce your carbohydrates in order to activate the glucagon and epinephrine hormones to burn the fat. There's just no avoiding low-carbohydrate nutrition if you want to obtain optimal health!

Another important, and often misunderstood, energy source in our cells are compounds called ketones. Ketones are generated from the breakdown of fatty acids in the mitochondria of liver cells and the addition of two acetyl-CoA molecules. These ketone "bodies," as they are sometimes called, are transported to various tissues through the bloodstream and converted back into acetyl-CoA to generate ATP again.

The presence of ketones in the blood and urine, a condition known as ketosis, has always been regarded as a negative situation, related to starvation. While it is true that ketones are generated during starvation conditions, they also are generated in times of plenty—but not plenty of carbohydrates. Since carbohydrate consumption suppresses lilt metabolism, ketones do not form. But in the absence of most car¬bohydrates in the diet, ketones will form from fat to supply energy. This is true even if large amounts of protein and fat are consumed in the diet, which is hardly a starvation condition.

Your brain, as well as other tissues, can use ketone bodies for energy. So here again we see that glucose is not necessary for energy, even for the brain. But Dr. Lutz has found that the benefits of low-carbohydrate nutrition only require 72 grams or so of carbohydrate per day. This amount is not usually low enough to require the body to make ketones for energy. Nonetheless, except in certain cases of people with metabolic diseases, ketosis is not something to fear. [a diet consisting of 90% of fats and proteins and 10% carbs is probably the amount required to be on ketosis, see for instance "Study finds eating fatty foods can help stop seizures"].

Remember that what is considered a "normal diet" today is based on a limited amount of data, all of which was acquired after humans already had begun eating too much carbohydrate. If you could take a trip back to the days before modern humans emerged, you might very well find that ketosis was more the normal metabolic state, and t hat today's human metabolic state is mostly abnormal.

The Heart and the Skeletal Tissue

It seems that no one really discusses energy in terms of organs other than the brain, which is always quoted as needing glucose. We never hear anything about the needs of the heart and Other organs. One of the body's best-kept secrets is that the heart uses fatty acids almost exclusively for energy, and these are saturated fat.1'2 This is a truly important point, and we think you can see why. How can people say that most healthy foods for the heart are low in fat, when the heart muscle is known to require fat in order to beat?

One reason could be that fatty acids can also be made from acetyl-CoA. Using this mechanism, the acetyl-CoA derived from glycolysis can make fatty acids as needed. However, it is known that fatty acid synthesis does not significantly contribute to the energy needs of the heart muscle cells.

The fact is, your heart needs fat from your diet to keep working. Low-fat diets that are also high in carbohydrate intake are probably the worst thing you could do for your heart, yet this is the prevail¬ing theory, promoted by numerous, often misinformed, organiza¬tions and people.

The single reason that the low-fat diet is so greatly promoted is this: fear of cholesterol. Yet this is but another widespread myth that's not really consistent with available information. The next chapter on heart disease will reveal just how weak the cholesterol theory is.

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Gary Taubes said:

The First Law

Body fat is carefully regulated, if not exquisitely so.

This is true even though some people fatten so easily that it's virtually impossible to imagine. What I mean by "regulated" is that our bodies, when healthy, are working diligently to maintain a set amount of fat in our fat tissue—not too much and not too little—and that this, in turn, is used to assure a steady supply of fuel to the cells. The implication (our working assumption) is that if someone gets obese it's because this regulation has been thrown out of whack, not that it's ceased to exist.

The evidence that fat tissue is carefully regulated, not just a garbage can where we dump whatever calories we don't burn, is incontrovertible. We can start with all the observations in chapter 5 about the wheres, whens, and whos of fattening. That men and women fatten differently tells us that sex hormones play a role in regulating body fat (as do Wade's experiments and what we know about estrogen and LPL). That some parts of our bodies are relatively fat free—the backs of our hands, for example, and our fore¬heads—and others not so, tells us that local factors play a role in where we fatten. Just as local factors obviously play a role in where we grow hair— in some places, but not in others.

That obesity runs in families (we're more likely to be fat if our parents were fat) and that the local distribution of fat itself can be a genetic attribute (the steatopygia of certain African tribes) tells us that body fat is regulated, because how else would the genes passed from generation to generation influence our fat and where we put it, if not through the hormones and enzymes and other factors that regulate it?

That the amount of fat (and even the type of fat) animals carry is carefully regulated also argues for this conclusion. We are, after all, just another species of animal. Animals in the wild may be naturally fat (hippopotami, for instance, and whales). They'll put on fat seasonally, as insulation in preparation for the cold of win¬ter or as fuel for annual migrations or hibernations. Females will fatten in preparation for giving birth; males will fatten to give them a weight advantage in fights for females. But they never get obese, meaning they won't suffer adverse health consequences from their fat the way humans do. They won't become diabetic, for instance.

No matter how abundant their food supply, wild animals will maintain a stable weight—not too fat, not too thin—which tells us that their bodies are assuring that the amount of fat in their fat tissue always works to their advantage and never becomes a hindrance to survival. When animals do put on significant fat, that fat is always there for a very good reason.* [*The camel's hump is another example of a large fat mass that exists for a purpose: the hump provides a reservoir of fat for survival in the desert, without the camel's having to keep that fat in subcutaneous deposits, as we do, where the insulation would present problems in the desert heat. The same goes for fat-rumped and fat-tailed sheep, and fat-tailed marsupial mice, all desert dwellers that carry their fat almost exclusively in the eponymous locations.] The animals will be as healthy with it as without.

Excellent examples of how carefully animals (and so presum¬ably humans, too) regulate their fat accumulation are hibernating rodents—ground squirrels, for example, which double their weight and body fat in just a few weeks of late summer. Dissecting these squirrels at their peak weight, as one researcher described it to me, is like "opening a can of Crisco oil—enormous gobs of fat, all over the place."

But these squirrels will accumulate this fat regardless of how much they eat, just like Wade's ovary-less rats. They can be housed in a laboratory and kept to a strict diet from springtime, when they awake from hibernation, through late summer, and they'll get just as fat as squirrels allowed to eat to their hearts' content. They'll burn the fat through the winter and lose it at the same rate, whether they remain awake in a warm laboratory with food avail¬able or go into full hibernation, eating not a bite, and surviving solely off their fat supplies.

The fact is, there's very little that researchers can do to keep these animals from gaining and losing fat on schedule. Manipu¬lating the food available, short of virtually starving them to death, is not effective. The amount of fat on these rodents at any particu¬lar time of the year is regulated entirely by biological factors, not by the food supply itself or the amount of energy required to get that food. And this makes perfect sense. If an animal that requires enormous gobs of fat for its winter fuel were to require excessive amounts of food to accumulate that fat, then one bad summer would have long ago wiped out the entire species.

It may be true that evolution has singled out humans as the sole species on the planet whose bodies do not work to regulate fat stores carefully in response to periods of both feast and famine, that some people will stockpile so much fat merely because food is available in abundance that they become virtually immobile, but accepting this conclusion requires that we ignore virtually everything we know about evolution.

A final argument for the careful regulation of body fat is the fact that everything else in our bodies is meticulously regulated. Why would fat be an exception? When regulation breaks down, as it does in cancer and heart disease, the result is often fatally obvious. When people accumulate excess fat, this tells us that something has gone awry in the careful regulation of their fat tissue. What we need to know is what that defect is and what to do about it.

The Second Law

Obesity can be caused by a regulatory defect so small that it would be undetectable by any technique yet invented.

Remember the twenty-calorie-a-day problem I discussed earlier? If we overeat by just twenty calories each day—adding just 1 percent or less to our typical daily caloric quota, without a compensatory increase in expenditure—that's enough to transform us from lean in our twenties to obese in our fifties. In the context of the calories-in/calories-out logic, this led to the obvious question: How do any of us remain lean if it requires that we consciously balance the calories we eat'to those we expend with an accuracy of better than i percent? That seems impossible, and assuredly is.

Well, these same twenty calories a day is all this regulatory system has to misdirect into our fat cells to make us obese. The same arithmetic applies. lf, by some unlucky combination of genes and environment, a regulatory error causes our fat cells to store an excess of just i percent of the calories that would otherwise be used for fuel, then we are destined to become obese.

If this misappropriation of calories into fat is only slightly larger, someone could end up grotesquely fat. Yet this would still seem like a relatively minor error in regulatory judgment—just a few percentage points, something exceedingly difficult to measure and yet not that hard to imagine.

The Third Law

Whatever makes us both fatter and heavier will also make us overeat.

This was the ultimate lesson of Wade's rats. It may be counter¬intuitive, but it has to be true for every species, for every person who puts on pounds of fat. It's arguably the one lesson we (and our health experts) have to learn in order to understand why we get fat and what to do about it.

This law is one fact we can count on from the first law of thermodynamics, the law of energy conservation, which health experts have been so determined to misapply. Anything that increases its, mass, for whatever reason, will take in more energy than it expends. So, if a regulatory defect makes us both fatter and heavier, it is guaranteed to make us consume more calories (and so increase our appetite) and/or expend less than would be the case if this regulation was working perfectly.

Here's where growing children help as a metaphor to under¬stand this cause and effect of getting fat and overeating. I'm going to use two photos of my oldest son to make this point. The photo below, on the left, was taken when he was not quite two years old and weighed thirty-four pounds.

The photo on the right was taken three years later, after he had gained nine inches in height and weighed fifty-one pounds.

He gained seventeen pounds in three years, so he certainly consumed more calories than he expended. He overate. Those excess calories were used to create all the necessary tissues and structures that a larger body needed, including, yes, even more fat. But he didn't grow because he consumed excess calories. He consumed those excess calories—he overate—because he was growing.

My son's growth, like every child's, is caused fundamentally by the action of growth hormones. As he gets older, he'll occa¬sionally go through growth spurts that will be accompanied by a voracious appetite and probably a fair share of sloth, but the appetite and the sloth will be driven by the growth, not vice versa. His body will require excess calories to satisfy the demands of the growth—to build a bigger body—and it will figure out a way to get them, by increasing his appetite or decreasing his energy expenditure or both. When he goes through puberty, he'll lose fat and gain muscle; he'll still be taking in more calo¬ries than he expends, and this, too, will be driven by hormonal changes.

That growth is the cause and overeating the effect is almost assuredly true for our fat tissue as well. To paraphrase what the German internist Gustav von Bergmann said about this idea more than eighty years ago, we would never even consider the possibility that children grow taller because they eat too much and exercise too little (or that they stunt their growth by exercising too much). So why assume that these are valid explanations for growing fat (or remaining lean)? "That which the body needs to grow it always finds," von Bergmann wrote, "and that which it needs to become fat, even if it's ten times as much, the body will save for itself from the annual balance."
The only reason to think that this isn't true, that the cause and effect go in one direction when we get taller (growth causes overeating) and the other when we grow fatter (overeating causes growth), is that this is what we grew up believing and we never stopped to consider if it actually makes sense. The far more rea¬sonable assumption is that growth in both cases determines appetite and even energy expenditure—not the other way around. We don't get fat because we overeat; we overeat because we're getting fat.

Since this is so counterintuitive but so critical to understand, I want to return to the examples of animals. African elephants are the world's largest land animals. The males typically weigh more than ten thousand pounds, although surprisingly little of this is fat. Blue whales are the largest animals, on or off land. They can weigh three hundred thousand pounds, and much of that is fat. African elephants will eat hundreds of pounds of food a day, and blue whales, thousands,* prodigious amounts, but neither species grow to be enormous because they eat so much. They eat prodigious amounts because they're enormous animals. With or with¬out large quantities of body fat, body size determines how much they eat.

The infants of these species also eat relatively enormous quan¬tities. They do so because they're born exceedingly large to begin with and because their genes predispose them to grow many thou¬sands of pounds (elephants) or hundreds of thousands of pounds (blue whales) larger still. Now both growth and body size are dri¬ving appetite. This is true whether these animals are using the calories to store fat, or to enlarge muscle and other tissues and organs. Whether or not they have enormous quantities of fat, the same cause and effect holds true.

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Psyche said:

Harold said:

Great thread... this plus what the C's have said in the recent transmition has me reevaluating my carb intake.... so thank-you. I eat gluten/wheat free bread, yeast free, allergenic bread, it is about 21grams of carbs each piece. I eat yams and onions and that is all I have in the veggie department. I eat lots of bacon, ham, and all other meats. I also have raspberry jam, which would fit into a hunter forager diet ie. berries yes? :)

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Jams are rich in sugar... I forgot how many Bread Units they had, but I remember thinking that I rather had more blinis with xylitol on them.

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Psyche said:

Gimpy said:

Psyche said:

There is a section of the book devoted to muscular spasms. They recommend L-carnitine supplementation during the first few weeks if there is muscular cramping. As the body adjusts to the high protein diet, it will be able to derive all the L-carnitine from the meat.

L-carnitine is the amino acid that helps carry fat into the mitochondria, where it will be used as an energy source.

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The new supplements I've been taking have L-carnitine in them, I'm going to go through the book today (Life without Bread) and see if adding more will help, though I'm wondering if its a matter of the pathways needing to heal? Does that make sense?

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Absolutely, they say that L-carnitine is only needed for a week or so, after that, you'll get all you need from the meat. Mouton, lamb and beef are specially rich in L-carnitine.

The other amazing thing to read was how mainstream organizations delierately stressed the mineral and vitamin content of fruits and veggies, whereas they tend to ignore meats and eggs, which turns out to be a complete source of all vitamins and minerals (except for vitamin C, which is still present in some animals).

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Gary Taubes said:

....

The evidence that fat tissue is carefully regulated, not just a garbage can where we dump whatever calories we don't burn, is incontrovertible. We can start with all the observations in chapter 5 about the wheres, whens, and whos of fattening. That men and women fatten differently tells us that sex hormones play a role in regulating body fat (as do Wade's experiments and what we know about estrogen and LPL). That some parts of our bodies are relatively fat free—the backs of our hands, for example, and our fore¬heads—and others not so, tells us that local factors play a role in where we fatten. Just as local factors obviously play a role in where we grow hair— in some places, but not in others.

That obesity runs in families (we're more likely to be fat if our parents were fat) and that the local distribution of fat itself can be a genetic attribute (the steatopygia of certain African tribes) tells us that body fat is regulated, because how else would the genes passed from generation to generation influence our fat and where we put it, if not through the hormones and enzymes and other factors that regulate it?
{...}

Excellent examples of how carefully animals (and so presumably humans, too) regulate their fat accumulation are hibernating rodents—ground squirrels, for example, which double their weight and body fat in just a few weeks of late summer. Dissecting these squirrels at their peak weight, as one researcher described it to me, is like "opening a can of Crisco oil—enormous gobs of fat, all over the place."

But these squirrels will accumulate this fat regardless of how much they eat, just like Wade's ovary-less rats. They can be housed in a laboratory and kept to a strict diet from springtime, when they awake from hibernation, through late summer, and they'll get just as fat as squirrels allowed to eat to their hearts' content. They'll burn the fat through the winter and lose it at the same rate, whether they remain awake in a warm laboratory with food avail¬able or go into full hibernation, eating not a bite, and surviving solely off their fat supplies.

The fact is, there's very little that researchers can do to keep these animals from gaining and losing fat on schedule. Manipu¬lating the food available, short of virtually starving them to death, is not effective. The amount of fat on these rodents at any particular time of the year is regulated entirely by biological factors, not by the food supply itself or the amount of energy required to get that food. And this makes perfect sense. If an animal that requires enormous gobs of fat for its winter fuel were to require excessive amounts of food to accumulate that fat, then one bad summer would have long ago wiped out the entire species.
{...}
Whatever makes us both fatter and heavier will also make us overeat.

This was the ultimate lesson of Wade's rats. It may be counterintuitive, but it has to be true for every species, for every person who puts on pounds of fat. It's arguably the one lesson we (and our health experts) have to learn in order to understand why we get fat and what to do about it.{...}

That growth is the cause and overeating the effect is almost assuredly true for our fat tissue as well. To paraphrase what the German internist Gustav von Bergmann said about this idea more than eighty years ago, we would never even consider the possibility that children grow taller because they eat too much and exercise too little (or that they stunt their growth by exercising too much). So why assume that these are valid explanations for growing fat (or remaining lean)? "That which the body needs to grow it always finds," von Bergmann wrote, "and that which it needs to become fat, even if it's ten times as much, the body will save for itself from the annual balance."

The only reason to think that this isn't true, that the cause and effect go in one direction when we get taller (growth causes overeating) and the other when we grow fatter (overeating causes growth), is that this is what we grew up believing and we never stopped to consider if it actually makes sense. The far more rea¬sonable assumption is that growth in both cases determines appetite and even energy expenditure—not the other way around. We don't get fat because we overeat; we overeat because we're getting fat.

Since this is so counterintuitive but so critical to understand, I want to return to the examples of animals. African elephants are the world's largest land animals. The males typically weigh more than ten thousand pounds, although surprisingly little of this is fat. Blue whales are the largest animals, on or off land. They can weigh three hundred thousand pounds, and much of that is fat. African elephants will eat hundreds of pounds of food a day, and blue whales, thousands,* prodigious amounts, but neither species grow to be enormous because they eat so much. They eat prodigious amounts because they're enormous animals. With or with¬out large quantities of body fat, body size determines how much they eat.

The infants of these species also eat relatively enormous quantities. They do so because they're born exceedingly large to begin with and because their genes predispose them to grow many thousands of pounds (elephants) or hundreds of thousands of pounds (blue whales) larger still. Now both growth and body size are driving appetite. This is true whether these animals are using the calories to store fat, or to enlarge muscle and other tissues and organs. Whether or not they have enormous quantities of fat, the same cause and effect holds true.

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Laura said:

Now, the point about the squirrels that get fat seasonally no matter what they eat, how much or how little, is supremely interesting in view of Wiley's hypothesis that people get fat because they are eating more carbs in summer than they do in winter and that they are supposed to do this. In fact, it contradicts that idea. If a person is supposed to get fat in summer, they will do so no matter what they eat. Therefore, eating more carbs in summer is probably NOT an evolutionary strategy.

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dugdeep said:

Laura said:

Now, the point about the squirrels that get fat seasonally no matter what they eat, how much or how little, is supremely interesting in view of Wiley's hypothesis that people get fat because they are eating more carbs in summer than they do in winter and that they are supposed to do this. In fact, it contradicts that idea. If a person is supposed to get fat in summer, they will do so no matter what they eat. Therefore, eating more carbs in summer is probably NOT an evolutionary strategy.

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Aha! Excellent point. I hadn't connected those dots. Thanks Laura!

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Carbohydrates are not required to obtain energy. Fat supplies more energy than a comparable amount of carbohydrate, and low-carbohydrate diets tend to make your system of producing energy more efficient. Furthermore, many organs prefer fat for energy.

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Mitochondria are the power plants of the cell. Because they produce most of the energy in the body, the amount of energy available is based on how well the mitochondria are working. Whenever you think of energy, think of all those mitochondria churning out ATP to make the entire body function correctly. The amount of mitochondria in each cell varies, but up to 50 percent of the total cell volume can be mitochondria. When you get tired, don't just assume you need more carbohydrates; instead, think in terms of how you can maximize your mitochondrial energy production through respiration.

If you could shrink to a small enough size to get inside the mitochondria, what would you discover? The first thing you'd learn is that the mitochondria are primarily designed to use fat for energy! This is a very important point that we need to examine further.

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loreta said:

I try to not feel sorry for them, this is an issue I have to work.

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Mr. Premise said:

This brings up a question I have, Psyche. I started my supplementation regimen before I was eating meat. It occurs to me that now I may not need some of the supplements. Is there a source to see what kinds of things are in red meat, for example. It is getting expensive to buy both supplements and local grass fed beef! A few months ago I listed what I take here: http://cassiopaea.org/forum/index.php?topic=21909.0

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Rethinking Thin: The New Science of Weight Loss--and the Myths and Realities of Dieting by Gina Kolata said:

Three obesity researchers were having breakfast at a medical meeting in Charleston, South Carolina, a few years ago when
their talk inevitably turned to the Atkins diet. It had reached a new peak of popularity, and they were simply annoyed with the diet and the whole low-carb movement. It just irked them that this seemingly irrational way to lose weight, this seemingly unhealthy, if not dangerous, diet scheme, was being hailed as the secret to effortless and permanent weight loss. The whole Atkins movement was built on testimonials, they groused.

"We kept saying, 'Nobody has any data,'" said Gary D. Foster, who was the clinical director of the weight loss center at the University of Pennsylvania. Finally, the three decided, Why not do a study? They had not applied for funds, but they were curious enough to do some research anyway. "It would be quick and dirty," Foster remarked, just a brief look at whether the Atkins diet had any value. The three fully expected to discredit it, showing it was no better, maybe even worse, than traditional diets for weight loss, and dangerous to boot. They just knew that the diet was going to do something awful to cholesterol levels and that people who followed it were going to be risking a heart attack.

And, they slowly realized, they also would be asking a question that, amazingly enough, had never been asked in a rigorous way: Is one diet any better than another? You might think that with all the years, all the decades, of obesity research, the answer would be obvious. It's a question that, of course, would have been well studied. But you would be wrong. That question, that fundamental question, had just been left dangling.

And so it began, the first attempt to compare the Atkins diet with something more traditional, the standard low-calorie, low-fat diet beloved of academic weight loss clinics.

The study took place at three medical centers—the University of Pennsylvania, the University of Colorado, and Washington University in St. Louis—and was directed by the three doctors who conceived it. It was small, involving just sixty-three obese men and women, people whose average weight was 216 pounds. And it lasted for one year. The subjects were randomly assigned to follow the Atkins diet—the researchers handed them the book Dr. Atkins' New Diet Revolution— or to follow a diet and behavior modification plan written by Kelly Brownell, a Yale psychologist who publishes an earnest textbook-like manual called The LEARN Program for Weight Management. "We picked LEARN because it is the most frequently used manual [at weight loss centers]," Foster explained. "It is the gold standard for weight loss and behavioral weight control."
No one could have been more surprised than these researchers when they saw the results.

The Atkins diet, they discovered, seemed better than the usual diet program, at least for the first six months; the subjects' weight loss, an average of 7 percent of their body weight, was twice as good as with the low-calorie diet. Granted, no one lost much weight, and granted, 40 percent of each group dropped out, and granted, by the time a year was up, the two groups were about equal in their total weight loss and almost everyone in either group who lost weight had regained most of it. The Atkins dieters ended up, on average, losing 4.4 percent of their body weight, or about 9.5 pounds, and the low- calorie dieters lost about 2.5 percent, or about 5.5 pounds, but the difference between the groups was not statistically different. Still, the Atkins diet, to the investigators' astonishment, led to higher levels of HDL cholesterol, which is linked to protection against heart disease, and lower levels of triglycerides in the blood, which also indicate a reduced heart disease risk. The conventional diet did just the opposite.

"That's not what we expected," Foster said. "How did it happen? Was it good? Was it bad? Was it indifferent?" And, most important, "What IS the best way to lose weight?"

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The three researchers published their results in the May 22, 2003, issue of the New England Journal of Medicine, one of the most prestigious medical journals. Their paper was accompanied by an editorial that ended with the usual platitudes. "The recipe for effective weight loss is a combination of motivation, physical activity, and caloric restriction," it said. "Until further evidence is available regarding the long-term benefits of a low-carbohydrate approach, physicians should continue to recommend a healthy lifestyle that includes regular physical activity and a balanced diet."

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The editorial, of course, dodged the question. Is it possible for most people to permanently lose weight? And, if so, how? If "a healthy lifestyle" were enough, would two-thirds of the nation have a weight problem? Would the nation be gripped by what is often called an obesity epidemic, as evidenced by the grim statistics of a growing national girth? The percentage of people who are overweight or obese was a whopping 47 percent in the period from 1976 to 1980, but now it is an even more whopping 64 percent.

The overweight say it is not that they don't try to be thin. All they do is try, many say, but nothing seems to help.
They may never have asked whether there is any scientific evidence that one diet is better than another, but most have, in a sense, experimented by themselves, trying diet after diet, hoping to find one that will lead them to their dream weight....

"Obese people get a level of abuse now that could not even be considered with any other group," says Jeffrey Friedman, an obesity researcher at Rockefeller University. Looking like a stereotypical rumpled scientist, long and lanky with no significant weight problem, Friedman is speaking not from personal experience but from his own research that showed him that sustained and substantial weight loss is problematic for nearly everyone. And he despairs over the plight of fat people.

"We have this naive view that the whole system of weight control can be controlled by willpower," Friedman says. He likes to cite weight loss advice from two millennia ago—eat less and exercise more. "We have to do better than repeating two-thousand-year-old mantras," he says.

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During World War II a remarkable experiment began at the University of Minnesota, one that would deeply trouble its
researchers and would become a classic in the annals of medicine. The question it asked was disarmingly simple: What would happen if young, healthy men deliberately lost a lot of weight?

The study was directed by the late Ancel Keys, a public health researcher at the University of Minnesota whose many accomplishments included inventing the K ration (the K was from his last name) for the army when it asked him to find a lightweight food that was packed with nutrients for paratroopers to carry. He also directed a pathbreaking study, the Seven Countries Study, comparing heart disease and diet among twelve thousand men. It began in 1958 and lasted for decades, and its conclusion—that people who ate lots of unsaturated fats, like olive oil, fared better than those whose diet was heavy in saturated fats, like butter—was the origin of the so-called Mediterranean Diet that is promoted today by many nutritionists.

But Keys's weight loss study was very different from his other research. It involved thirty-six young men, conscientious objectors, who took part in lieu of military service. The men were of normal weight and had been carefully selected from a group of one hundred who had applied to participate. The men Keys chose were the healthiest, both physically and psychologically.

For three months, the men were simply studied and observed. Then they started the diet—eating half as much as they normally ate and exercising, walking 22' miles a week. It was the sort of regimen that obese people often undertake when they try to lose weight, and it worked—the men lost 25 percent of their weight over six months. They spent the next three months re-feeding, as Keys put it, increasing their caloric intake and gaining back the weight they lost. Finally, those who remained—four of the men dropped out along the way— were followed for another nine months, when they were allowed to eat as they pleased.

The results were shocking.

While they were dieting, the men were obsessed with food; they could not stop thinking of food and eating. They licked their plates to get every last morsel. Food became the subject of their conversations and their fantasies. They hoarded food; they fixated on it.

Keys wrote: "Those who ate in the common dining room smuggled out bits of food and consumed them on their bunks in a long-drawn- out ritual. Cookbooks, menus, and information bulletins on food production became intensely interesting to many of the men who previously had little or no interest in dietetics or agriculture." The men "often reported that they got a vivid vicarious pleasure from watching other persons eat or from just smelling food."

They struggled over urges: to "gulp their food down ravenously" or "consume it slowly so that the taste and odor of each morsel would be fully appreciated." They poured on salt and spices; they started drinking so much coffee and tea that the researchers finally limited them to nine cups a day. They chewed gum nonstop, with one man chewing forty packs a day.

It got worse.

Some of the men began collecting cooking implements, like coffeepots or hot plates. One man found himself poking around in garbage cans. The men began bingeing.

"Several men were unable to adhere to their diets and reported episodes of binge eating followed by self-reproach. During the eighth week of starvation, one volunteer flagrantly broke the dietary rules, eating several sundaes and malted milks; he even stole some penny candies. He promptly confessed the whole episode, [and] became self- deprecatory."

Keys went on: "While working in a grocery store, another man suffered a complete loss of will power and ate several cookies, a sack of popcorn, and two overripe bananas before he could 'regain control' of himself. He immediately suffered a severe emotional upset, with nausea, and upon returning to the laboratory he vomited. . . . he was self-deprecatory, expressing disgust and self-criticism."

The men, previously so emotionally healthy, suffered bouts of depression, irritability, and mood swings. They lost interest in sex—all they cared about was food.

One man wrote, "I am one of about three or four who still go out with girls. I fell in love with a girl during the control period but I see her only occasionally now. It's almost too much trouble to see her even when she visits me in the lab. It requires effort to hold her hand. Entertainment must be tame. If we see a show, the most interesting part of it is contained in scenes where people are eating."

The men's metabolisms slowed to 40 percent of what they were before the study began. Their body temperatures dropped; their heart rates slowed. It was as though their bodies were doing everything possible to conserve calories.

Even when the dieting ended, and the twelve-week re-feeding period was under way, the men had problems. Normal meals were no longer enough. They would eat a huge meal and say they were still hungry.

One man's meals had as many as 5,000 to 6,000 calories, but he "started 'snacking' an hour after he finished a meal." Some of the men consumed 8,000 to 10,000 calories a day. Keys describes the scene:

Subject No. 20 stuffs himself until he is bursting at the seams, to the point of being nearly sick and still feels hungry; No. 120 reported that he had to discipline himself to keep from eating so much as to become ill; No. 1 ate until he was uncomfortably full; and subject No. 30 had so little control over the mechanics of "piling it in" that he simply had to stay away from food because he could not find a point of satiation even when he was "full to the gills." ... "I ate practically all weekend," reported subject No. 26. . . . Subject No. 26 would just as soon have eaten six meals instead of three.

Soon afterward, when men who had been starved as prisoners of war during World War II began describing their ordeals, they spoke of the same almost insane behavior, finding themselves dreaming of food and cooking and recipes. One prisoner, Private First Class Risto Milosevich, wrote of his fellow inmates: "They were very hungry. Food—that's the only thing that interested them. Most of the time, you get GIs together and they start talking about girls and ass and screwing, but the only thing they were doing was taking recipes down. In hindsight, it was comical."

An oddity, perhaps. Observations that were ones for the history books, perhaps.

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.... a decade later, those troubling behaviors of starving men began to haunt a young researcher at Rockefeller University. They were, he realized, just what he was seeing in obese people who had lost a lot of weight.

The Rockefeller scientist was Jules Hirsch, a man who, like Mickey Stunkard at Penn, has found himself discovering inconvenient truths about obesity and learning that those truths were all too often ignored or forgotten, perhaps because they simply were not what most people wanted to hear.

But if Mickey Stunkard, with his studies of large populations, with his data analyses, was taking one view of obesity, Jules Hirsch, his iconoclastic counterpart at Rockefeller University in New York, was looking at the obesity problem from the opposite perspective. His focus was on individuals and, especially, very fat people who would do anything—even live for months in a hospital on liquid meals—in order to get thin.

In those days, more than half a century ago, the world of research was a different place than it is today. The tools of molecular biology had not been invented, and some physician researchers, like Hirsch, specialized in a very laborious, painstaking kind of work that required taking just a few patients and studying them in minute detail.

The Rockefeller Institute for Medical Research, as Rockefeller University was then called, was a lavishly funded institution on the banks of the East River on the elite Upper East Side of Manhattan, and it had been established for just such studies. The university even had a gray stone hospital, high on a hill on its verdant campus, where patients would live, free of charge, while they participated in research. Then, as now, the only patients in the hospital were people participating in medical studies. Hirsch came to Rockefeller as a young scientist in 1954, lured by what he describes as "a remarkable institution" that gave young physicians time and resources to study diseases or medical conditions for years, allowing them "the extraordinary opportunity of time to reflect on the nature of the disease."

But the hospital and the style of research were not the only attractions for Hirsch. He also wanted to work with E. H. Ahrens, Jr., known as Pete Ahrens, an eminent scientist at Rockefeller who was one of the icons in the then-popular field of clinical investigation. Ahrens was known for his patience and for having the curiosity to embark on long, meticulous studies looking for individual differences in physiological responses. When Hirsch joined his group, the focus was on finding ways to prevent heart disease.

At that time, the powerful cholesterol-lowering statin drugs had not yet been discovered, and diets with very little animal fat were urged upon heart patients and people whose cholesterol levels were high. Hirsch began the work thinking only of heart disease—obesity was the farthest thing from his mind. He had never considered questioning the idea that anyone can be thin if they really want to. Nor did he wonder about the truth of the prevailing wisdom that said that people who never lose weight, or lose and regain, must have some psychiatric issues, some deep-seated need to be fat. In fact, he did not even have a personal interest in obesity—a medium-sized man with a compact body and a square-shouldered stance, he had never had a weight problem. The relationship between diet and heart disease was going to be his research problem.

"The question was, Are vegetarian diets good for preventing heart disease?" Hirsch explains. To find out, the scientists began by asking whether there was a way, other than asking people to recall their diets, to determine what sort of oil or fat they had been eating. It turned out that there was—the fat in food showed up in the globules of fat that float like bubbles in the body's fat cells. Oddly enough, when it comes to fat, you are what you eat.

Ahrens discovered this strange fact by investigating study subjects who had lived in the Rockefeller University Hospital, existing for months on diets that used corn oil as a source of fat. Their fat cells, n turned out, had increased amounts of linoleic acid, the fatty acid found in corn oil. "If you eat corn oil, your adipose tissue gets corn oily," Hirsch says. "We used to make a joke that if you eat ham, you turn into the Smithfield man."

There had been an epidemic of heart disease in the twentieth century. Had there been a corresponding change in Americans' diets? Ahrens and Hirsch asked. They looked for studies that described American diets, and data from the U.S. Department of Agriculture, which told what Americans ate. And they acquired samples of fat tissue, obtained at autopsies, and analyzed them. Their conclusions were that the American diet had changed from one that emphasized animal fat, and particularly fat from pork, to one with more corn or vegetable oils.

The data did not fit with the dogma—if the source of the diet was so important and if people had switched from lard to corn oil, there should have been less heart disease. Maybe obese people, who were more prone to heart disease, were eating more animal fats. Maybe, in fact, animal fat was helping to make the obese grow fat and stay that way.

But no, the investigators reported. They did not just ask obese people what they ate—they examined fat tissue from obese people. And, they discovered, obese people were eating the same fats as the non-obese. "Therefore, their diets, at least in the kind of fat being consumed, were not a significant factor in the production of obesity," Hirsch remarks.

But once he started looking at fat cells from obese people, Hirsch noticed something peculiar. Those fat cells were huge and numerous, very different from the compact, almost petite, and much less plentiful fat cells of people of normal weight.
That was interesting, he thought. What would happen to fat cells if obese people lost weight? Would there be fewer of them and would they be smaller, or would the formerly fat people keep all their fat cells but deflate the cells down to almost nothing?

It should be a straightforward study. Hirsch decided to advertise for a few obese people who would agree to live at the Rockefeller University Hospital for eight months, during which time the scientists would control their diets and make them lose weight. Everyone would benefit—Hirsch would get his before-and-after samples of fat cells, and the obese patients would become thin.

Obese people, seeing the ad, eagerly volunteered, and Hirsch recruited four of them, each of whom had been fat since childhood or adolescence. These were not just slightly overweight people. They were fat, truly massive.

One man, C.E, was thirty-eight and weighed 350 pounds. A thirty-six-year-old woman, R.S., weighed 280. A forty-year-old man, C.A., weighed 340 pounds. The fourth patient was E.L., a man who weighed 320 but had weighed more than 400 pounds two years earlier before losing more than 100 pounds on his own.

The study subjects began with an agonizing four weeks of a maintenance diet to assess their metabolism and caloric needs. They lived in the hospital, and their food was limited to what the scientists provided, with diets that were carefully adjusted to keep their weight steady, high as it was. Only then, after Hirsch knew how many calories each of them needed and how quickly each burned calories, could the diet begin. Although no one realized it at the time, that initial maintenance phase would be critically important in understanding what happened to those fat people during and after the study.

The weight loss phase that followed the maintenance phase was difficult—a period of four to five months when the subjects' only nourishment was a liquid formula providing 600 calories a day. Finally, the subjects spent another four weeks on a diet that maintained them at their new weights.

The long ordeal seemed worth it, though. Everyone lost weight, 100 pounds on average. Everyone was delighted with their new, slimmer selves. And everyone, including Hirsch, assumed that the subjects would leave the hospital permanently thinner.

That did not happen. Instead, Hirsch says, "they all regained." He was horrified. What an incredible setback, what a terrible consequence for people who had spent more than half a year living in a hospital and who had endured most of that time subsisting on just 600 calories a day. And they certainly wanted to be thin, so what went wrong? Why, Hirsch wondered, did the pounds come back?

He found himself mulling over the problem. Was it that fat tissue grows back, restoring itself when you take it away, much in the way that the liver regenerates when you remove part of it or that skin grows back over a wound? But no, that could not be, Hirsch realized, because he knew of a situation in which surgeons remove a large chunk of fat and it does not regenerate. "I often reflected that people who have large fatty tumors, called lipomas, and had the tumor removed did not regain the weight," he said. That means that a large mass of fat tissue can be removed and the fat never returns. But what happened with dieting could not be the same, he decided. His subjects kept their fat cells, but the cells had lost their fat globules and shriveled in size. "Shrunken adipose tissue over the entire body behaves in a very different way and restores itself," Hirsch observed.

There was, of course, another possibility that could explain the shocking weight gain without evoking some mysterious process in which fat tissue restores itself. Maybe it was just that those four people had some deep-seated psychological need to be fat. Perhaps other fat people would stay thin once they got their weight down.

So Hirsch and his colleagues, including Rudy Leibel, who, at the time, was working with Hirsch at Rockefeller, repeated the experiment and repeated it again.

Every time the result was the same. The weight, so painstakingly lost, came right back. But since this was a research study, the scientists looked at more than just weight loss; just as in the first study, they measured metabolic changes and psychiatric conditions and body temperature and pulse. And that led them to a surprising conclusion: Fat people who lose large amounts of weight may look like someone who was never fat, but they are very different. In fact, by every measurement, they seemed like people who were starving.

On every count, the weird, bizarre, almost depraved behavior that Ancel Keys reported when he studied the young men who were deliberately starved in his experiment during World War II was just like what Hirsch observed among the formerly obese subjects at Rockefeller University Hospital. Something was driving those people to regain their weight, and it was not a deep-seated desire to be fat.

Their bodies, for example, had changed so that they hung on to, clung to, every calorie that was eaten, making it harder and harder for them to stay thin. Before the diet began, the fat people had a normal metabolism—the number of calories burned per square meter of body surface was no different than it was for people who were thin and had never been fat. That changed substantially when they lost weight, with the formerly fat people burning as much as 24 percent fewer calories per square meter of their surface area than the calories used by those who were naturally thin.



The Rockefeller subjects also had a psychiatric syndrome that had been termed "semi-starvation neurosis." Hirsch's patients dreamed of food; they fantasized about food or about breaking their diet. They were anxious and depressed—some had thoughts of suicide. They secreted food in their rooms. They daydreamed about food. And they binged, looking for all the world like ordinary dieters who binge, looking like Mickey Stunkard's patient Hyman Cohen, who had told the stunned Stunkard that he had completely lost control of himself.

That story had shaken Stunkard, making him doubt the power of psychotherapy. But Hirsch's study was saying that perhaps there was another explanation. Cohen, like the fat people who had lost weight in the Rockefeller studies, was behaving just like someone who had been starved.

The Rockefeller researchers explained their observations in one of their papers: "Perhaps the most intriguing aspect of this study was that the removal of obesity by means of caloric deprivation led to behavioral alterations similar to those observed in the starvation of non-obese individuals. It is entirely possible that weight reduction, instead of resulting in a normal state for obese patients, results in an abnormal state resembling that of starved non-obese individuals."

Eventually, more than fifty people went through the months-long process of living at the hospital and losing weight, and every one of them had these physical and psychological signs of starvation, Hirsch reports. There were a very few who did not get fat again, but they made staying thin their life's work, becoming Weight Watchers lecturers, for example, and always counting calories and maintaining themselves in a permanent state of semi-starvation.

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