After visiting the doctor for the umpteenth time about my cough, I was given two options: one, to start exercising or two, to be prescribed a medication to help lower my blood pressure.
It was only after I read “Good Calories, Bad Calories” by Gary Taubes did I suspect that my high-carb diet was keeping me from reaching my ideal weight.
To overhaul my diet, I focused initially on cutting all refined carbs and grains, which were overloading my pancreas and causing my body to accumulate fat. The Rosedale Diet is the most scientifically advanced diet in the world, that has been shown to mimic the amazing effects of caloric restriction on health and life extension, without having to even think about restricting calories.
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.
Well, we talked about insulin, hyperinsulinemia, what causes it, and it’s not too great a mystery.
It gets very muddied when you’re talking about sugar, and complex carbohydrates versus simple carbohydrates.
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. They also measured insulin resistance via something called the euglycemic clamp method, which is a very accurate way of measuring insulin resistance. Let’s talk about some of the scientific studies that compare high-carbohydrate diets, low carbohydrates, and what it does to us. Ignoring insulin is like holding on to a ledge for dear life, and hoping gravity will go away. 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?
This entry was posted in Articles, Medical, Science Papers, Studies and tagged insulin and leptin, insulin resistance, rosedale, type III diabetes. Do you have any ideas about how to explore these seemingly contradictory empirical findinds?
The insulin tolerance test with 15 minutes of glucose measurements sounds like a real winner. Artemisia herba alba was widely used in traditional medicine for the treatment of diabetes.
Houda Ben Jemaa, Sarra Khlifi, Halima Ben Hmed, Inchirah Karmous, Anis Benzarti, Jalila Elati and Abdallah Aouidet, 2015. Diabetes is the most common metabolic disorders characterized by hyperglycemia resulting from defects in insulin secretion, or its action (ADA., 2003). Type II diabetes is characterized by hyperglycemia with biochemical alterations of glucose and lipid peroxidation.
In this study the effects of Artemisia herba alba extract on four different lots were carried out. Blood samples and tissues preparation: After two months of treatment, the animals were sacrificed by decapitation and the blood was collected in tubes containing EDTA.
Antioxidant enzymes activity: The activity of superoxide dismutase (SOD) was measured according to the epinephrine method, based on the capacity of SOD to inhibit autoxidation of adrenaline to adrenochrome (Misra and Fridovich, 1972).
Effect of Artemisia herba alba treatment on body weights in (a) High fat diet rats and (b) Diabetic rats.
Levels of plasma glucose: The mean fasting blood glucose level of the HF untreated group was not significantly higher than that of the rats treated with Artemisia herba alba and also control group (Fig.
The same result was observed in the kidneys with a decrease of 38% for the DI group and 45% for the DII (Fig. Antioxidant enzymes activities: Tissue antioxidant enzymes activities of treated with Artemisia herba alba and untreated rats are presented in Fig. In kidneys the same results were observed in DI and DII groups for the catalase enzyme but not for the SOD. The first purpose of this study was to design obese and diabetic animals models that would imitate the physiopathology characteristic of human syndrome. However organs and body weights of the low double dose of STZ combined with high fat diet group doesnt differ significantly compared to those of the control group. The Revolution Is You!: Your 6-Step Method for a Happier Mind, Healthier Life and Unlimited Results! Hashimoto's Thyroiditis Explained: A Guide with Delicious Recipes to Overcoming Symptoms and Living a Healthy Life! Today we have a guest post from my friend Adrian who changed his life on a low-carb, high-fat diet. When I visited the doctor, he would give me the same cough syrup and pills to suppress my cough, fever and joint aches. I ran more, ran faster and even introduced resistance training into my exercise regime but the weight refused to budge. In his book, Taubes argued that the best diet is one loaded with protein and fat but very low in carbohydrates. A typical dinner would consist of a slab of meat – be it chicken thigh, grass-fed steak or pork chop – and accompanied by some greens and a handful of nuts.
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.
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. It causes all sorts of cardiovascular disease, and we give them another chance to kill themselves.
In an increased carbohydrate diet, you know about poor glycemic control, high blood sugar, increased cholesterol, and increased triglycerides. Or would you temper your language somewhat about satruated fat were you to give this presentation today? Rosedale, in support of his continued research and support of communities and individuals in need. The objective of this study was to evaluate the antidiabetic, antihyperlipidemic and antioxidant effects of Artemisia herba alba extract on high fat diet and diabetic models. Antidiabetic, Antihyperlipidemic and Antioxidant Effects of Artemisia herba alba Extract on Experimental Diabetes.
Adipocytes are dynamic insulino-sensitive cells that have endocrine properties and contribute to whole-body energy homeostasis (Kim et al., 2007). Oxidative stress has been implicated in the pathogenesis of type II diabetes mellitus and its complications (Rahimi et al., 2005). It has been used in folk medicine by several cultures many years ago, in Iraq folk medicine, Artemisia herba alba was known as an anti-diabetic therapeutic agent (Wang and Ng, 1999). The plant material was dried at room temperature and stored in a dry place prior to use.The dried aerial parts of plants were crushed to a fine powder.
The plasma was immediately separated by low-speed centrifugation (for 1500 g for 15 min, 4°C). Glucose concentration was measured by an oxygen rate method employing a Beckman Coulter Oxygen electrode. The MDA activity was expressed as mmoles per milligram of protein.Proteins concentrations were determined according to the method of (Bradford, 1976) by using bovine serum albumin as a standard. Catalase activity was determined by measuring the decomposition rate of H2O2 at 240 nm (Jurczuk et al., 2004). The differences were examined by the one way analysis of variance (ANOVA) followed by the Test of Mann-Whitney using the SPSS 15 program (SPSS Inc., Chicago, IL, USA). The supplementation of Artemisia herba alba decreases significantly the LDL cholesterol in HF groups by 26.7%. The induction of diabetes caused a significant decrease in Ca and P and significant increase in iron levels in plasma compared to control groups. Our results showed that HF diet groups which consumed high saturated fat (tallow) have demonstrated a disturbance in lipid profile and an increase of organs and body weights in comparison to normal rats. It is suggested that the high fat diet might be a better way to initiate the insulin resistance which is one of the important features of type II diabetes (Kim et al., 2000).
At that time, I was still eating the typical USDA-recommended diet, with more than two-thirds of my calories coming from rice, pasta and bread.
Most health problems are due to refined carbohydrates, which raise insulin levels and promote the storage of fat.
For breakfast, I would eat eggs, a lot of unsweetened cheese, such as gouda, brie, cheddar, camembert, port salut, emmental, comte, sausages, full-fat Greek yoghurt or Paleorina’s grain-free bread with peanut butter. 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? In fact, most of the experts in the field are still trying to brainwash us into believing that. Well, actually, it kind of is; insulin resistance keeps you from getting fatter and fatter and fatter, so you don’t blow up. With time, some adaptation to the low glycemic index diet took place, resulting in a more rapid and larger insulin response.
I basically eat small meals,little carbs, salads mostly,with meat, and exercise 3x a week at the gym (resistance machines) and walk the rest of the time. Wistar albinos male rats were divided into four groups, the first was fed with high fat diet, the second was mimetic diabetes type II with high fat diet combined with double low dose of streptozotocin , the third was a model of type I diabetes with high dose of streptozotocin and the fourth was a control group.
10 g of plant materiel was soaked with 50 mL of 80% ethanol for twice 24 h, with occasional shaking. All the rats were provided with commercially available rat normal pellet diet (Almes, Mateur, Tunisia) and water ad libitum. Liver, heart and kidneys were removed immediately, rinsed with cold saline solution and weighed.
1, the administration of Artemisia herba alba to diabetic rats decreases the blood glucose levels. No significant difference in LDL and cholesterol levels was found between treated and untreated DI and DII groups (Table 2).
Diabetes caused progressive accumulation of lipid peroxidation in liver and kidneys in both DI and DII groups.
However, under these conditions, the administration of Artemisia herba alba extract attenuated these changes.For the diabetic type I group, there was a significant difference in the Ca, P and Fe between the treated with Artemisia herba alba and untreated group. As reported by others, consumption of high fat tallow diet induced early and persistent leptin resistance compared to the unsaturated fat diets (Flanagan et al., 2008). At the same time, STZ is widely used to reproducibly induce both insulin-dependent and non insulin dependent type II diabetes presently by inducing beta cell death through alkylation of DNA (Szkudelski, 2001). We know that there is a high correlation between serum levels of DHEA and incidence of aging.
Eventually, you get insulin resistant, so that the insulin cannot continue to do all its damage. Determining what is complex and what is simple is much more complex.” Now, this is kind of interesting.
Again, when it comes to fats, they can either be the most beneficial nutrients, or the most toxic. I would like to follow your health plan but I had to have my gall bladder removed a few years ago do to severe gall bladder infection and a large number of gall stones.
The Low-Density Lipoproteins (LDL) and the Very Low-Density Lipoproteins (VLDL) were calculated by the formula of Friedewald et al.
The administration Artemisia herba alba extract decreased significantly this peroxidation by 30% in the liver of DI rats and by 45% for the DII rats. 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.
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. 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).
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.
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. There were small but significant differences between the high glycemic index and low glycemic diets in insulin action at high insulin concentration.
Most of the fats we eat are toxic, but vitamin E is there to prevent that essential fatty acid oxidization. I have not been able to find out much about how that affects my digestion but I my understanding is that produced substances to help my body process cholesterol.
Our data showed that heart, kidneys, liver and body weights were significantly decreased by high dose of STZ.
We know that there is a greatly increased member of peroxide radials with insulin resistance. It can either go to series I eicosanoids and have all the great beneficial affects of that, or it can go to series II.
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. He was showing me this, I think it was mentioning a new drug that works by inhibiting glucose absorption; the Olestra of carbohydrates.
In the opposite direction, one would expect the high glycemic index diet to result in low insulin sensitivity. If you have enough vitamin E on board, the essential fatty acid can be an extremely healthy food. HDL concentration has been known to decrease in women consuming a low-energy, low-fat, high-carbohydrate diet.” Diabetes Care.
The plasma lipoproteins HDL, LDL-cholesterol and the triglyceride levels were altered by high fat diet and also by streptozotocin injection. The yield of dried plant extract was 153 g kg1 of powdered material and was stored at room temperature in opaque bottles.
Three days after administration of STZ, the tail vein blood glucose level was measured in all animals.
This effect may be due to lack of insulin which leads to the degradation of lipids and structural proteins which are known by their contribution to body weight (ADA., 2003). 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. The only actually laboratory finding hat they really correlated were low levels of insulin.
Why don’t we just cut out the pancreas and the gallbladder, and the stomach, and we can inhibit all that stuff. The High Fat (HF) diet tallow diet provides 4493 kcal kg1 of food and contains 22% fat. Now, the fat this is manufactured in these animals is very saturated fat; it’s a very poisonous, toxic fat.
Many people feel that it is due to the increased consumption, due to the increased formation of free radicals. 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. 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. All of these metabolic changes may be deleterious, and have the potential to accelerate atherosclerosis, as well as microangiopathy.
He has taken a lot of animals, and he has obliterated certain areas of the hypothalamus is involved in obesity. Next, the muscle tissues, and next, the fat tissues, and the endothelium, probably not at all. 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. 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. Is your recommendation of a high fat diet appropriate for someone without a gall bladder and if so is there something from a nutritional supplement stand point that I should do to compensate for the lack of a gall bladder?
Treatment with investigational drug increases antioxidant enzymes activities (superoxide dismutase and catalase in liver and kidneys) for type I and type II diabetic groups. Each of these batches (HF, DI, DII and C) was divided in two groups with seven rats per groups: Treated with the Artemisia herba alba extract and untreated rats. It is because most of the fat that we are eating is a byproduct of carbohydrate metabolism.
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. EPA, another essential fatty acid (the omega III fatty acid), and glucagon will keep it turned off.
So, insulin can continue to do the damage on the endothelium, endothelial cell proliferation. 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. In conclusion, this study suggests that the Artemisia herba alba has a beneficial effect in controlling diabetes by reducing lipid peroxidation and increasing antioxidant enzymes activities, which reduces the risk of developing diabetes complications.
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.
It is very important in the etiology of chronic diseases (arthritis, cardiovascular disease, asthma, autoimmune disease).
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.
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).
This may be related to generally higher plasma fatty acid concentration when the carbohydrates are slowly absorbable.” Things get really confusing now. Other culprits that can increase insulin resistance are thiazide diuretics, and beta blockers.
As demonstrated in the Table 1, however for the heart and kidney there was no significant difference.In DI group, we have noted a significant loss of organ weights compared to the control group.
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.
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. Due to the complex low glycemic index diet, it may show that it actually increases insulin resistance. 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. However, the Artemisia herba alba treatment increases significantly the weights of heart (+15%), kidney (+14%) and liver (+21%).For DII group, there was no significant difference in organ weights between treated and untreated rats and also with the control group.
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.
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.
Why should we advocate a diet that the majority of which is a totally nonessential nutrient.
Glucose caused the greatest glucose rise, sucrose caused the slowest rise, and both cereals fell in between, causing about the same glucose rise.
The American Diabetes Association diet, high complex carbohydrate diet, and again, complex, simple, what is that?
Free radicals damage to the insulin receptors is a large contributor to insulin resistance, especially those caused from heavy metals.
Decrease carbohydrates, and a good fat diet lowers blood sugar, lowers cholesterol, lowers triglycerides, and it leads to low degenerative diseases. 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. Sucrose, and other sucrose-containing foods, for example, cakes, pies, and cookies, may now be substituted for other carbohydrates, according to the ADA.
When you eat a very low-fat diet, you are also eating very few essential fatty acids, and you cannot manufacture eicosanoids. 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. 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? 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. It decreases your DHEA, it increases your cortisol, it decreases growth hormone, and most importantly, growth hormone effectiveness. 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.
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. White table sugar actually raised blood glucose very slowly, to a glycemic index of approximately 32, compared to 100 for glucose. We have seen tons of patients that have normal fasting blood sugars who have horrendous insulin levels. 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.
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.
All that sugar that is being produced in the liver, and it cannot be burned in the muscle, is shunted towards the fat cells. They’re looking at the glycemic index 15 years later, and they have totally misinterpreted it. 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. 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. 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.
That takes time, and during that time, you are exercising, and metabolism is going on, and your blood sugar doesn’t rise as rapidly. 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? 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.
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. They are still maintaining this very high carbohydrate diet, so they are requiring large doses of insulin. It is entitled “Glycerol Production and Utilization During The Early Phase Of Human Obesity.” April 1992, in JOURNAL OF DIABETES. Brown rice actually has a little bit higher glycemic index than white rice, for some reason or another; not much, they are both bad.
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. 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.
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.
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.
Other than fructose, essentially what determines a carbohydrate’s glycemic index, has to do with the fiber content.
What they did is, they measured insulin response to eating a high glycemic index, or a low glycemic index diet.
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.
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. 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.
They kept the carbohydrate content actually a bit lower that we eat, and we have been recommended a very high carbohydrate diet.
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. It doesn’t absorb as rapidly, and those foods that are particularly high in fiber have a lower glycemic index. John Nessler is saying that we could use the insulin tolerance test, and this is an interesting one, and it is very quick. If you’re becoming insulin resistant, then your fat cells should become insulin resistant, everything becomes insulin resistant; it should be okay.
Those are mostly the legumes; beans have a relatively low glycemic index in the 30’s and 40’s.
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. One group of people was fed a high glycemic index of 46%, and the other group a low glycemic index of 46%. 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. There were 35% or 40% fats, and the rest was protein, and they remained the same in both groups. For 15 minutes, you’ve got a window, and you can see how rapidly that sugar level is going to fall with that insulin.
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. Spread it throughout the day, and you won’t have these big, huge rises in blood sugar, and therefore, the compensatory increases in insulin. 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. 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. 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. 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. Proper nutrition, proper supplementation, and a bit of exercise, and he requires no insulin.
Even under the best parameters, even looking in the Smith-Kline labs, a normal fasting insulin is somewhere between 5 and 30. 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. 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. 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.
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