Metabolic syndrome (also known as metabolic syndrome X) is a grouping of cardiac risk factors that result from insulin resistance (when the body's tissues do not respond normally to insulin). A person with metabolic syndrome has a greatly increased risk of developing type 2 diabetes, cardiovascular disease and premature death. In fact, another name for metabolic syndrome is pre-diabetes. https://www.clairekerslake.com/wp-content/uploads/2011/11/candles.jpg
Data from the Seventh Report of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure (JNC 7), which was released in 2003, were relatively similar to the NHANES data. The JNC 7 noted that approximately 30% of adults were unaware of their hypertension; up to 40% of people with hypertension were not receiving treatment; and, of those treated, up to 67% did not have their BP controlled to less than 140/90 mm Hg. 
Metabolic syndrome is thought to be caused by adipose tissue dysfunction and insulin resistance. Dysfunctional adipose tissue also plays an important role in the pathogenesis of obesity-related insulin resistance.  Both adipose cell enlargement and infiltration of macrophages into adipose tissue result in the release of proinflammatory cytokines and promote insulin resistance. 
The exact cause of metabolic syndrome is unknown. It is frequently influenced by diet and lifestyle, but also seems to be genetically driven. As stated, many features of metabolic syndrome are associated with “insulin resistance,” which causes cells to lose their sensitivity to insulin, the hormone needed to allow blood sugar to enter cells for use as fuel. As glucose levels in the blood increase, the pancreas tries to overcompensate and produce even more insulin, which ultimately leads to the characteristic symptoms of metabolic syndrome. When insulin levels spike, a stress response occurs that leads to elevations in cortisol, the body’s long-acting stress hormone. This in turn creates an inflammatory reaction that if left unchecked begins to damage healthy tissue.
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.
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.
Although the first formal definition of metabolic syndrome entered medical textbooks not so long ago (1998), it is as widespread as pimples and the common cold . According to the American Heart Association, 47 million Americans have it. That's almost a staggering one out of every six people. The syndrome runs in families and is more common among African-Americans, Hispanics, Asians, and Native Americans. The risks of developing metabolic syndrome increases as you age. https://www.healthshare.com.au/storage/avatars/34553.png.60x60_q85_box-0,0,256,256.png
When you have type 2 diabetes, your cells don't get enough glucose, which may cause you to lose weight. Also, if you are urinating more frequently because of uncontrolled diabetes, you may lose more calories and water, resulting in weight loss, says Daniel Einhorn, MD, medical director of the Scripps Whittier Diabetes Institute and clinical professor of medicine at the University of California in San Diego.
Glucose is a simple sugar found in food. Glucose is an essential nutrient that provides energy for the proper functioning of the body cells. Carbohydrates are broken down in the small intestine and the glucose in digested food is then absorbed by the intestinal cells into the bloodstream, and is carried by the bloodstream to all the cells in the body where it is utilized. However, glucose cannot enter the cells alone and needs insulin to aid in its transport into the cells. Without insulin, the cells become starved of glucose energy despite the presence of abundant glucose in the bloodstream. In certain types of diabetes, the cells' inability to utilize glucose gives rise to the ironic situation of "starvation in the midst of plenty". The abundant, unutilized glucose is wastefully excreted in the urine.
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.
Insulin serves as a “key” to open your cells, to allow the glucose to enter -- and allow you to use the glucose for energy. Without insulin, there is no “key.” So, the sugar stays -- and builds up-- in the blood. The result: the body’s cells starve from the lack of glucose. And, if left untreated, the high level of “blood sugar” can damage eyes, kidneys, nerves, and the heart, and can also lead to coma and death.
That means doing full-body workouts in a superset, tri-set, barbell or kettlebell complex, or circuit format with non-competing exercises that create the biggest metabolic demand. But it must be done in a rep range that generates lactic acid and pushes the lactic acid threshold. Training legs, back, and chest will burn more calories and elevate metabolism more than an isolated approach training one of them. The rep range that works the best is the 8-12 hypertrophy range.
Practice relaxation or slow, deep breathing. Practice taking deep, slow breaths to help relax. There are some devices available that promote slow, deep breathing. According to the American Heart Association, device-guided breathing may be a reasonable nondrug option for lowering blood pressure, especially when anxiety accompanies high blood pressure or standard treatments aren't well-tolerated. https://www.clairekerslake.com/wp-content/uploads/2012/05/claire3.jpg
Hypertension is the most important preventable risk factor for premature death worldwide. It increases the risk of ischemic heart disease, strokes, peripheral vascular disease, and other cardiovascular diseases, including heart failure, aortic aneurysms, diffuse atherosclerosis, chronic kidney disease, atrial fibrillation, and pulmonary embolism. Hypertension is also a risk factor for cognitive impairment and dementia. Other complications include hypertensive retinopathy and hypertensive nephropathy.
Lipodystrophic disorders in general are associated with metabolic syndrome. Both genetic (e.g., Berardinelli-Seip congenital lipodystrophy, Dunnigan familial partial lipodystrophy) and acquired (e.g., HIV-related lipodystrophy in patients treated with highly active antiretroviral therapy) forms of lipodystrophy may give rise to severe insulin resistance and many of metabolic syndrome's components.
Obstructive sleep apnea (OSA) is a common but frequently undiagnosed sleep-related breathing disorder defined as an average of at least 10 apneic and hypopenic episodes per sleep hour, which leads to excessive daytime sleepiness. Multiple studies have shown OSA to be an independent risk factor for the development of essential hypertension, even after adjusting for age, gender, and degree of obesity.
^ Jump up to: a b Go, AS; Bauman, M; King, SM; Fonarow, GC; Lawrence, W; Williams, KA; Sanchez, E (15 November 2013). "An Effective Approach to High Blood Pressure Control: A Science Advisory From the American Heart Association, the American College of Cardiology, and the Centers for Disease Control and Prevention". Hypertension. 63 (4): 878–85. doi:10.1161/HYP.0000000000000003. PMID 24243703. Archived from the original on 20 November 2013. Retrieved 20 November 2013.