This is kind of interesting. This is an article in 1925 by the Frenchman Jean Oslem Rilit Savard. He wrote a book called THE PHYSIOLOGY OF TASTE. That’s not this; this is another article.
The article was written in 1825. “It has been clearly shown that it is only because of grains and starches that fatty congestion can occur, as much in a man as in animals. This affect plays a large part in the commerce of fattened beasts for our markets, and it can be deduced as an exact consequence that a more or less rigid abstinence from everything that is starchy or floury will lead to the lessening of weight.” How do we get animals fat quickly? Grain-fed diet. We know we can make them fat very quickly by feeding them carbohydrates. We haven’t figured that out for ourselves yet? So what do we do then? Now, the fat this is manufactured in these animals is very saturated fat; it’s a very poisonous, toxic fat. We eat these animal products then, and this is why the fat they we eat is toxic to us. It is because most of the fat that we are eating is a byproduct of carbohydrate metabolism. Fat in itself is not bad; I really want to hammer that home. Fat is not toxic; the fat that we eat in this country is toxic, for the most part. It is artificially manufactured. Greenberg, (that’s this one), is entitled –I don’t know what this is entitled. “Under circumstances of increased fat intake, the size of an individual aft cell increases. Carbohydrates may influence adipogenesis through insulin mediated regulation of fat cell number.”
Decreased insulin sensitivity is associated with decreased concentrations of polyunsaturated fatty acid, and he goes on to say that accordingly, the relationship between carbohydrate-containing diet and fat cell number could represent one way for carbohydrates to not escape a relationship to obesity. There are still lots of people out there saying that carbohydrates don’t make you fat. In fact, most of the experts in the field are still trying to brainwash us into believing that. Let’s talk a bit more about obesity. Peter Campbell writes in THE JOURNAL OF CLINICAL ENDOCRINOLOGY METABOLISM, and he showed that as body mass index is a relationship of size, it correlates height, and as body mass index goes greater than 27, your insulin resistance increases proportionately. So insulin resistance and obesity are directly correlated. George Bray is considered one of the pioneers in obesity research. He does a lot of work with the brain and obesity. He has taken a lot of animals, and he has obliterated certain areas of the hypothalamus is involved in obesity. You learned that way back in medical school, if you wipe out the ventromedial nucleus of the paraventricular nucleus, the hypothalamus animals will eat and eat and eat, and they will get fatter and fatter. What he has found recently is that before they get fat, when you wipe out those nuclei of the hypothalamus, insulin levels go way up. That occurs before the fattening process. He has done a lot of experiments where they have obliterated the beta cells of the pancreas, and they’ve taken out of the cells, and they’ve put it under the kidneys so that there was different neuroconnections, and same femoral connections, and found out that the islet cells are under autonomic control. So even hypothalamic obesity is medicated through insulin. Everything goes through insulin. It is the master hormone of metabolism. You cannot get around it. There are other affects of insulin. It decreases your DHEA, it increases your cortisol, it decreases growth hormone, and most importantly, growth hormone effectiveness. John Nessler, pioneer in insulin research; he is at Medical College of Virginia. He has been working on insulin research for 20 years. “Insulin mediated a decline in serum DHEAS and DHEA levels, previously reported in men, as well as the decline in serum DHEAS and DHEA in women, may be in part due to decreased synthesis.”
Another article, John Nessler. “The Effects of Insulin Reduction on Serum DHEA,” from JOURNAL OF CLINICAL ENDOCRINOLOGY AND METABOLISM, 1995. “These findings strengthen the idea that insulin acts as a physiological regulator of DHEA and DHEA sulfate metabolism in men, and confirm that insulin reduces serum DHEA and DHEA sulfate in elderly, as well as middle-aged men.” I think most of us have heard about the influence of DHEA on all the chronic degenerative diseases of aging. We know that there is a high correlation between serum levels of DHEA and incidence of aging. It is increased to free radical production. We know that there is a greatly increased member of peroxide radials with insulin resistance. The type III diabetics especially have very decreased vitamin E levels, and effectiveness. Many people feel that it is due to the increased consumption, due to the increased formation of free radicals. Gerald Ravin, another biggy at Stanford, writes in his article, “Syndrome X: Six Years Later.” “The very facets of Syndrome X are involved to a substantial degree in the cause and clinical course of the major diseases of Western civilization.” What else does insulin do? It is one of the main regulators of eicosanoids in the body. What are eicosanoids? Every cell produces eicosanoids. Every animal life form, from one cell to animals, produces eicosanoids. They are formed from essential fatty acids. That is one reason why essential fatty acids are so vital to the diet. When you eat a very low-fat diet, you are also eating very few essential fatty acids, and you cannot manufacture eicosanoids. There are some so-called good eicosanoids, and some so-called bad eicosanoids. I don’t know if you can read that; I’m sure you can’t, because I can’t. Series I eicosanoids (PGE I), cause vasodilatation. They reduce clotting, they cause dilatation of the bronchi, they cause and enhanced immune response, inhibit cell proliferation, they are an anti-inflammatory, they reduce cholesterol synthesis. They are anti-depressive, and they lower pain. Series II eicosanoids (PGE II), cause vasoconstriction, they are pro-clotting, they cause bronchial constriction, they increase cell proliferation, they suppress the immune system, they are extremely pro-inflammatory, they increase cholesterol synthesis, they increase triglyceride synthesis, and they increase your sensations of pain. What are the benefits of PGE I? These are kind of self-explanatory by the previous slide: Cardiovascular inhibiting, platelet aggregation, increases dilation, reduces cholesterol synthesis, immune system, the endocrine system, the nervous system it controls, neurotransmitters, it is an anti-depressive, a respiratory endocrine, stimulates AMP, and it controls almost all of the other hormones. Now, the detriments of PGE II are virtually the opposite. All of our systems have checks and balances. This is called the so-called good eicosanoids, and PGE II is the so-called bad eiconsanoids, but there is really nothing good and bad; why are they there if they’re bad? Well, again, that’s an evolutionary thing. The series II prostaglandins were there to help us heal. We’re supposed to be out fighting for food, and killing the wooly mammoth. If we get cuts in fights, we need inflammation to heal. You need your blood to clot; you don’t want to bleed to death. The problem is, we’re not doing that any more. We don’t need that much PGE II; we need much more PGE I, and we don’t have it. Our diet (you’ll see in a little bit, in fact, right now), is very conducive towards the production of the series II prostaglandins, and not the series I prostaglandins.
What is insulin’s role? It controls Delta-5 desaturates. Here is a chart. If you take one of the more important essential fatty acids (that’s linoleic acid). Its’ first step in conversion is GLA (gamalinoleic acid), and then it goes to dihomogammalinoleic acid, and from there, it can go one of two ways, and this is one of the most important steps in human metabolism, as far as I’m concerned. It can either go to series I eicosanoids and have all the great beneficial affects of that, or it can go to series II. What determines that is an enzyme called Delta-5 desaturate. What controls Delta-5 desaturates is the ratio between insulin and glucagon. High insulin will turn it on. EPA, another essential fatty acid (the omega III fatty acid), and glucagon will keep it turned off. It is very important in the etiology of chronic diseases (arthritis, cardiovascular disease, asthma, autoimmune disease).
Now, if high insulin is bad, why isn’t insulin resistance good? Insulin resistance means that high insulin isn’t able to do its dirty work. Well, actually, it kind of is; insulin resistance keeps you from getting fatter and fatter and fatter, so you don’t blow up. Eventually, you get insulin resistant, so that the insulin cannot continue to do all its damage. The problem with insulin resistance (and this answer is just recently being uncovered, and I have been looking for this answer for a year, and finally found some information, and talked to Robert Eckles at the University of Colorado and his group, who is doing a lot of research on the steps of insulin resistance, “the rest of the story”; Paul Harvey). Tissues become insulin resistant at different rates. First, the liver becomes insulin resistant, as you constantly eat sugar meals, high carbohydrate meals, and insulin is put out by the pancreas, the first pass is to the liver. It gets exposed to that insulin right away, and the first receptors to become resistant probably end up being in the liver, and there is recent documentation to that. Next, the muscle tissues, and next, the fat tissues, and the endothelium, probably not at all. So, insulin can continue to do the damage on the endothelium, endothelial cell proliferation. What happens when insulin causes resistance at the hepatocyte level? What does insulin do at the hepatocyte? It inhibits gluconeogenesis. When it becomes resistant, it can no longer inhibit gluconeogenesis. So the liver keeps putting out a bunch of sugar, and you have high blood sugar. Next, the muscle becomes resistant. The insulin cannot do the good stuff that it does in muscles. What does it normally do in muscles? It allows you to take in the amino acids to make more muscles. That’s being inhibited now. Fat tissue is a last tissue to become resistant. That doesn’t become resistant until you weight 500 pounds. All that sugar that is being produced in the liver, and it cannot be burned in the muscle, is shunted towards the fat cells. It continues to turn on lipoprotein lipase, and you continue to get fat. Eventually, you plateau. After you reach 230 pounds, you stop gaining weight… maybe. There are differences; not everybody is the same. Sure, there is some genetic variability in all this. This is out of Paris. C’est Le ——-. It is entitled “Glycerol Production and Utilization During The Early Phase Of Human Obesity.” April 1992, in JOURNAL OF DIABETES. “The mechanisms generating insulin resistance in the liver and muscles of recently obese children appear not to affect adipose tissue. The initial deposition of excess fat is associated with hyperinsulinemia, insulin resistance of liver and muscles, with normal, or supra-normal insulin sensitivity of glucose transport into white adipose tissue. John Eckle’s group. I talked with Michael Pagliosati over the phone at length, and it was very interesting. This is yet-to-be published (it’s up for publication, and will be published in a few months, probably), but in summary, he used a high-sucrose diet and noted insulin resistance in liver prior to peripheral tissue. This is a very important concept, because it really explains a lot. I could never figure out how you really get fat with insulin resistance. If you’re becoming insulin resistant, then your fat cells should become insulin resistant, everything becomes insulin resistant; it should be okay. The problem lies in the order of insulin resistance in the different tissues. That is creating all our diseases. Well, not all of them, but a major portion.
Do you live longer if you have lower insulin? That’s really the bottom line. Well, we don’t know, because nobody in this country really has very low insulin, it seems. There are some clues. In the Annals of The New York Academy Of Sciences, they show that centenarians (people who live to be 100 or longer), generally present lower concentrations of insulin. They did a lot of variability studies; they checked a lot of different variables on those people who are 100 years old or older, trying to find out what type of laboratory data could they gather to indicate whether a person might live a long life. The only actually laboratory finding hat they really correlated were low levels of insulin. There were also associated conditions that are associated with low levels of insulin; they had low blood pressure, they had low cholesterol, things like that, but there were signs of low insulin, and low blood sugar.
Well, we talked about insulin, hyperinsulinemia, what causes it, and it’s not too great a mystery. Sugar, what it is? That is where things become actually a little bit muddied. Still, what is sugar? Everybody thinks of white table sugar. We think of honey, we think of all the things that are sweet, and not sugar. We have been recommending diets for diabetics for hundreds of years. There are just certain things in medicine that just totally amaze me! We have been recommending diets for diabetics, and it wasn’t until 1981, when a diabetic researcher in Toronto, Canada, David Jenkins, decided to see what happens to people’s blood sugar when they eat different foods. Truly, nobody studied this before 1981. He fed a bunch of different people – hundreds of people, actually thousands of people, hundreds of different foods, and then measured their blood sugar afterwards. He fed them potatoes, he fed them glucose, he fed them sucrose, he fed them wheat bread and white bread, rice, pasta, cantaloupe, peas, beans, and everything you can think of, and measured their blood sugar. It was called The Glycemic Index. I didn’t put a glycemic index up here, and there is a reason for that. In the glycemic index, what he did, you feed somebody glucose (obviously, not much has to be done, it just has to be absorbed), and measured what the blood sugar was after a certain length of time, and gave that an arbitrary number of 100, and compared everything to it. Now, if you have a piece of wheat toast, and wheat toast has to be digested, and the so-called complex carbohydrates in wheat have to be converted into blood glucose, it takes a little bit longer. It has a glycemic index in the 70’s: 71 or 72. It has a lower glycemic index. It is considered a complex carbohydrate. If you take sucrose (that’s white table sugar), you get a rather surprising result. White table sugar actually raised blood glucose very slowly, to a glycemic index of approximately 32, compared to 100 for glucose. The reason for that is really not a great big mystery. Sucrose is a combination of glucose and fructose. Fructose is an odd sugar. It has to be extensively metabolized in the liver before it can be turned into glucose. That takes time, and during that time, you are exercising, and metabolism is going on, and your blood sugar doesn’t rise as rapidly. He fed somebody a white potato. Blood sugar skyrocketed. Glycemic index of 98, glucose is 100 – not much difference. It’s like feeding somebody pure glucose. Spaghetti is in the 70’s; white bread is about the same as wheat bread. Brown rice actually has a little bit higher glycemic index than white rice, for some reason or another; not much, they are both bad. All of the starches, with the exception of beans and fructose generally have glycemic indexes between 60 and 80, with a few up there in the 90’s. A lot of this has to do with the fiber content. Other than fructose, essentially what determines a carbohydrate’s glycemic index, has to do with the fiber content. Fiber cannot turn into glucose. Fiber holds the sugar in the intestines longer. It doesn’t absorb as rapidly, and those foods that are particularly high in fiber have a lower glycemic index. Those are mostly the legumes; beans have a relatively low glycemic index in the 30’s and 40’s. Those foods that do not have very much fiber raise your blood sugar very rapidly. You can slow absorption by chewing foods very well. You can effectively lower the glycemic just by spacing meals out. Don’t eat very much at one time; eat small meals. Spread it throughout the day, and you won’t have these big, huge rises in blood sugar, and therefore, the compensatory increases in insulin. By eating foods that are low on the glycemic index scale, you are really only buying time. It’s slowing absorption, but it’s all turning into sugar. In a 24-hour period, you eat 20 grams of sucrose, you eat 20 grams of beans (non-fiber, if you don’t count the fiber portion) 20 grams of carbohydrates turns into 20 grams of sugar, other than the metabolism that you are burning to that. Recently, they are figuring this out.
It gets very muddied when you’re talking about sugar, and complex carbohydrates versus simple carbohydrates. Go out and eat a high complex carbohydrate meal. That’s the diet that is really being recommended. That’s been going on for a long time. The American Diabetes Association has been saying for 20 years: “Eat a high complex carbohydrate diet.” Potatoes, pasta. Is that really complex carbohydrates? That’s raising your blood sugar faster than if you eat white table sugar. There was a symposium recently. An entire journal of THE AMERICAN JOURNAL OF CLINICAL NUTRITION was devoted to this symposium, moderated by a gentleman by the name of Edwin Beerman.
In the closing remarks of the symposium, he quotes: “The potential down side is the increased post prandial glucose and insulin responses to a higher carbohydrate meal. Once absorbed, glucose molecules circulating in the blood stream are indistinguishable from each other, whether from honey, rice, sucrose, whereas one of the speakers at this conference suggested dropping the term complex carbohydrates, and I could not agree more.” Carbohydrates are sugar. “Higher plasma in the glucose concentrations are obtained when the structure is changed from raw to cooked, from whole to ground, or hydrolyzed. Determining what is complex and what is simple is much more complex.” Now, this is kind of interesting. A couple of weeks ago (I see a lot of diabetics, and they love to show me articles and prove me wrong), and there is something called THE DIABETES WELLNESS LETTER, and a lot of diabetics get this. He was showing me this, I think it was mentioning a new drug that works by inhibiting glucose absorption; the Olestra of carbohydrates. Why don’t we just cut out the pancreas and the gallbladder, and the stomach, and we can inhibit all that stuff. It would be a lot cheaper. Anyway, he showed me this article, and this is what really caught my attention. It said the case against no sugar builds. In other words, they are looking at this glycemic index (and this is 15 years later, by the way; David Jenkins published all this stuff in 1981). They are looking at this glycemic index business, and they are figuring it out: “The 1994 American Diabetes Association nutrition recommendations now state that there is very little scientific evidence supporting the assumption that simple sugar should be avoided, based on the assumption that sugars are more rapidly digested and absorbed than our starches. In a study reported at the 1995 American Diabetes Association meeting, for example, researchers observed the rise in blood glucose from pre-sweetened cereal and unsweetened cereal, glucose, and sucrose. Glucose caused the greatest glucose rise, sucrose caused the slowest rise, and both cereals fell in between, causing about the same glucose rise. Sucrose, and other sucrose-containing foods, for example, cakes, pies, and cookies, may now be substituted for other carbohydrates, according to the ADA. Sure! Now, they are telling diabetics: “You can eat sugar!” Go for it! It’s no worse than the other carbohydrates. They are not saying that the other carbohydrates are as bad as sugar; they’re saying that sugar is no worse than the other carbohydrates. We’re feeding all our diabetics sugar! That makes a lot of sense. Anyway, that’s where they are. They’re looking at the glycemic index 15 years later, and they have totally misinterpreted it. It gets worse, believe it or not. Things get more complicated. Carbohydrates, simple, complex, I don’t care what you call it, are sugar. Carbohydrates are sugar. Your body makes it into sugar. They increase your blood sugar, they increase your insulin, and by now, we have figured out that insulin can do a lot of nasty things to us. I just came across a very interesting article. This is from THE AMERIAN JOURNAL OF CLINICAL NUTRITION, January 1996. This is by Dr. Benji Kings and Eric Riktor, of The University of Copenhagen, in Denmark. This is a very important study. What they did is, they measured insulin response to eating a high glycemic index, or a low glycemic index diet. They fed people a diet that is very typical of American diet. They kept the carbohydrate content actually a bit lower that we eat, and we have been recommended a very high carbohydrate diet. Worldwide is a bit lower than that. The carbohydrate diet in this study was a 46% carbohydrate diet. One group of people was fed a high glycemic index of 46%, and the other group a low glycemic index of 46%. There were 35% or 40% fats, and the rest was protein, and they remained the same in both groups. What you will see, is that after three days, the insulin response in the high glycemic index foods was quite a bit more than in the low glycemic index. It is predictable; after breakfast, if you eat a high glycemic index with more simple sugars, it is going to raise your blood sugar faster, and it should lead to greater insulin response. Same thing after lunch, and even more so, high glycemic index/low glycemic index, big difference. High glycemic led to much more insulin. After 30 days on this diet, they note almost the same. After lunch, there is also a narrowing.
Let’s see what they found. Initially, blood glucose and plasma insulin concentrations were lower during part of the day with the low glycemic index than the high glycemic index diet, but after 30 days of the diet, glucose and plasma insulin were not significantly lower with the low glycemic index than the high glycemic index. With time, some adaptation to the low glycemic index diet took place, resulting in a more rapid and larger insulin response. This adaptation can also reflect decreased insulin sensitivity. There were small but significant differences between the high glycemic index and low glycemic diets in insulin action at high insulin concentration. In the opposite direction, one would expect the high glycemic index diet to result in low insulin sensitivity. They did expect the high glycemic index diet to lead to greater insulin resistance. This was not the case. “In conclusion, the present study shows that the type of carbohydrate in an ordinary western diet influences whole body insulin action. When total carbohydrate intake provides 46% of energy, then insulin action at a high plasma concentration is lower (insulin action is lower, insulin resistance is higher), when the carbohydrates are primarily slowly absorbable, lower on the glycemic index. This may be related to generally higher plasma fatty acid concentration when the carbohydrates are slowly absorbable.” Things get really confusing now. Due to the complex low glycemic index diet, it may show that it actually increases insulin resistance. So, where are we? The American Diabetes Association diet, high complex carbohydrate diet, and again, complex, simple, what is that? We are telling our diabetic now to eat a whole bunch of sugar. I think it is part of population control. We’re trying to kill our diabetics. That’s the only explanation I can come up with. They are eating a bunch of sugar, and we know that leads to poor glycemic control. They are stuck on a bunch of oral hypoglycemics, and you know how they work. They work by whipping the pancreas into trying to produce more insulin. We have pancreases going overtime trying to keep up with the insulin resistance, putting out sometimes ten times as much insulin as otherwise we have to. It cannot keep up, so the sugar levels are rising, so we put people on drugs to try and squeeze a little bit more insulin out of that pancreas. What does that do? That leads to beta cell burn out. It dies. You’re whipping that horse to death, and it gives up. So, then, they become insulin dependent. They are still maintaining this very high carbohydrate diet, so they are requiring large doses of insulin.
What does that insulin do? It causes all sorts of cardiovascular disease, and we give them another chance to kill themselves. What are the other culprits for insulin? Carbohydrates aren’t the only culprits. They are the main one. Macronutrient intake is extremely important. We are all concerned about micronutrients, and that’s important. I take tons of them; I take handfuls of them. This keeps me from eating carbohydrates. You have to pay attention to the macronutrients. Other culprits that can increase insulin resistance are thiazide diuretics, and beta blockers. We have all these essential hypertensive patients due to hyperinsulinemia, and we stick them on beta blockers and thiazide diuretics, and we make them worse. Another huge contributor to insulin resistance is free radicals. Free radicals damage to the insulin receptors is a large contributor to insulin resistance, especially those caused from heavy metals. That is something to keep in mind. Measuring insulin resistance, I hope we are figuring out at this time that insulin resistance is very important, so, what do we do about it? How do we measure it? You can do several things. Measuring sugar levels doesn’t really tell you much. You need to know what is happening with the insulin. We have seen tons of patients that have normal fasting blood sugars who have horrendous insulin levels. Catch them early, and you can save their lives. Prevention! A good test is a glucose insulin tolerance test. We’ll show you a few of those, but that’s like a glucose tolerance test, except you measure insulin levels right along with it. It’s very simple. It is kind of time-consuming, and patients, unless you put it in a little catheter, have to be stuck a bunch of times, and they don’t like that. It’s a five-hour test. There is another test called the insulin tolerance test. John Nessler advocates this. I have not done this yet, but I think I may. I have been reading about it, and it is relatively new. There is recent data that shows that it correlates extremely strongly with the goal standard for insulin resistance, and that is called the euglycemic clamp technique. I won’t go into that, but it is used in research centers, and it’s a very involved technique. You basically wipe out the islet cell production of insulin, and infuse a certain rate of insulin, and infuse glucose to keep a blood sugar at a constant area. If they want to keep your blood sugar at 120, and you’re being intravenously given insulin, the more sugar that is required to keep your blood sugar level at 120 means the more insulin-sensitive you are. That is used at university studies, and it’s really the gold standard for insulin resistance, but it’s a very technically demanding test, and not used in the office. John Nessler is saying that we could use the insulin tolerance test, and this is an interesting one, and it is very quick. Take a patient fasting, measure their blood sugar, and intravenously you give them 0.1 units of insulin per kilogram of body weight, and measure their blood sugar every three minutes for 15 minutes. You don’t do it longer than 15 minutes because as the blood sugar gets low, the body starts putting out compensatory hormones like cortisone and epinephrine, and it is going to raise the blood sugar, and that throws it all off. For 15 minutes, you’ve got a window, and you can see how rapidly that sugar level is going to fall with that insulin. The more rapidly it falls, the greater the insulin sensitivity, and you get a constant. That is a 15-minutes test. It ought to work very well, and I don’t expect the blood sugars are going to fall any more than we see during the insulin tolerance test that we have been doing. You can do a fasting insulin, and you can catch late stages of insulin resistance, but the fasting insulin doesn’t really go up until you have become very insulin resistant. By that time, you have already got all the diseases. An insulin-dependent diabetic is a little bit more trouble. You cannot measure insulin, because you don’t know whether it is endogenous, or whether it is exogenous, but you can measure C-peptide. If you have a type II diabetic (if you have any diabetic), and they are on insulin, measure their fasting C-peptide level. Get a C-peptide level of 4 or 5, and that is in the normal range. They are producing as much insulin as you or I; they are just getting 100 extra units. They are very hyperinsulinemic, and that hyperinsulinemia is being caused from us. We are giving them all the diseases that they are dying from. Most of them die from vascular complications due to hyperinsulinemia. They don’t need to be on 120 units of insulin. Most of them don’t need to be on insulin at all. If they have normal levels of C-peptide, you know that if they follow a correct life-style, if they eat a proper diet, and if they get minimum exercise, they could get off that insulin altogether, and it doesn’t take long. We have got people who are on 200 plus insulin, and get off insulin totally within a few months. They feel a whole lot better. I have just a few examples of glucose insulin tolerance tests. This is a typical type I diabetic. The red line here, no insulin production. This is a diabetic that would normally be considered virtually type I. This is a very thin fellow. He is producing a maximum; the most his insulin rose was to 15. Normal would be up to 40 or 50, and it would come down real quickly. He only got up to 15. Guess what? Proper nutrition, proper supplementation, and a bit of exercise, and he requires no insulin. This is all you need. You really don’t need any more than that. He functions very well. He is very healthy. This is a gentleman who came in for obesity. He had a fasting blood sugar of 90, and fasting insulin of 6. Even under the best parameters, even looking in the Smith-Kline labs, a normal fasting insulin is somewhere between 5 and 30. That’s ridiculous! It should be below 10. If they just picked people off the street, sick people or well people (three-quarters of us have insulin resistance), and they can include those people. By all standards, he has normal fasting glucose, normal fasting insulin, and look what happens to his insulin in an hour. It goes up to 440. It doesn’t really get back to normal range for a long time. In six hours it was still elevated. It goes down to 17 in three hours. This guy looks at piece of toast and his insulin goes sky high. What is wrong with him? He was obese. He was 30-some years old. If you don’t control that insulin, there is no way you are going to cure his obesity. There is something called the Yo-yo Diet Syndrome. Many people are aware of this. People go on diets, they lose weight, and then they gain it back immediately, and more. The reason for that is that they aren’t paying attention to their insulin. Insulin remains high, because most of these diets are high-carbohydrate diets. You have a high-carbohydrate diet, you have high insulin, and you cannot burn fat properly. You burn your muscle tissue, you lean body mass goes down, and that is the most metabolically active tissue in your body, other than your brain. You cannot burn calories, and eventually, you get fat again, because insulin is telling you to. This is another one similar to the last one, but this is an 11-year-old boy. We caught it early. Normal fasting insulin, may be 15, and normal glucose. Again, his insulin rose very rapidly, and went down. This would be a type II diabetic. What you have is a much slower insulin response because of lost ability to manufacture granules, and a slow decline to maintain hyperinsulinemia for many hours.
So, what do you eat? There are three energy-producing foods, carbohydrates, fats, and proteins. Fats and proteins are found together in nature. Go on a high-carbohydrate diet, and you automatically go on a low-protein, low-fat diet. You can’t have it any other way. Two other ingestables would be fiber and water. That’s what there is to eat.
We are fat phobic. We ignore fat; we ignore good and bad fats. The essential fatty acids are probably the most efficient nutrients we can eat. Again, when it comes to fats, they can either be the most beneficial nutrients, or the most toxic. Most of the fats we eat are toxic, but vitamin E is there to prevent that essential fatty acid oxidization. If you have enough vitamin E on board, the essential fatty acid can be an extremely healthy food. What we are going to get into now is the meat. We talked about all the scientific background.
Let’s talk about some of the scientific studies that compare high-carbohydrate diets, low carbohydrates, and what it does to us. In an increased carbohydrate diet, you know about poor glycemic control, high blood sugar, increased cholesterol, and increased triglycerides. Is weight loss going to occur when subjects consume high or low-energy diets? “The consumption of the kid of diet advocated by the National Education Program seems to minimize the fallen insulin, and triglyceride concentrations. They both increase in proportion to dietary carbohydrate consumption. HDL concentration has been known to decrease in women consuming a low-energy, low-fat, high-carbohydrate diet.” Diabetes Care. “Low-fat, high-carbohydrate diets in non-insulin dependent patients led to higher plasma glucose, insulin, triglycerides, post prandial accumulation of triglycerides, increased VLDL, increased lipoprotein lipase, and demonstrated that multiple risk factors of coronary artery disease are accentuatedwhen individuals consume diets recommended to reduce this risk.“ “We conclude that high-carbohydrate diets may cause persistent increase in plasma, triglycerides, and VLDL cholesterol, hyperinsulinemia, and deterioration in glycemic control. All of these metabolic changes may be deleterious, and have the potential to accelerate atherosclerosis, as well as microangiopathy. “ Let’s use common sense. There are 50 or so essential nutrients in the human body. We’ve got vitamins, minerals, water, oxygen, amino acids, and essential fatty acids. There are no carbohydrates on that list. Why should we advocate a diet that the majority of which is a totally nonessential nutrient. Decrease carbohydrates, and a good fat diet lowers blood sugar, lowers cholesterol, lowers triglycerides, and it leads to low degenerative diseases. All of these quotes actually show that. Substitution of dietary protein for carbohydrates alters blood cholesterol, and cardiovascular risk profiles. The previous studies were showing the substitution of monounsaturated fats, and good quality fat is beneficial.
So I ask the AHA, The American Diabetes Association, The American Cancer Association, and any of you that still recommend a high-carbohydrate diet, what about insulin?