Metabolic syndrome is a collection of heart disease risk factors that increase your chance of developing heart disease, stroke, and diabetes. The condition is also known by other names including Syndrome X, insulin resistance syndrome, and dysmetabolic syndrome. According to a national health survey, more than 1 in 5 Americans has metabolic syndrome. The number of people with metabolic syndrome increases with age, affecting more than 40% of people in their 60s and 70s.
Diabetes is a chronic, metabolic disease characterized by elevated levels of blood glucose (or blood sugar), which leads over time to serious damage to the heart, blood vessels, eyes, kidneys, and nerves. The most common is type 2 diabetes, usually in adults, which occurs when the body becomes resistant to insulin or doesn't make enough insulin. In the past three decades the prevalence of type 2 diabetes has risen dramatically in countries of all income levels. Type 1 diabetes, once known as juvenile diabetes or insulin-dependent diabetes, is a chronic condition in which the pancreas produces little or no insulin by itself. For people living with diabetes, access to affordable treatment, including insulin, is critical to their survival. There is a globally agreed target to halt the rise in diabetes and obesity by 2025.
Metabolic syndrome increases your risk for coronary heart disease. Other risk factors, besides metabolic syndrome, also increase your risk for heart disease. For example, a high LDL (“bad”) cholesterol level and smoking are major risk factors for heart disease. For details about all of the risk factors for heart disease, go to the Coronary Heart Disease Risk Factors Health Topic.
^ Santaguida PL, Balion C, Hunt D, Morrison K, Gerstein H, Raina P, Booker L, Yazdi H. "Diagnosis, Prognosis, and Treatment of Impaired Glucose Tolerance and Impaired Fasting Glucose". Summary of Evidence Report/Technology Assessment, No. 128. Agency for Healthcare Research and Quality. Archived from the original on 16 September 2008. Retrieved 20 July 2008.
Taking this a step further, I'd note that there are exercises that might not be self-limiting initially, but reach that point eventually. For example, with a beginner, a suspension trainer inverted row is not self-limiting at all; there are several important technique elements that a lifter needs to master because doing the exercise under conditions of fatigue.
High blood pressure is classified as either primary (essential) high blood pressure or secondary high blood pressure. About 90–95% of cases are primary, defined as high blood pressure due to nonspecific lifestyle and genetic factors. Lifestyle factors that increase the risk include excess salt in the diet, excess body weight, smoking, and alcohol use. The remaining 5–10% of cases are categorized as secondary high blood pressure, defined as high blood pressure due to an identifiable cause, such as chronic kidney disease, narrowing of the kidney arteries, an endocrine disorder, or the use of birth control pills.
Hypertension with certain specific additional signs and symptoms may suggest secondary hypertension, i.e. hypertension due to an identifiable cause. For example, Cushing's syndrome frequently causes truncal obesity, glucose intolerance, moon face, a hump of fat behind the neck/shoulder (referred to as a buffalo hump), and purple abdominal stretch marks. Hyperthyroidism frequently causes weight loss with increased appetite, fast heart rate, bulging eyes, and tremor. Renal artery stenosis (RAS) may be associated with a localized abdominal bruit to the left or right of the midline (unilateral RAS), or in both locations (bilateral RAS). Coarctation of the aorta frequently causes a decreased blood pressure in the lower extremities relative to the arms, or delayed or absent femoral arterial pulses. Pheochromocytoma may cause abrupt ("paroxysmal") episodes of hypertension accompanied by headache, palpitations, pale appearance, and excessive sweating.
The exact mechanisms of the complex pathways of metabolic syndrome are under investigation. The pathophysiology is very complex and has been only partially elucidated. Most patients are older, obese, sedentary, and have a degree of insulin resistance. Stress can also be a contributing factor. The most important risk factors are diet (particularly sugar-sweetened beverage consumption), genetics, aging, sedentary behavior or low physical activity, disrupted chronobiology/sleep, mood disorders/psychotropic medication use, and excessive alcohol use.
Maturity onset diabetes of the young (MODY) is a rare autosomal dominant inherited form of diabetes, due to one of several single-gene mutations causing defects in insulin production. It is significantly less common than the three main types. The name of this disease refers to early hypotheses as to its nature. Being due to a defective gene, this disease varies in age at presentation and in severity according to the specific gene defect; thus there are at least 13 subtypes of MODY. People with MODY often can control it without using insulin.
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.
There is debate regarding whether obesity or insulin resistance is the cause of the metabolic syndrome or if they are consequences of a more far-reaching metabolic derangement. A number of markers of systemic inflammation, including C-reactive protein, are often increased, as are fibrinogen, interleukin 6, tumor necrosis factor-alpha (TNF-α), and others. Some have pointed to a variety of causes, including increased uric acid levels caused by dietary fructose.
But why does someone get to this point? For the chronic dieter they arrive with metabolic damage because they hold tightly to the “Eat less, exercise more” mantras they were taught. When weight loss slows down, they eat less and push harder in their exercise routine, pushing metabolism into the ground. For the person with the unknown metabolism problem their road to metabolic damage is much more subtle. This person simply isn’t feeling well, starts putting on weight, and progresses all the way to metabolic damage because no doctor was able to identify what was going wrong.
At the end of the twelve-week study both groups lost weight, but the difference in the amount of muscle vs. fat loss was telling. The aerobic group lost 37 pounds over the course of the study. Ten of those pounds came from muscle. In contrast, the resistance-training group lost 32 pounds. None of the weight they lost came from muscle. When the resting metabolic rate of each group was calculated, the aerobic group was shown to be burning 210 fewer calories per day. The resistance-training group avoided this metabolic decline and instead was burning 63 more calories per day.
Type 2 diabetes was also previously referred to as non-insulin dependent diabetes mellitus (NIDDM), or adult-onset diabetes mellitus (AODM). In type 2 diabetes, patients can still produce insulin, but do so relatively inadequately for their body's needs, particularly in the face of insulin resistance as discussed above. In many cases this actually means the pancreas produces larger than normal quantities of insulin. A major feature of type 2 diabetes is a lack of sensitivity to insulin by the cells of the body (particularly fat and muscle cells). http://www.clairekerslake.com/wp-content/uploads/2014/03/ipad_new.png
Because both yeast and bacteria multiply more quickly when blood sugar levels are elevated, women with diabetes are overall at a higher risk of feminine health issues, such as bacterial infections, yeast infections, and vaginal thrush, especially when blood sugar isn't well controlled. And a lack of awareness about having prediabetes or diabetes can make managing blood sugar impossible.
Insulin resistance also may increase your risk for metabolic syndrome. Insulin resistance is a condition in which the body can’t use its insulin properly. Insulin is a hormone that helps move blood sugar into cells where it’s used for energy. Insulin resistance can lead to high blood sugar levels, and it’s closely linked to overweight and obesity. Genetics (ethnicity and family history) and older age are other factors that may play a role in causing metabolic syndrome.
(As a side note, one tricky thing we are coming to find with leptin is that many obese people have very high circulating levels of leptin but some how their body still doesn’t listen to the signal. They are leptin resistant. This means that your metabolism slows and your hunger gets jacked up… even though you have plenty of fat stores on your body! Talk about frustrating… but solvable!)
Fortunately, since peaking in 2001-2002, the overall prevalence of metabolic syndrome in the United States has fallen, primarily due to decreases in the prevalences of hypertriglyceridemia and hypertension—and in spite of increases in the prevalences of hyperglycemia and obesity/waist circumference.  Data from the 2009-2010 National Health and Nutrition Examination Survey (NHANES) showed that the age-adjusted prevalence of metabolic syndrome had fallen to approximately 24% in men and 22% in women. 
Development of metabolic syndrome depends on distribution as well as amount of fat. Excess fat in the abdomen (called apple shape), particularly when it results in a high waist-to-hip ratio (reflecting a relatively low muscle-to-fat mass ratio), increases risk. The syndrome is less common among people who have excess subcutaneous fat around the hips (called pear shape) and a low waist-to-hip ratio (reflecting a higher muscle-to-fat mass ratio).
Place a Swiss ball in front of you on the floor. Place forearms and fists on the top of it and keep your body in a straight line from your ankles to head. Keep core engaged, elbows bent at 90 degrees, and naturally arch lower back as you roll the ball forward. Make sure your body doesn't collapse as you perform this movement. Pause here, then using your abs, pull the ball back toward knees to starting position. https://i.ytimg.com/vi/WJ6HyT4rCbs/hqdefault.jpg?sqp
^ Jump up to: a b Petzold A, Solimena M, Knoch KP (October 2015). "Mechanisms of Beta Cell Dysfunction Associated With Viral Infection". Current Diabetes Reports (Review). 15 (10): 73. doi:10.1007/s11892-015-0654-x. PMC 4539350. PMID 26280364. So far, none of the hypotheses accounting for virus-induced beta cell autoimmunity has been supported by stringent evidence in humans, and the involvement of several mechanisms rather than just one is also plausible.
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