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 Post subject: Insulin and Its Metabolic Effects By Ron Rosedale, M.D.
PostPosted: Fri Nov 09, 2012 1:35 am 
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Insulin and Its Metabolic Effects
By Ron Rosedale, M.D.

Presented at Designs for Health Institute's
BoulderFest August 1999 Seminar

This web site will prove that eating red meat and natural animal fats while restricting carbohydrates is not only healthy but will prevent and cure many diseases.

Click here to read the "Medical Disclaimer."

Let's talk about a couple of case histories. These are actual patients that I've seen; let's start with patient A. This patient who we will just call patient A saw me one afternoon and said that he had literally just signed himself out of the hospital "AMA," or against medical advice. Like in the movies, he had ripped out his IV's.

The next day he was scheduled to have his second by-pass surgery. He had been told that if he did not follow through with this by-pass surgery, within two weeks he would be dead. He couldn't walk from the car to the office without severe chest pain.

He was on 102 units of insulin and his blood sugars were 300 plus. He was on eight different medications for various things. But his first by-pass surgery was such a miserable experience he said he would rather just die than have to go through the second one and had heard that I might be able to prevent that.

To make a long story short, this gentleman right now is on no insulin. I first saw him three and a half years ago. He plays golf four or five times a week. He is on no medications whatsoever, he has no chest pain, and he has not had any surgery. He started an organization called "Heart Support of America" to educated people that there are alternatives to by-pass surgery that have nothing to do with surgery or medication. That organization, he last told me had a mailing list of over a million people, a large organization, "Heart Support of America."

Patient B is a patient who had a triglyceride level of 2200. Patient B was referred by patient A. He had a triglyceride of 2200, cholesterol of 950 and was on maximum doses of all of his medications. He was 42 years old, and he was told that he had familial hyperlipidema and that he had better get his affairs in order, that if that was what his lipids were despite the best medications with the highest doses, he was in trouble.

He was not fat at all, he was fairly thin.

Whenever I see a patient on any of those medications, they're off the very first visit. They have no place in medicine. He was taken off the medications and in six weeks his lipid levels, both his Triglycerides and his cholesterol were hovering around 220. Six more weeks they were both under 200, off of the medications. They have no place in medicine.

I should mention that this patient had a CPK that was quite elevated. It was circled on the lab report that he brought in initially with a question mark by it because they didn't know why. The reason why was because he was eating off his muscles, because if you take (gemfibrozole) and any of the HMG co-enzyme reductase inhibitors together, that is a common side effect that is in the PDR, and they shouldn't be given together.

So he was chewing up his muscles, including his heart which they were trying to treat. So if indeed he was going to die, it was going to be that treatment that was going to kill him.

Let's go to something totally different, a lady with severe osteoporosis. She is almost three standard deviations below the norm in both the hip femeral neck and the cervical vertebrae, and she is very worried about getting a fracture. A fairly young woman and she was put on a high carbohydrate diet and told that would be of benefit, and placed on estrogen, which is a fairly typical treatment.

They wanted to put her on some other medicines and she didn't want to, she wanted to know if there was an alternative. Although we didn't have as dramatic a turn around, we got her to one standard deviation below the norm in a year, taking her off the estrogen she was on, anyway.

Let's go to claudication.

That is severe angina of the leg when you walk, same thing as angina of the heart except of the leg. While walking, after walking a certain distance, there is pain. There was a gentleman who had extremely severe claudication, who happens to be my stepfather. It was a typical case, he would walk about fifty yards and then he would get severe, crampy pain in his legs. He was quite well off and was going to see the best doctors in Chicago, and they couldn't figure out what was wrong with him initially.

He went to a neurologist, they thought it might be neurological pain or back pain. He finally went to a vascular surgeon who said he thought it was vascular disease, so they did an arthrogram and sure enough, he had severe vascular disease. They wanted to do the typical by-pass surgery that they normally do on this. He was thinking of going in for the surgery for one reason, they had a trip planned to Europe in two weeks, and he wanted to be able to walk since they normally do a lot of walking.

Ten years previously he'd had an angioplasty for heart disease. At the time ten years ago, I told him he had to change his diet and he didn't of course. But this time he listened. I said that if he was not going to have a by-pass, then do exactly what I tell you to do and in two weeks you'll be walking just fine because by modulating this one aspect of his disease, I have never seen it not work, and it works very quickly to open up the artery.

We can talk about a patient with a very high cancer risk.

She had a mother and a sister who both died of breast cancer and she didn't want to, so she came in and I put her on the exact same treatment as the other cases I just mentioned. They were all treated virtually identically because they all had the same thing wrong with them.

What would be the typical treatment of cardiovascular disease? First they check the cholesterol. High cholesterol over 200, they put you on cholesterol lowering drugs and what does it do? It shuts off your CoQ10. What does CoQ10 do? It is involved in the energy production and protection of little energy furnaces in every cell, so energy production goes way down.

A common side effect of people who are on all these HMG co-enzyme reductase inhibitors is that they tell you their arms feel heavy. Well, the heart is a muscle too, and it's going to feel heavy too. One of the best treatments for a weak heart is CoQ10 for congestive heart failure. But they have no trouble shutting CoQ10 production off so that they can treat a number. And the common therapies for osteoporosis are drugs, and the common therapy for calaudication is surgery. For cancer reduction there is nothing. But all of these have a common cause.

The same cause as three major avenues of research in aging. One is called caloric restriction. There are thousands of studies done since the fifties on caloric restriction. They restrict calories of laboratory animals.

They have known since the fifties that if you restrict calories but maintain a high level of nutrition, called "C.R.O.N.'s:" Caloric restriction with optimal nutrition, or adequate nutrition, which would be CRAN"S, these animals can live anywhere between thirty and two-hundred percent longer depending on the species.

They've done it on several dozen species and the results are uniform throughout. They are doing it on primates now and it is working with primates, we won't know for sure for about another ten years, they are about half way through the experiment, our nearest relatives are also living much longer.

Then there are Centenarian studies.

There are three major centenarian studies going on around the world. They are trying to find the variable that would confer longevity among these people. Why do centenarians become centenarians? Why are they so lucky? Is it because they have low cholesterol, exercise a lot, live a healthy, clean life?

Well the longest recorded known person who has ever lived, Jean Calumet of France who died last year at 122 years, smoked all of her life and drank.

What they are finding on these major centenarian studies is that there is hardly anything in common among them. They have high cholesterol and low cholesterol, some exercise and some don't, some smoke, some don't. Some are nasty as can be and some nice and calm and nice. Some are ornery, but they all low sugar, relatively for their age. They all have low triglycerides for their age.

And they all have relatively low insulin. Insulin is the common denominator in everything I've just talked about. They way to treat cardiovascular disease and the way I treated my stepfather, the way I treated the high risk cancer patient, and osteoporosis, high blood pressure, the way to treat virtually all the so-called chronic diseases of aging is to treat insulin itself.

The other major avenue of research in aging has to do with genetic studies of so-called lower organisms. We know the genetics involved. We've got the entire genes mapped out of several species now, of yeast and worms. We think of life span as being fixed, sort of.

Humans kind of have an average life span of seventy-six, and the maximum life-span was this French lady at one-hundred and twenty-two. In humans we feel it is relatively fixed, but in lower forms of life it is very plastic. Life span is strictly a variable depending on the environment. They can live two weeks, two years, or sometimes twenty years depending on what they want themselves to do, which depends very much on the environment.

If there is a lot of food around they are going to reproduce quickly and die quickly, if not they will just bide their time until conditions are better. We know now that the variability in life span is regulated by insulin.

One thinks of insulin as strictly to lower blood sugar. Today in the clinic there was a patient listing off her drugs, she listed about eight drugs she was on and didn't even mention insulin. Insulin is not treated as a drug. In fact, in some places you don't even need a prescription, you can just get it over the counter, it's treated like candy.

Insulin is found as in even single celled organisms. It has been around for several billion years. And its purpose in some organisms is to regulate life span. The way genetics works is that genes are not replaced, they are built upon. We have the same genes as everything that came before us. We just have more of them.

We have added books to our genetic library, but our base is the same. What we are finding is that we can use insulin to regulate lifespan too.

If there is a single marker for lifespan, as they are finding in the centenarian studies, it is insulin, specifically, insulin sensitivity.

How sensitive are your cells to insulin. When they are not sensitive, the insulin levels go up. Who has heard of the term insulin resistance?

Insulin resistance is the basis of all of the chronic diseases of aging, because the disease itself is actually aging.

We know now that aging is a disease. The other case studies that I mentioned, cardiovascular disease, osteoporosis, obesity, diabetes, cancer, all the so-called chronic diseases of aging, auto-immune diseases, those are symptoms.

If you have a cold and you go to the doctor, you have a runny nose, I did Ear, Nose and Throat for ten years, I know what the common treatment for that is, they give you a decongestant. I can't tell you how many patients I saw who had been given Sudafed by their family doctors for a cold and they came to see me after because of a really bad sinus infection.

What happens when you treat the symptom of a runny nose from a cold and you take a decongestant? It certainly decongests you by shutting off the mucus. Why do you have the mucus, because you are trying to clean and wash out the membranes, and what else? What else is in mucus? Secretory IgA, a very strong antibody to kill the virus is in the mucus. If there is no mucus, there is no secretory IgA.

Decongestants also constrict blood vessels, the little capillaries, or arterioles that go to those capillaries, the cilia, the little hair-like projections that beat to push mucus along to create a stream, they get paralyzed because they don't have blood flow so there is no more ciliary movement. What happens if you dam a stream and create a pond?

In days you've got larvae growing. If the stream is moving, you are fine. You need a constant stream of mucus to get rid of and prevent an infection. I am going in to this in some detail because in almost all cases if you treat a symptom, you are going to make the disease worse because the symptom is there as your body's attempt to heal itself.

Now, the medical profession is continuously segregating more and more symptoms into diseases, they call the symptoms diseases. Using ENT for example, that patient will walk out of there with a diagnosis of Rhinitis which is inflammation of the nose. Is there a reason that patient has inflammation of the nose? I think so. Wouldn't that underlying cause be the disease as opposed to the descriptive term of Rhinitis or Pharyngitis?

Some one can have the same virus and have Rhinitis or Pharyngitis, or Sinusitis, they can have all sorts of "itis's" which is a descriptive term for inflammation. That is what the code will be and that is what the disease will be. So they treat what they think is the disease which is just a symptom.

It is the same thing with cholesterol.

If you have high cholesterol it is called hypercholesterolemia. Hypercholesterolemia has become the code for the disease when it is only the symptom. So they treat that symptom and what are they doing to the heart? Messing it up.

So what you have to do if you are going to treat any disease is you need to get to the root of the disease. If you keep pulling a dandelion out by it's leaves, you are not going to get very far. But the problem is that we don't know what the root is, or we haven't.

They know what it is in many other areas of science, but the problem is that medicine really isn't a science, it is a business, but I don't want to get in to that, we can talk hours on that. But if you really look at the root of what is causing it, we can use that cold as a further example.

Why does that person have a cold?

If he saw the doctor, the doctor might tell him to take an antibiotic along with the decongestant. You see this all the time because the doctor wants to get rid of the patient. Well we all know that in almost all cases of an upper respiratory infection it is a virus, and the antibiotic is going to do worse than nothing because it is going to kill the bacterial flora in the gut and impair the immune system, making the immune system worse.

The patient might see someone else more knowledgeable who will say no, you caught a virus, don't do anything, go home and sleep, let your body heal itself. That's better. You might see someone else who would ask why you caught a virus without being out there trying to hunt for viruses with a net. We are breathing viruses every day; right now we are breathing viruses, cold viruses, rhinoviruses.

Why doesn't everybody catch a cold tomorrow?

The Chinese will tell you that it is because the milieu has to be right, if the Chinese were to quote the French. Your body has to be receptive to that virus. Only if your immune system is depressed will it allow that virus to take hold.

So maybe a depressed immune system is the disease. So you can be given a bunch of vitamin C because your immune system is depressed and it is likely that the person has a vitamin C deficiency. That's where most of us are at right now, where we would give a bunch of vitamin C to try to pick up the immune system.

But why is the vitamin C not working. Vitamin C is make in almost all living mammals except humans and a couple other species. Vitamin C is made directly from glucose and actually has a similar structure and they compete for one another.

We've known for many years that sugar depresses the immune system.

We have known that for decades. It was only in the 70's that they found out that vitamin C was needed by white blood cells so that they could phagocytize bacteria and viruses. White blood cells require a fifty times higher concentration at least inside the cell as outside so they have to accumulate vitamin C.

There is something called a phagocytic index which tells you how rapidly a particular macrophage or lymphocyte can gobble up a virus, bacteria, or cancer cell. It was in the 70's that Linus Pauling knew that white blood cells needed a high dose of vitamin C and that is when he came up with his theory that you need high doses of vitamin C to combat the common cold.

But if we know that vitamin C and glucose have similar chemical structure, what happens when the sugar levels go up? They compete for one another upon entering the cells. And the thing that mediates the entry of vitamin C into the cells is the same thing that mediates the entry of glucose into the cells. If there is more glucose around there is going to be less vitamin C allowed into the cell and it doesn't take much. A blood sugar value of 120 reduces the phagocytic index seventy-five percent.

Here we are getting a little bit further down into the roots of disease. It doesn't matter what disease you are talking about, whether you are talking about a common cold or about cardiovascular disease, or osteoporosis or cancer, the root is always going to be at the molecular and cellular level, and I will tell you that insulin is going to have its hand in it, if not totally controlling it.

What is the purpose of insulin?

As I mentioned, in some organisms it is to control their lifespan, which is important. What is the purpose of insulin in humans? If you ask your doctor, they will say that it's to lower blood sugar and I will tell you right now, that is a trivial side effect. Insulin's evolutionary purpose, among others at least known right now, we are looking at others, is to store excess nutrients.

We come from a time of feast and famine and if we couldn't store the excess energy during times of feasting, we would all not be here, because we all have had ancestors that encountered famine. So we are only here because our ancestors were able to store nutrients, and they were able to store nutrients because they were able to elevate their insulin in response to any elevation in energy that the organism encountered.

When your body notices that the sugar is elevated, it is a sign that you've got more than you need right now, you are not burning it so it is accumulating in your blood. So insulin will be released to take that sugar and store it. How does it store it? (Someone in the audience suggest the answer glycogen)…Glycogen?

How much glycogen do you store?

Do you know how much glycogen you have in your body at any one time? Very little. All the glycogen stored in your liver and all the glycogen stored in your muscle if you had an active day wouldn't last you the day.

Once you fill up your glycogen stores how is that sugar is stored, as what particular kind of triglyceride, or fatty acid? Palmitic acid. Saturated fat, ninety-eight percent of which is palmitic acid.

So the idea of the medical profession to go on a high complex carbohydrate, low saturated-fat diet is an absolute oxymoron, because those high complex carbohydrate diets are nothing but a high glucose diet, or a high sugar diet, and your body is just going to store it as saturated fat. The body makes it into saturated fat quite readily.

What else does insulin do?

It doesn't just store carbohydrates, by the way. Somebody mentioned that it is an anabolic hormone, it absolutely is. Body builders are using insulin now because it is legal, so they are injecting themselves with insulin because it builds muscle, it stores protein too.

A lesser known fact is that insulin also stores magnesium. We mentioned it's role in vitamin C, it stores all sorts of nutrients. But what happens if your cells become resistant to insulin? First of all you can't store magnesium so you lose it, that's one effect, you lose it out the urine.

What is one of magnesium's major roles?

To relax muscles. Intracellular magnesium relaxes muscles. What happens when you can't store magnesium because the cell is resistant? You lose magnesium and your blood vessels constrict, what does that do?

Increases blood pressure, and reduces energy since intracellular magnesium is required for all energy producing reactions that take place in the cell. But most importantly, magnesium is also necessary for the action of insulin. It is also necessary for the manufacture of insulin.

So then you raise your insulin, you lose magnesium, and the cells become even more insulin resistant. Blood vessels constrict, glucose and insulin can't get to the tissues, which makes them more insulin resistant, so the insulin levels go up and you lose more magnesium. This is the vicious cycle that goes on from before you were born.

Insulin sensitivity is going to start being determined from the moment the sperm combines with the egg. If your mother, while you were in the womb was eating a high carbohydrate diet, which is turning into sugar, we have been able to show that the fetus in animals becomes more insulin resistant.

Worse yet, they are able to use sophisticated measurements, and if that fetus happens to be a female, they find that the eggs of that fetus are more insulin resistant. Does that mean it is genetic? No, you can be born with something and it doesn't mean that it is genetic. Diabetes is not a genetic disease as such. You can have a genetic predisposition. But it should be an extremely rare disease.

What else does insulin do?

We mentioned high blood pressure, if your magnesium levels go down you get high blood pressure. We mentioned that the blood vessels constrict and you get high blood pressure.

Insulin also causes the retention of sodium, which causes the retention of fluid, which causes high blood pressure and fluid retention: congestive heart failure.

One of the strongest stimulants of the sympathetic nervous system is high levels of insulin.

What does all of this do to the heart? Not very good things.

There was a study done a couple of years ago, a good, down to earth nicely conducted study that showed that heart attacks are two to three times more likely to happen after a high carbohydrate meal. They said specifically NOT after a high fat meal.

Why is that?

Because the immediate effects of raising your blood sugar from a high carbohydrate meal is to raise insulin and that immediately triggers the sympathetic nervous system which will cause arterial spasm, constriction of the arteries. If you take anybody prone to a heart attack and that is when they are going to get it.

What else does insulin do?

Insulin mediates blood lipids. That patient who had a triglyceride of 2200, one of the easiest things we can do is lower triglyceride levels. It is so simple. There was just an article in J.A.M.A. an article and they were saying that the medical profession doesn't know how to reduce triglycerides dietarily, that drugs still need to be used.

It is so ridiculous because you will find that it is the easiest thing to do. They come tumbling down. There is almost a direct correlation between triglyceride levels and insulin levels. In some people more than others. The gentleman who had a triglyceride level of 2200 while on all the drugs only had an insulin level of 14.7.

That is only slightly elevated, but it doesn't take much in some people, all we had to do was get his insulin level down to 8 initially and then it went down to six and that got his triglycerides down to under 200.

The way you control blood lipids is by controlling insulin.

We won't go into a lot of detail, but we now know that LDL cholesterol comes in several fractions, and it is the small, dense LDL that plays the largest role in initiating plaque. It's the most oxidizable. It is the most able to actually fit through the small cracks in the endothelium. And that's the one that insulin actually raises the most. When I say insulin, I should say insulin resistance. It is insulin resistance that is causing this.

Cells become insulin resistant because they are trying to protect themselves from the toxic effects of high insulin. They down regulate their receptor activity and number of receptors so that they don't have to listen to that noxious stimuli all the time. It is like having this loud, disgusting rap music played and you want to turn the volume down.

You might think of insulin resistance as like sitting in a smelly room and pretty soon you don't smell it anymore because you get desensitized.

You can think about it, its not that you are not thinking about it anymore. But if you walk out of the room and come back, the smell is back. You can get resensitized is what that is telling you. It would be like you are starting to go deaf and your are telling others to speak up because you can't hear them, so if I was your pancreas, I would just start talking louder, and what does that do to your hearing?

You would become deafer. Most cases of deafness, especially in old age is due to excessive noise exposure. All the noise exposure your ears have been exposed to, well the hair cells that end up triggering your brain to allow you to hear eventually get killed. Sometimes it just takes a single firecracker.

This is the same thing with insulin resistance. What happens is that if your cells are exposed to insulin at all they get a little bit more resistant to it. So the pancreas just puts out more insulin. I saw a patient today, her blood sugar was 102 and her insulin was 90! She wasn't sure if she was fasting or not, but I've seen other patients where their blood sugar was under 100 and their fasting insulin has been over 90.

That is a fasting insulin. I'm not sure how many people are familiar with seeing fasting insulins. But if I drank all the glucose I could possibly drink my insulin would never go above probably 40. So she was extremely insulin resistant.

What was happening was she was controlling her blood sugar. Statistically she was not diabetic. She is not even impaired glucose tolerant. Her glucose is totally normal supposedly. But her cells aren't listening to insulin, she just has an exceptionally strong pancreas.

Her islet cells that produce insulin are extremely strong and are able to compensate for that insulin resistance by producing thirty times more insulin than what my fasting insulin is. And just by mass action her pancreas is yelling so loud that her cells are able to listen, but they are not going to listen forever. Her pancreas is not going to be able keep up that production forever.

Well the usual treatment once she becomes diabetic, which would be inevitable, once her production of insulin starts slowing down or her resistance goes up any more, than her blood sugar goes up and she becomes a diabetic. For many years, decades before that her insulin levels have been elevated.

They have been elevated for thirty years probably and have never been checked. That insulin resistance is associated with the hyperinsulinemia that produces all of the co-called chronic diseases of aging or at least contributes to them. As far as we know in many venues of science, it is the main cause of aging in virtually all life.

Insulin is that important. So controlling insulin sensitivity is extremely important.

How else does insulin affect cardiovascular disease?

We've only just touched upon it. Insulin is a so-called mytogenic hormone. It stimulates cell proliferation. It stimulates cells to divide. If all of the cells were to become resistant to insulin we wouldn't have that much of a problem. The problem is that all of the cells don't become resistant.

Some cells are incapable of becoming very resistant. The liver becomes resistant first, then the muscle tissue, then the fat. When the liver becomes resistant, what is the effect of insulin on the liver, it is to suppress the production of sugar.

The sugar floating around in your body at any one time is the result of two things, the sugar that you have eaten and how much sugar your liver has made. When you wake up in the morning it is more of a reflection of how much sugar your liver has made. If your liver is listening to insulin properly it won't make much sugar in the middle of the night. If your liver is resistant, those brakes are lifted and your liver starts making a bunch of sugar so you wake up with a bunch of sugar.

The next tissue to become resistant is the muscle tissue. What is the action of insulin in muscles? It allows your muscles to burn sugar for one thing. So if your muscles become resistant to insulin it can't burn that sugar that was just manufactured by the liver. So the liver is producing too much, the muscles can't burn it, and this raises your blood sugar.

Well the fat cells become resistant, but not for a while. It is only after a while that they become resistant. It takes them longer.

Liver first, muscle second, and then your fat cells.

So for a while your fat cells retain their sensitivity. What is the action of insulin on your fat cells? To store that fat. It takes sugar and it stores it as fat. So until your fat cells become resistant you get fat, and that is what you see. As people become more and more insulin resistant, they get fat and their weight goes up.

But eventually they plateau. They might plateau at three hundred pounds, two hundred and twenty pounds, one hundred and fifty pounds, but they will eventually plateau as the fat cells protect themselves and become insulin resistant.

As all these major tissues, this massive body becomes resistant, your liver, muscles and fat, your pancreas is putting out more insulin to compensate, so you are hyperinsulinemic and you've got insulin floating around all the time, 90 units, more.

But there are certain tissues that aren't becoming resistant such as your endothelium, the lining of the arteries do not become resistant very readily. So all that insulin is effecting the lining of your arteries.

If you drip insulin into the artery of a dog, there was a Dr. Cruz who did this in the early 70's by accident, he was doing a diabetic experiment and found out that the femoral artery that the insulin was being dripped into was almost totally occluded with plaque after about three months.

The contra lateral side was totally clear, just contact of insulin in the artery caused it to fill up with plaque. That has been known since the 70's, it has been repeated in chickens, in dogs, it is really a well-known fact. Insulin floating around in the blood causes a plaque build up. They didn't know why, but we know that insulin causes endothelial proliferation, that's the first step, it causes a tumor, an endothelial tumor.

Insulin causes the blood to clot too readily.

Insulin causes the conversion of macrophages into foam cells, which are the cells that accumulate the fatty deposits. Every step of the way, insulin's got its fingers in it and is causing cardiovascular disease. It fills it with plaque, it constricts the arteries, it stimulates the sympathetic nervous system, it increases platelet adhesiveness and coaguability of the blood.

Any known cause of cardiovascular disease insulin is a part of. It influences nitric oxide synthase. You produce less nitric oxide in the endothelium. We know that helps mediate vasodilatation and constriction, i.e. angina.

I mentioned that insulin increases cellular proliferation, what does that do to cancer? It increases it. And there are some pretty strong studies that show that one of the strongest correlations to breast and colon cancer are with levels of insulin.

Hyperinsulinemia causes the excretion of magnesium in the urine. What other big mineral does it cause the excretion of? Calcium.

What is the cause of osteoporosis?

There are two major causes, one is a high carbohydrate diet which causes hyperinsulinemia. People walking around with hyperinsulinemia can take all the calcium they want by mouth and it's all going to go out in their urine.

Insulin is one of the first hormones that any organism ever developed, and as I mentioned in genetics, things are built upon what was there before. So all the other hormones we have in our body were actually built upon insulin. In other words, insulin controls growth hormone.

How does growth hormone work?

The pituitary produces growth hormone, and then it goes to the liver and the liver produces what are called IgF 1 thru 4, there are probably more. What does IgF stand for? Insulin-like growth factor. They are the active ingredients. Growth hormone has some small effects on its own, but the major growth factors are the IgF's that then circulate throughout the body.

Why are they called IgF's or insulin like growth factors? Because they have an almost identical molecular structure to insulin. When I said that insulin promotes cellular proliferation, it is because it cross reacts with IgF receptors. So somewhere in the evolutionary tree, IgF's diverged from insulin. Insulin can work very well all by itself, it doesn't need growth hormone. Growth hormone can't do anything without insulin.

Thyroid. How does thyroid work?

The thyroid produces mostly T4. T4 goes to the liver and is converted to T3, mostly there, other tissues too, but mostly in the liver. We are getting the idea that insulin controls a lot of what goes on in the liver, and the liver is the primary organ that becomes insulin resistant.

When the liver can no longer listen to insulin, you can't convert T4 to T3 very well. Usually in people who are hyperinsulinemic with a thyroid hormone that comes back totally normal, it is important to measure their T3. Their free T3 will just as often as not be low. Get their insulin down and it comes back up.

Sex hormones, estrogen, progesterone, and testosterone, does insulin help control them? Absolutely, in various ways. Insulin helps control the manufacture of cholesterol and where do all the sex hormones come from? All the stearic hormones are originally derived from cholesterol, so that's one way. Dr Nestler from the University of Virginia who has spent the last eight years doing multiple studies to show that DHEA levels are directly correlated with insulin levels, or I should say insulin resistance.

The more insulin resistant you are, the lower your DHEA levels. He firmly believes this and has a lot of studies to back it up, that the decline in DHEA is strictly due to the increase in insulin resistance with age. If you reduce the insulin resistance, the DHEA rises.

And how are these sex hormones carried around the body? Something called sex hormone binding globulins. The more that is bound, the less free, active hormone you have. Sex hormone binding globulin is controlled by what? Insulin. There is not a hormone in the body that insulin doesn't affect, if not directly control.

Let's talk about osteoporosis.

You take a bunch of calcium. The medical profession just assumes that it has a homing device and it knows to go into your bone. What happens if you high levels of insulin and you take a bunch of calcium. Number one, most of it is just going to go out in your urine. You would be lucky if that were the case because that part which doesn't does not have the instructions to go to your bone because the anabolic hormones aren't working.

This is first of all because of insulin, then because of the IGF's from growth hormone, also testosterone and progesterone, they are all controlled by insulin and when they are insulin resistant they can't listen to any of the anabolic hormones. So your body doesn't know how to build tissue anymore, so some of the calcium may end up in your bone, but a good deal of it will end up everywhere else.

Metastatic calcifications, including in your arteries.

Diseases are a result of a lack of communication. There are certain things that your cells need to be healthy. If you learn nothing else today, you should know that everything is at the cellular and molecular level and we are nothing but a community of cells. We are a commune of cells. We are a metropolis of cells that have been given instructions to cooperate.

When you have a large number of cells, like we are, ten trillion or so, there must be proper communication so that there will be proper division of labor. You can take most any cell in your body and under the right conditions you can put it in a petrie dish and it can live all on it's own. They each have a life of their own.

You can manipulate the genetics of a cell, and we've now made a blood cell in to a nerve cell. Pretty soon we are going to be able to take any cell we want and make it into any other cell, because every cell in your body has the identical genetics, all derived from that egg and that sperm that came together. Why is one cell different from another? Because they are reading different parts of the same library.

You can influence which part of that genetic library that every cell reads by the environment of that cell. The environment of that cell is going to be very much dictated by, number one, hormones, and what you eat. Eating is just internalizing the external environment. That is what you have circulation for, to bring that external environment to each and every one of those cells that is inside of you.

I hope that by now you have gotten the idea that high insulin resistance is not very good for you. So now let's talk about what causes insulin resistance. We have been talking about high carbohydrate diets, let's start talking about that a little bit more.

This is what causes insulin resistance.

That is definitely what worsens it. Any time your cell is exposed to insulin it is going to become more insulin resistant. That is inevitable, we cannot stop that, but the rate we can control. An inevitable sign of aging is an increase in insulin resistance.

That rate is variable, if you can slow down that rate you can become a centenarian, and a healthy one. You can slow the rate of aging. Not just even the rate of disease, but the actual rate of aging itself can be modulated by insulin. We talked about some of the lower animals and there is some pretty good evidence that even in humans we still retain the capacity to control lifespan at least partially. We should be living to be 130, 140 years old routinely.

Let's talk about carbohydrates, what are they? We talk about simple and complex carbohydrates, that is totally irrelevant, it means absolutely nothing. Carbohydrates are fiber or non-fiber. Few things in life are as clear-cut as this. Fiber is good for you, and a non-fiber carb is bad for you. You can bank on that.

There is not a whole lot of middle ground. If you have a carbohydrate that is not a fiber it is going to be turned into a sugar, whether it be glucose or not. It may be fructose and won't necessarily raise your blood glucose, fructose is worse for you then glucose, so if you just go by blood sugar, which is just glucose, it doesn't mean that you are not raising your blood fructose, or your blood galactose which is the other half of lactose.

All of those sugars are as bad or worse for you than glucose. You can't just go by so-called blood sugar which is just blood glucose, because we just don't measure blood fructose or blood galactose, but they are all bad for you. Why are they bad, well number one we know that it provokes insulin and every time you provoke insulin it exposes yourself to more insulin and just like walking in a smelly room it is going to become more resistant to insulin.

So every time you have a surge of sugar and you have a surge of insulin, you get more and more insulin resistant and all of the problems we've talked about.

What else is bad about sugar?

We know it increases insulin, but even by itself, sugar is bad for you. You can divide aging into basically two major categories, there is genetic causes of aging, we know that cells have a limited capacity to divide, normally we never get there, but the more rapidly you make cells divide, the more rapidly they age.

One of the effects of insulin is to stimulate cellular proliferation and division. So we know that it increases the rate of aging of a cell population just by that, that is another whole discussion. Let's go to the other half. Our cells accumulate damage with age we cannot help that.

When I say aging, we really are talking about something called senescence, or the damage associated with aging, but the common usage is the word aging. I cannot prevent you from being a day older tomorrow, that is aging, tomorrow you will be a day older than today, and that we cannot do anything about. When we talk about aging we normally think about the damage that is associated with that day.

We have accumulated more damage during that day, that is called senescence. What causes that damage? There is often an example of test tubes in a laboratory. You don't think of test tubes as aging, yet if you mark test tubes with a little red dot and counted the number of test tubes there were at the end of the year with a little red dot left, there would hardly be any, why, because they have encountered damage. They've broken, so even though there is not aging they do have immortality rates. Aging is an increase in the rate of mortality.

In humans, the rate of mortality doubles every eight years.

That is really how you gauge the rate of aging. We found in animal studies that the rate of aging can be largely controlled by insulin. But the damage that accumulates during that aging is caused by largely by sugar.

The two major causes of accumulated damage are oxygenation, and glycation. I'm not going to spend my time talking about oxidation. Most of you know all about that.

What is oxidation?

There are several definitions but we can use a very common one, whenever oxygen combines with something, it oxidizes. Oxygen is a very poisonous substance. Throughout most of the history of life on Earth there was no oxygen. Organisms had to develop very specific mechanisms of dealing with high levels of oxygen before there could ever be life with oxygen.

So we evolved very quickly, as plants arose and developed a very easy means of acquiring energy, they could just lay back and catch rays, and they dealt with that oxygen with the carbon dioxide by spitting it out, they didn't want it around. So the oxygen in the atmosphere increased. All the other organisms then had to cope with that toxic oxygen. Many perished if they didn't have ways of dealing with it.

One of the earliest ways of dealing with all that oxygen was for the cells to huddle together, so that at least the interior cells wouldn't be exposed to as much. So, multi-celled organisms arose after oxygen did. Of course, with that came the need for cellular communication.

So let's talk about glycation.

Everyone knows that oxygen causes damage, but unfortunately, the press has not been as kind to publicize glycation. Glycation is the same as oxidation except substitute the word glucose. When you glycate something you combine it with glucose. Glucose combines with anything else really, it's a very sticky molecule.

Just take sugar on your fingers. It's very sticky. It sticks specifically to proteins. So the glycation of proteins is extremely important. If it sticks around a while it produces what are called advanced glycated end products.

That acronym is not an accident; it stands for A.G.E.'s. If you can turn over, or re-manufacture the protein that's good, and it increases the rate of protein turnover if you are lucky. Glycation damages the protein to the extent that white blood cells will come around and gobble it up and get rid of it, so then you have to produce more, putting more of a strain on your ability to repair and maintain your body.

That is the best alternative; the worst alternative is when those proteins get glycated that can't turn over very rapidly, like collagen, or like a protein that makes up nerve tissue. These proteins cannot be gotten rid of, so the protein accumulates, and the A.G.E.'s accumulate and they continue to damage.

That includes the collagen that makes up the matrix of your arteries. A.G.E.'s are so bad that we know that there are receptors for A.G.E.'s, hundreds of receptors for every macrophage. They are designed to try to get rid of those A.G.E.'s, but what happens when a macrophage combines with an A.G.E. product?

It sets up an inflammatory reaction. We know that cardiovascular is an inflammatory process, any type of inflammation. You eat a diet that promotes elevated glucose, and you produce increased glycated proteins and A.G.E.'s, you are increasing your rate of inflammation of any kind. You get down to the roots, including arthritis, headaches.

When you start putting people on a diet to remedy all of this, my practice is largely diabetes, so my patients are more concerned with their blood sugar and their heart, things like that, but it is so common to have them come back and tell me they used to have horrible headaches and now don't have them anymore, or that they had a horrible pain in their shoulder, or terrible Achilles tendonitis that they don't have any more.

The glycated proteins are making the person very pro-inflammatory.

So we age and at least partially we accumulate damage by oxidation, and one of the most important types of tissues that oxygenate is the fatty component, the lipid, especially the poly-unsaturated fatty acids, they turn rancid. And they glycate, and the term for glycation in the food industry is carmelization.

They use it all the time, that is how you make caramel. So the way we age is that we turn rancid and we carmelize. It's very true. And that is what gets most of us. If that doesn't get us, then the genetic causes of aging will, because every cell in your body has genetic programs to commit suicide. There are various theories for this, one is that if they didn't, virtually every cell in your body would eventually turn cancerous.

Whether those so-called applopatic genes developed as a means to prevent cancer or not is open to speculation but it is a good theory. We know that all cancer cells have turned off the mechanisms for applotosis, which is the medical term for chemical suicide. So we know that it plays a role.

Let's get to diet.

Diet really becomes pretty simple. Carbohydrates we started talking about. You've got fiber and non-fiber and that's real clear-cut. Fiber is good, non-fiber is bad. Fibrous carbs, like vegetables and broccoli, those are great. What is a potato? A potato is a big lump of sugar. That's all it is. You chew a potato, what are you swallowing? Glucose. You may not remember, but you learned that in eighth grade, but the medical profession still hasn't learned that.

What is the major salivary enzyme?

Amylase. What is amylase used for? To break down amylose which is just a tree of glucose molecules. What is a slice of bread? A slice of sugar. Does it have anything else good about it? Virtually no. Somebody emailed me who had decided to do a little research. And there are fifty-some essential nutrients to the human body.

You know you need to breathe oxygen. It gives us life and it kills us. Same with glucose. Certain tissues require some glucose. We wouldn't be here if there were no glucose, it gives us life and it kills us. We know that we have essential amino acids and we have essential fatty acids. They are essential for life, we better take them in as building blocks or we die. So what he did is he took all the essential nutrients that are known to man and plugged it in to this computer data bank and he asked the computer what are the top ten foods that contain each nutrient that is required by the human body. Each of the fifty-three or fifty-four, depending on who you talk to, essential nutrients that there are were plugged in, and did you know that grains did not come up in the top ten on any one.

What is the minimum daily requirement for carbohydrates?


What is the food pyramid based on?

A totally irrelevant nutrient.

Let's go beyond Carbohydrates.

Let's back up even further? Why do we eat? One reason is energy. That's half of the reason. It is very simple, there are two reasons why we eat, one is to gather energy. We need to obtain energy. The other essential reason (Not just for fun! Fun is a good one, but you won't have much fun if you eat too much) is to replace tissue, to gather up building blocks for maintenance and repair.

Those are the two essential reasons that we need to eat. We need the building blocks and we need fuel, not the least of which is to have energy to obtain those building blocks and then to have energy to fuel those chemical reactions to use those building blocks.

So what are the building blocks that are needed, proteins and fatty acids. Not much in the way if carbohydrates. You can get all the carbohydrates you need from proteins and fats. So the building blocks are covered by proteins and fats.

What about fuel?

That's the other reason we eat. There are two kinds of fuel that your body can use with minor exceptions, sugar and fat. We mentioned earlier that the body is going to store excess energy as fat. Why does the body store it as fat? Because that is the body's desired fuel. That is the fuel the body wants to burn and that will sustain you and allow you to live. The body can store only a little bit of sugar.

In an active day you would die if you had to rely one-hundred percent on sugar.

Why doesn't your body store more sugar if it is so needed? Sugar was never meant to be your primary energy source.

Sugar is meant to be your body's turbo charger.

Everybody right here, right now should be burning mostly, almost all fat with minor exceptions. Your brain will burn sugar, it doesn't have to, it can do very well, even better by burning by-products of fat metabolism called ketones. That is what it has to burn when you fast for any length of time. They have shown that if your brain was really good at burning ketones from fat that you can get enough sugar that your brain needs actually from fat; just eating one-hundred percent fat.

You can make a little bit of sugar out of the glycerol molecule of fat. Take two glycerol molecules and you have a molecule of glucose. Two triglycerides will give you a molecule of glucose. The brain can actually exist without a whole lot of sugar, contrary to popular belief. Glucose was meant to be fuel used if you had to, in an emergency situation, expend and extreme amount of energy, such as running from a saber tooth tiger.

It is a turbo charger, a very hot burning fuel, if you need fuel over and above what fat can provide you will dig into your glycogen and burn sugar. But your primary energy source as we are here right now should be almost all fat.

But what happens if you eat sugar.

Your body's main way of getting rid of it, because it is toxic, is to burn it. That which your body can't burn your body will get rid of by storing it as glycogen and when that gets filled up your body stores it as fat. If you eat sugar your body will burn it and you stop burning fat.

We talked about a lot of the effects of high insulin. We talked about insulin causing the formation of saturated fat from sugar. Another major effect of insulin on fat is it prevents you from burning it. What happens when you are insulin resistant and you have a bunch of insulin floating around all the time, you wake up in the morning with an insulin of 90.

How much fat are you going to be burning? Virtually none. What are you going to burn if not fat? Sugar coming from your muscle. So you have all this fat that you've accumulated over the years that your body is very adept at adding to. Every time you have any excess energy you are going to store it as fat, but if you don't eat, where you would otherwise be able to burn it, you cannot and you will still burn sugar because that is all your body is capable of burning anymore.

Where is it going to get the sugar?

Well you don't store much of it in the form of sugar so it will take it from your muscle. That's your body's major depot of sugar. You just eat up your muscle tissue. Any time you have excess you store it as fat and any time you are deficient you burn up your muscle.

Getting back to the macronutrients, fuel, fat is your best fuel by far and the fuel that your body wants to use. So there are two reasons to eat, you need to gather the building blocks for maintenance and repair, that's protein and fat, no carbohydrate needed, and you eat for fuel, without question, fat is your most efficient fuel and the fuel that your body desires the most.

So where do carbohydrates come in?

They don't. There is no essential need for carbohydrates. SO why are we all eating carbohydrates? To keep the rate of aging up, we don't want to pay social security to everyone.

I didn't say you can't have any carbs, I said fiber is good. Vegetables are great, I want you to eat vegetables. The practical aspect of it is that you are going to get carbs, but there is no essential need. The traditional Eskimo diet for most of the year subsists on almost no vegetables at all, but they get their vitamins from organ meats and things like eyeball which are a delicacy, or were.

So, you don't really need it, but sure, vegetables are good for you and you should eat them. They are part of the diet that I would recommend, and that is where you'll get your vitamin C. I recommend Vitamin C supplements, I don't have anything against taking supplements, I use a lot of them.

Fruit is a mixed blessing. You can divide food on a continuum. There are some foods that I really can't say anything good about since there is no reason really to recommend them. And the other end of the spectrum are foods that are totally essential, like omega 3 fatty acids for instance which most people are very deficient in, and even those have a detriment because they are highly oxidizable, so you had better have the antioxidant capacity. So if you are going to supplement with cod liver oil you should supplement with Vitamin E too or it will actually do you more harm than good.

But most foods fall in the middle somewhere. Things like strawberries, you are going to get something bad with strawberries, you are going to get a lot of sugar with strawberries, but you are also going to get a food that is also the second or third highest in antioxidant potential of any food known, the first being garlic the second either being strawberries or blueberries. So, there is something good to be had from it. So I will let some patients put some strawberries in let's say a protein smoothie in the morning. But if they are a hard core diabetic, strawberries are out.

It doesn't take much, if you have a type I diabetic who is not producing any insulin they can tell you what foods do to their blood sugar. It doesn't take much. What is very surprising to these people once they really measure is what little carbohydrate it takes to cause your blood sugar to skyrocket.

One saltine cracker will take the blood sugar to go over 100 and in many people it will cause the blood sugar to go to 150 for a variety of reasons, not just the sugar in it.

When you are eating a high carbohydrate diet, when you are born, your mother, everbody is telling you to eat a bowl of Cheerios for breakfast. You eat that bowl of cheerios and that turns to sugar, and your sugar goes up very rapidly and that causes a big rush of insulin and your body all of a sudden senses a huge amount of sugar being delivered to it at once, of which it was never used to, in an evolutionary sense.

We only have one hormone that lowers sugar, and that's insulin. Its primary use was never to lower sugar. We've got a bunch of hormones that raise sugar, cortisone being one and growth hormone another, and epinephrine, and glucagon.

Our primary evolutionary problem was to raise blood sugar to give your brain enough and your nerves enough and primarily red blood cells, which require glucose. So from an evolutionary sense if something is important we have redundant mechanisms. The fact that we only have one hormone that lowers sugar tells us that it was never something important in the past.

So you get this rush of sugar and your body panics, your pancreas panics and it stores, when it is healthy, insulin in these granules, ready to be released. It lets these granules out and it pours out a bunch of insulin to deal with this onslaught of sugar and what does that do?

Well the pancreas generally overcompensates, and it causes your sugar to go down, and just as I mentioned, you have got a bunch of hormones then to raise your blood sugar, they are then released, including cortisone. The biggest stress on your body is eating a big glucose load.

Then Epinephrine is released too, so it makes your nervous and it also stimulates your brain to crave carbohydrates, to seek out some sugar, my sugar is low. So you are craving carbohydrates, so you eat another bowl of cheerios, or a big piece of fruit, you eat something else so that after your sugar goes low, and with the hormone release, and with the sugar cravings and carbohydrate craving your sugars go way up again which causes your pancreas to release more insulin and then it goes way down.

Now you are in to this sinusoidal wave of blood sugar, which causes insulin resistance. Your body can't stand that for very long. So you are constantly putting out cortisone.

We can talk about insulin resistance.

We hear a lot about insulin resistance, but stop and think a little bit, do you think our cells only become resistant to insulin? The more hormones your cells are exposed to, the more resistant they will become to almost any hormone. Certain cells more than others, so there is a discrepancy. The problem with hormone resistance is that there is a dichotomy of resistance, that all the cells don't become resistant at the same time.

And different hormones affect different cells, and the rate of hormone is different among different cells and this causes lots of problems with the feedback mechanisms. We know that one of the major areas of the body that becomes resistant to many feedback loops is the hypothalamus. The various interrelationships there I really don't have time to go in to here.

But hypothalamic resistance to feedback signals plays a very important role in aging and insulin resistance because the hypothalamus has receptors for insulin too. I mentioned that insulin stimulates sympathetic nervous system, it does so through the hypothalamus, which is the center of it all.

The receptors self-regulate.

If you want to know if insulin sensitivity can be restored to its original state, well, perhaps not to its original state, but you can restore it to the state of about a ten year old.

One of my first experiences with this, I had a patient who literally had sugars over 300. He was taking 200+ units of insulin, he was a bad cardiovascular patient, and it only made sense to me that you don't want to feed these people carbohydrates, so I put him on a low carbohydrate diet.

He was an exceptional case, after a month to six weeks he was totally off of insulin. He had been on 200 some units of insulin for twenty-five years. He was so insulin resistant, one thing good about it is that when you lower that insulin, that insulin is having such little effect on him that you can massively lower the insulin and its not going to have much of an effect on his blood sugar either. 200 units of insulin is not going to lower your sugar any more that 300 mg/deciliter.

You know that the insulin is not doing much. So we could rapidly take him off the insulin and he was actually cured of his diabetes in a matter of weeks. So he became sensitive enough, he was still producing a lot of insulin on his own, then we were able to measure his own insulin and it was still elevated, and then it took a long time, maybe six months or longer to bring that insulin down.

It will probably never get to the point of the sensitivity of a ten year old, but yes, your number of insulin receptors increases, and the activity of the receptors, the chemical reactions that occur beyond the receptor occur more efficiently.

You can increase sensitivity by diet, that is one of the major reasons you want to take Omega 3 oils. We think of circulation as that which flows through arteries and veins, and that is not a minor part of our circulation, but it might not even be the major part. The major part of circulation is what goes in and out of the cell.

The cell membrane is a fluid mosaic. The major part of our circulation is determined by what goes in and out. It doesn't make any difference what gets to that cell if it can't get into the cell. We know that one of the major ways that you can affect cellular circulation is by modulating the kinds of fatty acids that you eat. So you can increase receptor sensitivity by increasing the fluidity of the cell membrane, which means increasing the omega 3 content, because most people are very deficient.

They say that you are what you eat and that mostly pertains to fat because the fatty acids that you eat are the ones that will generally get incorporated into the cell membrane. The cell membranes are going to be a reflection of your dietary fat and that will determine the fluidity of your cell membrane. You can actually make them over fluid.

If you eat too much and you incorporate too many omega 3 oils then they will become highly oxidizable (so you have to eat Vitamin E as well and monounsaturates as well) There was an interesting article pertaining to this where they had a breed of rat that was genetically susceptible to cancer.

What they did was they fed them a high omega 3 diet, plus iron, without any extra Vitamin E and they were able to almost shrink down the tumors to nothing, because tumors are rapidly dividing. This is like a form of chemotherapy, and the membranes that were being formed in these tumor cells were very high in omega three oils, the iron acted as a catalyst for that oxidation, and the cells were exploding from getting oxidized so rapidly. So omega 3 oils can be a double edged sword.

Most food is a double edged sword.

Like oxygen and glucose, they keep us alive and they kill us, eating is the biggest stress we put on our body and that is why in caloric restriction experiments you can extend life as long as you maintain nutrition. This is the only proven way of actually reducing the rate of aging, not just the mortality rate, but the actual rate of aging, because eating is a big stress.

It has actually been shown by quite a number of papers that resistance training for insulin resistance is better than aerobic training. There are a variety of other reasons too. Resistance training is referring to muscular exercises. If you just do a bicep curl, you immediately increase the insulin sensitivity of your bicep. Just by exercising, and what you are doing is you are increasing the blood flow to that muscle. That is one of the factors that determines insulin sensitivity is how much can get there. It has been shown conclusively that resistance training will increase insulin sensitivity.

Back to the macronutrients because that is real simple, you don't want very much in the way of non-fiber carbs, fiber carbs are great, you are going to get some non-fiber carbs. Even if you just eat broccoli you are going to get some non-fiber carbs. That is OK since at least for the most part you are getting something that is really pretty good for you. Protein is an essential nutrient.

You want to use it as a building block because your body requires protein to repair damage and replenish enzymes. All of the encoded instructions from your DNA are to encode for proteins. That is all the DNA encodes for. You need protein, but you want to use it as a building block, but I don't believe in going over and above the protein that you need to use for maintenance, repair and building blocks.

I don't think you should be using protein as a primary fuel source. Your body can use protein very well as a fuel source. It is good to lose weight while using it a s a fuel source because it is an inefficient fuel source. Protein is very thermogenic, it produces a lot of heat, which means that less of it is going into stored energy, more is being dissipated. Just like throwing a log into a fireplace.

Your primary fuel should be coming from fat.

So you can calculate the amount of protein a person requires, or at least estimate it by their activity level. The book Protein Power actually went very well in to this. You have to calculate how much protein is required by their activity level and their lean body mass. There is still some gray area as to how many grams per kilogram of lean body mass, depending on the activity that person requires.

Anywhere perhaps one to two grams of protein per kilogram of lean body mass, maybe even a little bit higher if someone is really active.

You don't want to go under that for very long. I'd say that it is better to go over than to go under that amount for very long. But I especially don't want my diabetic patients, which means all of us, because in a very real sense we really all have diabetes, it is just a matter of degree, we all have a certain degree of insulin resistance.

If you can cure a diabetic of diabetes, you can do the same thing to a so-called non-diabetic person and still improve that person. I want to improve my insulin sensitivity just as much as I do my diabetics because insulin sensitivity is going to determine for the most part how long you are going to live and how healthy you are going to be. It determines the rate of aging more so than anything else we know right now.

What about supplements such as Chromium for example?

Chromium, it depends on whom you are dealing with, but are we talking about a diabetic patient, who is supposed to be the topic of this talk, yes, all my diabetics go on 1,000 mcg. of chromium, some a little bit more if they are really big people. Usually 500 mcg for a non-diabetic. It depends on their insulin levels.

I don't care so much what their sugar levels are, I care what their insulin levels are, which is a reflection of their insulin sensitivity. We are talking about hyperinsulinemia or non-hyper-insulinemia. Its insulin we should be concerned about.

I use a lot of supplements. What you really want to do, and my purpose mostly is to try to convert that person back into being an efficient burner of fat. We talked about when you are very insulin resistant and you are waking up in the morning with an insulin that is elevated, you cannot burn fat, you are burning sugar.

They don't know how to burn fat anymore and that is your best fuel.

One of the reasons that sugar goes up so high is because that is what your cell is needing to burn, but if it is so insulin resistant it requires a blood sugar of 300 so that just by mass action some can get in to the cell and be used as fuel. If you eliminate that need to burn sugar, you don't need such high levels of sugar even if you are insulin resistant.

So you want to increase the ability of the cells in the body to burn fat.

You want to make that glucose burner into a fat burner. You want to make a gasoline burning car into a diesel burning car. Did anyone ever look at the molecular structure of diesel fuel in your spare time? It looks almost identical to a fatty acid. There is a company right now that can tell you how to alter vegetable oil to use in your Mercedes. It's just a matter of thinning it out a little bit. It is a very efficient fuel.

You can look at other variables that will give you some idea too such as triglycerides. If they are very sensitive to high levels of insulin, they come in with insulin levels of 14 and they have triglycerides of 1000, then you would treat them just as you would if they had an insulin level of 50. It gives you some idea of the effect of the hyperinsulinemia on the body.

You can use triglycerides as a gauge, which I often do. The objective is to try to get the insulin level just as low as you possibly can. There is no limit. They classify diabetes now as a fasting blood sugar of 126 or higher. A few months ago it might have been 140. It is just an arbitrary number, does that mean that someone with a blood sugar of 125 is non-diabetic and fine? If you have a blood sugar of 125 you are worse than if you had a blood sugar of 124. Same with insulin. If you have a fasting insulin of 10 you are worse off than if you had an insulin of 9. You want to get it just as low as you can.

With athletes, let's think about that. What is the effect of carbohydrate loading before an event. What happens if you eat a bowl of pasta before you have to run a marathon. What does that bowl of pasta do? It raises your insulin. What is the instruction of insulin to your body?

To store energy and not burn it. I see a fair amount of athletes and this is what I tell them, you want everybody, athletes especially, to be able to burn fat efficiently. So when they train, they are on a very low carbohydrate diet. The night before their event, they can stock up on sugar and load their glycogen if they would like.

They are not going to become insulin resistant in one day. Just enough to make sure, it has been shown that if you eat a big carbohydrate meal that you will increase your glycogen stores, that is true and that is what you want. But you don't want to train that way because if you do you won't be able to burn fat, you can only burn sugar, and if you are an athlete you want to be able to burn both.

Few people have problems burning sugar if they are an athlete, but they have lots of problems burning fat, so they hit the wall. And for a certain event like sprinting it is less important, truthfully, for their health it is very important to be able to burn fat, but a sprinter will go right into burning sugar. If you are a 50 yard dash man, whether you can burn fat or not is not going to make a huge difference in your final performance.

Beyond your athletic years if you don't want to become a diabetic, and if you don't want to die of heart disease and if you don't want to age quickly…It is certainly not going to do you any harm to be able to burn fat efficiently in addition to sugar.

Vanadyl Sulfate is an insulin mimic, so that it can basically do what insulin does by a different mechanism. If it went through the same insulin receptors, then it wouldn't offer any benefit, but it doesn't, it actually has been shown to go through a different mechanism to lower blood sugar, so it spares insulin and then it can help improve insulin sensitivity. On someone who I am trying to really get their insulin down I go 25mg 3X/day temporarily.

I put people on glutamine powder. Glutamine can act really as a brain fuel, so it helps eliminate carbohydrate cravings while they are in that transition period. I like to give it to them at night and I tell them to use it whenever they feel they are craving carbohydrates. They can put several grams into a little water and drink it and it helps eliminate carbohydrate cravings between meals.

It is a high protein diet that will increase an acid load in the body, but not necessarily a high fat diet. Vegetables and greens are alkalinizing, so if you are eating a lot of vegetables along with your protein it equalizes the acidifying effect of the protein. I don't recommend a high protein diet. I recommend an adequate protein diet.

I think you should be using fat as your primary energy source, and fat is kind of neutral when it comes to acidifying or alkalinizing. In general, over 50% of the calories should come from fat, but not from saturated fat. When we get to fat, the carbohydrates are clear cut, no scientist out there is really going to dispute what I've said about carbohydrates.

There is the science behind it. You can't dispute it. There is a little bit of a dispute as to how much protein a person requires. When you get to fat, there is a big grey area within science as to which fat a person requires. We just have one name for fat, we call it fat or oil. Eskimos have dozens of names for snow and east Indians have dozens of names for curry. We should have dozens of names for fat because they do many different things. And how much of which fat to take is still open to a lot of investigation and controversy.

My take on fat is that if I am treating a patient who is generally hyperinsulinemic or overweight, I want them on a low saturated fat diet. Because most of the fat they are storing is saturated fat. When their insulin goes down and they are able to start releasing triglycerides to burn as fat, what they are going to be releasing mostly is saturated fat. So you don't want to take anymore orally. There is a ration of fatty acids that is desirable, if you took them from the moment you were born, but we don't, we are dealing with an imbalance here that we are trying to correct as rapidly as we can.

You have plenty of saturated fat. Most of us here have enough saturated fat to last the rest of our life. Truthfully. Your cell membranes require a balance of saturated and poly-unsaturated fat, and it is that balance that determines the fluidity. As I mentioned, your cells can become over-fluid if they don't have any saturated fat.

Saturated fat is a hard fat. We can get the fats from foods to come mostly from nuts. Nuts are a great food because it is mostly mono-unsaturated. Your primary energy source ideally would come mostly from mono-unsaturated fat. It's a good compromise. It is not an essential fat, but it is a more fluid fat. Your body can utilize it very well as an energy source.

Animal proteins are fine and are good for you, but not the ones that are fed grains.

Grainfed animals are going to make saturated fat out of the grains. Saturated fat in nature occurs to a very tiny degree. Not in the wild there is very little saturated fat out there. If you talk about the Paleolithic diet, we didn't eat a saturated fat diet. Saturated fat diets are new to mankind. We manufactured a saturated fat diet by feeding animals grains. You can consider saturated fat to be second generation carbohydrates. We eat the saturated fats that other animals produce from carbohydrates.

Zone was a good diet compared to the American diet it was unusual. Is it an optimal diet? No. Is it optimal for what is known today about nutrition, it is not. He is stuck in this mold he can't get out of but now he is trying to get out of it through the back door. Initially the author spoke about how it made no difference if you got your carbohydrate from candy or vegetables.

The Volkswagen was a good car, but eventually they had to change it to keep up with modern technology. What he is doing now is changing his recipes so that the 40% carbohydrates are coming primarily from vegetables, and the carbohydrates are going way down because he knows that if he doesn't it's not as good a diet.

I would go 20% of calories from carbs. Depending on the size of the person, 25 to 30% of calories from protein, and 60-65% from fat. You can get non-grain fed beef.

Insulin is not the only cause of disease.

There are other considerations such as iron. We know that high iron levels are bad for you. If a person's ferritin is high, red meat is out for a while, till we get their iron down. SO there are other things involved about if we are going to allow a person to eat red meat or not.

There is a great deal of difference between a non-grain fed cow and a grain fed cow.

Non-grain fed will have only 10% or less saturated fat. Grain fed can have over 50%.

There is a big difference. A non-grain fed cow will actually be high in Omega 3 oils. Plants have a pretty high percentage of Omega 3, and if you accumulate it by eating it all day, every day for most of your life, your fat gets a pretty high proportion of Omega 3. I would try for 50% oleic fat, and the others would depend on the individual, but about 25% of the other two.

In a fat diabetic I would probably go down on the saturated fat and go 60% oleic. I would go 1 to 1 on the omega 6 to 3, that would be therapeutic. The maintenance ratio would be about 2.5 to 1 omega 6 to 3. Arachadonic acid, DHA, to EFA. Therapeutic, I would go lesser on the saturated fats. I would try to do most of this through diet. There are some practicalities involved. I would ask the person if they like fish and if they practically puke in front of me they are going on a tablespoon of cod liver oil, the best brand is made by Carlson which doesn't taste fishy at all.

There are probably some others too that are okay. Most people end up going on a supplement of Omega 3 oils because most of them are not going to eat enough fish to get it, which would be about four days a week, and it can't be overcooked etc., it is a little hard to get that much entirely from diet.

I like sardines if they will eat them. Sardines are a very good therapeutic food. They are baby fish so they haven't had time to accumulate a bunch of metal. They are smoked so they are not cooked and the oil is not spoiled in them. You have to eat the whole thing. Not the boneless and skinless. You need to eat all the organs and they are high in vitamins and magnesium.

DNA glycates.

So if people are worried about chromosomal damage from chromium, what they should really be worried about instead is high blood sugar. DNA repair enzymes glycate as well. Insulin is by far your biggest poison. They disproved that study that was against chromium many times. They showed that it only happens if you put cells in a petrie dish with chromium but in vivo studies prove otherwise. The lowering of insulin is going to be better than any possible detriment of any of the therapies you are using. Insulin is associated with cancer, everything.

Insulin should be tested on everybody repeatedly, and why it is not is only strictly because there hasn't been drugs till recently that could effect insulin, so there is no way to make money off of it. Fasting insulin is one way to look at it, not necessarily the best way. But it is the way that everybody could do it. Any family doctor can measure a fasting insulin. There are other ways to measure insulin sensitivity that are more complex that we do sometimes.

We use intravenous insulin and watch how rapidly their blood sugar crashes in a fasting state in 15 minutes and that assesses insulin sensitivity, then you give them dextrose to make sure they don't crash any further. There are other ways that are utilized to directly assess insulin sensitivity, but you can get a pretty good idea just by doing a fasting insulin.

Ron Rosedale, M.D. 1999

 Post subject: Re: Insulin and Its Metabolic Effects By Ron Rosedale, M.D.
PostPosted: Fri Nov 09, 2012 1:39 am 
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Ron Rosedale – Protein: The Good, The Bad and The Ugly
Friday, May 7, 2010

Ron Rosedale recommends adequate protein and warns that excess protein is bad for health.

He gave this talk at the American Society of Bariatric Physicians (ASBP) meeting Oct 31, 2006. They’re medical experts who work to reduce obesity. As part of the 2006 presentations, the ASBP included a special segment that featured low-carb diets, researchers and scientists who are connected to the Nutrition and Metabolism Society. Special thanks to Instatapes for recording this presentation.

Listen to Ron Rosedale speech (40 minutes)

View PDF of keynote presentation that includes citations.
The good, the bad, and the ugly of protein.

The good, and that’s pretty good, is that we can’t live without it. It is a required nutrient. It’s an essential nutrient. Unlike carbohydrates, which is a nonessential nutrient, which means you don’t have to have any. With carboydrates, you can make whatever you need. With amino acids, you have to take some of them in.

Then we could go into a lot of the miscellaneous problems with proteins. I’m not going to go into that a lot. A lot of articles will show detriments to protein, and as Mike Eades mentioned, there’s a lot of articles will show it’s not detrimental. So it’s confusing. Whenever it’s confusing, it means you’re not going into it deep enough. You’re not go-ing deep enough into the basic science of it all.

Dairy products aside, when past and present meat consumption is factored in, there’s a three times risk of developing Alzheimer’s in meat eaters as opposed to vegetarians. Is that true or not? I don’t know. I don’t place a lot of emphasis on this kind of study. I want to go deeper because there is a lot of confusion. Here’s another study: High protein diet may precipitate a progression of coronary artery disease. Through an increase in lipid deposition and through inflammatory and coagulation pathways. Now if this is true, there must be underlying causes of this. That’s really what you want to get into to determine the truth of something.

We know that high protein can raise glucose. And I’m sure Mike Eades showed you studies where a high protein diet reduced blood sugars and was better for diabetics. But the question is, compared to what. If you compare a diet to the average American diet. If you change anything in the average American diet you’re going to improve it. Improving the American diet is not a trick. It’s like a race between a one-legged man and a grandmother. Who cares who wins that?

Here we’ve seen, if you eat a high protein diet, we’re going to go deeper and deeper and deeper into the science of all this. To see if there’s something to really tell us whether excess protein is good or bad. If you eat a high protein diet, there is excess stimulation of the transport to the liver. You flood the liver with amino acids, and it’s got to do something with them. You can do two things with protein. You can make protein, you can replenish the parts that have been torn down, or you can burn it for fuel. Hopefully, you’re not going to excrete it. Food was too precious in our evolutionary his-tory to waste it. Certainly, if you have protein in your urine, something is wrong. Burn it, or use it.

Rapid stimulation of the liver glycine cleavage system in rats fed a high protein diet. In other wods, you’re going to break down a lot of it if you eat a lot of it.

Glycine metabolism is stimulated by high protein feeding.

Effect of high protein intake on Insulin secretion and glucose. Hepatic glucose was sig-nificantly increased with high protein intake. It makes sense. If you have a bunch of amino acids floating around, your liver breaks extra protein into glucose forming carbon shells.

Insulin mediated suppression of hepatic glucose production was impaired with high protein intake but not in patients with a normal protein intake. Gluconeogensis was increased with a high protein diet. We conclude that a normal protein diet is accompanied by delayed progression of the continuous loss of endogenous insulin. We know that in diabetics, there’s a loss of islet cell function over time, and here they’re saying that high protein may contribute to that.

After adaptation to a protein restricted diet, if you restrict protein, diabetics experienced a 30% decrease in daily glucose concentrations, and I know from my practice, and this wasn’t in everybody, but if I had a diabetic, and I put all of them on a low carbohydrate diet. It doesn’t make sense to feed diabetics sugar. But in those that had more trouble processing sugar, the next step was reducing their protein, and I’d restrict it a lot, for an average size adult, I’d put them down to 50 grams a day, maybe 30 grams a day, and their sugar would then go down. So this isn’t just theoretical.

We conclude that severe protein restriction decreases insulin requirements in Type 1 diabetics and fasting hepatic glucose output and basal insulin levels in normal people. Not just diabetics.

We know that protein increases levels of insulin. We know that there’s an insulingenic effect in eating high protein. That’s well known. There’s also a leptin increase with pro-tein. Amino acids increase leptin. Continual high levels of insulin and leptin cause insulin resistance and leptin resistance. So you might get a short term benefit from high protein, but it may be at a price of a long-term detriment, If you keep those levels high. If you raise insulin you’re going to lower sugar temporarily until you become more insulin resistant, and if you raise leptin, you’re going to be less hungry, temporarily, until your hypothalamus becomes more resistant to its action. Which is will become by overexposure. It’s like if you’re in a smelly room, after a while you can’t smell it, the longer you stay in there.

Your cells work the same way. If they’re over-stimulated, they just put in earplugs. They don’t want to be yelled at.

Central nervous system. There’s a more critical role for leptin than insulin in mammalian energy homeostasis. People are ignoring leptin, but it’s probably more important than insulin in diabetes. And in all of the energy storage diseases. Metabolic syndrome, aging.

Why isn’t this really being told? Because there are no drugs that control leptin. So drug reps aren’t telling you about this. But, It can easily be controlled through diet. It is what tells you how to eat. You eat to control insulin and leptin. It’s very simple. Certain eating behaviors extend lifespan. They’ve shown that with dietary restriction. They thought it was calorie restriction, but it’s not. It’s restricting certain elements in the diet. Sugar and protein. Not fat. That’s a critical thing to understand.

In obesity, results of several studies show that chronically elevated central leptin, decreases hypothalamic leptin receptor expression and impairs receptor protein levels and impairs leptin signaling. So chronically elevated leptin contributes to leptin resistance, and leptin resistance leads to further obesity, leading to a vicious cycle of escalating metabolic devastation.

You can find a vicious cycle in almost any chronic disease. That’s why your body can’t deal with it. The way it deals with it ends up worsening the problem.

Lower leptin concentrations appeared to occur without evidence of increased hunger. If you lower leptin you improve leptin sensitivity. It’s suggesting a functional improvement in the resistance to leptin. The way to fix leptin and therefore obesity and therefore aging and diabetes and all sorts of things is by chronically keeping leptin down, your hypo-thalamus can increase sensitivity to it and listen to it. Not just by trying to up it. When leptin was first discovered that’s what they tried to do. Just give more leptin. How have they been treating diabetes? Give more insulin. Just up and up and up the insulin. No! You have to down and down and down the insulin. And give the cells more room to listen.
Communication is more dependent on listening actually, than speaking. Cells have to be able to listen to the signal.

If I were to start screaming at you, how many people will stay in this room? You’d cover your ears.

Response to energy restriction involving leptin concentrations is affected by dietary composition, not drugs. Macro-nutrient composition of the diet affects leptin. This is just saying that different protein compositions, different macro-nutrient compositions affected leptin.

On the high protein diet, the leptin messenger RNA did not decline upon fasting after a meal. It stayed up for a while. Chronically elevated leptin causes leptin resistance and leads to metabolic devastation.

Regulation of leptin secretion from white adipocytes by insulin glycolated substrates and amino acids. So the two things that will cause leptin spikes and chronically elevated leptin are sugar through a pathway called the hexosamine pathway and amino acids.

Amino acid precursors of citric acid cycle intermediate potently stimulates basal leptin secretion, insulin having an additive effect.

Ron Rosedale - mTOR is activated

And the MTOR is one most people don’t know about yet, which is unfortunate. Because the MTOR pathway is intriguing, and may be one of the most, if not the most, important nutrient sensing pathway in the body, aside from insulin. And here, if you get nothing out of this talk, but this one sentence, MTOR is activated by free amino acids. MTOR is a pathway that senses protein concentrations. More specifically, amino acid concentrations. MTOR is also linked to leptin, and amino acids stimulates MTOR stimulates leptin.

Protein increases leptin, also triggers the hexosamine pathway, and the ugly. High protein apparently accelerates aging and therefore all the chronic diseases associated with aging.

The role of specific nutrients in caloric restriction. Dietary restriction has been shown to increase longevity which indicates it’s having positive results. However, it appears it is not caloric restriction but the carbohydrate and protein restrictions in the diet, the medi-ate the effects, at least in flies, and it appears in other organisms, also.

Why would protein be so important in the regulation of aging. Life is a constant battle between damage and damage control. If we could repair damage as fast as it occurs, we would live forever. Ultimately, unfortunately, we damage the damage control mechanisms, and that’s really what does us in.
Excess protein actually increases damage and reduces our ability to repair it, so it’s a double whammy.

Life at higher temperatures leads to a greater accumulation of irreversible damage that leads to death. One of the advantages you’ll hear all over the place is that it’s good to be thermogentic. If you go to a health food store, there are thermogenic aids all over the place. And one of the advantages given to a high protein diet is that it’s thermogenic. And it is. Without question, protein is the most thermogenic nutrient you can eat. It will produce the most heat. Well producing heat and living a long life are just not compatible.

If you went to a gas station and there were two pumps, and one said this pump will produce the most fuel efficiency and give you the most mileage, and this other pump will cause your car to run hotter . . .

Which one are you going to get? You’d never get the one that makes your car run hotter because what’s that going to do to your engine. Not good things. That’s why you have a radiator.

Protein increases glycation, oxidation damage, and we know that protein increases growth hormone and IGF-1. In the last talk, I constantly hammered that high IGF-1, and insulin promotes aging, through a separate pathway. We know that protein increases IGF 1 and AGES, the short term for Advanced glycated end products. There are two major causes of aging. One is oxidative damage and the other is advanced glycated end products, that’s when glucose combines with proteins and DNA. Basically glucose is a sticky molecule that changes the shape and function of whatever it sticks to. It forms what are called advanced glycated end products, the acronym being AGES and that was intentional because it plays such a major role in the chemistry of aging.

In some cells AGES increase with amino acids. In another study, profibrotic injury response occurred in messengial cells exposed to amino acids with or without high glucose by formation of AGES, oxidative stress and activation of the protein kinase Beta and Map Kinase pathways. Which are cell proliferation pathways. Calorie restriction slowing aging and extending life. Mice with pituitary glands devoid of growth hormone producing cells exhibit a remarkably extended lifespan, as do genetically altered mice where they targeted the disruption of the growth hormone receptor, which results in low concentrations of IGF. Andre Barke has done a lot of work on this. Wonderful man, and he’s now head of the American Aging Associaton. And he’s shown convincingly that when you keep insulin and IGF down, animals live a lot longer. And he recently won the Methuselah prize for the longest lived mouse.

Rosedale MR animals

Reducing protein extends life. If you restrict methionine, you decrease visceral fat mass and you preserve insulin action. Reduced dietary methionine and caloric restriction pro-long lifespan. In other words, it isn’t just caloric restriction. If you reduce dietary methionine without caloric restriction, you get the same thing, Methionine restricted rats shows reduced visceral fats, with decreases in insulin, glucose and leptin. Insulin responses in older methionine-restricted animals as measured by oral glucose challenge are similar to young animals. By 16 weeks, methionine restricted animals show a 40% reduction in IGF, which is sustained throughout life.

For 60 years, the only dietary manipulation showed to retard aging was Calorie restriction, and more recently, they’ve shown that it isn’t necessarily calories. If you decrease tryptophan, and you decrease cystine and methionine, you get the same thing. Methionine restriction is not a consequence of reduced energy intake. The intervention alters the rate of aging and not by correcting a single defect.

Recent work has shown that dietary restriction in fruit flies is a product of acute effect on genetic transcription that causes fully fed flies to adopt the mortality profile of lifelong dietary restricted flies within 40 hours of initiation. In other words, you don’t have to do this starting from an infant. If you adopted some of these today, you can get the same genetically healthy profile, the same healthy genetic transcription profile, as if you had been dietary restricted all your life.

In other words, you can do this at any time. You can experience the benefits of this. You can go back in time, essentially.
You can reduce your aging to a certain extent and therefore the diseases associated with aging, if you just adopt this now.

Alterations in nutrient related signaling pathways are thought to initiate the cascade of changes that underlie longevity assurance by dietary alterations.

The nutrient sensing pathways, that’s what is critical.

Insulin and IGF alter lifespan in rodents and many other species. Insulin is known to be involved in regulation of homeostasis in response to a diet, and is know to be a link between the calorie of the diet and extended action. However, two lines of evidence indicate that insulin and IGF are not the only pathway. If you reduce insulin IGF activity and then put them on a dietary restricted program, you have an added effect. They seem to function by two separate, parallel pathways. Reducing insulin and IGF are definitely good. You go further and what’s that pathway? MTOR. It’s a parallel pathway that operates alongside the insulin pathway, but apparently, separately.

These studies provide further support to the argument that protective effects of dietary restriction are not limited to calories alone but involve an aspect of protein metabolism as well. Sugar and protein. That’s what was available when all these signals arose, evolutionarily.

Lifespan is important not because Nature cares about you, but it cares about reproduction, and it wants you to reproduce at a future, more opportune time, if the nutrient availability isn’t good now. But we can use that knowledge. We can still dig into pathways that affect aging and health by what we eat.

A little more on MTOR. The amino-sensitive MTOR pathway from yeast to animals. The target of rapamycin, which is a drug being investigated for cancer, and heart disease and autoimmune diseases and many things. It’s a natural substance discovered by accident. They didn’t know how it worked, but that’s how MTOR pathway was found. Maybe less than 10 years ago. They found it was extremely important, and we’re going to understand that any effect of rapamycin is paralleled by low amino acids. Rapamycin inhibits MTOR. That’s what it does. That’s how it works. How it works to reduce cancer.

In a 2002 study, they reported that the process through which nutrients, amino acids, activate MTOR are largely unknown. They said then that evidence exists for both an intracellular and membrane bound sensor for the amino acid. Since then, they have a clearer idea of how it works.

Studies performed in fat cells, in ovarian cells, in liver cells, in muscles, pancreatic beta cells all show a sensitivity of phosphorylation status of MTOR subtrates and amino acid concentrations. In other words, it appears to work everywhere. All cells have apparently an MTOR signaling pathway that is sensitive to amino acid concentrations.

Indeed, activity of MTOR was determined by amino acid availability in each cell line tested. That is the main thing that will stimulate MTOR. It is an amino acid sensing pathway.

Here’s an interesting comment: Future studies that examine the link between amino acid transports and MTOR activity will resolve the initial signaling events that result in the activation of MTOR targets and will provide insights into the scavenging of nutrients by malignant cells. Malignant cells try to hoard amino acids, and when they do so, they upregulate MTOR, and when they up-regulate MTOR, they stimulate cell division.

Here we show that inhibition of MTOR activates apoptosis. One of the ways that cancer is allowed to progress by shutting off P53. P53 is one of the ways that we kill cancer. It’s a checkpoint. P53 triggers cell suicide, which is known as apoptosis. Course, cancer cells don’t want that. So they mutate, or inIn some way, P53 got mutated, and it can’t trigger that cell suicide. And here, it’s showing that rapamycin, by down-regulating MTOR, can trigger cell suicide without P53. It’s another checkpoint. In other words, keep amino acids low, and you can check that cancer in its tracks.

The TOR pathway regulates genetic expression by linking nutrient sensing to histone acetylation, and the promise of rapamycin as a cancer drug is being explored. This is in 2003. It’s been showing remarkable antitumor activity in cells. We therefore find it intriguing that rapomycin results in a gene profile seen in amino acid limitation.
There are two things seen in cancer cells require to keep going.

Two things any cell requires. Fuel and parts, the main parts being protein. It’s a requirement for cancer. It doesn’t take a lot of intelligence to know that if you want to suppress it, just don’t eat it.

Don’t give it sugar. Sugar can be used as an anaerobic fuel. You can burn sugar without oxygen. You have to have oxygen to burn fat. Cancer cells are rapidly dividing, and they mostly will outplace the supply of oxygen. The most aggressive cancer has to use sugar as a fuel source. One way to suppress cancer is just not to feed it sugar. But this isn’t some elegant drug, or some profit induced therapy, so it’s not being used. I’ve seen remarkable results by just eliminating sugar form the diet. And that means potatoes, pasta, rice and all that stuff that turns into sugar immediately. Another way is by toning down the amino acids. Now you have to have some. But we know that if you restrict amino acids, your body goes into an amino acid conservation mode.

Rosedale TOR extension of life

Extension of chronological lifespan in yeast by decreased TOR signaling. TOR signaling regulates multiple cellular processes in response to nutrients, especially amino acids, raising the possibility that decreased TOR signaling mediates extended lifespan in caloric restriction. In support of this possibility, removal of either aspartame or glutamine from the media feeding the yeast significantly increased survival. Pharmacological Inhibition of TOR by rapomycin also increased lifespan.

We propose an up-regulation of a highly conserved response to starvation-induced stress is important lifespan extension by decreased TOR signaling in yeast and higher eukaryotes. Us.

There’s distinct signaling down stream. A lot of research going into MTOR. Key roles in regulating cell and animal growth. The cell cycle, gene expression. Recent studies have shown that MTOR is essential for cell growth and proliferation Rapamycin as a specific inhibitor of MTOR is in clinical use or potential use in graft rejection, restonosis after angioplasty, cancer angiogenesis, liver fibrosis and many other diseases. There is general agreement that amino acids do indeed stimulate the phosphorylation of MTOR downstream targets. Amino acid infusion during a euglycemic hyperinsulemic clamp in fasted humans decreased rather than increased glucose disposal. Raising glucose. Although these data may be explained by substrate competition. Ie, the Amino acids were oxidized instead of glucose. Which it is. Certainly partially. But there are indications the amino acids cause a time dependent rapamycin sensitive down regulation of protein kinase B and of glucose transport by insulin. In other words, it causes insulin resistance.

Another example suggesting that amino acids may cause insulin resistance is that of glutamine. This amino acid, which is a potent stimulator of glycogen synthesis is also a substrate for the hexose monophosphate shunt, and has been shown to highly regulate insulin sensitivity.

The importance of amino acid signaling in the coordination of whole body metabolism is also indicated by its involvement in the regulation of leptin production by adipocytes. Amino acids upregulate MTOR. Cause spikes in leptin.

There is an amino acid dependent signaling that controls lepin production via adipocytes.

The MTOR signaling pathway is frequently over-activated during cancer. Thus, the importance of amino acid signaling in cancer is evident.

When we’re talking about life extension in animals, we’re generally talking about reduction of cancer. Most laboratory animals die of cancer or autoimmune disease, so if you extend lifespan in laboratory animals, it’s synonymous with reducing cancer.

Another way that lifespan appears to be enhanced is by regulating protein turnover. You have to get rid of rotten proteins. We talked about AGES, and how glucose sticks to proteins and cause Proteins become malformed and do nasty things, so we have to get rid of them. Tear them down. We know with caloric restriction and other methods that enhance lifespan, you accelerate the breakdown of old proteins and manufacture of new proteins.

Proteozome mediated proteolysis and autophagic proteolysis declined with age. However, the last two pathways can be considered an anti-aging repair mechanism because they remove aberrant proteins and defective cellular organelles.

Caloric restriction not only increases proteozome proteolysis. But also autophagic proteolysis, which may contribute to increased longevity. When you upregulate MTOR you down regulate proteolysis.
The best drug to reduce MTOR signaling, to slow aging and the chronic diseases associated with it is already available. Avoid high protein.

But what is that? What is high protein. You can go to a lot of textbooks that talk about .6 grams per kilogram. But one study that I think is very interesting . . . You can get into a ballpark. When you talk about 2 to 3 grams of protein per kilogram of lean body mass, that is certainly too much protein.

But what is the requirement in an infant, infant, being breastfed. Young infants, 2 months old, have the highest protein need. They’re growing rapidly. Brain is growing. The protein content in breastmilk is about 1 gram per 100 milliliters, and the daily intake is approximately on 1 gram per kilogram per day. That’s what nature says is the requirement of a growing, breast-feeding infant.

When other foods are introduced during the weaning period the protein intake Increases remarkably to 3 or 4 grams of protein per kilogram per day in spite of the fact that the protein requirements are decreasing. The long-term consequences are obscure. Although I think the MTOR signaling are telling us what those long-term consequences might be. A high protein intake has endocrine effects such as it increases insulin, increases IGF, and we know these hormones increase the rate of aging. Furthermore the metabolic effect of high urea and many amino acids may exceed the kidney and hepatic system’s ability to metabolize and excrete the excess nitrogen.

In other words, when you use protein as a fuel, you take off the excess nitrogen, and then you have to do something with it. Because, it’s a poison. If you take too much, It causes acidosis in the blood and that causes redistribution of calcium and magnesium, and all sorts of things, and what the consequence are for that is manifold.

So what’s high. Certainly above 1 gram per kilogram of lean mass is probably high.
Most people, I’ll put on .7 or .75 grams per kilogram of lean body mass.

But if I’ve got a diabetic, and I really want to reverse their aging, which means reverse their diabetes, because diabetis is a model of aging, I’ll put them down to .5 or .6 grams per kilogram of lean body mass per day.

So what’s left to eat?

We know that sugar, foods that turn into sugar, raise insulin, IGF accelerate aging, worsens diabetes. It’s horrible for you. Now I’m telling you that extra protein isn’t good for you either. It appears to accelerate the MTOR pathway and has all kinds of debilitating effect, not the least of which is stimulating cancer.
Fat. Eat fat.

Fat appears not to stimulate insulin. It does not stimulate the MTOR pathway. It does not cause an increase of leptin and in fact it keeps it down. And our health is going to be dependent on what our hormones tell our brains to do, whether to be hungry or not. If you keep leptin down and your hypothalamus can listen to leptin, you are not going to overeat. When leptin is down it stimulates fat burning. It helps diabetes. It helps all sorts of things. I’ve been doing this for over two decades now, and I can tell you for sure it happens.

You have to regulate the hormones that regulate your brain, and you do this by diet, and then you can affect the rate of aging and the incidence of the diseases associated with aging.

 Post subject: Re: Insulin and Its Metabolic Effects By Ron Rosedale, M.D.
PostPosted: Fri Nov 09, 2012 1:40 am 
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Thermogenesis – Not So Good For Health – Ron Rosedale
Sunday, September 16, 2012

LISTEN (30 Minutes)

Ron Rosedale, there are about a thousand ways that a person can look at health research and a thousand details to check. It’s so confusing. To understand how we work and how our metabolism works, what if we start by figuring out what questions to ask?

RON ROSEDALE: - Sorting through confusion—that’s really the way to go. Number one is to ask the right questions. If you don’t ask the right questions, you’re never going to get a useful answer. That’s why, for instance, in my blog on the “safe starch” debate, I posed four questions that really to me summarize what the debate is about, and then I answered them. People often ask the wrong questions, and so they keep getting answers that create a wild goose chase, or bad information. Getting the questions right – that’s a major key.

When it comes to questions, and what “kind of animal” are we, I’m thinking about the recent debates about metabolism. One question that few people ask is, “What’s the point of seeking a high metabolism? Instead, most people simply assume that a higher metabolism is a better one. For instance, in discussions of the recent Harvard study regarding the merits of high carb/low fat, versus other ways to eat, many experts and reporters focused on how many calories the test subjects burned. As background, in the Harvard Study, people ate one of three ways. Two were higher in carbs. The third was high in protein and fat and lower in carbs.

High Thermogenic Meal

ALL the people were fed a deficit of calories that meant they lost weight, and then they were returned to a weight-stable level of calories, but rotated throughout the three different kinds of diets, keeping the calories the same on each diet. The researchers measured plenty – inflammatory markers, hormone signaling, and so on. What many researchers and reporters focused on is that people eating a lower-carbohydrate diet tended to burn more calories than people whose diets included more carbs. I’ll say that again: On the low-carb diet, the test subjects burned more calories a day than people burned on other kinds of diets. That caught people’s attention. Many praised that finding, saying a high metabolism is a good thing, because then, someone can eat more without gaining weight. Does that make sense? Is asking whether someone’s metabolism is higher, with the assumption that higher is a good thing, well, is that the right question?

High Thermogenic Car (from


No, not at all. We shouldn’t be asking the question, “How do I get a higher metabolism?” We should be asking the question, “How do I improve the quality of my metabolism?” Which is a very different story. Anybody can have a higher metabolism. You can do it, for instance, with recreational drugs and diet pills, many of which have been taken off the market,. These for the most part, will actually increase the rate of aging and its symptoms, as will many other ways to “raise” metabolism just for the sake of raising it such as the many “thermogenic aids” in “health food” stores. If you simply seek to increase metabolism, you’re just going to increase the rate of whatever kind metabolism you’ve got going, good or bad. So if you’ve got a less than optimal metabolism, and you just increase the rate of it, you’re just going to increase the damage that it’s doing. That’s what you see in many, many people. And that’s a major problem.

A related problem is a misunderstanding about how the thyroid, and diet, interact with metabolism. One of the major issues that one sees in the so-called safe starch debate, is that the advocates of eating more starches often warn that when you don’t eat carbs, you end up with a lower amount of the thyroid hormone, T3, in the blood, and this is a warning sign of hypothyroidism–meaning too little thyroid function. And that’s just such a wrong way of looking at it. Certainly when you eat a very low-carbohydrate, high-fat diet, the amount of T3 in your blood goes down—but in most cases, even though T3 goes down, your TSH – thyroid stimulating hormone – does not go up. TSH is a kind of thermostatic regulator. When the body actually needs more thyroid hormone, TSH generally rises, and pushes the thyroid to make more T3. When the body is getting enough thyroid, TSH generally stays low. So if your thyroid hormone levels go down while your TSH also stays in the low to normal ranges, it’s probably not because your thyroid is sick, any more than your pancreas is sick when your insulin level goes down on a very low-carbohydrate diet, and your blood sugars stay low as well. When insulin levels go down and blood sugar becomes more normal as well, it’s a clue that your cells are finally becoming less insulin resistant and are getting sensitive to a healthy, low level signal of insulin. In a similar way, a low TSH, coupled with a lower T3 level, is indicative, not of a sick thyroid, but more of proper signaling. You might say it indicates that your cellular resistance to the signals of thyroid is letting up. Your cells are getting more sensitive to thyroid signals, and your T3 level is going down precisely because cells can finally hear the signal properly. So a lower thyroid level, with low- to normal TSH, can indicate that your metabolism is now functioning at a higher-quality level. In other words, you’re getting more bang for each energy buck.

More bang for the buck is also happening, for instance, in calorie-restricted animals who live longer than animals fed a regular amount of calories. In calorie-restricted animals, researchers generally see a lower free T3. They also see lower T3 in centenarians, people who live past 100. When you see a lower free T3, it’s really indicative of kind of a longevity phenotype. It’s indicative of what you might even call, non-hibernating hibernation. And one clue that this lower T3 is healthy is that people who have it generally report that they function better. If it happens to you, on a low-carb diet that you’ve become adapted to over time, you’re not weak. You generally have more energy.

Having your T3 level go lower, in a healthy way, is like being able to turn down the idle of a car when it’s tuned properly, so that at rest it doesn’t have to waste as much energy. In an efficiently running car, the resting “metabolism” of the car is lower. And if you want to get power from that car, if you want to accelerate, that’s better too. When a car is well tuned, it allows for a lower idle speed, and it will actually accelerate faster, and the engine itself certainly will have a much longer lifespan. It’s functioning better.

Well, I suppose that metabolism can go TOO low. For instance, if we wanted our cars to have as low a metabolism as possible, we should keep them in the garage all the time and never drive them.

Zero Thermogenic Car


That’s true. Certainly one would have to then get into the depths of a discussion on what is life, and is the car really being a car if it’s really not doing anything? Is it being any more than a rock? It’s not functioning at all. That gets into more of a philosophical argument, and actually a scientific argument, but that’s probably a story for another day.

That’s a story for another day, but this issue regarding, how do we tell if our metabolism is at the right “idle speed”, it isn’t a question that most people ask. And it’s a concept that’s often missing in debates among experts about what kind of diet is the healthiest. For instance, in the Harvard study, their “low-carb/high fat diet” was actually a rather high protein diet. For years, high-protein advocates said that eating a high level of protein is wonderful, because when you eat a lot of protein, it burns with more heat, and since it burns with more heat, you can eat more of it and not gain as much weight. Does that make sense to you?


It makes sense, but again, it’s the wrong question. Improving health is not whether we gain or lose weight, it’s the kind of weight, number one. For instance, I don’t think anybody really wants to lose just any kind of weight. They don’t want to lose their muscle or their brain or their bones. They want extraneous adipose belly fat to be lost, typically. And if you’re seeking health, it’s not a matter of whether heat is produced, but really where that heat is going. If your body makes extra heat, you want to get rid of heat, number one. You have to get rid of it quickly. Inside the body, excess heat destroys. How about a fever?

High Thermogenic Human

A normal body temperature is less damaging for the body than the higher temperature of a fever. However, our body can handle a fever better than many invading organisms do, because a multicellular creature, such as a human, has more ways to protect against excess heat such as having heat shock proteins than, for instance, a virus does. Furthermore, the temporary higher temperature increases the activity of our immune system, and helps a body produce white blood cells faster. For all these reasons, occasionally, the body will produce a fever in order to kill an invader. If the fever goes too high, it kills too much of us as well. But if it stays at a level the body can handle, it kills off the invader faster. So short-term bursts of high fever, for our bodies, can be a valuable tool. But bodies don’t maintain a fever as a regular thing. Heat is a double-edged sword. It’s part and parcel of any type of energy exchange, and in some cases, we can use heat as a weapon for our body defense, but certainly excess heat destroys. That’s because our bodies, including each and every cell, need to work in a healthy, coordinated way. In contrast, heat is totally random, nonsensical motion that promotes incoordination.

Now, if heat-generation such as a fever, is only good for a short-term battle, it surprises me that some very well-respected scientists will say that it’s good news that eating protein causes thermogenesis, meaning it increases heat. The most common reason that many health experts praise thermogenesis is that, they say it means you can eat more food without gaining weight. Those same experts tend to say that the plague of modern society is that people get too fat when they eat as much as they want and so, the question to answer is, “How can people continue to eat as much as they want, and still keep their weight down?” And for them, the answer is, “Eat foods that take more energy to metabolize, because they make heat in the body and then the body supposedly stores less of the fuel as energy–that is, as fat.” Do you think it’s time for people to stop saying that this approach is healthy?


Yeah, it is.

So, whether it’s a car or a person, simply “fueling up” on something to increase the heat isn’t improving metabolic quality.


It isn’t a good thing. Producing excess heat can contribute to a whole lot of damage.

High Thermogenic Human - from

On the other hand, is it always bad to produce extra heat? As an example, an athlete who’s exercising is making heat. Is that okay?


That’s part of their training, to adapt to getting rid of heat fast. In other words, as they adapt to training, they will sweat more than they did when they began training. They’ll have better circulation to get rid of heat. It’s certainly part of the training, part of what will adapt them to being a better athlete, adapting to excreting heat.

And that’s true with ourselves as well, you think?


That’s true.

Now, some studies indicate that when people exercise more, their resting metabolism actually goes down. So they’re sort of like that car you described, which can idle at a lower speed, but performs faster and better when it’s time to put the pedal to the metal. That is, when they exercise, they produce more heat than someone who’s not exercising as hard. But when they’re resting, they have a lower metabolism. But is an athlete’s way of generating heat a reason to say that producing heat by eating more protein –ie– eating a more thermogenic diet — is that a good thing?


No, not at all. Again, it’s not—I think what you’re referring to then is the rate of metabolism. When a person switches to a low-carb diet, their metabolism overall isn’t necessarily increasing. The rate of metabolism might increase somewhat if they feel more energetic and start exercising more, and resting on the sofa less. And they might lose weight not because they’re burning more calories but instead because their hormones are signaling correctly and they’re less hungry. In other words, what’s happening on a very low-carbohydrate diet is, they’re improving the quality of their metabolism such that they’re able to burn fat properly and more importantly, ultimately enable better leptin and insulin signaling that will more appropriately apportion which fuel to burn when, in other words, when to burn fat and when not to. Most people are not able to burn fat — certainly not as readily as they need to or would want to. And the reason for that is because of inappropriate—or inaccurate, really—leptin signaling and even insulin signaling, more widely known as leptin and insulin resistance.

If somebody switches to eating fewer carbohydrates and they feel wiped out, do you wonder whether that person has adapted to fat-burning yet?


That’s correct. They’re not. For most of the people, and I’ve questioned a number, including many who attended the August, Ancestral Health Symposium at Harvard, most people who mention that they felt poorly when they went on a very low-carbohydrate diet, when you question them in detail, you find they were eating way too much protein–two, three, four times as much protein as I normally recommend. People have within themselves such a fear that fat is a bad thing to eat, unconsciously they avoid it, and the only thing you can eat if you’ve eliminated most carbs and you don’t eat fat, is protein. So when people go on a very low-carbohydrate diet, unless they consciously think about it all the time, they go high-protein, which can make them miserable.

So when people report feeling poorly when they go on a very low-carbohydrate diet—and by the way, most people don’t feel poorly, and many feel much more energetic. But among those who report they feel bad, it’s usually either that they haven’t given the switch to low carb, high fat eating a long enough time to get through the physiological adaptation this switch requires, or, they never get through that adaptation because they’re eating too much protein, or too much carbohydrate. Excess of either of these will prevent you from actually getting through that adaptation. For instance, they lower their carbohydrate some but not enough to really start burning fat. It only takes 100 grams of carbohydrate a day to prevent a person from properly going into ketosis, and therefore supplying the necessary “ketone” fuel for many different body functions that can’t simply burn fatty acids, such as the brain. Or, they eat so much protein, the excess protein raises insulin and also leads the excess protein to be burned or transformed by the body into sugar, and all that keeps them out of ketosis as well. And if you’re not generating ketones because you’re eating too many carbohydrates, or you’re eating too much protein, then certainly initially you’re going to have a difficult time and you’re not going to feel well.

And I wonder whether some people, for instance, Type 1 diabetics who give themselves shots of insulin and also shots of sugar to balance out the insulin, I wonder if the shots and the sugar mean that they never get to the point where their bodies are resilient about adapting to just burning fat.


I totally agree. What you really have to do is, you have to maintain low-sugar in your blood long enough to kind of turn down the glucostat. It’s like a thermostat, only with sugar, with glucose, so that the glucose goes down because you don’t need it so much. You’re training your body so that it’s just keeping a minimal amount of sugar available, and the ability to produce sugar if needed, for anaerobic emergencies, such as running from a tiger. But you’re not keeping excess sugar stores at the ready, because you have to burn sugar all the time because you’re unable to burn fat. Unfortunately, the vast majority of people on earth have trouble burning fat, meaning that they have too much sugar in their diets and in their blood, so they crave sugar all the time because they’re unable to properly burn fat, and I think it really is the base cause of the mass amounts of chronic diseases and premature aging that people are experiencing. These chronic diseases, such as diabetes and heart attacks, wouldn’t be happening if people would eat foods that are very low-sugar-forming carbohydrates, and if they would eat appropriate protein, but not high protein, and then fill in the appetite gaps by eating fat when necessary.

In addition to asking what foods improve hormone signaling, you’re also asking another question. You’re asking “What foods generate the most metabolic heat, simply to digest them, and what foods generate the least amount of heat? The answer to that question gives you a good strong predictor of what is going to lead to the least wear and tear on the body.


It is as simple as that. I don’t know if you read my last blog post on safe starches, where I posed four questions about “safe starches” and then answered them. Afterwards, some people posting comments about my blog brought forth the correct biochemistry, which is that you get many more ATP molecules from an equivalent gram amount of fat compared to glucose or protein. This supported my simple premise that fat is by far the most preferable fuel to burn. Fat producing the least heat and the most usable energy is taken right out of biochemistry textbooks.

High Carb Hummingbird

Well, even if burning fat is so “useful”, is it healthy for everything? Could you feed fat to a hummingbird?


I think you probably could, actually, and perhaps it would live longer. I wouldn’t say it would live necessarily better–for it might have to give up the life of flitting from one flower to another–and eating fat wouldn’t necessarily be ideal to perpetuate a hummingbird genome – for if you could adapt a hummingbird to live off of fat, and you kept it near a great fat source, that individual hummingbird might live longer. But if all wild hummingbirds required fat, they would probably starve to death for lack of available food. They probably wouldn’t have babies. So Nature has adapted hummingbirds to be sugar eaters. And that’s the “nature” of Nature. Nature is not concerning itself totally with longevity. It doesn’t care. It’s concerned about the longevity of the genome, not about the temporary caretakers of that genome, the soma, that is, the cells that keep our body going — in contrast to the cells that are designed to make new babies. Nature’s only concern with our soma, our body, is to keep it going long enough for us to get to the next generation going and help it stand on its own two feet.

What’s natural, I think, is not necessarily what’s healthiest for one particular hummingbird, or person — after all, most people would consider health as meaning that you, as an individual, lead a long, healthy—including post-reproductive-life health—life. Nature, I don’t think, ever really cares much about post-reproductive health and longevity, other than as it pertains to parenting and perhaps grand parenting so that the baby can grow old enough to essentially fend for itself. If you ask the question, “How does longer life of the parents affect survival of the next generation?” then you can answer some puzzles. For instance, why do humans live much longer than chimpanzees?

We take longer to grow up?


That’s right. Human babies are helpless when they’re born, and it takes a long time for them to have a reasonable chance of survival. Longer than it takes for a chimpanzee baby. So Nature has endowed human parents and even grandparents with a long enough lifespan to enable to children to grow old enough to take care of themselves. That’s probably why humans live longer than chimpanzees. But even among humans, there’s a time when the advantages of living longer don’t clearly add benefit to the lives of our offspring. So I think that we have to get away from constantly thinking that what’s natural is what’s best for individual health. So, just looking at the the idea of what’s natural. Just do what’s natural. Eat what’s natural. There’s a big argument about what “natural” actually is. And simply asking the question, “What has been mankind’s ‘natural’ way to eat?” is not the same as asking, “How can I eat to maintain my health and life as long as possible?” But that question of individual longevity is a question we can strive to answer. We can work to use the best science that tells you how nature allowed a human, or perhaps any life, to live a long and healthy lifespan, especially during the time period before reproduction begins, when the needs are highest to preserve vitality. As we find out more about what those secrets are to living a healthy life before the time comes to produce offspring, then we can apply those secrets to both the reproductive and the post-reproductive years. You can apply them at any time of life. For instance, what we’re seeing is that nature has endowed virtually all animal life with a means of outliving a famine so that it could then reproduce at a future, more opportune time. As part of this, all life maintains chemical sensors, hormonal pathways that tell the genes and the genome, and every cell, what the nutrient availability is. And when a body senses food is low, it up-regulates instructions to virtually every cell, making maintenance and repair of that cell a greater priority. It increases each cell’s DNA repair and intracellular antioxidant systems and heat shock proteins and what’s called autophagy, which kind of cleans up the garbage inside the cell faster and better.

One can take what you just said about gearing up to survive a famine to assume that humans are doomed to have to eat and eat and eat because we’re programmed to deal with famines. Is that what you’re saying?


Not really. In fact, eating low-carb/high fat tends to keep appetite very low. When it comes to health, and longevity, and maintaining an ideal body weight, the major secret to this way of eating, is that the “famine signal” that leads to hunger and all the rest is extremely ancient. It must have arisen shortly after life began itself, even with single-cell organisms in the ocean, which means it occurred before there was oxygen in the atmosphere. And life was flourishing for millions, even billions of years, before there was enough oxygen in the atmosphere that “life” was allowed to even use fat as fuel. You have to have oxygen to be able to burn fat. You don’t need oxygen to burn glucose. And therefore these famine signals are dependent on two major nutrients, glucose and protein, certain amino acids, but not fat. And that’s a real key. In other words, if you keep your glucose intake low, such that insulin signaling and leptin signaling stay down, and yes, by the way — the secretion of leptin is largely dependent on how much glucose a person ate. Leptin signaling is influenced by sugar more than fat, even, and that’s something that everybody just argues about, but it’s very, very clear in the literature. But in any event, if you keep your sugar levels low, and also if you don’t eat excess protein, such that you don’t raise a pathway known as MTOR, which senses amino acid and protein availability, you keep those low, it then mimics calorie restriction. Caloric restriction increases longevity in all kinds of animals. But you don’t have to be calorie restricted to gain those benefits, because you can eat fat. It’s kind of a free ride. It doesn’t get the body into believing that you’ve got nutrient excess that needs to be stored away in order to survive a famine, or used to produce a new generation of cells or offspring. It allows the body to stay in the mode of maintenance and repair.

You’re talking about the evolution of our signaling pathways, and how fat helps them stay settled down and promotes more health in us. But could it also be that eating and storing fat is also doing something even more basic? Could it be causing less heat damage in terms of how it’s stored and how it’s metabolized?


That’s exactly true. So one can look at fat as being a much cleaner-burning fuel than sugar, which it is. It does cause less damage than if you were to burn sugar as your everyday fuel. But people around the world are being forced to burn sugar all the time because they can’t burn fat properly, and the reason for that is because the signals that tell you whether to burn fat or glucose, namely leptin and insulin, have been so corrupted over time because of our modern, high-carb diets, in particular, that their bodies can’t properly so-call “fuel partition.” They can’t switch over between fat and sugar properly.

Many animals DO have the ability to switch between fat and sugar fuels very quickly. For instance, a hummingbird drinks basically soda water, and during the day, its blood sugars are sky-high. Over 600-a blood sugar that could kill a human. But a hummingbird burns the sugar fast, and any excess goes into its liver. The liver gets incredibly fatty, but then at night, the hummingbird burns most of that fat away. So it’s got an incredibly balanced system for switching from sugar burning to fat burning.


So when you look at a lot of the animal examples, number one, the key is that nature isn’t really caring if they live a long life. Nature is just trying to get them to live long enough to be able to reproduce. But two, they continue to have proper fuel partitioning, like you mentioned. They can burn fat where and when appropriate. So even though they might store fat in their livers, they can then get it out of their livers very easily and readily. In modern people, the problem with leptin resistance,, is that they can’t easily switch from burning sugar to burning fat. And then they store a lot of abdominal fat that they’re not able to access properly. So it continues to build and then infringe on the vital organ system, such as liver function and heart function, etc. So that is the main problem, and that might take a long time to develop, but once it’s there, it’s a problem. And humans face another challenge that many animals don’t, simply because most animals don’t live long enough to get stuck with this long-term problem. For instance, in humans and in hummingbirds, certain molecular processes, like, advanced glycated end products, take a while to accumulate, and it could be that some of these animals that survive on high-carb fuels just don’t live long enough to be able to accumulate glycation to any great degree that would impair their insulin and leptin signaling.

We know, for instance, that humans live a fairly healthy life through childhood, although now we’re starting to get even so-called adult-onset diabetes in the young. But for the most part, children are much healthier than adults. They can eat, and they do eat lots of junk food, but they don’t suffer from diabetes and obesity and heart disease generally until later in life. And the reason for that is because a young body can make proper compensations for eating poorly. It can burn the excess off faster. Their bodies can increase thermogenesis, so to speak. That extra burning off of energy is not necessarily healthy, but the kids don’t notice it at the moment. But what it does is, it starts the leptin and insulin signaling going wrong at an early stage, which increases the chance that later in life, their bodies can no longer make the appropriate compensations for eating poorly. And then they get problems that we currently call diseases. Their blood sugars go up, and we call it diabetes. They become obese. If we started measuring insulin and leptin resistance or sensitivity early in life, you’d find that there was a progression almost from a moment they were born, in fact even before they were born, depending on what their mothers ate. If a mom is eating a high carb diet, her child can be born already insulin and leptin resistant.

Are some people more fortunate, and their bodies are more resilient at dealing with the hit of transitioning back and forth between fat burning and sugar burning? After all, some athletes say that all their exercise keeps their bodies strong and more resilient at dealing with different foods and also dealing with the generation of heat.


That’s exactly true. The statement that I made decades ago now I think still holds true. The more fat you burn, the healthier you’ll be, and the more sugar you burn, the less healthy you’ll be. Provided you don’t get hit by a Mack truck.

 Post subject: Re: Insulin and Its Metabolic Effects By Ron Rosedale, M.D.
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Insulin, Leptin and the Control of Aging
By Ron Rosedale, M.D. | Published: November 8, 2011

Insulin, Leptin and the Control of AgingHe gave this talk at the American Society of Bariatric Physicians (ASBP) meeting Oct 31, 2006. They’re medical experts who work to reduce obesity. As part of the 2006 presentations, the ASBP included a special segment that featured low-carb diets, researchers and scientists who are connected to the Nutrition and Metabolism Society. Special thanks to Instatapes for recording this presentation.

SPEAKER’S INTRODUCTION: Dr. Ronald Rosedale is an internationally renowned expert on the biology of aging. He was at the International Conference on Aging Medicine at Rio de Janiero, and the first European Conference on Longevity Medicine and many more. He is the author of The Rosedale Diet: Insulin and its metabolic effects. He will be speaking to us this morning on the detrimental effects of too much protein. Please welcome Dr. Ronald Rosedale.

We might give a different view on protein intake and nutrition and actually health in general. First, you hear a lot about paleolithic nutrition, the idea being that ancient man can tell us how to be healthy. That we need to go back to our ancient roots and eat like they did, and then we’ll be healthy. But you have to go back even further and understand what Nature is after. And there are two prime prerogatives of all life, since the beginning of life. And they both involve making more life.

How do you make more life? Reproduce. What do you do to reproduce? You have to eat. You have to eat and reproduce. It’s all life does, and we evolved with those dictums.

We can’t use Paleolithic Man. We evolved with a diet to not allow a man to live a long healthy life.
Nature does not care about us living a long healthy life, or any life, for that matter. Nature wants “Life” to live.

It’s like, you don’t care if there’s a little cell on your hand that dies, as long as the whole remains. Nature doesn’t care if you or I dies, or if all mankind dies. Nature wants life to live. The diet that ancient man grew up with was to maximize reproductive sense. Not necessarily the life of each individual.

We do know, there is a powerful connection between energy stores, reproduction and longevity. Certainly, we know that it takes a lot of energy to make babies. And if there was not a lot of energy around, Nature would put off reproduction, and it is that trick that we want to use. It puts off reproduction by allowing the organism to live longer. It appears that all organisms have genetic mechanisms to delay aging, to delay dying so that the organism can reproduce at a future more opportune time. And generally this is genetically controlled, and it’s controlled by the availability of nutrients, whether it’s good to reproduce now or put off reproduction into the future.

Because of this, we know now that there are nutrient sensors that tell the body and tell the genetics how much nutrition is available right now, and it is a liaison between nutrient stores and genetic expression that determines whether the body will move toward reproduction or maintenance and repair. This is on an organism level and on a cellular level. On a cellular level, increasing reproduction might not be such a good thing because when you push growth and reproduction too far, you stimulate cancer.

We’ll talk a little about diabetes because it’s the quintessential disease of nutrient stores. Ask anyone what is diabetes, and they’ll say it’s a disease of blood sugar. Diabetes is not a disease of blood sugar. If you get nothing else out of this talk today, realize that diabetes is not a disease of blood sugar. It is a disease of insulin signaling. What we have hear is a failure to communicate. Insulin tells the body a very vital message. Not how much sugar to have. The real purpose of insulin has to do with being a switch, a nutrient sensor, that is one of the pathways that will dictate whether a cell reproduces or whether it lives.

Caloric restriction, metabolism, IGF and insulin are integrated into this longevity pathway, and this pathway appears to be conserved through all of evolution.

It’s found in yeast and flies and worms. Everything down to yeast. Not bacteria. Bacteria has a different definition of life. In fact, it never dies. It just keeps reproducing. So you can’t throw bacteria in there. But yeast, flies, worms, rodents, primates, and certainly humans, it appears. Since the discovery of insulin, most studies have focused on the role of insulin in the metabolism of glucose, however a failure of insulin signaling is certainly associated with a shorter lifespan. What we’re seeing over the last decade is a central role of insulin signaling in lifespan. The discoveries indicate that aging is a programmed and well controlled process regulated by the same pathways that affect growth, metabolism and lifespan. It is an evolutionarily conserved process, so you can extrapolate, it appears, to humans, since it appears ubiquitous.

Calorie restriction also appears to ubiquitously extend lifespan in laboratory animals, and so far, it appears to extend lifespan in humans, too. It extends lifespan in yeast, flies, fish, worms, mice, rats, monkeys, and perhaps humans. Some common, consistent effects of caloric restriction include lower fat mass, particularly visceral fat–remember that–lower circulating insulin and IGF concentrations, increased insulin sensitivity, lower body temperature. Flowers live longer if you keep them cooler. It appears to be a universal truth. Lower fat free mass. Lower sedentary energy expenditure. Decreased levels of thyroid hormone and decreased oxidative stress. Reduced metabolism and therefore free radical production is another possible explanation. And there Other effects such as lower body temperature, decreased insulin, decreased IGF, decreased sympathetic nervous system activity, altered gene expression have all been suggested as mechanisms that explain the extended lifespan associated with calorie restriction.

There’s also a connection between calorie restriction and chromatin structure. Genes are wrapped around chromatin, and their expression is often dictated by how well they’re wrapped. Basically, you uncover the genes to read them. Genetic expression is really the importance of genetics. It’s not the genes you have. Every cell in your body other than your sperm and eggs have the same genes. What makes a heart cell a heart cell and a kidney cell a kidney cell depends on which genes are read. That depends on chromatin structure and other molecular mechanisms such as methylation and acetylation and things like that.

This is talking about an important part of genetic expression dictated by a gene called SIR-2 which in the humans, the homologue is SIRT-1, and research at MIT and Harvard has looked and determined this pathway is NAD and NAHD dependent, meaning energy stores, and when SIRT-1 in humans and SIRT 2 in so called lower forms of animals goes up, animals tend to live longer, and it appears it does this by turning off detrimental pathways that can accelerate aging and turns on maintenance and repair pathways that extend lifespan, and at least partially, you can up-regulate SIRT expression and therefore, by suggestion, lifespan, by amino acid restriction.

Interestingly also, SIRT-1 protein binds to and represses genes controlled by the fat regulator PPR. Where have you heard that before? That’s Avandia, Actos. The first one was Rezulun but they had to take it off the market because it killed too many people. They still kept the other drugs on the market. These are supposedly insulin sensitizers. They are NOT insulin sensitizers. That’s just marketing hype. These PPR agonist drugs such as Actos and Avandia actually work by increasing fat mass. They multiply fat cells. They give you a bigger dumping ground to put sugar. So yes, it lowers blood sugar. Only because you turn it into fat. But is that a healthy thing to do?

Okay? You have to ask the right questions.

Is reducing kidney disease a healthy thing to do?
If I could snap my fingers and create a pill that cuts heart disease in half. Is that a healthy thing to do? Well not necessarily if it increases cancer. You have to look at mortality rate. What is the end result?

If you dig deeper into the answers, you always end up face to face with the biology of aging. Because it will give you the answers. If you slow the again process, and that doesn’t mean getting older, longer. that means staying younger longer, it’s probably a good thing to do, and then you’re going to repress the symptoms of aging. You’re going to repress diabetes and obesity and osteoporosis and cancer and arthritis. The diseases and symptoms we associated with aging. The only way we can really make a dent in that is to treat the underlying disease. And that is aging and that is a disease. In laboratory animals we can manipulate the process of aging to step back in time to a time when it no longer had diabetes. So it isn’t just to prevent disease. You treat disease this way.

Insulin/IGF represents a family of growth factors that regulate metabolism, growth, cell differentiation and survival. It links insulin action to the map-kinase pathway of cell division. Here’s a very important gene, one of the first genes that was discovered that can extend lifespan is DAF-2 discovered by Cynthia Kenyon at University of California in San Francisco that amazed everyone. They didn’t know at the time what it did, but they did know that DAF-2 mutants can live four times longer. They found a moderate decrease in insulin IGF-1 signaling has been shown to extend lifespan in mice. It’s associated with lower levels of insulin, and it’s similar to the improved insulin sensitivity that you see in caloric restriction.

In mouse models, decreased food intake can extend lifespan, and there’s a special role for insulin signaling in fat in the longevity process. Reduced fat tends to lower insulin and protects you from diabetes. They found, by testing various tissues that if you just reduce fat levels, and you enhance insulin sensitivity while reducing fat levels in fat tissue, you extend lifespan. So it doesn’t have to be all over. Fat tissue is a particularly important part of this process. Just a moderate decrease in insulin and IGF signaling has been shown to extend lifespan in mice. This was done by a friend of mine, Andre Bartke and he’s done a lot of studies in mice and shows that if you down regulate insulin and IGF signaling, and you increase insulin sensitivity, you can increase lifespan in mice. A couple of years ago he won the Methusula award. It’s given to the researcher who can extend the life of a mouse the longest. I think he’s extended lifespan about six years now in mice. The normal lifespan is two years. What they’re doing in these laboratories is amazing. They’re tripling lifespan. They’re doing it by the same pathways of genetics that we have in humans. They’re going into the genetics of it, which we can’t quite do in humans yet. The genetics are altered by nutritional stores and nutrient sensors. We do have a way to dig into these genes. Maybe not with pliers yet, but by what we put in our mouths.

Centenarians, people who live to be 100 or older, have lower insulin and IGF levels. One of the nice ways to study aging in humans is on centenarians. Centenarians, they’ve been showing now for quite a few years that there are differences among centenarians. They eat different diets, they smoke and have different personalities. There are not a lot of similarities between centenarians. But they universally have lower IGF, lower insulin, lower temperature and lower thyroid levels. Those go together.

Conclusions: Strong similarities exist between insulin and IGF systems. Maybe linked to oxidative stress, lifespan. It suggests that the Insulin-IGF system arose early in evolution and it is an essential component of anti-aging systems which is conserved from yeast to humans.

Now let’s look at a slightly different view on how insulin works. The typical thinking is that the most important organs that will determine whether a person will become diabetic is how insulin sensitive the muscles, fat and liver are. But that doesn’t seem to be the case. In mice, they turned on and off genes of insulin receptors in different tissues of the body. They determined that the two organs most important by far in determining whether an organism will be diabetic or not are whether it has insulin sensitivity in the brain and liver. Two big keys in determining health and diabetes. These researchers say that we’ve overestimated how important insulin is in muscle and fat and underestimated its importance in other tissues.
This is where we get to leptin.

How many people have heard of leptin? Unfortunately there hasn’t been as much publicity on leptin as there probably should because there aren’t yet any drugs to control it. But leptin is very critical to your health. We’re going to spend time talking about it and its connection to the diseases of aging and actually aging itself. It has a key role in regulating glucose. We get to the brain-liver circuit, which regulates glucose. Brain will tell the liver how much sugar to make. About half the sugar you have floating around in your body on a day to day period depends on how much your liver manufactures. The other half is how much sugar you put in your mouth. I agree with Mike and Mary Dan Eades and many other people about the importance of not putting a bunch of sugar in your mouth. If you want to keep your insulin and sugar low, it doesn’t take an Einstein to figure out, just don’t eat it. You want to keep low the amount of sugar you put in your mouth. That means all the foods that turn into sugar, even rice, potatoes, cereal, pasta, bread. Those are just other names for sugar. Bread is just a slice of sugar, potatoes are just a lump of sugar. Within minutes after swallowing it you just digest these foods into sugar. Fastest way to up-regulate IGF and insulin and sugar and accelerate aging and all the diseases associated with aging is by eating sugar. We’re not going to go there. The mountains of evidence that show that a high carbohydrate diet is bad could fill this room. We’re going to assume we’re on common ground, that eating sugar is bad for you. One of the reasons is because of the up-regulation of insulin and IGF which accelerates aging. One of the ways you up-regulate sugar is that your brain takes signals and tells your liver to manufacture a bunch of sugar. That’s why diabetics can wake up and find their sugars are higher than when they went to bed. They haven’t eaten for twelve hours and their sugars are high, sometimes higher than when they went to bed. It’s because the liver is pumping out glucose. The major control of the liver is the brain. What controls the brain? The hypothalamus. There is cross talk between the brain and liver that couples central nutrient sensing to peripheral nutrient production, ie, glucose. Disruption may lead to hyperglycemia, and that crosstalk between the brain and liver, and the central nutrient pathway involves leptin, your fat. Leptin modulates the meal regulated food intake. It leads to Increased vagal outflow to the liver which produces more sugar. Your fat speaks to the brain via leptin, and is supposed to tell it how much sugar to produce.

We go back to the beginning.
What we have here is a failure to communicate. That’s how you get sick.

We’re ten trillion cells. They have to communicate with one a other. We think of ourselves as a single individual. Well, we’re not. We’re more like a beehive or an ant colony. There has to be constant and really harmonious signals hitting each and every cell, all the time, and when the communication goes awry, you get sick. That’s the difference between life and death. If I died right now, I’d have the same parts. But they wouldn’t be speaking to each other properly.

Leptin modulates glucose by acting as an insulin-sensitizing factor in most insulin-target tissues. Leptin can modulate, in an inhibitory manner, insulin sensitivity, Directly as an autocrine signal and indirectly through neuroendocrine pathways. These pathways may be relevant to conditions caused by hyperleptinemia, such as in aging. As we get older, and as indicated in accelerated aging, and in people who are older chronologically, they have higher levels of leptin, due to leptin resistance. Almost all fat people have high levels of leptin. Fat is associated with diseases of aging. Leptin is a pro-aging hormone. You want to keep it down. Not up.

Are people here familiar, cause I’m skipping over and assuming people are familiar with what leptin usually does.

Here’s a very brief review. Leptin was discovered about ten years ago. Produced by fat. It’s supposed to tell your hypothalamus how much fat you’ve got and whether to produce more fat. And whether you should keep eating to produce more fat or get rid of some excess. In our evolutionary history, it was good to store some fat. All of our ancestors encountered a famine. You needed to have a good energy source. Fat’s a good, efficient energy source, but it wasn’t good to be too fat, because if you were too fat, you were going to end up as a meal for another organism. Because if you are running from a lion in a group of people, which one is it going to catch? If you got too fat, the lion catches you, because you can’t run up a tree. And those genes would have been eliminated from the gene pool. Leptin tells the brain how much fat there is, and whether you should get more fat or you shouldn’t..

Which means, leptin controls whether or not you’re hungry.

It, leptin, knows people are only going to do what they feel like doing. The only way to get people to lose weight is, which means to lose fat, is to get people to not eat too much. That means they can’t be hungry. Trying to not eat in the face of hunger is an impoosibility, it’s bound to fail. That’s why you see this yo yo dieting. If you’re hungry, ultimately, you’re going to eat. It’s like holding onto a cliff. You look down two miles, and you know if you let go, you’re going to die. Gravity is unrelenting. So is hunger.

Therefore, there are signals to the brain that will tell you how hungry you are. These are the same things that will control, also fat storage. The same master signal that controls hunger also controls your ability to store and burn fat. It also controls how much sugar is available. It also controls through the nutrient sensing pathways, the rate of aging, and therefore the diseases associated with aging.
I can’t stress how important that is, because no drugs control it. You can control it by what you eat. Very important, because you dig right into the same genes that are regulating all these aging process in all these laboratory animals.

If you inject leptin into the brain, right into the hypothalamus, you increase glucose uptake. All those people who are hyper-leptinemic, they have high levels of leptin because their brains can’t listen to leptin. If your hypothalamus can’t hear the leptin signal. If you’re a fat slob, and the fat signal’s trying to yell, quit eating, and the brain can’t hear the signal, it’s getting a whisper, and it’s not hearing the signal to stop being hungry. It’s hearing that you’re too skinny and there’s a famine and you need to eat more fat, and so that’s what you’ll do. There’s a disconnect. A failure to communicate. So you make more fat, you make more leptin, until finally the volume goes high enough that your hypothalamus can hear it, but in the meantime, you’ve increased your set point for how much leptin it takes, and how much fat you have,df before your hypothalamus can hear the signal. You’ve got much more fat than you should have had, if your thalamus had better hearing. You have to restore that hearing.

It appears that with insulin resistance, that’s because your cells can’t listen to insulin, so your pancreas produces more insulin so your pancreas can yell at your cells. Because speaking normally wasn’t getting the message through, so your pancreas has to yell. That’s not a good thing because you raise insulin and accelerate aging.

Same thing appears to happen with leptin. Hypothalamus can’t listen to leptin. You have to yell at it. Well, Increasing leptin so it can be heard has detrimental effects. One of the things is increased glucose.

Leptin prevents triglyceride accumulation, provided it can be heard. Well, fat regulates insulin sensitivity. Leptin also regulates glucose homeostasis independent of energy balance. Leptin has a direct effect in promoting glycemic control. It acts directly on insulin production by the pancreatic beta cells, apparently through signals sent through the vagus nerve. Leptin goes up, you make more sugar.
Just remember, your fat apparently is in charge of your brain.

We kind of thing of the brain as being in control. Fat influences your brain. It’s not just an ugly energy storage tissue you’ve got to get rid of. With the discovery about ten years ago that fat is an endocrine organ that produces hormones that regulate lots of important processes in the body, we now know that your brain listens to fat. When I say we’re ten trillion cells that need to listen to communication signals, it’s kind of like the military. You’ve got generals and colonels and lieutenants and captains. It appears from what we know thus far, that leptin is a four-star general. I put insulin as a three star general. Reproductive hormones and insulin listen to leptin. Thyroid listens to leptin. And ovarian hormones. They listen to instructions from above. Leptin appears to integrate everything, including aging. Your lifespan will be determined by the communication of hormones, primarily insulin and leptin.

Hypothalamic arcuate nucleus . . . Leptin signaling in the arcuate nucleus is an affect on glucose. The restoration of leptin signaling remarkably improves the homeostasis of the mouse. Eight weeks after treatment blood glucose levels fell.

Deficits of leptin activity in certain regions of the central nervous system might underlie type 2 diabetes. We think of diabetes being a disease of blood sugar. No. Insulin signaling? That’s what I thought. Now, It appears that leptin might actually supercede insulin in causing or treating diabetes.

Here’s a study that raised eyebrows. After you’re born, everybody thought your brain had fixed neuron connections and they showed that leptin actually changes nerve endings in the brain to do its bidding. If it wants to make you hungry, it doesn’t just do it by neurotransmitters. The “fat brain” actually changes the anatomy of the brain, and leptin is a crucial regulator, including synaptic plasticity and axon guidance within the hypothalamus. Links between nutrition and adipocyte driven instructions from leptin . . . leptin makes you hungry, it actually changes the anatomy of the brain. It’s talking about the fat brain accesses a new dimension in the journal science. Axon guidance within the hypothalamus.

Very important clinical implications. Leptin controls not only how fat your are, but where you’re fat. For a long time we’ve heard about the apple shape versus the pear shape. The apple shape is associated with much more detrimental physiological processes. The pear shape might look ugly, but it’s not particularly unhealthy. It’s visceral fat versus subcutaneous fat. Visceral fat is a totally different organ than subcutaneous fat. It produces different hormones. Visceral fat is really bad for you. If you’ve got visceral fat, it’s because of leptin resistance.

Islets within the pancreas can get fat. We think of ourselves as a single individual. We have to think that we’re 10 trillion cells, and cells can get too fat. Just as getting fat is not good for us, being fat is not good for cells. Beta cells in the pancreas can get fat, and when they do, they can’t produce insulin properly. That’s another way that leptin controls glucose and determines whether you’re a diabetic or not. Whether the cells are getting fat or not is being proposed to be caused by leptin. We propose the signal is leptin and its function is to create for adipocytes a monopoly on fat storage, to maintain a constancy of intracellular triglycerides and adipocytes. So when things are working properly, you store fat in fat cells. When the signals or getting messed up, you start storing fat in other places,and it’s when you start storing fats in other places you get really unhealthy.

Bears get really fat prior to hibernating. But bears don’t get heart disease, because their fat is stored almost all in subcutaneous fat, not in visceral tissues. So being fat doesn’t make you sick. Being fat in the viscera makes you sick. Being fat in places other than the subcutaneous tissue makes you sick. And that’s determined by leptin.

The other tissue that’s very importantly regulated by leptin is the liver, via the vagal nerve from the hypothalamus, but it also determines how fat the liver is, and a few studies here talk about non-alcoholic fatty liver disease. Fatty liver is grossly under-diagnosed. It affects at least two thirds of obese people, perhaps more, and also some people who are not obese. It almost totally parallels the incidence of the so-called metabolic syndrome, and many people believe that metabolic syndrome is actually caused by fatty liver. Which is determined by leptin.

Fatty liver disease is strongly associated with diabetes. High cholesterol. Hypertension. The process starts when there’s so much dietary fat in the blood it can no longer be stored in normal places such as fat cells.

Leptin treatment decreased visceral fat specifically, supporting the role of leptin in determining fat distribution. That’s a very important role of leptin. Determining not only whether you’re fat, but where you’re fat. Perhaps more important.

We’re talking about cardiovascular disease now. There’s a link between insulin action and cardiovascular disease. And Insulin resistance in the development of diabetes can be reduced by preventing the age-dependant accumulation of visceral fat.

When you do liposuction, it doesn’t really help health by taking out subcutaneous fat. It didn’t really help diabetics. But if they took out the omentum in mice, they could totally reverse diabetes in mice. So they’re starting to do this in humans, at Vanderbilt. Leptin activity increases aromatase activity, in visceral fat (not subcutaneous), which converts testosterone and estrogen, which is why you see all these overweight men with breasts. That’s because of an increase in aromatase, and that’s not good because it’s also a powerful increaser of cancer, particularly prostate cancer.
Leptin is linked to autoimmune diseases.

Some of this has to do with how it promotes hypoandrogenicity. Leptin is also a powerful pro-inflammatory agent. You’ve heard of the link between chronic inflammation and cardiovascular disease. Leptin is itself an inflammatory cytokine. But it also dictates the production of interleukins and TNF alfa, Which are pro-inflammatory agents linked to heart disease and diabetes.

Leptin is a novel independent risk factor for coronary heart disease. Leptin enhances the calcification of vascular cells. This was new to people. Leptin also helps control osteoporosis. It helps control where you put calcium. We think of osteoporosis, and women are being given the dictum to take a bunch of calcium. As if osteroporosis is caused by a lack of calcium. That is ridiculous. That’s like saying, I’m going to put a bunch of bricks on an empty lot, and stand back and watch a house be built. I could take a cup calcium carbonate or coral calcium, any type of calcium you want, and dissolve it in a bucket of your blood and stand back and watch for the better part of eternity and I would never see a bone form. And you won’t see a bone form. It won’t happen. You have to have the right signals to make bone. And there’s a powerful correlation between ostereoporosis and calcium buildup and plaque in arteries. You’ve got the calcium but you’re putting it in the wrong place. Just as you can end up with fat in the wrong place, with calcium, whether it’s put in the right place or the wrong place, lot of it is apparantly controlled by leptin. Leptin kind of dictates where you put calcium.

How can one hormone make a difference in all these different things? It has to do with leptin’s ability to control the rate of aging. Aging, or the lack of it, is determined by proper communication. When that communication goes awry, all kinds of things go wrong.
They have shown leptin inhibits bone formation.

Leptin controls osteoblastic activity in bones and vascular cells. High leptin inhibits bone formation via the hypothalmus. And the arterial wall may be an inportant target for leptin action. All the treatment for osteoporosis has to do with osteoclastic activity. Osteoclasts break down bone. They want to prevent the breakdown of bone. The drug treatments don’t make new bones.

But bone strength is determined by the protein content, not the calcium content of bone. It’s the flexibility of bone, which has nothing to do with bone density. It’s the protein content of bones. You want to have protein, you need protein, but you want it in the right places, and you want it in the right amount. High leptin levels are a potent inhibitor of bone formation.

Life is not in the parts. We’re all made of the same stuff. it’s what you, or more accurately, your hormones, do with the parts, that will will determine whether you’re healthy or not. That’s really the way to think.

By changing leptin sensitivity, the Hypothalamic set point can be reversed. In regards to leptin levels, there’s a Possible role of protein.

You know, leptin controls sweetness. I’m just recognizing that this is my next talk.

It doesn’t matter. The problem was, they’re both so linked. You got off easy. I really blast protein in the next one!

I just talked about leptin regulating inflammatory responses. So this is a talk about hormones and aging. The next talk is going to go into problems with proteins and aging. And we’ll go a bit deeply, through a pathway called the M-TOR pathway.

How many people have heard of M-TOR? A couple of people. Not too many. It’s extremely important. It’s another nutrient sensing pathway. You have insulin that senses sugar stores, and leptin that senses fat stores. M-TOR senses the amount of amino acids available and also regulates aging similar to insulin but using amino acids as the key to energy stores. The two major sources of nutrition that determine whether an organism will reproduce or live longer, you have to have fuel available and you have to have parts available. The fuel early on was glucose and not fat. These signals arose in evolution was very long ago. It’s a very ancient mechanism when there wasn’t oxygen in the atmosphere. Life had to flourish before there was oxygen in the atmosphere. Plants had to flourish before they put out oxygen, so these pathways arose with glucose as the fuel availability, and amino acids for the parts availability, and those are the two things you need to make more cells.

So the next talk, we’re going to talk about the MTOR pathway that dictates the amino acid availability and how it plays into the aging process.

Getting back to hormones — Reduced leptin concentrations lead to reduced temperature. You live longer. Temperature kills. You heat something up and it disrupts molecules. It denatures proteins. If you’re going to live longer, one of the ways is by toning down the temperature. In dietary restriction, there may be diverse mechanisms, often known as calorie restriction.

How many people have heard of caloric restriction as a way to enhance lifespan. The dictum has been that it’s strictly a reduction of calories. It doesn’t matter where they come from. As long as you restrict them, you’ll live longer. What they’re showing in more recent studies is that is not true. There are specific nutrients that you can restrict that mediate the effects of dietary restriction. In this particular study by Linda Partridge in London, who’s done a lot of work with aging, the reduction of either dietary yeast or sugar can reduce mortality and extend lifespan by an amount that’s unrelated to the calorie content of the food, with yeast having a much greater effect per calorie than sugar. Get that. Yeast having a much greater effect per calorie than does sugar. Yeast was the form of protein they were feeding these animals. So when you reduce protein, you live longer.

Here, they’re showing that a fall in leptin is one of things that mediates dietary restriction. If leptin doesn’t fall, you’re not going to live longer. In normal men, a fall in leptin in fasting may be both a necessary and sufficient physiological adaptation of these axes, which has to do with hypthalaumus, pituitary, gonads, IGF, thyroid. You have to drop leptin, or dietary restriction is not going to help.

Dietary restriction explained from an evolutionary viewpoint is an adaptive response by the neuroendocrine and metabolic response systems to maximize survival during times of food shortage. Adipose tissue is recognized as an endocrine organ, and leptin secreted by the adipocytes seems to be an especially important factor for the adaptive response to fasting and neuroendocrine response under caloric restriction.

The one known way to extend lifespan of every species studied since 1933 has been to reduce calories. Since that time, the emphasis has been to figure out why. Ten years ago, they discovered a gene that can control aging, Age-1 gene, discoered by Tom Johnson at the university of Colorado, and Cynthia Kenyon with DAF-2 expanded on this. These all link to nutrient sensors and it all links into a pathway that governs maintenance and repair or growth. They’re all linked to nutrient receptors, and it appears that in mammals, leptin plays a key role, and those animals that use fat as a prime energy store, leptin plays a key role in the aging process.

Prior to leptin, and it appears that they’re cousins, it was Insulin and IGF. Insulin and IGF in ancient organisms, insulin and Insulin like Growth factor were the same. Over time they evolved to have separate duties. Now insulin is more metabolic, and IGF is more anabolic.

Leptin has been proposed as a potential candidate for the adaptive response to Caloric restriction.

This was a longer talk than the other one.

So we’ll have to hurry.

A hypothesis for interpreting the extension of life from caloric restriction posits that normal food intake is geared toward optimizing the internal milieu for reproduction. That’s what Nature is after. Not after health. Nature doesn’t care whether you’re healthy or not. We have to use this trick, however. Nature wants us to live long if it thinks we can reproduce better in the future.

In our ancient life, that was dictated by fuel availability. We can use the science to regulate the nutrient sensing pathways to improve our lifespan and our health.

Here it’s showing that leptin is very much involved in reproduction.

Skinny women, women marathon runners stop ovulating. Inject them with leptin and they’ll start ovuating again. Reproduction and eating are the two main endeavors or all life, and they’re both controlled by leptin.

DAF-16, I don’t have the time. Here, it’s showing that Daf-16 is one of the genetic components that mediates caloric restriction. They’re finding that just activity in the intestines — In C-elegans, the intestines is where it stores fat. DAF-16 in fat, Determines lifespan in the worm.

Signals from fat regulate genetic expression.

Here again, talking about the importance of fat tissue in longevity. Leptin controls whether you’re satiated or not. It also has to do with life extension. With PPAR alpha. Not PPAR gamma. PPAR gamma is what people are taking drugs for. PPAR gamma accelerates life and reduces lifespon. PPR Alpha enhances lifespan. Exactly the opposite. Leptin modulates this through the PPR system because PPR gamma influences a lot of what happens in fat.

Failure of leptin suggests leptin plays a major role in dietary restriction. There’s a link between leptin concentration, with higher levels linked to telemere shortening, which is another theory for aging, that shorter telomeres reduces lifespan, and telomere shortening is controlled by leptin. Waist-to-hip ratio correlates with leptin levels. Centenarians have lower waist to hip ratio. Longer lifespan was predicted by lower levels of leptin. Here, they’re showing that a bunch of amino acids stimulated leptin production.

One of the ways that leptin is elevated that causes hyperleptinemia is caused by high levels of amino acids.

Whereas a high fat diet is associated with low leptin.
In membrane composition, insulin and leptin regulate the types of fat found in membranes.

Talking about IGF again and membranes, that omega three fatty acids improve leptin sensitivity.

This is a study that hasn’t been published yet, that is a collaboration between myself and Eric Westman and John Konhilas. What we’re showing is that a high fat, adequate protein, low carbohydrate diet with nutritional supplements in an outpatient setting, resulted correlates of aging. There were reductions in body weight, triglycerides, insulin, glucose, leptin, free T3 The same things you see with caloric restriction. But we were not restricting calories. The reduction in insulin and leptin levels was strongly correlated with reduction in weight, but the reduction in leptin levels was far greater than the initial weight loss. In other words, leptin is not dictated by how fat you are. It’s dictated by what you eat. Sugar increases leptin output, and amino acids increase leptin output.

You don’t have to have any sugar, but you have to have some protein. But you don’t want too much. Too much protein raises leptin and accelerates aging.
Your brain is a servant of your fat, your brain is what fat uses to do its bidding, and your fat’s bidding will determine your lifespan.


 Post subject: Re: Insulin and Its Metabolic Effects By Ron Rosedale, M.D.
PostPosted: Thu Nov 15, 2012 1:55 pm 
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A Conclusion to the ‘Safe Starch’ Debate
Ron Rosedale M.D.
A more complete version with additional comments about Kitavans, thyroid, nature, and more…

I understand where Paul Jaminet, Chris Kresser and other ‘safe starch’ advocates are coming from, sort of; that if we have to maintain a certain level of blood glucose anyway, then why not eat it? I don’t need to hear more arguments that say that glucose is necessary for mucus; glucose is necessary for protein, etc. I could even add that glucose is needed much more importantly for self-recognition to help prevent autoimmunity (and I believe non-enzymatic glycation can mess that self recognition up), and many other purposes. I agree. I repeat; I agree that glucose is a necessary component of life. Few, I believe, deny that. However, this does not imply that glucose is an essential dietary nutrient or that we must, or even should, eat it. Being a necessary component of life and being a dietary necessity are far from the same. Cortisol is necessary for human life yet you don’t need to eat it, and rarely should. As with so many biomolecules, it’s far preferable to let the body adjust the levels depending on needs.

Paul Jaminet correctly states, as an example of glucose’s importance, that even in a state of starvation blood glucose is maintained right up until death. However, what this really shows is that even if you are starving, and eating no carbohydrates, or fat, or protein, there is no such thing as “glucose deficiency” (unless insulin toxic or relatively rare conditions where glucose cannot be made sufficiently, such as cortisol deficiency, but the ‘safe starch’ advocates are not referring to this). The body can easily make what it needs.

When you eat starch it is digested into glucose and before it goes anywhere it first enters the bloodstream. All you will accomplish then by eating starch is to raise the blood glucose further. Therefore, one cannot correctly talk about a glucose deficiency from not eating enough.

One needs to rephrase the question from, “Are ‘safe starches’ necessary to eat or even beneficial?” to…

Question #1;

Is it better to eat the requisite glucose, or let the body make it?

The ‘safe starch’ debate boils down to whether it is better to eat the requisite glucose, or let the body make it when necessary. I believe strongly in the latter. We can never know exactly how much and when we will need extra glucose depending on environmental circumstances.

Furthermore, when you eat the glucose, there are different effects than if your liver made it, namely it circulates for hours and leads to a spike in insulin and leptin, that circulates for hours, that over time will contribute to insulin and leptin resistance…that ultimately contributes to metabolic chaos and resulting chronic diseases of aging including obesity, diabetes, cardiovascular disease, osteoporosis, autoimmune disease, cancer, and others.

I have long summarized health by the ability to burn fat… or not.

Eating glucose i.e. “safe starches” will spike insulin and will, at least temporarily, prevent one from burning fat…anyone.. a worm, a mouse or any human. It will raise leptin and will remove one from the healthy calorie restriction phenotype (see below).

Glucose, like all parts, must be orchestrated; where, when, how it is used is what will determine health and life. The use of glucose, just like cholesterol and all biochemicals in our body, must be orchestrated. Let’s not mess that orchestration up by forcing that glucose on us at a time, place, or purpose that is likely not in tune with what the body, or brain, wants or needs. Let’s not mess with the orchestra unless we are absolutely sure that we totally know the score.

When we talk about significance of starches, safe or otherwise, the most important factor is their effect on hormones and other biochemical pathways that affect the harmony of 15 trillion cells needing to act as one for life and health. And all starches raise insulin and leptin levels…a lot…having a long term adverse effect of insulin and leptin resistance; cells not being able to properly hear their life-giving messages.

Paul Jaminet and all the other safe starch advocates concentrate on blood sugar…and though it is unwise, to say the least, to eat glucose when one is trying to keep blood glucose down, diabetes is not a disease of BS, but of insulin, and more importantly, leptin resistance. It is the effect of eating “safe starches” on insulin and leptin resistance that must be acknowledged and stressed.

Disease is not as much from the parts but much more from the misinformation given them.

Life is in the instructions, not the parts. It is not a lack of substrates, parts, that is generally the problem, but the instructions of what to do with the part; the effect on hormones that tell the part what it needs to be doing to maintain the health of the republic of parts and cells..

It is not an excess of cholesterol that causes heart disease.

It is not a lack of calcium that causes osteoporosis.

Disease is not due to glucose, excess or deficiency, but the communication that tells it what to do…and sugars, more than most anything, by non-enzymatic glycation and insulin and leptin resistance, messes up that communication.

Question #2;

If the body can make all the glucose it needs from other biochemicals, called gluconeogenesis, are there potential adverse effects from this?

This is a whole different story than talking about glucose deficiency. Furthermore, any potential adverse effect of gluconeogenesis would be determined from the initial precursor; whether one is using amino acids to manufacture glucose or other substrates that are extremely benign such as from ketones, the glycerol backbone of fats, or from lactate recycling. Those latter sources of glucose substrates separate from amino acids, under adapted carbohydrate and protein restricted conditions, can virtually make up the entirety of precursors for whatever glucose might be necessary.

Most people on my diet actually gain lean mass without increasing exercise, via protein sparing and increased sensitivity to insulin. Therefore, one can’t be burning much of their lean mass/protein, if any. They are deriving their fuel from ketones, glycerol, recycled lactate and pyruvate. This is perfectly healthy, more so than burning glucose.

Fat is a great fuel, the best fuel, furnishing fatty acids, ketones, and glycerol (that can turn into glucose if necessary), to burn. I encourage you to see the fine summary of the great advantages of burning ketones at AHS 2012 by Nora Gedgaudas. However, one needs at least two weeks to adapt to properly burning fat, more if older or overtly metabolically challenged. I maintain that the symptoms that people are experiencing occasionally and calling glucose deficiency are nothing but inadequate adaptation to properly burn fat by either consuming too much carbohydrate or eating excess protein.

Gluconeogenesis from protein requires deamination (cutting off the nitrogen), and the nitrogen molecule is then used to manufacture ammonia and urea that are both poisonous. This is why urine is called urine. Burning protein is not healthy, but if you can’t burn fatty acids or ketones and you are limiting carbohydrates you will have no choice but to make glucose from protein, either from what you eat, or from your muscles, bone, or other protein sources. You will not be too happy. The trick then is to not eat more sugar/starch, but to adapt to burning ketones and fats…by eating less sugar, not eating too much protein, and eating fat if hungry. You learn to ski by skiing. You learn to burn fat by burning fat.

Question #3;

Is it that important to eat less than 100 gm starch?

Answer; Yes; that is where the deeper benefits lie. That is when one gets into ketone burning and when one can get into the calorie restriction, longevity phenotype.

The worst diet to be on is high fat along with moderate and sometimes even low (as opposed to very low) carb. If you are going to eat fat, you have to be able to burn it, and as little as 100 gm non-fiber carb/day can prevent one from adequately burning fat and ketones. If one is going to properly follow my high fat diet, one must go all the way; very low sugar forming carbohydrates, and no more than adequate protein.

According to George Cahill, perhaps the world’s foremost expert on the metabolism of ketones and starvation, 100 gms/day of sugar forming carbohydrates i.e. starches is all it takes to prevent one from burning and therefore adapting to burning, ketones.

The best diet allows for maximal burning of fat and ketones. This is also a high fat diet, but where non-fiber carbs are kept very low and protein is not consumed in excess. (For most, this is between 50-70 gm protein/day depending on lean mass, exercise, growth and pregnancy.) There is a tipping point where a high fat diet goes from not so good to great as non-fiber carbs and protein are further lowered.

As one follows my diet more closely, meaning as little non fiber carbs as possible and avoiding excess protein (above 1 gm/day/kg lean mass for most), the beneficial returns not only increase, but accelerate.

In a diabetic, as one lowers their sugar intake, one will generally lower their blood glucose, at least to some extent. But don’t get fooled into believing that the greatest results possible have been obtained. Do not confuse better with best or even good. It is easy to do better. The typical diet is so bad that most any change will lead to improvement.

You won’t see the really deep benefits of actually lowering the “glucostat” and reversing hormone signaling resistance in the hypothalamus and morphing into a longevity phenotype until you get into what the brain and body thinks is not necessarily starvation in general but glucose starvation, whereby genetic expression will be totally shifted towards maintenance, repair, and longevity that would relate to both disease prevention and reversal. This metabolic adaptation to nutritional availability was set during extremely ancient times shortly after life began around 4 billion years ago and long before fat was used as a fuel, long before paleolithic man, when glucose dominated the oceans and was what to eat.

Question #4;

Is the VLC diet only better for “sick” people?

What I said 20 years ago is just as true today; Carbohydrates should be defined as fiber or not fiber. Any carb that is not a fiber will turn to sugar and will cause harm…for any and everyone, males, females, monkeys and worms. The only difference among the sugars and non-fiber carbs is how fast and how much harm will be caused.

In everyone, when one eats starches it quickly turns to sugar, glucose, fructose, galactose, etc. that will circulate and glycate the collagen that lines the arteries causing inflammation and cardiovascular disease and all of the other adverse effects of glycation. This causes inflammation secondary to the AGE-RAGE reaction. Raising glucose raises insulin increasing risk of cancer. This is not safe and should not be called a safe starch. ‘Safe starches’ is an oxymoron.

One should not discuss effects of starch only on blood glucose. What about intracellular glucose? If you eat that sugar and it’s not in the circulation, where is it? Much gets pushed inside cells causing intracellular glycation and cellular harm. Lots will turn into liver fat. It has to go somewhere, and wherever it goes it will do damage. This is why it is better to talk about glycemic load than glycemic index. All sugar eaten will cause damage.

EVERYONE who eats starch will raise their glucose and/or insulin…a lot. Keeping glucose down by raising insulin is doing one no favors; just trading one evil, elevated glucose, by an even worse evil, high insulin. (See “Insulin and its Metabolic Effects“). This was shown clearly by the ACCORD study.


If diabetes were properly diagnosed as improper metabolic signals, especially from insulin and perhaps even more importantly from leptin, then we all have diabetes to one degree or another..

Paul Jaminet and Chris Kresser have stated that maybe a very low carb diet is better for those who are sick with metabolic diseases, but not for ‘healthy’ people. However, we all are in various stages of metabolic disease. We all have some degree of insulin and leptin resistance. Most wake up recovering from their dietary insults and are the most insulin sensitive they will be the whole day. In other words, we all have some degree of diabetes, if it were diagnosed properly.

When you eat a so-called ‘safe starch’ meal, many people’s blood glucose, if not most, will go above 126 mg/dl, meaning that if they were fasting, they would by definition be called a diabetic. The fact that they were not fasting does not mean that the glucose does not do the same harm as if they were fasted. Eating several such meals/day would mean that the supposed ‘healthy’ person was ‘diabetic’ most of the day and perhaps only upon awakening was the BS at a healthier range…and this is saying nothing about insulin and leptin levels and resistance, where the underlying disease actually resides.

Life’s commonalities are much more critical to life than the differences, since life can’t live without them. (See my next blog, an essay I had written a few years back called “The Transcendence of Commonality Amongst Individuality”.)

The basics of metabolism are true for all people, in fact virtually all life. This is why worm studies are important to us. Human insulin and glucose will work in a worm just as it does in a human, causing damage and shortening lifespan when elevated.

Starches, “safe” or otherwise turn quickly to glucose in any animal that can digest them and all will get the same side effects; it will cause glycation, AGEs, raise insulin, leptin, whether you have blue eyes, brown eyes, are a mouse or a worm… This is the advantage of getting further down, closer to the roots of disease; differences fade away and the commonalities are left to see…and treat.

Yes people are different, but the basics that we are talking about here are not only true for all people but transcends humans and are true for virtually all animal life. It is worth repeating; if you eat a non-fiber carbohydrate (sugar or starch), it will raise your blood sugar, as it would your neighbor’s blood sugar, and it will raise virtually every person’s blood sugar in the world…and every dog’s, and every worm’s blood sugar… In turn, raising glucose raises insulin and leptin and accelerates the rate of aging, and the symptoms of aging, including cardiovascular disease, diabetes, obesity, osteoporosis, and cancer.


Kitavans and Okinawans are poor examples to use in defense of carbohydrates.

I have consistently heard those in the Paleo, higher carbohydrate camp refer to the Kitavans as an example of a population eating a high carbohydrate diet and supposedly being much healthier, and the conclusion often made is that their high carbohydrate diet is causing the improved health of Kitavans.

It’s interesting to look at small subpopulations such as the Kitavans, but not more. Basing dietary recommendations on that is fraught with error. They are a very small, isolated group of people that easily could have certain genetic anomalies that might allow for longevity (even though they don’t particularly live a long life). Kitavans also mostly eat one major meal a day and that offers benefits in spite of any starches since most of the day they are calorie and protein restricting. Both are highly correlated with longevity in many animal studies. Partly because of this they’re much smaller than the average Western population, the average male being 5’4″ tall and female being 5’1″. It is known that smaller members of a species such as dogs live longer, and there is evidence that this may also apply to humans. This is likely related to lower IGF-I levels, a well studied longevity factor in animals. Was this measured in the Kitavans? How about mTOR, also associated with lower protein intake and strongly associated with longevity?

Little mentioned of the Kitavans is their high intake of coconut oil. This is very high in medium chain triglycerides that have been shown to have numerous and powerful metabolic advantages. That is the trouble with population studies. It is impossible to control all of the variables in diet and lifestyle.

But do Kitavans have extended longevity? That’s quite debatable. They do not have a higher number than average of centenarians (if any) and do not apparently have higher than (even post 50 year old to account for high infant death rate) average lifespans.

A serious mistake so frequently made in health and medical studies is confusing correlation with causation. This is well illustrated with virtually all of the studies that correlate cholesterol with heart disease. But even here, in the Kitavan study, the most one can say is that their health and longevity, if indeed they have increased longevity, is correlated with a diet and not caused by it. It could be that the diet is an innocent bystander and that the real cause of their enhanced health is from their short stature and the possibly related low IGF-1 and mTOR. They may even be healthier in spite of their diet.

Being short and thin, with likely low IGF-1 levels, eating a somewhat protein restricted diet high in MCT’s, the Kitavans have several known reasons to live long, healthy lives. Even so, they do not have remarkably long lifespans. It is this that needs to be explained. Why not? Perhaps because they are eating high amounts of starches. In other words, rather than the notion that is being perpetuated by starch proponents that Kitavans live a long, healthy life secondary to eating starches, it could be that whatever health benefits that are being experienced by Kitavans are in spite of the starches rather than because of them. It is very possible, in fact probable, that they would live even longer and healthier lives if they ate a high-fat, very low carbohydrate diet in addition to their other advantages, thus keeping glucose and insulin lower to go along with their likely lower IGF and mTOR.

All one can say is that Kitavans, with their diet of far less junk food, higher (cellulose) vegetables, high MCTs, lower protein, that may help result in short and lean stature likely secondary to lower IGF-1and mTOR (known longevity factors in animals), with their less stressed lifestyle gives them low rates of heart disease and diabetes but with only an average lifespan with few centenarians, that may likely be despite eating starches than because of it. And this is the best example that ‘safe starch’ advocates can come up with??

As far as the Okinawans; simple. They are calorie restricted, eating a diet higher in fish and vegetables, and lower in rice than their mainland counterparts. In the most comprehensive study pertaining to the Okinawan diet and longevity, the following was found;

“Findings include low caloric intake and negative energy balance at younger ages, little weight gain with age, life-long low BMI…and survival patterns consistent with extended mean and maximum life span.”

The study concluded…

“This study lends epidemiologic support for phenotypic benefits of CR in humans and is consistent with the well-known literature on animals with regard to CR phenotypes and healthy aging.”

I have not seen a breakdown of the calories eaten, but since they eat more fish and fibrous vegetables than their mainland counterparts and lower calories, simple logic could conclude that they eat fewer non-fiber carbohydrates, which, along with reduced stress, may account for their increased average lifespan.

Caloric Restriction, the Traditional Okinawan Diet, and Healthy Aging, Annals of the New York Academy of Sciences, Volume 1114, Healthy Aging and Longevity: 3rd International Conference, p 434–455, October 2007

We must understand the limited information allowed by laboratory tests to interpret them properly.

Lowering thyroid (or raising rT3) is not hypothyroidism.

Lowering WBC does not mean impaired immunity, but perhaps less stress on the immune system, or stronger WBCs as far as phagocytic activity, therefore requiring fewer of them. Lowering insulin does not necessarily mean T1 diabetes.

Centenarians and CR (calorie restricted) animals including humans have lower free T3.

I don’t doubt that Paul’s diet is a good one. There lots of good diets and virtually any diet that is different than the typical American diet will be better. But we are not just talking about better. We’re not talking about improving diabetes but reversing diabetes, heart disease, and slowing down the aging process itself. The major benefit of a very low carbohydrate, moderate protein, high-fat diet, and what will get you to the next level of health, is the adaptation to constantly burning fat and ketones and thus requiring less glucose. By forcing the intake of 100 gm or more of glucose into the body you would prevent that adaptation (according to George Cahill) and would prevent experiencing the truly deep benefits of a very low carbohydrate, high-fat diet.

The lowering of free T3 is a sign of that deep adaptation, and, according to Paul, when you follow his diet you prevent the lowering of free T3. That is powerful indication that following a “safe starch” diet is preventing one from changing into a calorie restriction phenotype and preventing the genetic expression and adaptation to deeper maintenance and repair that equates to health and longevity that a very low carbohydrate, high-fat diet would otherwise allow the opportunity for.

Age and Ageing 2010; 39: 723–727

“Down-regulation of thyroid hormones, due to either genetic predisposition or resetting of thyroid function favours longevity.” [emphasis mine]

It is important to understand nature, and to understand what its primary directive is…and its primary directive is not longevity, and certainly not post reproductive health and longevity. For that we have no footsteps to follow. As far as I know, no other species is purposely trying to live a long, healthy post reproductive lifespan. For that we only have the best science go by.

What, or even whom, is evolution selecting for? Evolution does not select for (somatic) longevity. However it wants to keep the genome immortal. If one looks at an individual human or any animal or any life, it can be broken down into the soma, the body, and the germline. The soma is there to take care of the germline and see it through to the next generation. The soma is taking the chromosomal baton that had been handed to it and passing it to the next soma to take care of that chromosomal information so that it too can do the same to the next generation. As such, our germline has stayed immortal since the beginning of life. The soma becomes expendable and takes the environmental hits, the oxidation and glycation and other insults. It is the shield that protects your genetic information from that damage. It is why we even age. Therefore, the only longevity that can be talked about is the immortal longevity of our germline and the “expendableness” of our soma. The longevity of the soma becomes, at least for nature, irrelevant outside of that.

Until we understand that nature cares little for us living a long and healthy life and until we go beyond what is typically “natural”, we will continue to do what is very natural, and it is inevitably natural to get sick and die soon after our children can stand on their own two legs, as it were.

Any discussion of health and medicine should at least take into account the biology of aging.

Life is a constant battle between damage and repair. It is repair that we have the most control over, and is therefore the most important.

As far as damage; there are at least 2 major sources. We have only limited control over oxidation. This, by definition is from oxygen. However, you shouldn’t stop breathing.

Glycation. Don’t eat glucose. Any excursion increases glycation.

Repair; The biology of aging convincingly shows nutrient sensors including insulin for glucose and mTOR for protein, control a genetic pathway that is almost universally conserved among all animal life from single celled yeast onward to humans. Science also is showing that leptin controls the healthy phenotype imparted by calorie restriction in so-called higher organisms that use fat as a primary fuel.

It appears that nature has all sorts of tricks up her sleeve to allow the members of the species to live as long as necessary to impart a reasonable chance of reproductive success. Tricks such as intracellular antioxidant up regulation, DNA repair, increased autophagy (cellular garbage collection), are all enhanced when nature believes this is necessary, including times of hardship such as perceived famine. Those nutrient sensors are controlled by the amount of macronutrients in each meal, sugars and proteins raising all of them…but not fat. When these nutrient pathways are raised, cells are told to multiply and repair is diminished, accelerating aging and increasing risk of cancer in complex multi-celled people.

Paul Jaminet and the other ‘safe starch’ advocates seem to be concentrating only on the on potential damage, or lack thereof, secondary to glucose, including mitochondrial damage. I, along with many biology of aging experts, believe strongly that glucose is a major cause of molecular damage in all life and that it contributes to aging. However, the “accumulated damage” school of aging, especially as it pertains to reactive oxygen species is really quite archaic today. Being ignored is the effect of eating glucose on the above extremely important nutrient sensing pathways that help regulate the genetic expression of extremely powerful repair mechanisms. To dig into this ancient health-promoting pathway, one must simulate glucose deprivation and eat far less glucose forming carbs than recommended by ‘safe starch’ advocates.

Controlling intake of protein is very important. I believe that I was the first low carb advocate to disavow high protein and instead recommend higher fat. I was then and am now extremely confident that I am right. I had plenty of friendly disagreements with the Eades about protein when we worked together, as they believed high was good as did almost all low carb advocates. My public talk/debate with the Eades at ASBP (American Society of Bariatric Physicians) in 2006 that is posted on my site – Protein: The Good, The Bad and The Ugly and several others, where I introduced the science of mTOR and the relationship between protein, cancer, and aging changed a lot of minds about high protein including apparently Jeff Volek and Steve Phinney who are now embracing the lower protein and higher fat diet in their books.

A quote by Oscar Wilde that is very apt, “Everything popular is wrong”…quote everything popular is wrong1 A Conclusion to the Safe Starch Debate by Answering Four Questions

A low fat diet to lose weight and treat diabetes and even that diabetes is a disease of blood sugar…

Take calcium to strengthen bones…

Cholesterol causes heart disease…

Even low carb advocates pushing high protein…

I have long said these were all wrong, and I have argued against them all for 2 decades…and I will be shown ultimately to be correct on all counts…

I have used my diet to save many lives. I have been fighting for my VLC, high fat and no more than adequate protein diet and the importance of insulin, leptin and mTOR to be accepted, since I am certain this can save millions more. No offense, but comparatively ‘safe starches’ is just a speed bump.

© Copyright 2012 Ron Rosedale, M.D.


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