The last two centuries saw Americans transforming from fit to fat and from overweight to obese. Heart disease, cancer, autoimmune disease, obesity, and metabolic syndrome plagued the whole American society with very little sign of statistic improvement. Maybe you have heard of metabolic syndrome, or maybe not, but according to recent statistics, 27 percent of all American adults and 40 percent in their 60s and 70s, fit the criteria of having the syndrome.
Syndrome X is seen as the common cаuѕe of premаture deаth and diѕаbility, leading to аccelerаted and preliminary аging. Despite, insulin resistance is considered the main culprit behind the metabolic syndrome appearance, there are few other hormones involved in its pathogenesis. One of them is the hormone leptin. Its discovery (1994) marked one of the most significant changes in conventional medical theories and practice.
Leptin is a major and powerful hormone that sends impulses to a specific structure in the human brain (hippocampus) suggesting resistance to the temptation of foods. When food is consumed, leptin is secreted by the adipose (visceral and subcutaneous) tissue into the blood where it sends impulses to the brain. There is a structure in the human brain known as “nucleus caudatus,” armed with specialized receptors that respond to leptin.
Actually, leptin is a hunger-mediator, causing feelings of satiety and is proven critical in controlling the caloric intake. It can be easily compared to a natural appetite suppressant, while insulin- to an appetite stimulant. Leptin can be also compared to the principle violin in the philharmonic orchestra – the “concertmaster”– who controls (tunes) the other instruments (hormones) - to function- or – not. The hormone works to increase energy expenditure, thus being particularly responsible for the body fat warehouse. Rosenbaum is one of the first researchers whose attention stayed focused mainly on the paradigm “leptin and leptin resistance.” Its discovery helped scientists to start “in vivo” clinical trials with leptin that caused mice to eat less and lose weight. According to the author, leptin may explain why people who lose weight often have a hard time keeping it off, and by restoring leptin to its pre-diet levels may reverse the problem. The article published in the International Journal of Obesity (2004; 28, p.1344–48) proved that “obese subjects are almost uniformly hyperleptinemic, but the hypothalamus is unable to transduce this leptin signal to reduce body weight, termed 'leptin resistance'.” Explained differently, leptin resistance occurs when the body is no longer efficient at carrying the hormone across the blood-brain barrier to the brain. By offering completely “new way” for dieters to treat obesity, Rosenbaum et al. concluded that “when someone looses weight it is created about the ‘perfect storm’ for regaining weight,” and that “after a significant weight loss, the metabolism not only becomes more efficient, but the brain becomes more vulnerable, as there are areas of the brain that seem to be less active-thus, one becomes more responsive to food and in less control of it, as per his final conclusions.” (Rosenbaum et al., 2004) http://www.nature.com/ijo/journal/v28/n10/full/0802753a.html Several other teams of researchers pointed out to the fact that hormonal imbalance may have everything to do with being overweight or obese. Hart abd Grossman (2007) believed that the fat cells do not and cannot develop insulin resistance to the degree other body and organ’s cells do, and as a result of insulin resistance, all muscles and organs are being starved, while fat cells are being fed. They were working on leptin resistance, as the main culprit behind the syndrome appearance. That was the new “missing link” that surfaced in the field of weight loss. Insulin was just seen as a co-promoter in the appearance of the “apple shape” obesity— main marker of the metabolic disorder. Researchers agreed that the more insulin the pancreas secretes— the more likely is the appearance of the “apple shape” around the waist. It was also proved that the more “leptin resistant” the body becomes— the more likely is the metabolic syndrome appearance. Apparently, hyperinsulinemia combined with insulin and leptin resistance can make anyone obese.
You may request our "Leptin Restore" program or an on line or by phone alternative consultation, as well as newly written article that can suit your business purposes:: (715) 392-7591; (218) 213-6167; (218) 213-7087 These statements have not been evaluated by the Food and Drug Administration. The material in this newsletter is provided for informational purposes only. Thus our intentions are not to diagnose, cure, mitigate, treat or prevent any disease. If you use the information in this newsletter without the approval of your health professional, the authors of this letter do not assume any responsibility. Copyright @ 2009, Natural Health-Wellness LLC. All rights reserved. You may visit us at:http://www.examiner.com/x-49392-Milwaukee-Diets-Examiner
Metabolic syndrome is highly prevalent in the today’s Western World, and the number of people who struggle with it and its deadly consequences continues to rise. The reason for the increased incidence of metabolic syndrome in the highly industrialized countries is mainly due to the high level of stress, malnutrition, use of over processed food, and physical inactivity. The metabolic derangement includes cardiovascular disease, diabetes 2, abdominal obesity (increased waist circumference), hypertension, high triglycerides, low levels of high density lipoprotein (good cholesterol), and high levels of low density lipoprotein (bad cholesterol) combined with high fasting glucose levels (insulin resistance). The terms “metabolic syndrome,” "insulin resistance syndrome,” dysmetabolic syndrome”, “syndrome X," “Syndrome X,” “Raven’s syndrome,” and CHAOS (in Australia) are all synonyms used specifically to define the syndrome as a constellation of symptoms or conditions associated with increased risk for the development of type 2 diabetes and atherosclerotic vascular disease (e.g. heart disease, coronary artery disease and stroke). The cluster of metabolic abnormalities has been also named the “Deadly Quartet” by Kaplan (1989), due to the fact that metabolic syndrome can lead to type 2 diabetes (the most common type of diabetes mellitus), high blood insulin levels, high blood pressure, obesity and poor lipid profile (dyslipidemia) - elevated LDL (“bad”) cholesterol, elevated triglycerides, low HDL (“good”) cholesterol, with increased risk for clotting-heart attack, stroke, gout, kidney failure and Alzheimer disease. The syndrome comprises an accumulation of different and mutually intensifying diseases and risk factors, which mostly share the same causes. Actually, metabolic syndrome is a known as a cluster of disorders, affected by both genetics and lifestyle intrinsic and extrinsic factors. It affects a large number of people in a clustered fashion. In some studies it is calculated as being up to 25% of the population in USA. It increases the risk of type 2 diabetes (the most common type of diabetes) anywhere from 9-30 times that of the normal population and despite studies vary the risk of heart disease increases 2-4 times over the normal population. There are also other concerns as well as fat accumulation in the liver (also known as fatty liver), resulting in chronic inflammation and the potential for degenerative cirrhosis. The kidneys can also be affected, as there is an association with microalbuminuria- the leaking of protein into the urine, a subtle but clear indication of kidney damage. Other problems associated with metabolic syndrome include obstructive sleep apnea, polycystic ovary syndrome (POOS), increased risk of dementia with aging, and rapid cognitive decline in the elderly. The main features of metabolic syndrome include insulin resistance, obesity, hypertension (high blood pressure), cholesterol abnormalities, and an increased risk for clotting. It is a cluster of conditions that occur together in one the same person. It is increasing the risk of heart disease, stroke and diabetes. Having just one of these conditions- increased blood pressure, elevated insulin levels, excess body fat around the waist or abnormal cholesterol levels- is not a guarantee that you have metabolic syndrome, but it does contribute to the risk of it. If more than one of these conditions occurs in combination, the risk is even greater. What remains yet controversial is whether metabolic syndrome should be considered a coronary equivalent or not. There is also a debate as to whether it is obesity or insulin resistance that causes metabolic syndrome, or if the syndrome is a result of a greater metabolic cause. Insulin resistance refers to the diminished ability of cells to respond to the action of insulin in promoting the transport of the sugar glucose, from blood into muscles and other tissues. Because of the main role that insulin resistance plays in the metabolic syndrome, a separate part of the study as devoted to insulin resistance. The literature research depicts that long with regular medical checkups few tests will help to diagnose and monitor the syndrome (Grundy et al., 2005). Excess of insulin can cause fat storage. When excess insulin is secreted in response to excess sugar consumption, the blood sugar (glucose) is stored in fat cells. Normally, the glucose is used by the cells of the body and mostly stored in the muscles and the liver. But when there is more than the body can use, insulin forces fat cells to take in blood lipids called triglycerides and fat cells grow. Metabolic syndrome can remain latent for years, masquerading as other diseases like: Chronic Fatigue Syndrome (CFS), attention deficit disorder (ADD), obesity, kidney failure with edema (fluid retention), bipolar disorder, etc. Despite the serious cardiovascular risk posed by metabolic syndrome, there is currently no standard, accepted interventional treatment regimen to prevent the disorder. However, for those at greatest risk for metabolic syndrome, phenotypic nutrition allows nutritionists to tailor a nutrient and supplement strategy to amplify beneficial biochemical pathways as well as gene expression. Mechanism of appearance (Pathogenesis): An important pathogenic factor is the insulin-resistance which is often a consequence of increased obesity. Metabolic syndrome is a cluster of: 1. Abdominal obesity (waist circumference: Men — waist greater than 40 inches; Women — waist greater than 35 inches 2. Triglycerides — greater than 150 mg/dl 3. HDL Cholesterol — less than 50 mg/dl in women, and less than 40mg/dl in men 4. Blood pressure — greater than 130/ 85 mm Hg 5. Fasting glucose — greater than 110 mg/dl To be diagnosed with Metabolic Syndrome one must present the following: Central obesity (waist circumference) greater than 40 inches for men and greater than 35 inches for women Fasting blood triglycerides greater than or equal to 150 mg/dl Blood high-density lipoprotein (HDL) of less than 40 mg/dl for men and less than 50 mg/dl for women Blood pressure greater than or equal to 130/85 mmHg Fasting glucose greater than or equal to 110 mg/dL. Fasting plasma glucose test. This convenient test measures blood glucose after at least 8-12 hours of fasting. It is used to detect diabetes or pre-diabetes Oral glucose tolerance test. This highly sensitive test, which is used to diagnose diabetes or pre-diabetes, measures blood glucose after fasting for at least 8 hours and 2 hours after a glucose-containing beverage. Casual (random) plasma glucose test. This test measures blood glucose no matter when last meal was eaten. This test, along with other symptoms, is used to diagnose diabetes but not pre-diabetes. Tests you must request: 1. Fasting blood sugar or three-hour glucose tolerance test (diagnoses pre-diabetes). 2. Iron panel — includes ferritin, tranferrin, iron-binding capacity and free iron level. 3. Cholesterol (with complete breakdown of subtypes) -- LDL, HDL, VLDL, and Triglycerides levels. 4. Independent risk factors: homocysteine, Lp(a), fibrinogen and CRP. 5. Blood pressure frequent monitoring. 6. Waist measurement and Body Mass Index (BMI) calculation. 7. C-reactive protein test (CRP) and Homocysteine test. The above tests measure the rate of inflammation. 8. Total cholesterol, HDL, LDL and triglyceride test. The above tests measure the level of dyslipidemia. 9. Urine test for microalbuminuria. 10. Hemoglobin A1C (measures the chronic blood sugar glycation control). Hb (A1) or glycosilated (glycated) test. This Hb is a form that is implicated in the diabetic nephropathy, retinopathy and neuropathy and Type 2 diabetes. Note* Test-results that come back positive for diabetes should be confirmed by repeating the fasting plasma glucose test or an oral glucose tolerance test on a different day. If one has been diagnosed with prediabetes or diabetes, there are a number of different ways to monitor it. Your MD will select the right drug, or procedure, while the ND- the correct diet, nutraceutical, herb or lifestyle changing approach.
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http://www.examiner.com/x-49392-Milwaukee-Diets-Examiner?showbio If you would like to learn more on the above topic, to request an on line or by phone alternative consultation, or a newly written article that can suit your business purposes, please call: (715)392-7591; (218) 213-6167; or (218) 213-7087 These statements have not been evaluated by the Food and Drug Administration. The material in this newsletter is provided for informational purposes only. Thus our intentions are not to diagnose, cure, mitigate, treat or prevent any disease. If you use the information in this newsletter without the approval of your health professional, the authors of this letter do not assume any responsibility. Copyright @ 2009, Natural Health-Wellness LLC. All rights reserved.
Insulin is an important polypeptide hormone secreted by the islets of Langerhans in the pancreas that is central to regulate the metabolism of carbohydrates and fats in the human body. Its main role is in the conversion of glucose to glycogen, which lowers the elevated blood glucose to normal levels. Insulin causes body cells in different organs and tissues (e.g. liver, muscle, and fat tissue) to utilize glucose from blood, storing the restful amount as glycogen in the liver and muscle. It helps controlling the metabolism of foods you eat and levels of glucose in the blood as an authentic “key keeper."
The function of insulin seems rather simple. During digestion, sugar is absorbed into the blood stream and elevated blood sugar levels stimulate the production of insulin in the pancreas. Insulin allows glucose to diffuse from the blood into essential body organs and tissues in order to be utilized for energy. While regulating glucose and glycogen in the liver, insulin also controls blood sugar by promoting protein synthesis in the cells. There are two reasons the blood glucose to stay unutilized properly by the body cells- when insulin is absent (type 1 diabetes) and in case of a relative insuline deficiency or “insulin resistance” (type 2 diabetes). Type 2 diabetes can also occur as a result of a partial failure of the pancreas. Thus, glucose builds up in the blood, resulting in an excessive amount of circulating blood glucose (hyperglycemia). Even people with diabetes who take oral medication or require insulin injections to control their blood glucose levels can have higher than normal blood insulin. The phenomena “insulin resistance” occurs when the normal amount of insulin secreted by the pancreas is not able to unlock the door to cells. In some cases (about 1/3 of the people with insulin resistance), do not respond to elevated levels of insulin. In metabolic syndrome, the body cells become resistant to normal effects of insulin and the cells do not absorb glucose from the blood properly to use for energy. In case that a person is affected by metabolic syndrome, his body is becoming resistant to normal levels of insulin secreted by the pancreas, making impossible the future utilization of glucose by the mitochondria in the cells. To maintain normal blood glucose, the pancreas secretes additional insulin, but not in sufficient quantities to meet the body’s needs. In order to balance the above disorder, the pancreas keeps producing additional amount of insulin, but as the body is becoming “deaf” to insulin stimulation or “insulin-resistant”- the last one cannot be used for future glucose assimilation. Constantly elevated levels of insulin are responsible for the abdominal "apple shape" obesity - as a consequence of insulin resistance, leading to a high blood pressure, dyslipidemia, persistent hyperglycemia (high blood glucose), ischemic or hemorrhagic stroke, heart attack, type 2 diabetes, vision problems, gout, kidney insufficiency and Alzheimer's disease. Hence, metabolic syndrome can result in a variety of serious health problems, linked mainly to the central disorder – insulin resistance. Central obesity and insulin resistance (glucose intolerance) are thought to represent the common underlying factors of the Syndrome X, whose other features are chronic low-grade proinflammatory state and a common prothrombotic state. Another missing link in the pathogenesis of metabolic syndrome is the long time unrecognized hepatic insulin resistance that appears to mediate the cascade of glucose intolerance, hyperglycemia, high level of triglyceride, and HDL-cholesterol abnormalities that contribute to the constellation of heart-disease risk factors called metabolic syndrome and it does represent a newly discovered pathophysiology link in CVD development. If you would like to learn more on the above topic, to request an on line or by phone alternative consultation, or a newly written article that can suit your business purposes, please call: (715) 392-7591; (218) 213-6167; or (218) 213-7087 These statements have not been evaluated by the Food and Drug Administration. The material in this newsletter is provided for informational purposes only. Thus our intentions are not to diagnose, cure, mitigate, treat or prevent any disease. If you use the information in this newsletter without the approval of your health professional, the authors of this letter do not assume any responsibility. Copyright @ 2010, Natural Health-Wellness LLC. All rights reserved.
The Key to a long and healthy life is weight loss, no doubt about it. How you eat may influence your health, as well as your figure. No matter how skinny you are if you aren’t healthy, it will not match your longevity criteria. Obesity is a major public health problem that is becoming more common among adults, increasing rapidly in children and adolescents, and has been linked to a broad range of physical, emotional and socioeconomic problems. The Center for Disease Control (CDC) has found that obesity affects close to 100 million American adults- that is one in three and an increase of more than 57 percent since 1991. Being overweight can have a devastating effect on human well-being both physically and emotionally. An increasing number of Americans are becoming overweight, which can lead to many serious health problems, including premature death. Obesity has been linked to a growing complex of health conditions including type 2 diabetes, coronary heart disease (CHD), metabolic syndrome, cancer, osteoporosis, and depression. Fueling the problem is a growing amount of misinformation about obesity itself, as well as serious confusion over the connection and understanding between dietary fat and body fat. Getting obesity and overweight epidemic under control will involve more than just telling everyone to go on a diet. It is quite obvious that there is no single magic bullet that can overcome obesity as a condition. Fortunately, obesity can be reversed with proper nutrition, dietary and lifestyle changes. Exercise, weight management, and optimum nutritional supplements such as chromium polynicotinate, vitamin C, proline, lysine, and other antioxidants help to normalize sugar and increase insulin sensitivity. Every attempt should be made to reduce total body weight to within 20% of the "ideal" body weight calculated for age and height. If this is done obesity will improve significantly. Despite that there is no unified treatment or a disease cure, right diet, nutritional and herbal supplementation, aggressive lifestyle changes can help support healthy blood sugar levels and to control obesity and metabolic syndrome. Several vitamins, minerals, herbs and antioxidants have been studied for their efficacy at promoting healthy blood sugar and protecting cells from the damage of elevated oxidation with favorable results. The high cost of managing morbid obesity, together with the recent economical situation have led to a growing interest in potentially gentler modalities and methods presented as a strategy by the alternative medicine. If you would like to learn more on the above topic, please call and require a personal consultation: (715) 392-7591; (218) 213-6167; or (218) 213-7087 These statements have not been evaluated by the Food and Drug Administration. The material in this newsletter is provided for informational purposes only. Thus our intentions are not to diagnose, cure, mitigate, treat or prevent any disease. If you use the information in this newsletter without the approval of your health professional, the authors of this letter do not assume any responsibility. Copyright @ 2009, Natural Health-Wellness LLC. All rights reserved.
Nausea (Latin, nausea) is a sensation of unease and stomach discomfort in the upper zone of the stomach with the urge to vomit. The attack of nausea is known as a qualm. The specific odor and flavor of ginger is caused by a mixture of zingerone, shogaols and gingerols, volatile oils that compose one to three percent of the weight of fresh ginger. In laboratory animals, the gingerrols increase the motility of the GI tract and have antiinflammatory, analgesic, sedative, antipyretic and antibacterial properties. Ginger has a sialagogue action, stimulating the production of saliva, which makes swallowing easier. Factors which can trigger nausea are listed here: Food Poisoning is the main reason behind nausea. Stomach indigestion is another main reason behind nausea. Clustered headaches can trigger nausea. Stomach infection (enteritis) or gastroenteritis can be reason behind nausea. Enteroviruses (stomach flu) are another reason behind the symptom-nausea. Motion or sea-sickness may also lead to nausea and vomits. Food intolerances (lactose, gluten) can also provoke nausea. Holistic & Home Remedies for Nausea Nausea can be easily treated with the natural remedies and above all they are completely safe. In case you are interested to receive our holistic "Fight Nausea The Natural Way" please call (715) 392-7591, 218-213-7087, 218-213-6167 or connectdoctors@naturalhealth-wellness.com and http://naturalhealth-wellness.com/
The medical team I worked for had made quite many efforts investigating what exactly were the causes of obesity as main promoter for metabolic syndrome appearance and vice versa. The focus of ours was at first on identifying the bacterial and viral etiology of the obesity as triggers to the road of prediabetes, and Type 2 diabetes. At the same time most of the world famous researchers consider insulin resistance as the main cause behind obesity and started to look for auto-antibodies or mutations in genes and insulin receptors. It was extrapolated that these antibodies will bind to the insulin receptor and consequently will block them. From our studies we could see that increased cardiovascular risk factors precede the onset of type 2 diabetes. An issue is whether it is glucose or insulin that increases the CVD risk. In nondiabetic subjects, people who are insulin resistant always have slightly elevated glucose levels. Metаbolic Syndrome is a combination or a cluster of disorders chаrаcterized by the presence of severаl of the following risk fаctors: hyperglycemiа, hypertension, low high-density lipoprotein (LDL), high low-density lipoprotein (HDL), high triglyceride, аbnormаl body mаss index (BMI), micro-аlbuminuriа, endotheliаl dysfunction, prothrombotic stаte, based on general proinflаmmаtory process (Bаusell, 2007) (Although not аll these criteriа need to be met before the syndrome will be found). In fаct, three of the above symptoms are found to be an indicаtive of the syndrome. It is estimаted thаt over 22% of the аdult U.S. populаtion hаve Metаbolic Syndrome аnd the incidence is rаpidly increаsing eаch yeаr. Prediabetes is a phase known as the condition of having abnormal elevated levels of glucose, insulin, and triglycerides in the blood. In fact “prediabetes” is a term-synonym for metabolic syndrome. Prediabetes is found in cases when blood glucose (sugar) levels are elevated beyond normal but are not considered high enough to indicate true Type 2 diabetes. Generally, the ‘prediabetic’ phase should be defined as combination of insulin resistance, glucose intolerance, elevated insulin secretion, and subclinical inflammation as predictors of the metabolic syndrome, beta-cell dysfunction, chronic inflammation, increased insulin resistance and decreased insulin secretion, as shown in the Framingham Study (FS) and the Insulin Resistance Atherosclerosis Study (IRAS). The prediabetic phase is seen as an early attempt metabolic syndrome to be defined as already available.
What makes metabolic syndrome quite dangerous is that is converting in the 21st century modern pandemic, constantly escalating in numbers around the world, and especially in US, where morbid obesity is on a rise. With other words, prediabetes is diagnosed when the level of glucose is abnormal but below the well known diabetic values: fasting values of 100-125 mg/dl, and 140-199 mg/dl two hours after a glucose load. For diabetes, the values are 126 mg/dl (fasting) and 200 mg/dl (two hours after a glucose load). Old аge, postmenopаusаl stаtus, ethnicity, higher body mаss index, current smoking, low household income, high cаrbohydrаte intаke, аnd physicаl inаctivity аll hаve been connected with the increаsed odds of the onset аnd or deterioration of metаbolic syndrome. Аn аdditionаl 12 million аdults will likely develop the diseаse аs а result of аging аlone by 2022 (Feinstein, 2008). Not а single cаuse аt the moleculаr level cаn be trаced to the origin of metаbolic syndrome (Diаmond, 2001). However, increаsing evidence suggests this enigmatic syndrome originаtes from a combination of insulin resistаnce аnd the аctivаtion of vаsculаr inflаmmаtory mechаnisms relаted to increаsed oxidаtive stress. For exаmple, insulin resistаnce results in preferentiаl metаbolism of free fаtty аcids which leаds to reduced glucose utilizаtion (Ford, 2002).
Insulin resistаnce is identified in children prior to the development of the dyslipidemiа, hypertension аnd hyperglycemiа thаt occur lаter in life. Аs one аges, pаncreаtic betа cell exhаustion is not аble to meet insulin resistаnce demаnds, аnd this might eventuаlly leаd to the progression of metаbolic disturbаnce including dyslipidemiа, hypertension (Feinstein, 2008). On the other hаnd, the infiltrаtion of аdipose tissue by inflаmmаtory mаcrophаges is indicаted аs а common feаture of obesity. Аdipose mаss аs meаsured by weight, BMI or viscerаl obesity correlаteѕ quаntitаtively with genetic expression of mаcrophаges thаt produce inflаmmаtory mediаtors аnd mаrkers. Therefore, while Syndrome X mаy shаre some common chаrаcteristic feаtures with diаbetes, despite it's not а diаbetes or prediаbetic condition per se as other distinct fаctors аnd cаuses аre аlso involved (Bаrclаy & Lie, 2004).
The insulin resistance, insulin secretion, and the phase of subclinical inflammation are claimed as predictors of the metabolic syndrome. Many researchers noted that there is some controversy about insulin levels as a predictor of CHD, although most of the data indicate a positive correlation. It is known that insulin concentrations predict metabolic syndrome and many others metabolic disorders. High absolute concentrations of LDL are not related to baseline insulin levels, but high insulin concentrations predict the development of small dense VLDL. In the San Antonio Heart Study (SAHS), people with normal glucose tolerance were followed to see whether they developed Type 2 diabetes. At baseline, they had higher triglycerides, higher HDL, higher systolic blood pressure (BP) than prediabetics, slightly higher glucose levels but the differences were really very small, although significant, and much higher insulin concentration.
The argument was that it was hyperinsulinemia and IR that drove this pre-diabetic issue. After some time, the San Antonio data were reviewed and an attempt made to develop a model for IR versus glucose. From the San Antonio study, where there was information on IR and low insulin secretion, and from earlier studies of the Pima Indians, it was shown that low insulin secretion and IR do predict the onset of Type 2 diabetes. Furthermore, when these factors were combined, there was about a 20-fold excess of incidence of Type 2 diabetes. The United Kingdom Prospective Diabetes Study(UKPDS) data suggest that the relationship between glucose concentrations, while clearly significant related to myocardial infarction (MI) is not as significant in its relationship to microvascular disease. Pyorala at all (1998) also presented data from a 25-year follow-up study reported in (Circulation, 1998; p. 398-404) that showed that nondiabetic men with the highest IR are at greatest risk for a major CHD event. Major clinical feature of the metabolic syndrome is the abdominal (visceral) obesity. Obesity sets the stage for metabolic syndrome which then itself increases one's chances of diabetes, heart disease, stroke and other diseases. Therefore, everyone in our Western society should be concerned about obesity as well as our government must take care on developing preventive programs. What is good, the government is already starting to take substantial meassures to fight the above mentioned pandemic. Of course people are different. Those in whom the disorder is quite severe will accumulate fat extremely quickly, when those in whom it is moderate - will gradually increase in weight and those in whom it is mild- may be able to keep their excess weight stationary for long periods. Despite of the aggressiveness in many weight loss programs (plans), based on restrictive diets, multiple drug treatment strategies, active exercise, sauna and massage techniques, the results seem temporary and quite unsatisfactory. The pounds seem to come back immediately, after months and even years or as soon as the treatment programs are forgotten or relaxed.
BMI is a measure of how much weight anyone carries for a given height. Basically one is considered "overweight" when their body mass index is greater than the upper range of the normal ranges. In order to meet the criterion for frank "obesity" one's BMI needs to be 30 or higher. The entity known as "morbid obesity" also known as clinically severe obesity, is defined as a BMI of greater than or equal to 40.
However, one can also be labeled as morbidly obese if body mass index is 35 or higher and the individual has one or more "co morbid" conditions. The following co-morbid conditions can be formulated as metabolic syndrome (diabetes, high blood pressure, high cholesterol, stroke and cardiovascular disease). Being overweight is, alongside diabetes, a leading cause of increased cholesterol levels, high blood pressure and coronary artery disease. Hence, obesity increases chances of developing all the above risk factors. One of the missing links in the pathogenesis of metabolic syndrome is the long time unrecognized hepatic insulin resistance that appears to mediate the glucose intolerance, hyperglycemia, high level of triglyceride, and HDL-cholesterol abnormalities that contribute to the constellation of heart-disease risk factors called metabolic syndrome and it does represent a newly discovered pathophysiology link in CVD development (Biddinger et al., 2008). Kahn R., (2005) proved that insulin resistance is related to dyslipidemia, and insulin resistance- to glucose intolerance, while is not related to obesity. Actually, it is already known that obesity causes insulin resistance, but is not related to high blood pressure. Except insulin there are few other hormones involved in the etiology and pathogenesis of metabolic syndrome. One of them is the hormone- leptin.
Leptin is a hormone that works as natural appetite suppressant secreted by fat cells in the body. Its discovery in the 1990s helped researchers to start experimenting with leptin that caused mice to eat less and lose weight while this rarely happens in humans. Falling levels of this hormone, that helps the brain resist tempting foods, may explain why people who lose weight often have a hard time keeping it off. Restoring leptin to its pre-diet levels may reverse this problem, concluded Rosenbaum, offering a new way for dieters to finally win the weight battle. "When you lose weight you've created about the perfect storm for regaining weight," as per Rosenbaum of Columbia University Medical Center in New York, whose research appears in the Journal of Clinical Investigation. After significant weight loss according to him the metabolism not only becomes more efficient, so the body needs fewer calories, but the brain becomes less vulnerable to tasty-looking treats. "Areas of the brain involved in telling not to eat seem to be less active. "When you are obese, you are more responsive to food and you are less in control of it," states Rosenbaum. Since then researchers started to look for the best methods to use human hormones to help healing obesity. In several earlier studies, researchers found out that when people lose weight, leptin levels decrease, as the body tries to protect its proper stored energy.
Rosenbaum was interested to investigate the impact of the leptin loss on the brains of people who had lost weight, and whether replacing leptin might help them keep off the weight. He used functional magnetic resonance imaging that shows activity in the brain. The researcher studied six obese patients before and after going on a hospital-supervised diet that reduced their body weight by 10 percent. People were shown pictures of food and non-food items. The author found that after weight loss, areas in the brain responsible for regulating food intake were less active when people were shown food images, while areas in the brain responsible for emotion were more active. When the researchers restored leptin to the levels before dieting, these changes were largely reversed. Similar results have been seen in people with a rare genetic condition in which their bodies do not make leptin. Rosenbaum believed leptin could be useful tool in helping people maintain weight loss. According to him the idea was to create a whole new class of therapies to help people with obesity keep weight off after they have lost it.
Making the situation worse, insulin resistance or low level of insulin secretion from the pancreas co-promote the formations of an additional third type of adipose tissue. It seems that the more insulin the pancreas secretes, the more likely is the appearance of the “apple shape” around the waist. Apparently hyperinsulinemia (too much insulin in the blood) can make anyone not only fat but also preliminary aged. And in fact insulin is the hormone that makes us fat and preliminary aged, despite we need it for energy supply. An even more insidious reason for this is that the fat cells do not develop insulin resistance to the degree other body cells do. The final result is that, in insulin resistance, all muscles and organs are being starved while the fat cells are being fed. Already knowing that adipose tissue also produces increased levels of pro-inflammatory signaling factors (eicosanoids and interleukins) cellular substances – hormones and other bioactive substances referred to as adipocytokines (Hotamisligil, 2004), as a vicious circle of all of these factors insulin sensitivity in organs like muscle and liver is decreasing (Matsuzawa, 2004).
It is also hypothesized that secondary factors as for example: nonesterified fatty acid liberation and adipokine (e.g., adiponectin) production (Carr et al., 2004), independent of obesity and other risk factors (Egan, Greene, and Goodfriend, 2001; Janssen, Katzmarzyk and Ross, 2002) may also play a significant role in the metabolic syndrome pathogenesis. Obviously the conglomeration or the convergence of these risk factors elevates the risk for this disease (Pladevall at al., 2006). As it is already cited in the literature- adipokines are a variety of proteins with signaling properties produced in body fat cells. While in the past white adipose tissue (one type of body fat) used to be regarded as a passive energy warehouse which is also used to provide a buffer and protection to all internal organs, lately this concept has been turned 180 degrees up and it is now understood that white adipose tissue is highly active and dynamic organ being involved in a multitude of physiological and metabolic biochemical reactions and processes. Research also suggests that appetite-regulating hormones are affected by sleep and that sleep deprivation could lead to weight gain. In two separate "well randomized" studies, people who slept five hours or less had higher levels of ghrelin - a hormone that stimulates hunger - and lower levels of the appetite-suppressing hormone leptin than those who slept eight hours per night. Prof. Cappuccio of the University of Warwick has proved that short sleep duration may also lead to obesity, through an increase of appetite via hormonal changes. Lack of sleep produces secretion of ghrelin, which stimulates appetite and creates less leptin, which suppresses appetite. The hormonal relationship and obesity is shown also in HERS study published in JAMA (2000).
The hyperinsulinemia in women has been shown to stimulate the release of testosterone from the ovaries (HERS study). It is a well known fact that people who are obese are suffering from this disorder regardless of whether they eat normally, excessively, or less than normal. At the same moment it is quite obvious that there are people who are constantly overeating but are free of the above disorder. It is easy to conclude that obesity in all its multiple forms is due to an abnormal damage in the hypothalamic area of the brain- a center that is the main regulatory mechanism of a hunger, thirst and the sexual desire. Most adults who develop “prediabetes” have insulin resistance as its main culprit. The human body uses sugar as a fuel (energy) to function, and reproduce. To this end, sugar has to be transported from the bloodstream across cell walls into the cells, where the sugar is actually burned and turned into energy. Insulin is a key hormone produced by the pancreas, primarily as a response to the sugar absorbed into the bloodstream after you eat a meal. Insulin acts on cell walls in such a way that the cells can take up and metabolize sugar. If the cell walls don't allow insulin to do its job, a person is said to have insulin resistance.
Insulin resistance refers to the mechanism by which one develops prediabetes or metabolic syndrome. They're not two different conditions. They are cause and effect — insulin resistance is a synonym for metabolic syndrome which is the preamble of the prediabetes state. To make things worse, lipid metabolism is also affected as a consequence of the insulin resistance and the blood pressure consequently elevates. Above all the rate of blood clotting increases- thus, the danger of a stroke and heart attack in the future. In order to overcome resistance, the pancreas produces more and more insulin — and unfortunately, the increased levels of insulin are detrimental to our arteries leading to the vicious circle of elevated blood pressure. In fact, only a small proportion of individuals who have prediabetes have insulin deficiency, but all of them show insulin resistance. If cells such as those of the liver and muscles are becoming resistant to insulin, then sugar cannot enter cells easily and remains in the bloodstream exceeding its normal values. A relationship between severe stress or emotional drama (loss of a loved one, divorce, etc.) and the onset of metabolic syndrome had been noted by few clinical studies since the first descriptions of metabolic syndrome as an entity. It seems in the way how it's described--that the presence of extended emotional disturbance or elevated stress, especially in individuals who can't handle stress, is a good enough indicator for the onset of metabolic syndrome. I am not surprised, as most of the chronic degenerative diseases start immediately after severe psychological drama and the above phenomena continues to be seen as main reason in cancer, autoimmune disease and many other diseases ethiopathogenesis. However, the presence of elevated stress or emotional shock is not the only reason beind the metabolic syndrome appearance, but for its treatment resistance as well. Practical research experience shows that the relative resistance of treatment of most of the metabolic syndrome cases rests upon the inability to deal with anger, to gain love, respect or affection and at a certain point separate clinical symptoms (e.g. obesity, high blood sugar) start to manifest on different levels. Contrary the syndrome seems to improve by finding or giving love to the others.
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