The key sign of metabolic syndrome is central obesity, also known as visceral, male-pattern or apple-shaped adiposity. It is characterized by adipose tissue accumulation predominantly around the waist and trunk.[5] Other signs of metabolic syndrome include high blood pressure, decreased fasting serum HDL cholesterol, elevated fasting serum triglyceride level, impaired fasting glucose, insulin resistance, or prediabetes. Associated conditions include hyperuricemia; fatty liver (especially in concurrent obesity) progressing to nonalcoholic fatty liver disease; polycystic ovarian syndrome in women and erectile dysfunction in men; and acanthosis nigricans.
Hypertension is rarely accompanied by symptoms, and its identification is usually through screening, or when seeking healthcare for an unrelated problem. Some people with high blood pressure report headaches (particularly at the back of the head and in the morning), as well as lightheadedness, vertigo, tinnitus (buzzing or hissing in the ears), altered vision or fainting episodes.[20] These symptoms, however, might be related to associated anxiety rather than the high blood pressure itself.[21]
Central obesity is a key feature of the syndrome, being both a sign and a cause, in that the increasing adiposity often reflected in high waist circumference may both result from and contribute to insulin resistance. However, despite the importance of obesity, patients who are of normal weight may also be insulin-resistant and have the syndrome.[27]
The symptoms similar to symptoms of patients with hypertensive crisis are discussed in medieval Persian medical texts in the chapter of "fullness disease".[155] The symptoms include headache, heaviness in the head, sluggish movements, general redness and warm to touch feel of the body, prominent, distended and tense vessels, fullness of the pulse, distension of the skin, coloured and dense urine, loss of appetite, weak eyesight, impairment of thinking, yawning, drowsiness, vascular rupture, and hemorrhagic stroke.[156] Fullness disease was presumed to be due to an excessive amount of blood within the blood vessels.
This content is provided as a service of the National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK), part of the National Institutes of Health. The NIDDK translates and disseminates research findings through its clearinghouses and education programs to increase knowledge and understanding about health and disease among patients, health professionals, and the public. Content produced by the NIDDK is carefully reviewed by NIDDK scientists and other experts.
The distribution of adipose tissue appears to affect its role in metabolic syndrome. Fat that is visceral or intra-abdominal correlates with inflammation, whereas subcutaneous fat does not. There are a number of potential explanations for this, including experimental observations that omental fat is more resistant to insulin and may result in a higher concentration of toxic free fatty acids in the portal circulation. [21]
The brain is crucial in development of metabolic syndrome, modulating peripheral carbohydrate and lipid metabolism.[33][34] The metabolic syndrome can be induced by overfeeding with sugar or fructose, particularly concomitantly with high-fat diet.[36] The resulting oversupply of omega-6 fatty acids, particularly arachidonic acid (AA), is an important factor in the pathogenesis of metabolic syndrome.
Broyles, S., Katzmarzyk, P. T., Srinivasan, S. R., Chen, W., Bouchard, C., Freedman, D. S., & Berenson, G. S. (2010, May). The pediatric obesity epidemic continues unabated in Bogalusa, Louisiana. Pediatrics, 125(5). Retrieved from http://pediatrics.aappublications.org/content/125/5/900?sso=1&sso_redirect_count=1&nfstatus=401&nftoken=00000000-0000-0000-0000-000000000000&nfstatusdescription=ERROR%3a+No+local+token
Gary Edward Sander, MD, PhD, FACC, FAHA, FACP, FASH is a member of the following medical societies: Alpha Omega Alpha, American Chemical Society, American College of Cardiology, American College of Chest Physicians, American College of Physicians, American Federation for Clinical Research, American Federation for Medical Research, American Heart Association, American Society for Pharmacology and Experimental Therapeutics, American Society of Hypertension, American Thoracic Society, Heart Failure Society of America, National Lipid Association, Southern Society for Clinical Investigation
How to treat metabolic syndrome is controversial. Because there are several potential markers, the public health community has struggled with the decision of how best to define, diagnose and treat it. Nutritional approaches have generally been downplayed in favor of multiple medications that target the individual markers. Conventional recommendations tend to emphasize caloric restriction and reduced fat intake, even though metabolic syndrome can best be described as carbohydrate intolerance. The most effective treatment for metabolic syndrome is to control the intake of carbs, not fat. In fact, restricting dietary fat and replacing it with carbohydrate actually makes many of the problems of metabolic syndrome worse. The metabolic syndrome paradigm has therefore caused a great deal of distress—and pushback—among those advocating low-fat diets. For more on how to prevent metabolic syndrome, see How to Reduce Your Risk for Metabolic Syndrome.
People with glucose levels between normal and diabetic have impaired glucose tolerance (IGT) or insulin resistance. People with impaired glucose tolerance do not have diabetes, but are at high risk for progressing to diabetes. Each year, 1% to 5% of people whose test results show impaired glucose tolerance actually eventually develop diabetes. Weight loss and exercise may help people with impaired glucose tolerance return their glucose levels to normal. In addition, some physicians advocate the use of medications, such as metformin (Glucophage), to help prevent/delay the onset of overt diabetes.
Diabetes can also result from other hormonal disturbances, such as excessive growth hormone production (acromegaly) and Cushing's syndrome. In acromegaly, a pituitary gland tumor at the base of the brain causes excessive production of growth hormone, leading to hyperglycemia. In Cushing's syndrome, the adrenal glands produce an excess of cortisol, which promotes blood sugar elevation.

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Home blood sugar (glucose) testing is an important part of controlling blood sugar. One important goal of diabetes treatment is to keep the blood glucose levels near the normal range of 70 to 120 mg/dl before meals and under 140 mg/dl at two hours after eating. Blood glucose levels are usually tested before and after meals, and at bedtime. The blood sugar level is typically determined by pricking a fingertip with a lancing device and applying the blood to a glucose meter, which reads the value. There are many meters on the market, for example, Accu-Check Advantage, One Touch Ultra, Sure Step and Freestyle. Each meter has its own advantages and disadvantages (some use less blood, some have a larger digital readout, some take a shorter time to give you results, etc.). The test results are then used to help patients make adjustments in medications, diets, and physical activities.
The symptoms may relate to fluid loss and polyuria, but the course may also be insidious. Diabetic animals are more prone to infections. The long-term complications recognized in humans are much rarer in animals. The principles of treatment (weight loss, oral antidiabetics, subcutaneous insulin) and management of emergencies (e.g. ketoacidosis) are similar to those in humans.[123]
^ Sacks, F. M.; Svetkey, L. P.; Vollmer, W. M.; Appel, L. J.; Bray, G. A.; Harsha, D.; Obarzanek, E.; Conlin, P. R.; Miller, E. R. (2001-01-04). "Effects on blood pressure of reduced dietary sodium and the Dietary Approaches to Stop Hypertension (DASH) diet. DASH-Sodium Collaborative Research Group". The New England Journal of Medicine. 344 (1): 3–10. doi:10.1056/NEJM200101043440101. ISSN 0028-4793. PMID 11136953.
Type 2 diabetes: Type 2 diabetes affects the way the body uses insulin. While the body still makes insulin, unlike in type I, the cells in the body do not respond to it as effectively as they once did. This is the most common type of diabetes, according to the National Institute of Diabetes and Digestive and Kidney Diseases, and it has strong links with obesity.

Kidney damage from diabetes is called diabetic nephropathy. The onset of kidney disease and its progression is extremely variable. Initially, diseased small blood vessels in the kidneys cause the leakage of protein in the urine. Later on, the kidneys lose their ability to cleanse and filter blood. The accumulation of toxic waste products in the blood leads to the need for dialysis. Dialysis involves using a machine that serves the function of the kidney by filtering and cleaning the blood. In patients who do not want to undergo chronic dialysis, kidney transplantation can be considered.
This is an incredibly important, but commonly overlooked factor that heavily influences a metabolic resistance training program's success. While you can usually get by with minimal equipment with a MRT program, body weight only can get old very quickly.  Fortunately, just adding a kettlebell, band, suspension trainer, barbell, or other implement can quickly expand your exercise selection pool.  It's important to realize that a little bit can go a long way, especially if you're training in a busy gym and can't monopolize pieces of equipment for too long without someone walking off with them! https://www.healthshare.com.au/storage/avatars/35489.png.60x60_q85_box-0,0,256,256.jpg
In most people with established essential hypertension, increased resistance to blood flow (total peripheral resistance) accounts for the high pressure while cardiac output remains normal.[52] There is evidence that some younger people with prehypertension or 'borderline hypertension' have high cardiac output, an elevated heart rate and normal peripheral resistance, termed hyperkinetic borderline hypertension.[53] These individuals develop the typical features of established essential hypertension in later life as their cardiac output falls and peripheral resistance rises with age.[53] Whether this pattern is typical of all people who ultimately develop hypertension is disputed.[54] The increased peripheral resistance in established hypertension is mainly attributable to structural narrowing of small arteries and arterioles,[55] although a reduction in the number or density of capillaries may also contribute.[56]
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