Introduction:
If you have high abdominal fat and your Blood pressure is slightly elevated, you need to worry even if your BMI is normal because this may be a sign of impending diabetes. Let us understand how the diabetes is developed and further progressed. Understanding how the diabetes is developed and further progressed is the key to cure it, so let us first understand the mechanism of its development. Diabetes is caused by a problem in the way human body makes or uses insulin. Insulin is needed to move blood sugar (glucose) into cells, where it is stored and later used for energy.
Beta cells produce insulin in response to blood glucose. These beta cells produce insulin in precise proportion to the level of glucose in the blood stream. Following a meal, blood sugar levels rise significantly, and the beta cells release a large amount of insulin. This insulin causes body cells to grab the sugar, causing blood sugar to quickly return to its normal range. Once blood sugar is in the normal range, the beta cells reduce the output of insulin to an idling state. In this way, the beta cells adjust their production of insulin on a real time basis, producing just enough insulin to deal with the amount of blood sugar currently in the blood stream.
In type 1 diabetes, the beta cell islets are destroyed. Once the islets are killed, the ability to produce insulin is lost, and the symptoms and consequences of diabetes begin. In type-II diabetes Insulin resistance is the prime cause of diabetes. Insulin is a chemical messenger signalling proteins called GLUT-4 transporters (residing within the cell) to rise up to the cell’s membrane, where they can grab on to glucose and take it inside the cell. In patients with insulin resistance, the cells do not get the message that the glucose is available. Cells are unable to hear insulin “knocking” on the door resulting in elevated blood levels of both insulin and glucose
In the early stages of insulin resistance, the pancreas compensates by producing more and more insulin, and so the “knocking” becomes louder and louder. The message is eventually “heard”, enabling glucose transportation into the cells, resulting in the eventual normalization of blood glucose levels. This is known as “compensated insulin resistance”. The liver helps regulate glucose levels by reducing its secretion of glucose in the presence of insulin. This normal reduction in the liver’s glucose production may not occur in people with insulin resistance.
Over time, the stress of excessive insulin production burns out the beta cells unable to keep pace with accelerated output. As a result, glucose levels remain elevated for prolonged periods. This is called “uncompensated insulin resistance” and is the essence of advanced type 2 diabetes.
Gradually, increased insulin resistance and various other factors discussed later diminish the ability of pancreas to produce sufficient insulin and the classification line between type-I and type-II diabetes becomes blurred.
Insulin Resistance
As explained above Insulin resistance (IR) is a physiological condition where the natural hormone insulin , becomes less effective at lowering blood sugars. The resulting increase in blood glucose may raise levels outside the normal range and cause adverse health effects, depending on dietary conditions . Certain cell types such as fat and muscle cells require insulin to absorb glucose. When these cells fail to respond adequately to circulating insulin, blood glucose levels rise.
It is well known that insulin resistance commonly coexists with obesity . However, causal links between insulin resistance, obesity, and dietary factors are complex and controversial
In experiment carried out on rodents, large quantities of saturated, monounsaturated, and polyunsaturated (omega-6) fats all appear to be contributing to Insulin Resistance to some degree, compared to high-starch food, but saturated fat appears to be the most effective at producing IR. This is partly caused by direct effects of a high-fat diet on blood markers, but, more significantly high-fat diet has the tendency to result in caloric intake far exceeding animals’ energy needs, resulting in rapid weight gain. The effect of dietary fat is largely or completely overridden if the high-fat diet is modified to contain nontrivial quantities (in excess of 5-10% of total fat intake) of polyunsaturated. omega-3 fatty acids. This protective effect is most established with regard to the so-called “marine long-chain omega-3 fatty acids”, EPA and DHA , found in fish oil; evidence in favor of other omega-3′s, in particular, the most common vegetable-based omega-3 fatty acid, ALA is more limited. Some studies find ALA only effective among people with insufficient long-chain omega-3 intake and some studies fail to find any effect at all . ALA can be partially converted into EPA and DHA by the human body, but the conversion rate is thought to be 10% or less, depending on diet and gender, limiting its effectiveness.
Elevated levels of free fatty acids and triglycerides in the blood stream and tissues have been found to contribute to insulin resistance. Triglyceride levels are correlated with excess body weight, overeating and trans fat intake. They are strongly inversely correlated with omega-3 intake and fat loss again highlighting the importance of omega-3 rich diet and exercise.
Intake of simple sugars, and particularly fructose , is also a factor that contributes to insulin resistance. Fructose is metabolized by the liver into triglycerides, tends to raise their levels in the blood stream. Therefore, it may contribute to insulin resistance through the same mechanisms as the dietary fat. Experiments on rodents suggest that, high levels of fructose and/or sucrose induce insulin resistance similar to that of fats, and, this insulin resistance is ameliorated by fish oil supplementation. A low-fat diet high in simple sugars (but not in complex carbohydrates and starches) stimulates fatty acid synthesis, primarily palmitate , therefore, resulting in the plasma fatty acid pattern that is similar to that produced by a high-saturated-fat diet. However, very little is known about effects of simple sugars in whole fruit and vegetables. Epidemiological studies suggest that their high consumption is associated with somewhat lower risk of insulin resistance.
Another mechanism contributing to Insulin resistance is leptin resistance. An important role of leptin is long-term inhibition of appetite in response to formation of body fat. In some individuals this mechanism is disrupted and their appetite and caloric intake is not reduced despite elevated level of leptin. Once leptin resistance is developed, the individual becomes prone to further overeating, weight gain, and insulin resistance. Experiments on rats suggest that leptinresistance can be triggered by chronic consumption of fructose or consumption of energy-dense, highly palatable food over a period of several days.
Insulin itself leads to a kind of insulin resistance; every time a cell is exposed to insulin, the production of GLUT4 (type four glucose receptors) on the cell’s membrane decreases. In the presence of a higher than usual level of insulin (generally caused by insulin resistance), this down-regulation acts as a kind of positive feedback, increasing the need for insulin. Exercise reverses this process in muscle tissue.
Some scholars propose that insulin resistance and obesity are not really metabolic disorders per se, but simply adaptive responses to sustained caloric surplus, intended to protect bodily organs from lipotoxicity (unsafe levels of lipids in the bloodstream and tissues). It has been suggested that exclusion of glucose from lipid-laden cells by developing insulin resistance is a compensatory defence against further accumulation of lipogenic substrate.
Fast food meals are energy-dense, palatable, and cheap, increasing risk of overeating and leptin resistance. They are simultaneously high in dietary fat and fructose, and low in omega-3. These characteristics have independently been linked to insulin resistance.
In most cases, therefore, development of diabetes is nature’s way of maintaining energy and mass balance in response to the sustained high Caloric intake (mostly in the form of carb and fat) for many years without expenditure of those calories, resulting in metabolic changes causing insulin resistance and subsequent beta cell destruction in pancreas. Our system begins to adjust to the high calorie diet and low activity level five to seven years before we are ever diagnosed with diabetes. Our body seems to recognise that it is surplus of calories and stored fat and reprograms itself not to absorb the energy from food as efficiently as it used to. Insulin resistance is developed which prohibits the cells to listen to the insulin signal. This results in rising of the blood glucose level due to non-absorption in the cells. Excessive amount of glucose circulation in the blood plasma is called hyperglycaemia.
Main Symptoms when left undiagnosed:
People with hyperglycaemia feel hungry because their cells are unable to absorb the sugar in the blood, and the body reacts as if it needs more food (Polyphagia). All the excess sugar in the blood eventually winds up in the urine, and this acts as a diuretic, as the body tries to bring more water in to dilute the urine. This is why polyuria occurs. Because the hyperglycemic person is producing so much urine, they naturally feel thirsty as their body tries to replace the water resulting in the classical symptom of Polydipsia.
Other Dangers of Insulin Resistance
Insulin resistance causes high level of circulatory insulin due to compensatory mechanism, drugs for type-II diabetes or externally administered insulin or simply due to chronic high calorie diet. This may pose several other dangers to the health.
Cancer
Insulin stimulates cell growth, and unfortunately cancer cells have six to 10 times the number of insulin receptors–molecules that grab on to the hormone–as do normal cells. So if extra hormone hits a pre-existing cancer cell, it makes a bad thing much, much worse. “For cancer, insulin is like pouring gasoline on a fire.
Cardiovascular Disease
High levels of insulin in the blood damage the lining of arteries, increase bad blood fats such as triglycerides and LDL cholesterol, and clump blood cells together so they are more likely to block up vessels
Polycystic Ovary Syndrome
High level of insulin causes Polycystic Ovary Syndrome which causes infertility and dramatically raises the risk for heart disease.
In addition to above some studies also link Alzheimer’s, Parkinson’s, and Huntington’s diseases to insulin resistance
Mechanisms of Beta-Celldestruction
Insulin resistance often leads to Beta-Cell destruction through various mechanism listed below. However, some individuals may have limited Beta-Cellmass early in life because of genetic factors predisposing them to diabetes.
Central Obesity is the main risk factor for the development of diabetes. It is often accompanied by an elevation of lipids in the blood (dyslipidemia) and increased circulating leptin and cytokine levels. All of these factors have been shown to modulate Beta-cell function and survival. The influence of dyslipidemia on the Beta-cells of an individual will depend on his or her specific lipid profile. Whereas some free fatty acids and lipoproteins have been shown to be pro-apoptotic for the Beta-cell, others are protective. Thus, long-term exposure to saturated fatty acids such as palmitate (a saturated fatty acid that is found in humans, animals and plants and is a major component of palm oil) appears highly toxic, whereas monounsaturated fatty acids such as oleate protect against both palmitate- and glucose-induced Beta-Cellapoptosis. It is interesting to note that similar toxic effects are also observed in non-Beta-cells such as cardiac cells. Lipoproteins may affect Beta-Cellsurvival in a similar way, whereby VLDL and LDL are pro-apoptotic and HDL is protective.
Mitochondrial dysfunction has also been proposed as a common feature of both impaired insulin responsiveness of peripheral tissues and defective Beta-Cellsecretory function and survival.
Oxidative stress affect insulin sensitivity, insulin secretion, Beta-cell survival, and also play a role in the development of the secondary complications of diabetes These effects are mainly catalyzed by the generation of reactive oxygen species and reactive nitrogen species, which ultimately activate stress-induced pathways (transcription factor nuclear factor (NF-kB), stress kinases, and hexosamines) to manipulate cell fate.
Some in vitro studies suggest that closure of the KATP channels by the sulfonylureas tolbutamide and glibenclamide (commonly prescribed drug for type-II diabetes) may induce Ca2+-dependent Beta-cell apoptosis in rodent and human islets. In an important recent clinical study comparing insulin and sulfonylurea treatment of type 2 diabetes, it was shown that treatment with insulin preserved Beta-cell function more effectively than glibenclamide. It remains to be established whether it is the beneficial effects of insulin or the possible Beta-cell toxicity of glibenclamide that accounts for this observation.
Summing up, High energy food, rich in carbohydrates, fats and simple sugars coupled with low activity level appear to be contributing to Insulin Resistance and Beta-cell destruction. Hyperglycaemia plays a central role among those factors contributing to both Beta-cell “burnout” and insulin resistance. While transient postprandial hyperglycaemic excursions may predominantly induce Beta-cell proliferation in insulin-resistant individuals, this adaptive mechanism fails in the long run and is overridden by Beta-cell destruction (apoptosis). In addition this, hyperglycaemia also impairs Beta-cell secretory function. This glucotoxic effect is evident before apoptosis leads to a significant decrease in Beta-cell mass. Glucotoxicity does not act alone. Saturated fatty acids, lipoproteins, leptin, and circulating and locally produced cytokines further burn out the Beta-cells and are also prominent factors in developing insulin resistance. Increasing evidence in both experimental and clinical studies suggests that oxidative stress plays a major role in the pathogenesis of both types of diabetes mellitus. Abnormally high levels of free radicals and the simultaneous decline of antioxidant defense mechanisms can lead to damage of cellular organelles and enzymes, increased lipid peroxidation, and development of insulin resistance. Studies suggest that some therapeutic agents prescribed for type-II diabetes may also negatively influence the fate of the Beta-cells. Insulin resistance causes high level of circulatory insulin due to compensatory mechanism, drugs for type-II diabetes, externally administered insulin or simply due to chronic high calorie diet even in healthy individuals. This may pose several other dangers to the health including proliferation of pre-existing Cancers, Obesity, Cardiovascular Disease, Polycystic Ovary Syndrome, and is also linked to Alzheimer’s, Parkinson’s, and Huntington’s diseases.
Cure
Knowing the mechanism of insulin resistance and Beta-Cell destruction, it is easy to understand how this deadly disease can be cured. As explained above diabetes is nature’s way of maintaining energy and mass balance in response to the sustained high Caloric intake (mostly in the form of carb and fat) without the matching activity level for many years, resulting in metabolic changes causing insulin resistance and subsequent beta cell destruction in pancreas. The key to cure this disease is to reduce calorie intake and increase physical activity to burnout the excessive storage of body fat primarily in abdominal region. In addition to this, as oxidative stress and dyslipidemia are also major factors in developing insulin resistance and beta cell destruction, A diet comprising of antioxidants and “marine long-chain omega-3 fatty acids”, EPA and DHA , will be specially useful in reverting the disease. Although less effective, those who are vegetarian may consume omega 3 fatty acids of plant origin. Some Yogic exercises are said to regenerate Beta-Cells and should be practiced if possible. The three pronged approach comprising of increasing physical activity, practicing yoga to regenerate pancreatic beta cells and restore there secretory functions and modifying the diet is explained below.
Physical Activity
To restore mass and energy balance in our body in order to help prevent or reverse insulin resistance is exercise. If high abdominal fat exist and body mass index (BMI) is high, initially more calories are required to be burnt than what is consumed so that stored fat reserves get depleted. Once the body mass index (BMI) is reached in the range of 22-23, try to maintain that weight by adjusting the exercise intensity and caloric intake.
Increase in daily activity level can be useful. Some of the ideas to increase the activity level are to use stairs instead of lift if health permits, parking car away so that small walk is needed to reach the destination and including some light sports in daily activity schedule
Brisk walk can be a safe exercise for adults of all age groups. Four km of brisk walk ( 2 km each in morning and evening is recommended. However, distance and speed should be increased gradually to avoid fatigue, stress and injuries. Highest speed of 6 to 6. 5 km/hr is sufficient. This will burn about 300-325 kcal per day. Once the target weight fat reduction is achieved, duration of walk can be reduced. Brisk walk will not only burn calories but will also improve cardio-vascular health.
Yoga
Some asana are helpful in regenerating pancreatic beta cells. The list includes Halasan, Naukasan, ArdhNaukasan, Ardh Badh Padm Paschimottanasan, Paschimottanasan, Dhanurasan, Urdhwa Dhanurasan, Bhujangasana, Shalabhasana, Ardhmatsyendrasana, Matsyendrasana, Mayurasana, Padm-mayurasana, Hansaasana, etc. These should be practiced according to once capacity and should be tried gradually in supervision of an expert to avoid injury.
Diet
Only exercise cannot restore the energy and mass balance required for healthy living. It is required to cut the unwanted calories without cutting essential nutrients. A normal adult man doing light work needs about 2200 kcal per day and a normal adult women doing light work need at least 1900 kcal per day. The Dietary Guidelines recommends distribution for the energy nutrients from Fat: 20 – 35% of total calories (average 30%), from Protein: 10 – 35% (average 15%) and from Carbohydrates: 45 – 65% (average 55%). Some healthy diets, like the Mediterranean Diet, promote 40% of calories from fat, but the fat must be olive oil, fish oil and nuts. Alcohol is the fourth energy-producing nutrient, and it is recommended in moderation, if at all.
Replace bad fat by good fat
Replace saturated fat such as ghee (purified butter) and butter from your diet with oils rich in monounsaturated and poly unsaturated fatty acids such as mustard, peanut, olive, sunflower or safflower oils. Monounsaturated fatty acids (MUFAs) and Poly unsaturated fatty acids (PUFAs) may help lower your risk of diabetes and heart disease by improving related risk factors. For instance, MUFAs may lower your total cholesterol and low-density lipoprotein cholesterol levels. MUFAs may also help normalize blood clotting. And some research shows that MUFAs may also benefit insulin levels and blood sugar control, which can be especially helpful if you have type-II diabetes. MUFA such as oleate also protect against both palmitate- and glucose-induced Beta-Cellapoptosis.
Use Olive Oil
The Mediterranean diet, which is abundant in antioxidants, is associated with a relatively low incidence of coronary heart disease and diabetes. Olive oil and olives, which contain the antioxidants hydroxytyrosol, oleuropein, and tyrosol, are important components of this diet and may have beneficial effect in type-I and type-II diabetes by reducing oxidative stress.
The main type of fat found in all kinds of olive oil is monounsaturated fatty acids (MUFAs). MUFAs are actually considered a healthy dietary fat. Use unsaturated fats, such as MUFAs and polyunsaturated fats (PUFAs), instead of saturated fats and trans fats.
But even healthier fats like olive oil are high in calories, so use them only in moderation. Choose MUFA-rich fats such as olive oil instead of other fats – particularly butter and margarine – not in addition to them. And remember that you can’t make unhealthy foods healthier simply by adding olive oil to them.
Remember that heat, light and air can affect the taste of olive oil and possibly its health-promoting nutrients. Store olive oil in a dark, room-temperature cupboard, or even in the refrigerator. The fats and healthy phytonutrients in olive oil – as well as the taste – can slowly degrade over time, so it’s probably best to use it within a year or within six months once opened.
Never Use Trans-fats
Trans fat is the common name for unsaturated fat with trans-isomer (E-isomer) fatty acid (s). Because the term refers to the configuration of a double carbon-carbon bond, trans fats may be monounsaturated or polyunsaturated but never saturated .
No trans fats are essential fatty acids ; indeed, the consumption of trans fats increases the risk of coronary heart disease by raising levels of “bad” LDL cholesterol and lowering levels of “good” HDL cholesterol. Health authorities worldwide recommend that consumption of trans fat be reduced to trace amounts. Trans fats from partially hydrogenated oils are more harmful than naturally occurring oils
Consume food rich in Omega-3 Fatty Acids:
Oily fish are rich source of omega 3 fatty acids DHA and EPA. Omega 3 fatty acids of plant origin ( found in flaxseed, almonds and walnuts, The 18 carbon α-linolenic acid (ALA) has not been shown to have the same cardiovascular and anti-diabetic benefits as DHA or EPA due to conversion efficiency in mammals from ALA to DHA and EPA. DHA and EPA are made by marine microalgae. These are then consumed by fish and accumulate to high levels in their internal organs. However, it is recommended to limit the fish intake up to two serving per week for adult healthy man and to even lower level in pregnant woman and children to avoid dangers of mercury contamination found in fish.
Aspartame
Aspartame has been the subject of several controversies, hoaxes and health scares since its initial approval by the U. S. Food and Drug Administration (FDA) in 1974. Critics allege that conflicts of interest marred the FDA’s approval of aspartame, question the quality of the initial research supporting its safety, and postulate that numerous health risks may be associated with aspartame. Veracity of these claims could not be verified, however, warning on its label that Aspartame is not recommended for children indicates that it is not a healthy product and may have some side effects. I therefore, recommend that aspartame or the food items containing aspartame should be better avoided.
Avoid processed and fast food
Say no to namkeens, kurkure, pop tarts, commercially prepared fish sticks, stick margarine, cake, candy, cookies, readymade or ready to cook microwave popcorns, burgers, and pizzas, as they are high in calories and often contain transfats. A 100 gm portion of a popular namkeen contains about 560 kcal whereas one hour of brisk walk will only burn about 400 kcal. Fast food meals typically possess several characteristics which have independently been linked to insulin resistance. They are energy-dense, palatable, and cheap, increasing risk of overeating and leptin resistance. They are simultaneously high in dietary fat and fructose and low in omega-3; and they usually have high glycemic indices. Consumption of fast food has been proposed as a fundamental factor behind the coronary heart diseases, diabetes and obesity.
Cut on calories from refined sugar and high simple carbohydrate food:
As a balance between calorie intake and expenditure is required to be met without cutting on essential nutrients, it is therefore recommended to replace simple carbohydrates like refined sugar, and sweet beverages with complex carbohydrates and proteins. Adequate amount of protein will ensure synthesis of adequate muscle mass due to increased level of exercise. Recommended amount of protein in grams is about 0. 5 to 0. 9 times your body weight in kg depending upon the exercise level.
Food with large amounts of complex carbohydrates include legumes, starchy vegetables like potatoes and corn, rice and grain products. Other vegetables such as green beans, broccoli and spinach contain less starch, but they have more fiber.
Complex carbohydrates should supply about half the calories in diet. However, the best complex carbohydrates come from legumes, vegetables, breads, pasta and cereals. Choose 100% whole wheat or 100% whole grain brad cereal and pasta products over refined flour products because they contain more fiber. The extra fiber slows down the absorption of the carbohydrates so you feel full longer and be less likely to over-eat throughout the day.
Eat Ample Quantity of Vegetable Salad
Every meal should include plentiful of salad and it should be consumed before main course. This helps satiate your stomach and reduces chances of overeating. Salad may be dressed with olive oil. In addition to this fruit shall be consumed in moderation once a day as they often have enough oxidants and essential nutrients which are essential for overall well being. Once you are able to manage your overall calories you should not be afraid of sugar from fruit in moderate amount.
Type-II diabetes can be delayed, prevented or reversed with safe, inexpensive therapy such as losing weight, changing eating habits, and exercising. It is true that it does take a serious commitment on your part to certain lifestyle changes, but these changes are possible to achieve and the results will be extremely gratifying.
