Blood pressure was traditionally measured using a stethoscope and a blood pressure cuff (called a sphygmomanometer), a device that includes a cuff, a bulb, and a pressure dial that reads the pressure in millimeters of mercury (mm Hg). This is still considered the best method but, more commonly, devices that combine a blood pressure cuff with electronic sensors are used to measure blood pressure.
Not so anymore. Thanks to the rising obesity epidemic in young people, kids and teens are getting these conditions — and they're getting them earlier than ever before. Some estimates say that nearly 1 in 10 teens — and over a third of obese teens — have metabolic syndrome. And a study of 375 second- and third-graders found that 5% had metabolic syndrome and 45% had one or two risk factors for it.
(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!)
Metabolic syndrome is a cluster of metabolic risk factors that come together in a single individual. These metabolic factors include insulin resistance, hypertension (high blood pressure), cholesterol abnormalities, and an increased risk for blood clotting. Affected individuals are most often overweight or obese. An association between certain metabolic disorders and cardiovascular disease has been known since the 1940s.
Hypertension is defined as elevated blood pressure and is the leading cause globally of death and disability. It is the major risk factor for heart attack and stroke, and is also a significant risk factor for for chronic kidney disease and chronic heart failure. Because individuals with hypertension usually don’t have any symptoms, it is a disease that is often under-diagnosed. Diagnosis relies upon routine blood pressure screening to monitor and detect affected individuals.
Picking up where HIT legends such as Arthur Jones and Mike Mentzer left off, Chris Lutz is carrying the torch of evidence based, scientific resistance training into the future.The author produces further, more up to date evidence and the proper techniques and order of operation for successful use of HIT methodology. This is a must read for any HIT enthusiast, aspiring trainer, or even the beginner trainee.
It is common for there to be a development of visceral fat, after which the adipocytes (fat cells) of the visceral fat increase plasma levels of TNF-α and alter levels of a number of other substances (e.g., adiponectin, resistin, and PAI-1). TNF-α has been shown not only to cause the production of inflammatory cytokines, but also possibly to trigger cell signaling by interaction with a TNF-α receptor that may lead to insulin resistance.[31] An experiment with rats fed a diet with 33% sucrose has been proposed as a model for the development of metabolic syndrome. The sucrose first elevated blood levels of triglycerides, which induced visceral fat and ultimately resulted in insulin resistance. The progression from visceral fat to increased TNF-α to insulin resistance has some parallels to human development of metabolic syndrome. The increase in adipose tissue also increases the number of immune cells present within, which play a role in inflammation. Chronic inflammation contributes to an increased risk of hypertension, atherosclerosis and diabetes.[32]
Weight loss surgery in those with obesity and type two diabetes is often an effective measure.[14] Many are able to maintain normal blood sugar levels with little or no medications following surgery[95] and long-term mortality is decreased.[96] There is, however, a short-term mortality risk of less than 1% from the surgery.[97] The body mass index cutoffs for when surgery is appropriate are not yet clear.[96] It is recommended that this option be considered in those who are unable to get both their weight and blood sugar under control.[98]
Some cases of diabetes are caused by the body's tissue receptors not responding to insulin (even when insulin levels are normal, which is what separates it from type 2 diabetes); this form is very uncommon. Genetic mutations (autosomal or mitochondrial) can lead to defects in beta cell function. Abnormal insulin action may also have been genetically determined in some cases. Any disease that causes extensive damage to the pancreas may lead to diabetes (for example, chronic pancreatitis and cystic fibrosis). Diseases associated with excessive secretion of insulin-antagonistic hormones can cause diabetes (which is typically resolved once the hormone excess is removed). Many drugs impair insulin secretion and some toxins damage pancreatic beta cells. The ICD-10 (1992) diagnostic entity, malnutrition-related diabetes mellitus (MRDM or MMDM, ICD-10 code E12), was deprecated by the World Health Organization (WHO) when the current taxonomy was introduced in 1999.[53]
Set up a series of exercise stations that work muscles in a push/pull fashion, starting with the upper body and proceeding to the lower body (i.e. chest, back, shoulders, biceps, triceps, quads, hamstrings, calves and abdominals). Move from one exercise to the next with minimal rest (ideally less than 15 seconds). Perform three circuits in total. Don't pass out. Reap the rewards.
Because metabolic syndrome and insulin resistance are closely tied, many healthcare providers believe that insulin resistance may be a cause of metabolic syndrome. But they have not found a direct link between the two conditions. Others believe that hormone changes caused by chronic stress lead to abdominal obesity, insulin resistance, and higher blood lipids (triglycerides and cholesterol).
[Guideline] Skyler JS, Bergenstal R, Bonow RO, et al. Intensive glycemic control and the prevention of cardiovascular events: implications of the ACCORD, ADVANCE, and VA Diabetes Trials: a position statement of the American Diabetes Association and a Scientific Statement of the American College of Cardiology Foundation and the American Heart Association. J Am Coll Cardiol. 2009 Jan 20. 53(3):298-304. [Medline].