Nutrition Think Tank – Part 3 – Science of Health

“Any disease, any injury, anything that deviates from perfect health is due to miscommunication. There is either some sort of information that is not getting across or some that is getting across that shouldn’t.  And that produces all disease.”  – Ron Rosedale, MD  

– from first lecture at the 2004 Boulder Nutrition Think Tank.  (This recording is roughly 75 minutes)

 

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TRANSCRIPT:  

Hello everybody, my name is Ron Rosedale. Nice to meet all of you. To start, we’re going to use this session partly for education — mostly to educate myself. I’d like to become educated about all of you, your backgrounds, and what you hope to accomplish from being a part of this Nutrition Study Group.

My own background is that I’m a physician who specializes in metabolic diseases and diseases of aging. In fact, a large interest of mine over the last several years has been aging itself. I first began looking into diabetes as model of accelerated aging. And it’s not just diabetes — there’s also osteoporosis and cardiovascular disease. In fact, in the last decade or so, it’s been recognized that aging itself, or at least accelerated aging, is a disease and can be modified.

Ostensibly many people get interested in nutrition because they’re trying to improve their weight or, to be more specific, to reduce the level of excess fat they carry on their bodies. What you’ll learn as we go through the science is that when we do this through nutrition, in reality, we’re intervening in the aging process. We’re using nutrition to slow aging down and, in some cases, to even reverse it.

Many of you have mentioned goals both for your personal health and for the health of your communities. For instance, I think Marcus mentioned that one of his goals is to try to clear up confusion about diets. That’s one of my goals as well. And to achieve it, I also want to mention I’m here for selfish reasons. I’ve been treating patients mostly through nutritional approaches for most of my adult professional career, and it became pretty apparent a couple years ago that on an individual basis I can offer just a very limited amount of help, teaching one person at a time. My goal is no less than to change the way medicine is practiced in this country and to influence people on a global scale. You do that with little steps, and this is one of the little steps.

I want to show you as best I can what can be accomplished through changing your diet. I will describe the science behind how nutritional choices can affect whether you are healthier because of what you eat or whether you become more ill. I want to take into account what everyone has said about the personal health problems that they’re hoping to improve through diet. Cholesterol control, diabetes, weight control, confusion, auto-immune disease are common in many people; we’re going to address all of those. I want to show you that they all have fundamental, similar, common underpinnings. They’re all literally symptoms of the underlying disease of aging.

Some of you mentioned the phrase, “as you’re getting older–as we’re getting older, we’re gaining weight,” “as we get older, we get auto-immune disease,” “as we get older, we might get heart disease.” The common denominator is getting older. I can’t prevent you from getting a day older tomorrow, but we can help slow down the damage that’s associated with that day, and that’s what we want to talk about.

I would be very appreciative if you would help disseminate this knowledge. What we want to do is teach many teachers. The way to make a big dent is to teach the teachers, so that the teachers can pass it down and it can continue to spread that way. But it’s really the knowledge that we’re after. I’m not treating you, I’m just discussing. I’m trying to pass on knowledge that I’ve accumulated over the years about what I feel works best, and I’m going to give you the reasons why.

 

To begin with, there are two major diets right now duking it out. For a long time, the “gold standard” was the high-carb, low saturated fat diet. That diet has been kind of the mantra of the medical profession, the American Heart Association and the American Diabetes Association for decades. Over the last few years — finally — that mantra has come into question. And the question has been raised about a low-carb high-protein diet or a low-carb anything-else-goes diet.

 

There was a radio show where I was featured as the “opponent” to the standard American diet. It was a national show, so the talk show hosts assumed that since my so-called “opponent” was advocating the standard high-carb diet, naturally I would be advocating the well-known low-carbohydrate Atkins-type diet. Instead, I basically said that both those diets are wrong. In fact, some of the major confusion about nutrition right now is coming about because neither one is right. The diet I recommend is a bit different from both of those. And I’ll tell you about that diet soon.

 

But I think the main reason that there’s so much confusion about diet is because there have been literally thousands of books written about diet and health that say, “Do this to be healthy,” or, “Do that.” The symptoms they urge you to “improve,” along with the foods they recommend you eat, vary widely depending upon the author’s specialty, just as advice from your health care provider varies depending upon the specialist you see. You may want to improve your own health because you’re low on energy, or you’re in pain, or because a close relative has died young and you want to avoid that fate.

 

Your cardiologist may respond that to be healthier, you need to lower your cholesterol. You’ll get a different definition of health from a chiropractor, or from an MD, or from a gastroenterologist, or a neurologist. If you ask a thousand different health professionals what health is, you’ll get a thousand different answers. The confusion arises because all these experts most likely have a different view of health than you do, or than I do, or than each other. There’s no common denominator. If you have no common destination, how can they tell you accurately how to get there? To a cardiologist, health is often having as low a cholesterol as you possibly can, so being on cholesterol-lowering drugs will make you healthy. If you go by that definition, cholesterol-lowing drugs are good for health because they lower your cholesterol. But that begs the question: Is health really best measured through low cholesterol’ As we will discuss later, the answer is no. In fact, right now, the medical community is overplaying the benefits of lowering cholesterol, and seriously underplaying the side effects. We’ll talk more about that later. For now, the main point is, we need a much more basic definition of “health.”

 

What is “health” and how do you find it? After all, you really have to know your destination before you can ever know how to get there. That’s one of the things we’re going to be talking about. Because I don’t want confusion as to what our destination is. Only when we know the destination can I accurately then tell you how to get there by nutrition. Once you have a clear road map about where you’re going, then I think you’ll understand why nutrition is so powerful. I believe that you can accomplish more by changing your diet and maybe using a few supplements than with any combination of drugs and surgery. And I think you’ll understand that by the end of our conversation.

 

So what is health? That’s not such as easy question. I’ve been thinking about that question for a long time. First of all, when you say, “What is health”?, when I say, “What will make me healthy”? or “What will make you healthy”?, we can’t take much for granted. What do I mean when I say “me” or “you”? What is “you”? This is more than just a pedantic question.

 

You are not what you think you are. You are actually ten trillion lives. It’s fairly well accepted that the basic fundamental unit of life is the cell. And it’s pretty well accepted that each individual cell is a living entity. In your body, you’ve got about ten trillion of them, each one trying to live its own life, but also trying to be part of a community. Each one of us survives because our bodies are like a beehive, or an ant colony. We’re a society, a republic of cells, and it’s that republic that you’re trying to keep alive. Cells come and go — you’ve got a bunch of dead cells in you right now. You’re going to hopefully renew most of those. You’ve got almost as many dead cells as live cells. Whether living or dead, one thing they share in common is that they all have the stamp of your personal blueprint — your body’s DNA.

 

But you’ve got a whole bunch of visitors living in your gut: intestinal flora, some people estimate three pounds worth. Some might be abnormal bacteria and fungi, but most are probably so-called “normal” microbes, and since they aid digestion, you need these colonizers. You’d be dead if they weren’t living in your gut. It’s roughly three pounds of microbes total, but most are tiny, so that in a healthy person, there are at least three times as many bacteria living in your gut than the number of the cells that are normally considered your own body. Yet we don’t consider the intestinal flora to be part of you. Every time you go to the bathroom, you excrete some of those colonizers, and hopefully you’ll eat some more when you have some food, and they keep multiplying. They’re one example of how our life is really a republic of many different lives, considered part of ourselves and not part of ourselves. We breathe — why do we breathe? We take in oxygen; we need oxygen to burn food. Where do we get that oxygen? We use our lungs to process it, and it comes from plants. Our lungs would be worthless without plants. We could not live without plants. Plants could do very well without us, but we couldn’t live without plants. We’d be useless. There’s a fairly well-accepted scientific argument that plants are like an external organ. They manufacture a vital nutrient that we can’t live without. So where does our life begin, and where does it end? That’s not such an easy question.

 

We talk about being “healthy,” but what is that? To be healthy, you have to be alive, right? I mean, it’s hard to call a dead person healthy. Now that might not be sufficient, but certainly something fundamental to being healthy is staying alive. But this then begs the question, what is “life”” The answer seems simple. But if we want to keep you “alive,” we have to know what life is. And that’s actually a question that has been asked over the decades of many Nobel Laureates and never been answered. Nobody knows what life is.

 

You think you know. You have a gut feeling, as it were, about what life is, but it’s a very difficult question to answer. Trying gets into some pretty deep physics that we won’t go into now. For now, let me just say that the question can actually be answered. And as a preview of what that answer is, it really amounts to the fact that life comes, not from individual “things,” but from a way to organize information. Which means, what we’re trying to keep alive, when we’re striving for better health, is the information that tells our cells, our tissues, our bodies, “us” what to do — how to act in a coordinated manner so that we believe we are a single, well-functioning, healthy individual. And that’s really what life is all about. Life is in the instructions. It is the organization. It is the prevention of chaos that we’re trying to sustain. To stay alive, we need instructions. To maintain our body’s health, cells must stay in touch. Otherwise they’ll go off on their own. So they’re constantly sending messages and getting instructions. Every millisecond they’re getting sending out messages and getting thousands back, from hormones. That’s how cells communicate, via chemical messengers that they read via Braille. The shape of those messengers tells those cells what to do. They’ll tell a heart cell to keep pumping or a skin cell to keep external poisons out. In fact, those external messengers tell each cell just what it is.

 

What many people don’t realize is that every cell in your body has the same identical genetic structure. Your heart cells have the same genes as your kidney cells, the same genes as your skin cells. The only cells that don’t have identical DNA are the so-called gametes. Sperm and eggs have a bit of a different genetic apparatus. But every other cell in your body has the same genes. Why is that important? Because despite having the exact same DNA, the cells themselves are not all the same. Obviously a heart cell is not the same as a kidney call is not the same as a skin cell, and yet they have the exact same genes.

 

The point is that it is not the genes that make most cells different. It is the expression of the genes. Because, just as in a vast library not every book gets read at once, in the vast library of coding within each of your cells? DNA, not all the genes are read. In fact, in each cell, only a small fraction of the genes are being read, which means that only a small fraction of the potential instructions in the DNA is being used to help that cell express its function. This genetic expression is what will make a heart cell a heart cell and make it beat, or a skin cell a skin cell. It is the genetic expression that defines what it is and what it does. So when you hear, “Diabetes is a genetic disease,” or, “My parents had diabetes. All of my family was fat. Therefore, I’m doomed. I’m going to get fat. I’m going to get diabetes. I’m going to get breast cancer or heart disease, because I’ve been told by my doctors that they’ve measured my genes,” this does not have to be your fate — if you make choices that get clear instructions to your cells, so that their genetic expression is clarified.

 

If there can be greater understanding of genetic expression, then many fatalistic choices can be avoided. I’m just thinking of a patient right now who I was told yesterday was having a bilateral mastectomy because her doctor told her she had the genes that would predispose her to breast cancer. So she’s having a preventive bilateral mastectomy. What I want you to understand is, it’s not so much your genes that are important; it’s the expression of those genes.

 

We’re finding, for instance, that genes which increase cancer risk can be expressed or they can remain dormant. What makes the difference is the messages the cell receives. If the cell gets messages that it should become diabetic, it’ll be diabetic. If it gets messages that it should burn fat and it doesn’t need sugar, it will avoid diabetes and stay healthy. The messages are what matter. Think of your DNA as a library of books that contain all the knowledge, all the blueprint instructions that has been accumulated from the history of life. Thousands and millions and billions of years of instructions, depending on your point of view, has been accumulated in this library. But we don’t need all those instructions, all at once. The key is to make sure that the right ones are expressed.

 

Another way to underline the importance of genetic expression is to realize that we only use a fraction, maybe a few percent of our total genes, and the genes themselves are not that different from the genes of other species. We know, for instance, that we have 99.7 percent identical genes to a chimpanzee. We have a 70 percent homology of genes to a worm. But I would say there’s a big difference between a chimpanzee and a human, or a human and a worm, even though our genes are almost the same. So why are we different? Because the expression of our genes is different, just like the expression of genes in a heart cell differs from the expression of genes in an eye cell,  even though the DNA, the genes, in each of those cells are identical. Genetic expression is that important, and we have the power to alter our genetic expression.

 

As to how to alter genetic expression, it happens via the environment that a cell finds itself in, via the different instructions, with a powerful influence created by the quality of the nutritional environment. We know if you subject many different types of life forms to a famine, they’re going to try even harder to exist, because that is elemental. Everything in the universe today is trying to do the same thing: to exist. Just trying to be. Trying to remain alive. And those that are best at it, do. So everything you see out there has learned how to cope with a very hazardous universe, where sudden damage is common, and so is a lack of resources. Organisms that are subjected to famine might shift their genetic expression to turn into a spore, which is an effective strategy that can hold its life in suspended animation for anywhere between a few hours to, perhaps, millions of years. Life has many ways of suspending action. Scientists have found seeds of lotus plants that were hundreds, perhaps thousands, of years old that when placed in an environment of water and soil grew lotus plants. A bacteria has been discovered that was anywhere between 25 million and 250 million years old. It basically desiccated itself — dried itself out of water — to try to survive a very salty environment. Whether each cell of the bacteria survived for millions of years, or whether it was reproducing very slowly, that bacteria survived by changing its genetic expression to deal with the changes to its environment. It appears that over the years, every organism, every type of life, has gathered vast stores of knowledge about how to live a much longer, healthier life, because nature wants us to reproduce. Nature wants the information on how to make life persist to persist.

 

When it’s not a good time to reproduce right now, it appears that Nature has endowed every living organism with the knowledge of how to stay alive longer so that organism can reproduce at a future, more opportune time. Geneticists and researchers studying the biology of aging are using their awareness of Nature’s back-up plans to extend the lives of laboratory animals. Over the last ten years, they’ve been able to use what they’ve learned to do some remarkable things. In countless animals, they’ve been able to tweak the genes so that the creature lives between 30 and 600 percent longer. That’s the equivalent of a human living to be, perhaps, 800 years old. They’re able to make worms, flies, yeast, common laboratory rats live longer. There’s even a prize called the Methuselah prize that goes to the researcher who’s able to keep an organism alive the longest — recently, the prize went to a friend of mine, Andre Bark, who has been able to keep a mouse alive four times its normal life span, like a human living to be 500 years old. So there are amazing strides being made in the study of aging that the general public doesn’t know about yet. But it’s time for people to know that one of the most powerful ways to influence lifespan – a common denominator across all species — is to provide an ideal nutritional environment. The right nutrition increases an animal’s longevity.

 

Now let’s talk about sugar and insulin, two things that rise or fall in your body’s nutritional environment, depending largely upon what you eat. If you go to your doctor, the doctor is likely to say that the purpose of insulin is to regulate blood sugar. You’ll hear that from the top people in the world. And it is not true. In fact, it is very far from the truth. The purpose of insulin has almost has nothing to do with “regulating” blood sugar. Insulin has hundreds, maybe thousands of roles, including transporting vitamin C to white blood cells and transporting sugars to cells. Guiding all these deliveries is insulin’s primary role: to allocate energy. Which products, and how much of them, insulin delivers determines whether a cell will allocate energy toward maintenance and repair or toward reproduction. And which of these tasks is expressed by your cells has a tremendous influence over your health.

 

Allocating energy between maintenance and repair and reproduction has always been essential to life. It is so important that it’s become a driving theory about aging called the disposable soma theory. Among experts in the biology of aging, it’s really no longer a theory, it’s pretty well accepted as fact as you can get. It states that there are basically two lives within each of us: the so-called soma, which means “body” and is what you think of as yourself, and your germ line, your germ cells: your sperm and your egg. Now, all of our cells can reproduce — our skin cells can reproduce more skin cells to replace those that have worn out. Our lung cells, our muscle cells, can do the same. But only sperm and egg cells can become something that goes far beyond themselves — a completely formed, brand new creature, in our case, a human baby. And while a skin cell, or a lung cell, simply divides to “make” a new life, when male and female join their germ cells through sex, it gives a chance to reshuffle DNA, taking some from the sperm, some from the egg — creating fresh new possibilities for life.

 

The disposable soma says that we’re here just to temporarily care for the precious sperm and eggs that house the information on how to make life. Our purpose is to perpetuate that information. Keep those genes healthy, keep the germ cells healthy, so that we can reproduce, mixing our germ cells with those of another to refresh them and let them be born into a brand new package for moving forward in life. It’s a remarkably successful strategy, because life has remained alive ever since the very first earthly cell was created, over three billion years ago. That first cell divided and divided and continued to get more and more complex, and it found more ways to survive in a very hazardous world, until it made complex beings, like us, that are still here to see to it that our germ cells continue to divide. That very first cell has remained immortal. “We,” as the caretakers, are dispensable. Like a new car that carries precious passengers, it makes sense to allocate energy toward the maintenance and repair of the car, because it’s doing an important job, and for the most part, the repairs won’t cost a lot. When the passengers no longer need to be in that car, or when the damage to the car has become too extreme, it makes less sense to repair it. It makes more sense to buy a new car. In a similar way, after we reproduce and care for our young, and they become capable of reproducing young themselves, we become dispensable, which, according to the disposable soma theory, is why we age and die. It’s a question worth asking — why do we have to die? After all, some organisms don’t seem to die — for instance, when a single-celled organism “births” a new cell by dividing, it doesn’t die. If the original cell can live on through its divisions, why can’t we, also, both live and multiply? What’s the real purpose of human aging and dying? The disposable soma theory suggests that we, as the caretaker, take the brunt of wear and tear. We age, so that our germ cells don’t.

 

To delve more deeply into the disposable soma theory, we have a certain amount of energy that can be directed towards reproduction, including the perpetuation of our germ line, or toward maintenance and repair. To live longer, we need to minimize wear and tear on our body — our ‘soma” — just as you can extend the life of a car by taking care of it. To live more than a normal lifespan, we have to give Nature a reason to keep us alive and healthy that involves our germ line — we need to give Nature a reason to keep us healthy for the sake of the future life we carry inside.

 

One of the reasons Nature might want to give extra attention to our maintenance and repair is if we encountered a famine. During a famine, life has evolved to recognize that it’s not a good time to reproduce. Basically, it “asks,” why invest a whole bunch of energy into making babies, if there won’t be food around to feed to them? After all, creatures that are composed of cells — and we humans are among them — evolved in times, for the most part, that were much different than what we live in today. Food was never a guarantee. Today, you can go to King Super’s and buy food 24/7. That was not how it was 500 million years ago, or 10,000 years ago, or even 200 years ago. Encountering a famine was commonplace. You never knew whether you were going to eat tomorrow or not, and it became imperative to essentially make hay while you could. If there was a lot of food around, it was very important to eat that food; in fact, eat as much of it as you could, and store some that of that energy for tomorrow, or for next week, or even for next month, because you didn’t know the next time you would eat.

 

For animals, the signal for how to store sugars as fuel apparently comes from insulin. In fact, sugar was one of our first fuels. I won’t go into why that’s so, but we know that sugar was a fuel long before fat was — and when sugar rises in the blood stream, it’s a signal that you’ve got more energy than you can burn right now. That’s what allows it build up in your blood. Otherwise You’d be burning it. And that rise in blood sugar is a signal to secrete insulin, so it can give the body instructions for storing that sugar, so you’ll have fuel for tomorrow or next week or next month. But we only store a small amount as sugar, because it’s more efficient to convert that sugar into fat. We use fat as our stored form of energy. So right there you have a purpose for insulin that goes beyond the control of blood sugar: it’s actually the storage of energy. At the very least, the purpose of insulin is to store energy for times of need when there are times of plenty.

 

It goes beyond that. I was talking about aging, and life, and death, and the disposable soma theory because it appears that, at least in simple organisms, insulin is a signal that will tell each individual cell in your body whether that cell should reproduce right now or whether it’s time to conserve energy, keep the existing cell in good repair, and wait for a better time to reproduce. That is, when there’s plenty of fuel around, insulin helps give the signal to go ahead and reproduce now — to put extra energy into the process of dividing, rather than maintaining the cell in its present state. Or, when energy is short, then the signal is to wait, and keep the cell in good repair. When the signal is strong for building and repair, the cell has to up-regulate, which means increase the genetic expression of the mechanisms that allow you to stay healthy and alive.

 

Maybe people here have heard of antioxidants? Antioxidants reduce many kinds of damage that can happen in the body, which is why people take antioxidants such as Vitamin C and Vitamin E. But sometimes oxidation is good, because that’s how we kill cancer, that’s how we kill bacteria. So just flooding the body with global antioxidants might not be that great. It’s best to switch them on when you want them, and off when you don’t. And it turns out, each cell has antioxidant systems which they can fine-tune, because they can turn them on from the inside. For instance, within our cells are tiny proteins called heat shock proteins, which help instructions flowing throughout the cell maintain their clarity; there are DNA repair enzymes; there are all sorts of proteins and enzymes and other things you’ve probably never heard of that are required to keep the cell healthy and alive. And these all can be up-regulated or down-regulated via the genes, if they’re given the instructions to do so.

 

Where do the instructions come from? They come from hormones, including hormones that tell the cell that it must increase maintenance and repair because it’s not a good time to reproduce right now. We know that even in simple one-celled organisms, that signal comes from insulin. So there we’ve gone beyond insulin controlling blood sugar, and beyond insulin controlling the storage or use of energy, into controlling the actual aging process, and therefore symptoms of aging. As we age, and as we accrue damage, we get heart disease and diabetes, and we start getting auto-immune diseases and we get osteoporosis. These are symptoms of the damage we accrue as we age. We have a constant battle between the inevitable occurrence of damage and its repair. We cannot stop damage. It’s a part of life.

 

Take those antioxidants we mentioned earlier. We take antioxidants to try and prevent oxidation. But why do we oxidize? Because we are surrounded by oxygen, and we breathe it. It’s almost a built-in aging mechanism. We can’t tell you to not oxidize. That would require the cessation of breathing, which wouldn’t be such a healthy thing. So we know we’re going to oxidize. The best we can do is repair the damage which that oxidation does. And instead of just taking in antioxidants, we can actually turn up the repair mechanisms inside our own cells. But we have to give Nature a reason to do so, and one way is to influence the amount of insulin that is flowing to our cells.

 

So insulin is receiving a lot of notoriety among researchers working on the biology of aging. Last spring, we presented some of our findings on health and nutrition at one of the major meetings in the world on the biology of aging. It seemed that every other talk at this conference had to do with insulin. Why? Roughly a decade ago, scientists discovered the first gene that was shown to modify aging, the “Age 1 gene,” discovered by Tom Johnson, a geneticist at the University of Colorado, who we spoke to at this conference, where he, too, was presenting. Tom’s discovery ten years ago set off an explosion in research. It included a gene that when mutated extended the life of a worm considerably. This was front-page news in all the scientific journals. This was a huge finding, that you could mutate one gene, and the worm would stay alive 50 percent longer and stay healthier. With this mutation, the worm didn’t just get older longer; it stayed younger longer. All the diseases associated with aging were slowed down. It’s as if time had slowed down for that organism.

 

The gene was called daph-2, and at first, researchers didn’t know what that mutation did. Then Cynthia Kenyon’s group at the University of California, San Francisco discovered what that gene did: it encoded an insulin receptor. Since then, scientists have continued to clarify the trails, and now they have the entire genetic pathway that controls aging mapped out in the worm, and the fly, and they’re doing it now in the rodent, and in yeast. And lo and behold, the really cool part is, they’re finding that the genes that control aging in worms and flies and rodents and even in single-celled creatures such as yeast are identical. It is a conserved mechanism that began early on in cellular life, and they’re finding the same genes in humans. In other words, this mechanism to actually regulate the aging process that regulates the symptoms associated with aging — obesity and diabetes and heart disease and osteoporosis and all those things — are encoded by all the same genes, and those genes all listen to insulin. How much insulin you have flowing around in your body is going to determine, to a large extent, how rapidly you age, and how rapidly you get the symptoms of aging.

 

But they’re finding even more: that in complex organisms like us, the total storage of energy in your body influences how rapidly you age, not just what energy comes along, cell by cell. The reason that this total storage makes a difference is because it, too, influences that balance between putting effort into reproduction or putting energy into maintenance and repair. If there’s a lot of energy stored on your body for your ten trillion cells, if you’ve got a whole lot of energy right now, it seems that our bodies assume that what you ought to be doing is reproducing, and not necessarily living a long life.

 

Now, insulin seems to have most influence on a cell-by-cell basis. But there is also influence coming from the total energy storage system of the body. How do the cells get this information, and how do they receive instructions about it? Again, your cells are told by hormones which task to choose. And in humans the hormone that gives the global messages about whether you should reproduce or live a long, healthy life appears to be leptin, which you’ve probably never heard of, but you will. You’ll be among the first to hear of this extremely important hormone.

 

With each passing day, scientists are finding more and more outstanding functions of leptin. We know that it controls osteoporosis. Keeping leptin low causes bones to build, to get stronger. It is the only known way to do that. Estrogen or Fosamax do not build bone. That is a misconception. They can help prevent the breakdown of bone, but that is not the same thing as building strong bones. When you rely on Fosomax and other drugs, what you end up with is old brittle dried bones. But controlling leptin allows an increase in maintenance and repair mechanisms from inside your body, which in turn allows you to build strong bones. Want to get off of cholesterol-lowering drugs? Simple. You want to get off of most high blood pressure medications? It’s relatively easy. Want to reverse diabetes? It’s relatively easy. But it’s not going to be from a drug, and therefore, since profits in our country are so dependent on selling a product, you haven’t heard of what the best solution to these diseases is.

 

To sum up: There are two major hormones that control the rate of aging in lab animals, and in humans they have been shown to greatly influence the degree and prevalence of all of the so-called chronic diseases of aging: heart disease, cancer, diabetes, auto-immune disease. A lot of people ask about auto-immune disease or malfunction of the immune system. The immune system is one of the major systems where information and knowledge and communication are really important. You want to communicate what that immune cell should be gobbling up — cancer cells and bacteria — but it should not gobble up yourself. When it gets confused, it starts gobbling up you. And that’s an auto-immune disease. It’s a definite sign of miscommunication, failure to communicate. All disease — there is no exception — any disease, any injury, anything that deviates from perfect health is due to miscommunication. There is either some sort of information that is not getting across or some that is getting across that shouldn’t. And that produces all disease. For some of the most severe forms of auto-immune disease, for instance, they’re finding that it’s preceded by a surge in leptin. Very interesting research that’s fairly new. That includes MS. And when they kept leptin levels low, it prevented the auto-immune disease. Whether it can then be used to treat existing auto-immune diseases, it’s too new to know. But obviously leptin plays a big role in the immune system. We know that leptin influences the sympathetic nervous system, which influences heart rate and blood pressure.

 

I mentioned calcium deposition in arteries, calcium deposition in bones, protein building of bones — there is no chronic disease that leptin has not been found to either strongly influence or, in fact, actually control. Much of the medical community is becoming aware of this, but it hasn’t been taught to them yet. These are research articles. They’re all from different specialties. People are amazed when they hear the different things that it does. How can something that controls fat deposition — and I’ll explain that in a minute — also control bone formation or heart disease or cancer, auto-immune diseases, so many different things? The common denominator is, it controls the genetic expression of maintenance and repair because it’s actually controlling the aging process.

 

Leptin was first discovered about ten years ago. There was a mouse model called the OB mouse. There’s a fat mouse. It’s used in a lot of experiments, for different drugs, different diets, mostly drugs. It’s used as a model of human obesity. They didn’t know what made it fat until about ten years ago. They found that the reason this mouse was fat — it was called the “OB mouse” for “obesity” — is that it lacked a hormone called leptin. When Dr. Friedman at Rockefeller University in New York injected this mouse with leptin, it became thin and healthy and vibrant. It received lots of publicity. Front page USA Today, they showed a picture of this fat mouse and how after it received leptin it was thin. They figured this was the cure for obesity.

 

Literally within days, drug companies were researching how to genetically manufacture leptin. Obesity is a big deal. They could make trillions of dollars. They figured they would be the first to patent a genetic formulation of leptin before they started measuring leptin in people. Then they started measuring leptin in people, and they found out that in almost all overweight people, it was not due to a lack of leptin. It was due to — not necessarily ‘due to,” but it was correlated with very high levels of leptin. Giving extra leptin didn’t do anything. That stopped them in their tracks. They knew leptin had something to do with obesity, but they had no idea what to do about it. To this day, leptin is known as the “fat hormone.” Leptin is produced by fat cells. It has taken fat to new heights.

 

Fat was considered a nasty byproduct. People are fat. You don’t want fat. Now we know that fat produces a bunch of hormones. Your pancreas produces hormones. The pancreas produces insulin, so it’s considered an endocrine gland. Your adrenal gland produces hormones. It’s considered an endocrine gland. Your fat cells produce hormones. Your fat is considered an endocrine gland, just like your pancreas or your adrenal glands. It produces a lot of different hormones, leptin probably being the most important. And what it’s supposed to do “ and this is revolutionizing the thinking about obesity — is to regulate your weight.

 

It was no good to be fat in our history, and it was no good to be skinny. You wanted to store some energy. Our ancestors encountered periods of famine. If you didn’t store any energy, you wouldn’t survive that famine. If you were fat, you actually had a better chance of surviving a longer famine. All the skinny contemporaries would have died off. It was a selective advantage to be fat, and to get fat efficiently. So if you did encounter a bunch of fruit, let’s say, then eat that fruit, get fat quickly, so that if a tough winter hits, you’ll be able to survive it.

 

But the other side of the coin is, if you became too fat, you won’t be able to move very quickly, and our ancestors needed to be mobile. They had to hunt. They had to run after prey. And if you were too fat, You’d be the last one there. You wouldn’t get to eat. Almost self-limiting, to prevent you from getting too fat. But more importantly, you couldn’t prevent yourself from being prey. So if a lion was chasing a group of people, the fattest person is going to get caught. So there was a selective disadvantage to being fat, and it was selected against. There had to be a signal to tell your body how much fat to store. You wanted just enough to tide you through a reasonable famine, but not so much that you couldn’t run very fast. And that signal is from leptin.

 

What is supposed to happen is, as you get fatter, your fat cells produce leptin. It goes to your brain, to a particular sector in your brain called the hypothalamus — more specifically the arcuate nucleus of the hypothalamus — a tiny little portion of your brain that regulates hunger, its powerful center. If you electronically stimulate the portion of that hypothalamus that satiates hunger, for instance, an animal will not eat and will starve to death. On the converse, right adjacent to that, if you electronically stimulate the area that causes you to be hungry, that animal will stay hungry and will continue to eat and never stop until it dies.

 

It is really powerful, arguably the most powerful area of the brain that there is. And leptin controls it. Now, there’s a lot of feedback because hunger is so important it isn’t the only control. They’re finding a dozen or so hormones the regulate the feeding and hunger area. But still, it appears that leptin is the most powerful, and the others tend to depend on leptin.

 

What is supposed to happen is, as you get fatter, your fat cells produce leptin, and it goes to your hunger center and signals that you’ve got enough fat stored. Start burning it and quit being hungry and stop eating. The only way that a person will be able to stay away from food — especially in our society, when food is available everywhere — is if they are not hungry. Hunger is a powerful force. And we have built-in mechanisms to obey what we’re told to do. We think of ourselves as free-willed individuals. I would argue against that. We’re not really that free-willed. We do what our hormones tell our brain to do. The signals between nerves, the neuro-transmitters, are hormones. Every thought, every desire, every purpose, every behavior that you have is dictated by hormone signals.

 

The two most powerful signals that regulate feeding and behavior are the signals that regulate hunger and reproduction. The urge for sex and the urge for hunger are the most powerful signals that we have, because they are what allowed life to perpetuate. All of our ancestors gave in to those urges, or we wouldn’t be here talking today. If you’re told to eat, you’re going to find a way to eat.

 

You can control yourself. You can say, “I’m fat. I’m not going to eat.” You can do that for a day, for two days. You can count calories and say, “Once I reach 1500 calories, I can’t eat any more.” And you’ll do that. But then if you’ve got a hormone, leptin, telling you you’re going to eat — you’re going to eat. It’s like holding on to a cliff. That’s an analogy I use frequently. You can hold on to a cliff and look down ten miles. You’re at the top of Mount Everest. You look down, a you know that if you let go, you’re going to die. And you’re going to hold on as hard as you possibly can. And you will let go, eventually. Because gravity is unrelenting. And so is hunger.

 

That’s why diets haven’t worked. That’s why you see these yo-yo diets all the time. You’ve heard of the yo-yo diet syndrome? People will lose weight, gain it back, lose weight, gain it back. If you lose weight but you still have high levels of leptin, that indicates leptin resistance, which I’ll describe, telling you that you need to store more fat, and you will. Everything you think about will be food. You’ll be thinking about eating when you’re sleeping. And you will eat. The only way you’re not going to eat is if you don’t want to because you’re not hungry. The only way you’re not going to be hungry is if leptin is telling your brain that you shouldn’t be hungry and that you have more fat than you need, or at least enough, and that you can actually burn off some of it. Leptin has to be a clear signal to your brain.

 

So how do people get fat, if this is supposed to be working? I mentioned that all disease is a result of miscommunication, or malcommunication, or wrong communication. How many people here have heard of insulin resistance? The majority of people. That’s great. I first started talking about insulin resistance maybe a decade ago. I first talked to a big group of doctors in Chicago in the latter part of 1995. Not one doctor out of the several hundred that were there had ever heard of insulin resistance. It wasn’t known at all. Now it’s known to the general public.

 

Insulin resistance is what causes most cases of type 2 adult onset diabetes, which is most cases of diabetes. You have plenty of insulin, but your cells are resistant to it. It doesn’t hear the message. So sugar can’t get into your cells to get stored. Insulin lowers sugar as a byproduct of trying to store that sugar as fat, mostly. So it’s not really regulating sugar, it’s regulating energy storage. If your cells can’t hear insulin, then the sugar doesn’t go in your cells and your sugar is allowed to elevate and you get diabetes. But it’s not due to a lack of insulin. So giving more insulin perhaps allows the body to yell louder for a little while, but it’s only going to perpetuate the resistance. It doesn’t treat the underlying cause of insulin resistance.

 

Insulin resistance is like being in a smelly room. If you’re in a smelly room, pretty soon you can’t smell it. You become desensitized to the smell due to the strong odor. You’ve basically temporarily burned out your olfactory nerve. Now, you can smell it again if you go out of the room. In other words, make the smell diminish and then you can resensitize your olfactory nerve, so you come back in half an hour and you can smell it again. If your cells are exposed to high levels of insulin throughout your life, the same thing happens. Your cells become diminished in sensitivity. Pretty soon they can’t ‘smell? insulin, so to speak. And they can’t listen to insulin.

 

In most people, they don’t ever even get a chance to go out of the room. Every day they’re exposed to high levels of insulin, because of people’s diets. They eat a particular meal and it causes insulin to go way up, almost every meal. So they’re constantly, chronically exposed to high peaks of insulin. And they get more and more resistant to the action of insulin. Early on, your pancreas can compensate by producing more insulin. It would be analogous to just pumping more smell into the room, or yelling louder. That only causes your cells to become more resistant faster. And your pancreas will reach a limit as to how much insulin it can produce. It can’t continue to produce insulin indefinitely, certainly not higher levels, so it’s going to reach a peak. But your resistance in going to climb.

 

To reach that peak typically that took four, five, six decades, which is why it’s called adult onset diabetes. It started when you were zero days old. Actually, it started in the womb, when your mother ate foods that caused insulin surges. As a fetus, before you were ever born, you were exposed to high levels of insulin. You started becoming insulin-resistant in the womb. It shows that mothers who eat a high-carbohydrate diet will produce babies who are born with partial insulin resistance, setting you up for diabetes in later life.

 

Does that mean that diabetes is a genetic disease? No. You can be born with something without it being genetic but rather what the fetus was exposed to in the womb. The treatment would not be to make more insulin. You’ve got plenty around. The treatment is to resensitize the cells to insulin. The true diabetic treatment is not to give more insulin. The treatment is to eat a diet that minimizes insulin so that the cells can reacquaint themselves with insulin’s signal.

 

Insulin’s signal, as I mentioned, goes way beyond the control of blood sugar. It’s not sugar we’re concerned about in diabetes. The big concern in diabetes is the fact that your cells can’t listen to a hormone that regulates aging. That’s a problem; diabetics show a higher degree of cardiovascular disease, a higher degree of cancer, a higher degree of auto-immune disease, a higher degree of osteoporosis. They’ve got higher incidences of all of the chronic diseases of aging because they’re aging at an accelerated rate. So it’s really the aging process you need to slow down. I don’t really care about the sugar, other than it’s telling me that you can’t listen to insulin. And the consequences of that go way beyond blood sugar. If you regulate your insulin, get yourself to listen to insulin, sugar’s going to come down. That’s a given. The incidence of cancer’s going to go way down, heart disease is going to go way down. Your capacity to store extra fat is going to go down. That gets us back to leptin.

 

How do people get fat? Let’s say you start getting fat. Let’s say your brain can’t listen to leptin. Let’s say you start getting leptin-resistant, just like insulin resistance. Your brain is not hearing leptin. So it’s thinking that you’re starving to death. It’s thinking that if you don’t have any fat, you’re going to be in trouble. You won’t be able to survive a famine. So you need to be hungry. You need to eat more and make more fat. So you could be 5”2” and weigh 250 pounds, but you’re being disconnected from your brain. Your brain has no idea. Your brain has no idea that you’ve got 200 pounds of fat being stored on a 50-pound frame. And it’s telling you to store more. It’s saying, “Be hungry. Eat more.”

 

And so it tells you to keep getting fatter and fatter, until finally you produce enough leptin to get through the block. A little whisper can get through to your brain, saying, “All right. I’m a little bit fat.” And then your hunger goes away. People who get fat don’t usually get to a thousand pounds. They might level out at two hundred pounds, two hundred fifty, three hundred — whatever poundage is necessary to produce enough leptin to tell the brain that the body is storing some fat.

 

The only way you are going to effect a significant change in the amount of fat a person is storing on a permanent long-term basis is if you can get that leptin message heard louder. If you can restore leptin’s sensitivity, all of a sudden you’re having your brain get screamed at by leptin. Your brain is going to hear a message: “I’m really fat. I’m way too fat. I’d never survive a lion chasing me, and I need to get rid of some of that fat.” And the way you’re going to get rid of that fat is to be allowed to burn it through the sympathetic nervous system and to not be hungry so you don’t keep storing it. You become really satiated, and you’re allowed to dig into your fat stores. And if you dig into your fat stores, your cells are going to eat. I mentioned early on that I do not want you to think of yourselves as a single individual. You are not. You are a republic of cells. It is your cells that are living. You are a beehive. You are an ant colony. You are a society of cells. It is your cells that eat. When you put food in your mouth, when you digest food, you’re just continuing the refinement and the processing of that food.

 

When a farmer has a cow, for instance, he’ll take that cow to the feed lot and then they’ll kill it and chop it up into big pieces and it’ll go to the store and it’ll go to the butcher shop and they’ll chop it up into smaller pieces and you’ll buy it and you’ll take it home and then you’ll chop it up into smaller pieces and you’ll cook it and you’ll chew it. All you’re doing is chopping it up into smaller pieces. And it’s absorbed through your intestines and distributed through your blood stream. You’ll just continue to distribute that food, just like taking it from the farm to the grocery store, or taking it from the grocery store home, taking it from home to your mouth, taking it from your mouth to your cells — it is your cells that will sit down to the dinner table and eat.

 

Your cells can burn sugar or they can burn fat. That is their choice. You want your cells to burn fat. I am sometimes asked if I can summarize in a single sentence everything I’ve said so far, as if I were a college professor and I were going to be testing you. I always liked when my professors said, “This is what I’m going to ask on my test. This is all I want you to get out of today.” What will make you healthy, what will determine your health and how long you live is the proportion of fat versus sugar you burn over a lifetime. It’s as simple as that. The more fat you burn compared to sugar, the healthier you’re going to be, and the longer you’re going to live, other things being equal, provided you don’t get into a car wreck or something. But as far as nutrition goes, it is the proportion of fat versus sugar you burn over a lifetime.

 

People do not get fat because they eat it. People get fat because they don’t burn it. There’s a big difference. If you eat fat with sugar, you’re going to burn the sugar up first and store the fat. If you keep doing that, you forget how to burn fat. If you can’t burn fat, if you’re leptin-resistant, for instance, or if you’re insulin-resistant, they’re telling you to store fat and don’t burn it. You’re going to stay hungry and you’re going to crave sugar and carbohydrates, because you don’t store much sugar and carbohydrate. So you have to keep eating it. At night, if you don’t eat, and your hormonal milieu is telling you to make fat and don’t burn it, that means you have to burn sugar. Where are you going to get your sugar if you’re not eating? You’re going to get it from your muscle and bone. You can make sugar out of protein, easily, a process called gluconeogenesis. Diabetics wake up in the morning and they measure their blood sugar. Where is it? It’s high. And you wonder, “But I didn’t eat anything. Where did it come from”?

 

It came from your muscle and your bone. You want to know how you become osteoporotic? That is how. By turning your bone into sugar. The strength of your bone is determined by the protein matrix, not by the calcium. Calcium, by the way, has nothing to do with it whatsoever. That’s something perpetuated by the dairy industry. It’s the protein. What holds the building up? It’s the frame. You think the brick on the outside has much to do with it? Calcium is like the brick on the outside. In fact, it can actually impede signaling. I won’t get there right now. But you have to be able to burn fat.

 

If you have the ability to burn fat properly, if you can listen to leptin, if you can listen to insulin and your brain can finally detect that you’ve got plenty of fat around and that you should be burning it, you can dig into your pantry. You “ your cells “ can eat 24/7, without having to put anything into your mouth. You’ll have plenty of fuel, and they’re not going to make you crave food. You’re only going to crave food if you have to burn sugar. Because you don’t store much sugar. That means you’ve got to eat it. You’ve got to take carbohydrates and sugar because you’ve got to burn it and you don’t have much stored, and you’re not allowed to dig into your fat stores.

 

So you’ve got two ways to be satiated. When you become leptin- and insulin-sensitive, number one, it appeases a very powerful center in your brain to tell you that you’re not hungry, and number two, you’re allowed to burn fat so your cells have something to eat so they they’re not hungry either. That is how you lose weight. That is how you control diabetes. When you are leptin-resistant and your leptin levels end up being high, just like they are when you’re insulin-resistant — and you can measure these pretty easily — not only do you become fat, but you become fat in all the wrong places. We know that when you’re leptin-resistant, there’s a propensity to put fat around your middle, the so-called “apple shape,” visceral fat. It surrounds and permeates your liver. As such, your liver become partially deaf. It gets smothered in fat. So it can’t listen to insulin. One of the prime messages of insulin is to tell your liver to quit making sugar. When diabetics wake up in the morning and their sugar is high, they got it from their liver. Their liver was making sugar out of protein which originally came from your muscle and bone. That protein is delivered to your liver, and your liver makes sugar out of it.

 

Now, if your liver could listen to insulin, it wouldn’t do that. Only when it can’t listen to insulin does it make too much sugar. And it can’t listen to insulin if it has too much fat around it. So you get into these vicious cycles. You become leptin-resistant. Your liver becomes smothered in fat. It can’t listen to insulin. Therefore it makes too much sugar. You become insulin-resistant, and that sugar turns to fat. As that sugar turns to fat in your fat cells, it causes spikes in leptin. Those spikes in leptin cause further leptin-resistance.

 

You now know more about health than any doctor that you’ve ever seen. You can go back and tell your doctor that nobody knows this information, and yet it’s absolutely vital. You’ve got certain keys to health right now. The key thing I want you to take out of it is, you’ve got to be able to burn fat. The only way you’re going to be able to burn fat is if you can have proper insulin and leptin signaling. If you do that, you’re not only going to be able to burn fat, but you’ll be able to slow down the damage associated with being one day older tomorrow — otherwise known as aging. When you do that, you are going to slow down, and in fact, you can easily reverse heart disease and osteoporosis and diabetes. It’s really not hard to do.

 

(But you don’t want people to do it yet.)

 

Right. Now that you know how to do it, I consider this information so important, if this stuff was known, and if we could make the proper changes, the incidence of diabetes and heart disease and high blood pressure — obesity would take a little bit longer — could be cut in half, actually less than half, probably twenty-five percent, cut three-quarters worldwide in a month. I think it could go beyond that. Incidence of cancer would go way down. Amazing things can be done to the health of the entire world with very simple changes. But we have to be able to prove it. And the only way we can prove it is by showing — I don’t want you to just necessarily take my word for it. Maybe I’m full of BS. But I’ve been able to show this for a long time. I want to show it in black and white and I want to prove it to the medical and scientific community, and we can only do that by a lab test. We can measure your insulin and leptin and triglyceride and other things that are important. Cholesterol, by the way, I don’t consider to be very important. We could measure it, but there are so many aspects to cholesterol. I suppose I’ll mention it now because everybody’s going to ask, so I’ll go through just a very, very quick thing about cholesterol.

 

Cholesterol is not your enemy. It is required for life. You need cholesterol. There is no life on earth that can live without cholesterol. It is part of every cell membrane. The medical recommendation to get the cholesterol level as low as possible is the most ignorant recommendation that I have ever heard. It is killing more people than any other single recommendation in the history of mankind. You do not want to necessarily lower your cholesterol. Cholesterol is not only required to make any cell membrane, it’s required to make estrogen, cortisone, any of the steroid hormones. It is one of the few commonalities of all life that we know of. There are few elements to life in general that are more important than cholesterol. You don’t want to get rid of cholesterol.

 

Is cholesterol associated with disease? Yes, it probably is. But association and cause are not the same things. It’s very different. Cholesterol is associated with disease because cholesterol goes up when you’ve got disease because it is trying to save your life. It is like somebody who was in a car accident and a paramedic stops by to try to save that person’s life, and then they put that paramedic in jail for causing that car accident, even though he might have just been walking by. That’s what they did to cholesterol.

 

When you become injured, you become inflamed. Inflammation is a common mechanism to repair damage. You cut your hand. Certain things will happen to allow you to live. You’re going to see swelling. The swelling is there to try to stop the bleeding, to try to close the gap so that dirt and bacteria don’t get in. The inflammation causes white blood cells to rush to the area. It causes blood vessels to constrict so you don’t bleed to death. It causes your blood to clot so you don’t bleed to death. And it also causes stimulation of new cells to be manufactured to replace the ones that have been damaged.

 

These inflammatory signals go throughout your body. You cut your little finger and there’s an increase in inflammatory signals in your bloodstream, which goes everywhere. Some of those inflammatory signals go to your liver. It is your liver that manufactures cholesterol. That’s well known. That’s not debated. When we measure your cholesterol, it is the cholesterol manufactured by your liver. The amount you eat is almost irrelevant. That’s not really that debated any longer. That was found out 15 years ago. Your liver is manufacturing cholesterol, and when your cholesterol goes up, it’s an indication that you’ve got to repair damage. You’ve got a lot of inflammation around.

 

So the reason you have high cholesterol is because you’ve got damage going on that your body is trying to repair. What you really ought to be going after is the damage. Why do you have damage going on? What is causing the damage? It could be too much glucose around, because we know it damages tissues in a process called glycation. Glucose combines with proteins and causes that. We know it causes inflammation. A lot of things cause inflammation. Any time you have inflammation, you’re going to have signals going to your liver to manufacture cholesterol to fix tissue. So cholesterol is associated with disease, but in a more positive way.

 

When you lower cholesterol, what you’re doing is repairing the repair mechanism — while you’re augmenting the bank accounts of the pharmaceutical industry. The single product that has made the greatest profit in the history of mankind is what? It’s not Microsoft. It’s actually statin drugs. The recommendation to lower cholesterol has nothing to do with health. It has to do with the bank accounts of the pharmaceutical industry. Don’t even concern yourself with cholesterol. It shouldn’t even be measured in people other than as an indication of disease — but there are better indications.

 

And of course we know that there are different kinds of cholesterol. So even if you went by the usual medical thinking — for instance, 20 years ago there was just cholesterol. Then they found out there’s “good” and “bad” cholesterol. You’ve heard about good and bad cholesterol: HDL and LDL. HDL is supposed to be “good” cholesterol and LDL is supposed to be “bad” cholesterol. So in some cases, high cholesterol was good if a lot of it was HDL, right? Well, we know now that you can continue fractionating cholesterol. First of all, cholesterol is just cholesterol. It is only a single molecule. There’s no such thing as “good” and “bad” cholesterol. HDL stands for what? “High-density lipoprotein.” What is HDL? It’s a protein. It’s not cholesterol. It’s a totally separate entity. And yet we equate it with cholesterol. What does LDL stand for? “Low-density lipoprotein.” It’s a protein. What is cholesterol? It’s actually a fatty alcohol. It’s in an entirely different class of molecule from HDL and LDL.

 

We also know that HDL and LDL can be fractionated and that there are “good” and “bad” LDLs and “good” and “bad” HDLs. And only the small, dense LDLs are potentially bad, not even bad. You can have LDL A, LDL B, LDL C. That can all be measured, but it’s somewhat costly to do. It’s only LDL C that could be bad for you if it became oxidized. It’s more oxidizable, and it can cause more inflammation. So oxidized LDL C is more inflammatory and can cause damage. So just measuring HDL and LDL is worthless. You would need to measure the oxidized fraction of LDL C.

 

Cholesterol is a fat. Fat turns rancid, right? You can’t leave fish out on a counter for very long. They’re pretty smelly. Fat is one of the molecules that oxidizes pretty readily. So cholesterol by itself is a vital aspect, not just important; you can’t live without it. But it can become damaged easily, become oxidized, and then it can be bad. Any fat, though, can oxidize and turn bad.

 

What is your brain mostly made of? Fat. Subsequently, what can happen to your brain? It oxidizes. It oxidizes fairly easily, which is why we get a lot of brain diseases. Because your brain oxidizes, should we recommend that everybody have their brain removed, because it can potentially oxidize? No. Why? Because your brain we consider to be fairly important to your life. Likewise, cholesterol can oxidize. But that mean we should remove your cholesterol? No. We do not want to remove your cholesterol from your cells. It’s required for your cellular life every bit as much as your brain is required for your life, actually even more so. The recommendation is a nonsensical recommendation, to lower cholesterol with cholesterol-lowering drugs.

 

What I would propose is, we are making certain tests available to all of you for as little as we possibly can. The battery of tests we’re proposing would normally run you about $500. If anybody can pay anything, that would be great. Those that can’t pay, we’re going to do for free. So you are all going to become my patients. There’s patient confidentiality, just like any patient. I’m not going to let anybody know — I mean, I’m not allowed to. It’s illegal for me to let anybody else know what your labs are.

 

(But on the other hand, the test results can be used as a kind of group portrait of what’s happening to people.)

 

Right. With your permission. Only with your permission. If you allow it, we’ll just do laboratory averages, just so we can maybe use it as a study.

 

(We also don’t want people to be eating totally healthy right now.)

 

Right. That’s actually a good point. (laughter) The changes that we’re talking about can occur very rapidly. Some of these changes can occur in one day. Big changes can occur in just a few weeks. We can turn somebody who can’t burn an ounce of fat into a really significant fat-burner in just three weeks.

 

(And there’s the dilemma, because most of these folks have been experimenting with their diets.)

 

Right. So what I want you to do is just eat like you normally would have eaten a month ago. Or a year ago. Eat your last supper.

 

(Again.) (laughter)

 

This’ll be your last guilt-free week. After that, I’m going to make you feel so guilty. (laughter) Go ahead and have your cheesecake. No, I mean, don’t go overboard. Just eat like you normally would have eaten, that’s all I’m asking.

 

(I’m Shelley Schlender. You’ve been listening to a weekly meeting of the Boulder Nutrition Think Tank, launched in 2004. For questions about medications, be sure to consult with your primary care physician. We recommend that whenever you make a lifestyle change, tell your doctor, including about any dietary or supplement changes. )