482. INSULIN - Insulin Resistance Treatment

Insulin Resistance Treatment

Reversing Insulin Resistance

The great news is that insulin resistance symptoms can be reversed simply by changing the diet and engaging in regular exercise. Yes, it's that simple. Experts like Dr. Charles Gant, Professor Loren Cordain, Dr. Joseph Mercola and Dr. Al Sears tells us that insulin resistance and type 2 diabetes can almost always be reversed with diet and exercise.
Since the primary cause of insulin resistance is sugar and the consumption of carbohydrates, when you remove these foods from your diet, and replace them with adequate fat and protein then the vicious cycle will stop.
If their is not excess sugar in the blood stream, then cells will start to burn off what is stored as fat, the pancreas will stop releasing insulin all the time and the glucose receptors will stop being resistant. Thus blood sugar and insulin levels will stabilize. When insulin restablizes, then triglycerides, blood pressure, cholesterol etc. stabilize as well.
Exercise will also be crucial because it burns glucose off and lowers insulin levels. Brief periods of intense exercise, such as that found in the PACE exercise program is the most effective form of exercise in this case because it helps stabilize the autonomic nervous system by telling the adrenals gland to stop releasing adrenalin that triggers the liver to dump glycogen into the blood stream.
However, exercise alone will not work because you'd have to exercise continually to burn off all the sugar if you continue to eat carbohydrates. But when used in combination with the removal of starchy carbohydrates it enhances the reversal. If you have a lot of stress in your life, then exercise is even more important.
Of course, other substances that trigger adrenalin and the liver to release glucose in the blood stream must cease as well, like smoking, drinking alcohol and caffeine.
Reduce stress and get adequate sleep. The regular practice of deep breathing exercises, mindfulness and mindfullness based meditation are simple yet powerful ways to bring blood sugar down triggered by stress, because they turn off the stress response system. Make time for eight or nine hours of sleep a night and take naps if needed.
Since nutritional deficiencies are a common cause of insulin resistance, a comprehensive nutritional supplement program designed with the help of your health care provider can be helpful. Three of the most common and beneficial include Chromium, B6 and glutamine. Each of these aids in the process of regulating blood sugar and assists during the process of changing the diet. Other important nutrients may include all the B vitamins, magnesium, manganese, vanadium, vitamin C and E. A health care provider who practices functional medicine can help advise you when designing a nutrient plan.

The Best Diet for Insulin Resistance

The bottom line is that all foods that cause blood sugar levels to rise need to be eliminated or at least greatly restricted. Dr. Charles Gant tells us that starchy carbohydrates are totally non-essential in the diet. You can acquire all the energy needed through protein and short-chained fatty acids.
All carbohydrates break down into glucose in the body. However, the most important factor is how rapidly they convert to sugar and how long the blood sugar remains high. All foods high in starch like whole grains, potatoes and beans cause a rapid and intense rise in glucose. Potatoes, for example, are about equal to sugar. Carbohydrates found in non-starchy vegetables and whole fruits have less impact on blood sugar.
One of the first steps you want to take when looking for the best diet for insulin resistance is to become familiar with the GI, also known as the glycemic index. Foods that are high on the glycemic index cause a higher spike in blood sugar, while foods that have a lower glycemic index are processed slower, which results in smaller amounts of sugar appearing in the blood stream at one time, which is easier for the body to manage.
Dr. Al Sears recommends that you don't eat foods that have a GI of more than 40. Marcelle Pick, OB/GYN NP, recommends keeping your carbohydrate consumption to no more than 22 grams per meal.
However, the easiest and truly the best diet for insulin resistance symptoms is to follow the Paleolithic Diet. as Professor Loren Cordain points out in his book, The Paleo Diet, All the components needed to reverse insulin resistance are inherent in the Paleolithic diet simply because you are eating the foods that natured intended you to eat. The foods you were genetically designed to eat do not result in disruption of blood sugar and insulin levels.

The best diet for insulin resistance is very simple:

·an abundance of lean meats and fish

·eggs

·an abundance of non-starchy vegetables

·small amounts of nuts and seeds

·small amounts of low-sugar fruits

·fat from meat, as well as olive oil, avocados or avocado oil, walnut oil, flax and fish.

·an abundance of clean water

·that's it. nothing more

Wheat, corn, rye, rice, brown rice, barley, beans, potatoes, sweet potatoes, peas or any other starchy food should be avoided or eaten only on occasion.
Fruit juices, caffeine, soda pop, alcohol etc., should be avoided.
Dried fruit should be eaten only on occasion as it is high in sugar as well.
A low-fat diet is the worse thing you can do for yourself.
Although not technically part of the Paleolithic diet, butter will not have a negative impact on blood sugar and yogurt won't either if eaten moderately without sugar.
        Food should be organic, because the presence of pesticides, herbicides, additives, preservatives etc., trigger the stress response system, which as we learned earlier releases adrenalin, which alerts the pancreas to release insulin.
        When we look over the list of foods that will reverse insulin resistance we clearly see that when we return to the diet that our ancestors ate we are giving our body exactly what it needs for optimal health.
        The best diet for insulin resistance is also the best diet for any other health condition and humanity in general.

Insulin Resistance Test

An actual insulin resistance test per se is not available. Instead diagnoses is made by looking at the comprehensive picture of your health using a variety of tools, including the presence of insulin resistance symptoms, health conditions you have and lab work. Your lifestyle, level of stress, type of diet you eat and patterns for exercising will be taken into account as well.
For example, if you have high triglycerides and low HDL which typically occur in insulin resistance then a knowledgeable physician would suspect resistance and pursue further testing like a glucose tolerance test.
Dr. Charles Gant recommends a blood test that measures insulin after fasting overnight and then again two hours after a high carbohydrate meal. He states a normal insulin level is 6 to 8, while 12 is problematic and 16 indicates a definite problem. Marcelle Pic recommends a glucose level no higher than 75 to 80. If fasting glucose climbs to 100 then we're talking about pre-diabetes, and if it hits 126 then we're looking at diabetes.
According to Marcelle Pick, OB/GYN NP, it is believed that at least 25% of the population has full blown insulin resistance, which amounts to more than 80 million Americans. However, due to the diet we consume, most everyone has some degree of resistance. She also tells us that the percentage is much higher in women who are in perimenopause. Other studies have prevalence as high as 44 percent in the elderly population.
These are alarming statistics and a clear indication that the diet most of society consumes is deadly. Ideally the time to make changes is before insulin resistance symptoms began to develop and testing is required. Insulin resistance is completely avoidable by making the right choice in food and exercising.
It's important to be aware that many traditional main-stream physicians are not educated about insulin resistance and therefore you should be seeking a health care provider who practices what is called functional medicine to make an accurate diagnoses and design a plan for recovery.

481. INSULIN - Physiologic Effects of Insulin

Physiologic  Effects  of  Insulin

Insulin Deficiency and Excess Diseases

        Diabetes mellitus, arguably the most important metabolic disease of man, is an insulin deficiency state.
        It also is a significant cause of disease in dogs and cats.
        Two principal forms of this disease are recognized:

·Type I or insulin-dependent diabetes mellitus is the result of a frank deficiency of insulin. The onset of this disease typically is in childhood. It is due to destruction pancreatic beta cells, most likely the result of autoimmunity to one or more components of those cells. Many of the acute effects of this disease can be controlled by insulin replacement therapy. Maintaining tight control of blood glucose concentrations by monitoring, treatment with insulin and dietary management will minimize the long-term adverse effects of this disorder on blood vessels, nerves and other organ systems, allowing a healthy life.

·Type II or non-insulin-dependent diabetes mellitus begins as a syndrome of insulin resistance. That is, target tissues fail to respond appropriately to insulin.

Typically, the onset of this disease is in adulthood.

Despite monumental research efforts, the precise nature of the defects leading to type II diabetes have been difficult to ascertain, and the pathogenesis of this condition is plainly multifactorial.

Obesity is clearly a major risk factor, but in some cases of extreme obesity in humans and animals, insulin sensitivity is normal.

Because there is not, at least initially, an inability to secrete adequate amounts of insulin,

insulin injections are not useful for therapy.

Rather the disease is controlled through dietary therapy and hypoglycemic agents.

Hyperinsulinemia or excessive insulin secretion is most commonly a consequence of insulin resistance, associated with type 2 diabetes or the metabolic syndrome.

More rarely, hyperinsulinemia results from an insulin-secreting tumor (insulinoma) in the pancreas.

Hyperinsulinemia due to accidental or deliberate injection of excessive insulin is dangerous and can be acutely life-threatening because blood levels of glucose drop rapidly and the brain becomes starved for energy (insulin shock).

Stand on a street corner and ask people if they know what insulin is, and many will reply, "Doesn't it have something to do with blood sugar?" Indeed, that is correct, but such a response is a bit like saying "Mozart? Wasn't he some kind of a musician?"
Insulin is a key player in the control of intermediary metabolism, and the big picture is that it organizes the use of fuels for either storage or oxidation.
Through these activities, insulin has profound effects on both carbohydrate and lipid metabolism, and significant influences on protein and mineral metabolism.
Consequently, derangements in insulin signalling have widespread and devastating effects on many organs and tissues.

The Insulin Receptor and Mechanism of Action

Like the receptors for other protein hormones, the receptor for insulin is embedded in the plasma membrane. The insulin receptor is composed of two alpha subunits and two beta subunits linked by disulfide bonds. The alpha chains are entirely extracellular and house insulin binding domains, while the linked beta chains penetrate through the plasma membrane.
The insulin receptor is a tyrosine kinase.
In other words, it functions as an enzyme that transfers phosphate groups from ATP to tyrosine residues on intracellular target proteins.
Binding of insulin to the alpha subunits causes the beta subunits to phosphorylate themselves (autophosphorylation), thus activating the catalytic activity of the receptor.
The activated receptor then phosphorylates a number of intracellular proteins, which in turn alters their activity, thereby generating a biological response.
Several intracellular proteins have been identified as phosphorylation substrates for the insulin receptor, the best-studied of which is insulin receptor substrate 1 or IRS-1.
When IRS-1 is activated by phosphorylation, a lot of things happen. Among other things, IRS-1 serves as a type of docking center for recruitment and activation of other enzymes that ultimately mediate insulin's effects.
A more detailed look at these processes is presented in the section on Insulin Signal Transduction.

Insulin and Carbohydrate Metabolism

Glucose is liberated from dietary carbohydrate such as starch or sucrose by hydrolysis within the small intestine, and is then absorbed into the blood. Elevated concentrations of glucose in blood stimulate release of insulin, and insulin acts on cells throughout the body to stimulate uptake, utilization and storage of glucose. The effects of insulin on glucose metabolism vary depending on the target tissue.

Two important effects are:

1.    Insulin facilitates entry of glucose into muscle, adipose and several other tissues. The only mechanism by which cells can take up glucose is by facilitated diffusion through a family of hexose transporters. In many tissues - muscle being a prime example - the major transporter used for uptake of glucose (called GLUT4) is made available in the plasma membrane through the action of insulin.

2.    When insulin concentrations are low, GLUT4 glucose transporters are present in cytoplasmic< vesicles, where they are useless for transporting glucose. Binding of insulin to receptors on such cells leads rapidly to fusion of those vesicles with the plasma membrane and insertion of the glucose transporters, thereby giving the cell an ability to efficiently take up glucose. When blood levels of insulin decrease and insulin receptors are no longer occupied, the glucose transporters are recycled back into the cytoplasm.

3.    The animation to the right depicts how insulin signalling leads to translocation of glucose transporters from the cytoplasm into the plasma membrane, allowing glucose (small blue balls) to enter the cell. Click on the "Add Glucose" button to start it.

It should be noted here that there are some tissues that do not require insulin for efficient uptake of glucose: important examples are brain and the liver. This is because these cells don't use GLUT4 for importing glucose, but rather, another transporter that is not insulin-dependent.
2. Insulin stimulates the liver to store glucose in the form of glycogen. A large fraction of glucose absorbed from the small intestine is immediately taken up by hepatocytes, which convert it into the storage polymer glycogen.

1.    Insulin has several effects in liver which stimulate glycogen synthesis. First, it activates the enzyme hexokinase, which phosphorylates glucose, trapping it within the cell. Coincidently, insulin acts to inhibit the activity of glucose-6-phosphatase. Insulin also activates several of the enzymes that are directly involved in glycogen synthesis, including phosphofructokinase and glycogen synthase.

2.    The net effect is clear: when the supply of glucose is abundant, insulin "tells" the liver to bank as much of it as possible for use later.

        A well-known effect of insulin is to decrease the concentration of glucose in blood, which should make sense considering the mechanisms described above.
        Another important consideration is that, as blood glucose concentrations fall, insulin secretion ceases.
        In the absence of insulin, a bulk of the cells in the body become unable to take up glucose, and begin a switch to using alternative fuels like fatty acids for energy.
        Neurons, however, require a constant supply of glucose, which in the short term, is provided from glycogen reserves.
        When insulin levels in blood fall, glycogen synthesis in the liver diminishes and enzymes responsible for breakdown of glycogen become active.
        Glycogen breakdown is stimulated not only by the absence of insulin but by the presence of glucagon, which is secreted when blood glucose levels fall below the normal range.

Insulin  and  Lipid  Metabolism

1.    The metabolic pathways for utilization of fats and carbohydrates are deeply and intricately intertwined. Considering insulin's profound effects on carbohydrate metabolism, it stands to reason that insulin also has important effects on lipid metabolism, including the following:

Insulin promotes synthesis of fatty acids in the liver.
        As discussed above, insulin is stimulatory to synthesis of glycogen in the liver.
        However, as glycogen accumulates to high levels (roughly 5% of liver mass), further synthesis is strongly suppressed.
        When the liver is saturated with glycogen, any additional glucose taken up by hepatocytes is shunted into pathways leading to synthesis of fatty acids, which are exported from the liver as lipoproteins.
        The lipoproteins are ripped apart in the circulation, providing free fatty acids for use in other tissues, including adipocytes, which use them to synthesize triglyceride.
        Insulin inhibits breakdown of fat in adipose tissue by inhibiting the intracellular lipase that hydrolyzes triglycerides to release fatty acids.
        Insulin facilitates entry of glucose into adipocytes, and within those cells, glucose can be used to synthesize glycerol.
        This glycerol, along with the fatty acids delivered from the liver, are used to synthesize triglyceride within the adipocyte.
        By these mechanisms, insulin is involved in further accumulation of triglyceride in fat cells.

1.    From a whole body perspective, insulin has a fat-sparing effect. Not only does it drive most cells to preferentially oxidize carbohydrates instead of fatty acids for energy, insulin indirectly stimulates accumulation of fat in adipose tissue

Other Notable Effects of Insulin

In addition to insulin's effect on entry of glucose into cells, it also stimulates the uptake of amino acids, again contributing to its overall anabolic effect. When insulin levels are low, as in the fasting state, the balance is pushed toward intracellular protein degradation.
Insulin also increases the permeability of many cells to potassium, magnesium and phosphate ions.
The effect on potassium is clinically important. Insulin activates sodium-potassium ATPases in many cells, causing a flux of potassium into cells. Under certain circumstances, injection of insulin can kill patients because of its ability to acutely suppress plasma potassium concentrations.

481, INSULIN - Training Clients With Diabetes

Training Clients With Diabetes Jeffrey Janot, M.S. and Len Kravitz, Ph.D. Introduction The incidence of diabetes mellitus, a metabolic disease, is a growing problem in the American population. To date, 16 million Americans have diabetes, either known or unknown, with 1,700 new cases being diagnosed everyday (Nieman 1998). Diabetes has been linked to the development of a variety of diseases including heart disease, stroke, peripheral vascular disease, and neurological disorders. The cause of death in individuals with diabetes is not the disorder itself, but from the diseases associated with it, most notably heart disease. Diabetes is classified into two categories: Type I and Type II. Typically, Type I diabetes occurs in younger individuals (not always!) and comprises approximately 10% of all diabetic cases. Thereby, 90% of the cases are Type II, which is most common in older individuals. Effective management and prevention strategies for diabetes are of utmost importance. As exercise professionals, you can play a crucial role within these strategies, working collaboratively with other skilled health professionals. It should be noted that there are a number of opportunities for personal trainers to enhance their professional knowledge, such as obtaining clinical-type certifications (ACE clinical exercise specialist, ACSM exercise specialist, etc.). This article will present recommendations and clinical considerations for the development of a safe strength training program for individuals with diabetes. A brief discussion of the pathophysiology behind diabetes will be presented first, followed by specific exercise prescription guidelines for strength training. In addition, Table 1 summaries some cardiorespiratory guidelines according to frequency, intensity, time and type (FITT) for the client with Type I and Type II diabetes. Pathophysiology of Type I and Type II diabetes The pancreas is the insulin-producing organ in the body. Insulin is made and stored in specialized cells within the pancreas and is released by various signals that are sensitive to the intake and digestion of food. In Type I diabetes, the specialized cells in the pancreas that produce insulin are destroyed, so that the production of insulin cannot occur in these individuals. In Type II, the specialized cells are able to produce insulin, but the insulin is ineffective at helping blood sugar (glucose) to enter the body tissues (most notably skeletal muscle) that need it for producing energy. This condition is called insulin resistance. In general, a normal resting blood glucose level ranges from 70 to 110 milligrams per deciliter (mg/dl) of blood. If two or more measurements of blood glucose levels (after a 12-hour fast) exceed 140 mg/dl, diabetes is typically diagnosed. The causes of diabetes are somewhat different between the two types. Heredity or a genetic pre-disposition to developing diabetes seems to be common to both types. Other factors related to Type I are environmental causes or viral infections that destroy the pancreas; whereas, increasing age, race, and obesity are related to Type II. Exercise training fits into the treatment scheme of diabetes by addressing the management of obesity. This is where exercise professionals can make the biggest impact on the treatment of diabetes. Strength training research and guidelines for diabetics The major benefits of resistance training in individuals with diabetes are: 1) improved blood cholesterol profiles, 2) increased heart function, 3) decreased blood pressure, 4) improved insulin sensitivity and blood glucose control, 5) improved muscular strength, power, and endurance, and 6) increased bone strength (Soukup et al. 1994). Two fairly recent studies by Eriksson and colleagues (1997) and Ishii and colleagues (1998) illustrate the benefits of strength training in the management of diabetes. In the study by Eriksson, eight participants who had Type II diabetes completed a 3-month progressive resistance program that consisted of two days a week of circuit weight training. One set of 15-20 reps was completed at each station with a 30-sec rest between stations. A variety of upper- and lower-body muscle groups were challenged. The researchers found that circuit weight training was responsible for improvements in blood glucose level control and that these improvements were significantly related to training-induced muscle hypertrophy. This study also showed that increases in muscle mass from strength training are important in the management of diabetes, as well as decreasing the risk for developing complications associated with diabetes. In the study by Ishii and colleagues (1998), 17 individuals with Type II diabetes were placed into two groups: a strength-training group and sedentary control group. The training group participants were instructed to train five times per week for 4-6 weeks at workloads corresponding to 40-50% of their 1 rep max. Two sets of 10 repetitions for upper body muscles and two sets of 20 repetitions for lower body muscles were done using the following exercises: arm curl, military press, bench press, squats, knee extensions, heel raises, back extensions, and bent knee sit-up. The researchers reported that the rate of blood glucose entry into the working muscles increased after training. This study demonstrates that moderate-intensity, high volume training improved insulin sensitivity by 48% in these individuals. Strength training prescription guidelines for clients with diabetes Determining resistance. In both groups, 1 rep maximum testing can be done provided that the person’s diabetes is stable and has no complications that can be affected by maximum exertion. In general, most people can tolerate 30-50% of 1 rep maximum for a workload during exercise training. Number of sets and repetitions. 1-2 sets per exercise is a good starting point for your client. Repetitions can be established in the same manner as you would for an individual without diabetes. Base your prescription on the client’s individual goals and their exercise tolerance. In general, use lower repetitions/higher resistance for strength and higher repetitions/lower resistance for endurance. Rest time between sets. Using 30-60 seconds for the rest period is appropriate in most situations. With greater intensity bouts a slightly longer (up to 2 minutes) rest period may be necessary. Frequency of strength training. Having your client strength train at least two days per week is appropriate in order to see beneficial results from the type of exercise, as shown in the study by Eriksson and colleagues (1997). Clinical considerations for exercising the individual with diabetes Some considerations regarding exercise prescription involve minimizing the risks involved with exercising individuals with diabetes. In cases where the individual has vascular problems and/or high blood pressure, consult the client’s physician before progressing. Also, use lighter workloads for these individuals, as they will not increase blood pressure as much as the higher loads. It is also important to attempt to minimize the risk of your client for developing hypoglycemia (low blood glucose) during exercise. Strategies such as eating 1-2 hours before exercise, eating a snack before exercise (and possibly during), having them check their blood glucose before exercising, and knowing the warning signs of hypoglycemia (dizziness, anxiety, shaking, and uneasiness) will help exercise tolerance. Knowing when to stop exercise and seek emergency care is a point that cannot be overstated by these authors. Clients should consult their dietitian or physician on what foods are appropriate to eat before, during, and after exercise. Lastly, follow general exercise guidelines such as proper warm-up and cool-down, appropriate footwear, adequate hydration, and avoid exercising in extreme environments. Major contraindications to exercise training with diabetics is presented in Table 2. Summary The main goal of the treatment of diabetes is to achieve good blood glucose control and avoid complications related to high blood glucose (Eriksson et al. 1997). Since exercise has an insulin-like effect on blood glucose levels, exercise should be considered as an adjunct to the medical management of diabetes. Strength training (when done correctly) has been shown to provide a safe and effective way to control blood glucose, increase strength, and improve the quality of life in individuals with diabetes.