Metabolic syndrome is believed to develop due to insulin resistance. Insulin is a hormone that is produced by the pancreas (an organ located near stomach). It helps blood sugar enter cells, where it is used for energy. With insulin resistance, the body fails to recognize the insulin that is produced, causing the sugar to accumulate in the blood instead of being absorbed into other cells. Because blood sugar levels remain high, the pancreas keeps producing more and more insulin, leading to high insulin levels. While blood sugar levels are not high enough to be classified as diabetes, they do increase the risk of developing serious health problems.

There are some interesting developments in blood glucose monitoring including continuous glucose sensors. The new continuous glucose sensor systems involve an implantable cannula placed just under the skin in the abdomen or in the arm. This cannula allows for frequent sampling of blood glucose levels. Attached to this is a transmitter that sends the data to a pager-like device. This device has a visual screen that allows the wearer to see, not only the current glucose reading, but also the graphic trends. In some devices, the rate of change of blood sugar is also shown. There are alarms for low and high sugar levels. Certain models will alarm if the rate of change indicates the wearer is at risk for dropping or rising blood glucose too rapidly. One version is specifically designed to interface with their insulin pumps. In most cases the patient still must manually approve any insulin dose (the pump cannot blindly respond to the glucose information it receives, it can only give a calculated suggestion as to whether the wearer should give insulin, and if so, how much). However, in 2013 the US FDA approved the first artificial pancreas type device, meaning an implanted sensor and pump combination that stops insulin delivery when glucose levels reach a certain low point. All of these devices need to be correlated to fingersticks measurements for a few hours before they can function independently. The devices can then provide readings for 3 to 5 days.
Researchers assigned overweight subjects to three groups: diet-only, diet plus aerobics, diet plus aerobics plus weights. The diet group lost 14.6 pounds of fat in 12 weeks. The aerobic group lost only one more pound than the diet group. Their training was three times a week starting at 30 minutes and progressing to 50 minutes over the 12 weeks. Nothing special. But the weight training group lost over 21 pounds of fat. That's 44% and 35% more than diet and cardio-only groups respectively. The addition of aerobic training didn't result in significant fat loss over dieting alone. Thirty-six sessions of up to 50 minutes is a lot of work for one additional pound of fat loss. But the addition of resistance training greatly accelerated fat loss results.
Many of you at this point know my story, for the entirety of my life I had tried diet after diet. I was active, I ate well, yet no one would believe that because I was obese. Indeed, my poor mother dragged me from doctor to doctor trying to figure out what was going on with me. She was desperately trying to help me understand why nothing I did worked and why year after year I gained more and more weight and felt less at home in my body. I know that I am not alone in this as so many of you have reached out to tell me that they are struggling with weight loss. This phenomenon, that I have titled weight loss resistance, is a huge concern to me! This was part of the reason I became a Naturopathic Doctor. In the days when no one could help me shed the extra 80lbs of body fat I had, I had to do my own research, I had to blaze my own trail and now I am compelled to share that!
Insulin is a hormone that is produced by specialized cells (beta cells) of the pancreas. (The pancreas is a deep-seated organ in the abdomen located behind the stomach.) In addition to helping glucose enter the cells, insulin is also important in tightly regulating the level of glucose in the blood. After a meal, the blood glucose level rises. In response to the increased glucose level, the pancreas normally releases more insulin into the bloodstream to help glucose enter the cells and lower blood glucose levels after a meal. When the blood glucose levels are lowered, the insulin release from the pancreas is turned down. It is important to note that even in the fasting state there is a low steady release of insulin than fluctuates a bit and helps to maintain a steady blood sugar level during fasting. In normal individuals, such a regulatory system helps to keep blood glucose levels in a tightly controlled range. As outlined above, in patients with diabetes, the insulin is either absent, relatively insufficient for the body's needs, or not used properly by the body. All of these factors cause elevated levels of blood glucose (hyperglycemia).
“Too often, doctors don’t set reasonable expectations,” says Lauren Harris-Pincus, RDN, of New York City. A blanket statement like "'Lose weight and go exercise' is not as motivating as 'If you lose a modest 5 percent of your body weight, you can make a significant impact on the important numbers like blood pressure, blood sugar, and cholesterol/triglycerides,'” Harris-Pincus says.
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. [27]  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. [28]

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Monitoring your caloric intake may be helpful if you’re overweight, but everyone with type 2 diabetes should track how many carbs they’re taking in. That can be tricky because carbs are in many of the common foods you may already eat, but there are both good and bad sources of carbs. Fruits and vegetables, for example, are good sources, while pretzels and cookies are bad sources. (29)
^ Kyu HH, Bachman VF, Alexander LT, Mumford JE, Afshin A, Estep K, Veerman JL, Delwiche K, Iannarone ML, Moyer ML, Cercy K, Vos T, Murray CJ, Forouzanfar MH (August 2016). "Physical activity and risk of breast cancer, colon cancer, diabetes, ischemic heart disease, and ischemic stroke events: systematic review and dose-response meta-analysis for the Global Burden of Disease Study 2013". BMJ. 354: i3857. doi:10.1136/bmj.i3857. PMC 4979358. PMID 27510511.

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). https://www.healthshare.com.au/storage/avatars/patricia-durning.jpg.60x60_q85_box-0,0,100,100.jpg
^ Jump up to: a b Gatta-Cherifi, Blandine; Cota, Daniela (2015). "Endocannabinoids and Metabolic Disorders". Endocannabinoids. Handbook of Experimental Pharmacology. 231. pp. 367–91. doi:10.1007/978-3-319-20825-1_13. ISBN 978-3-319-20824-4. PMID 26408168. The endocannabinoid system (ECS) is known to exert regulatory control on essentially every aspect related to the search for, and the intake, metabolism and storage of calories, and consequently it represents a potential pharmacotherapeutic target for obesity, diabetes and eating disorders. ... recent research in animals and humans has provided new knowledge on the mechanisms of actions of the ECS in the regulation of eating behavior, energy balance, and metabolism. In this review, we discuss these recent advances and how they may allow targeting the ECS in a more specific and selective manner for the future development of therapies against obesity, metabolic syndrome, and eating disorders.
Insulin is released into the blood by beta cells (β-cells), found in the islets of Langerhans in the pancreas, in response to rising levels of blood glucose, typically after eating. Insulin is used by about two-thirds of the body's cells to absorb glucose from the blood for use as fuel, for conversion to other needed molecules, or for storage. Lower glucose levels result in decreased insulin release from the beta cells and in the breakdown of glycogen to glucose. This process is mainly controlled by the hormone glucagon, which acts in the opposite manner to insulin.[61]
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.[18][19][20]
It has not been contested that cardiovascular risk factors tend to cluster together; the matter of contention has been the assertion that the metabolic syndrome is anything more than the sum of its constituent parts. Phenotypic heterogeneity (for example, represented by variation in metabolic syndrome factor combinations among individuals with metabolic syndrome) has fueled that debate. However, more recent evidence suggests that common triggers (for example, excessive sugar-intake in the environment of overabundant food) can contribute to the development of multiple metabolic abnormalities at the same time, supporting the commonality of the energy utilization and storage pathways in metabolic syndrome.
"Brittle" diabetes, also known as unstable diabetes or labile diabetes, is a term that was traditionally used to describe the dramatic and recurrent swings in glucose levels, often occurring for no apparent reason in insulin-dependent diabetes. This term, however, has no biologic basis and should not be used.[39] Still, type 1 diabetes can be accompanied by irregular and unpredictable high blood sugar levels, frequently with ketosis, and sometimes with serious low blood sugar levels. Other complications include an impaired counterregulatory response to low blood sugar, infection, gastroparesis (which leads to erratic absorption of dietary carbohydrates), and endocrinopathies (e.g., Addison's disease).[39] These phenomena are believed to occur no more frequently than in 1% to 2% of persons with type 1 diabetes.[40]
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.

Per the WHO, people with fasting glucose levels from 6.1 to 6.9 mmol/l (110 to 125 mg/dl) are considered to have impaired fasting glucose.[67] people with plasma glucose at or above 7.8 mmol/l (140 mg/dl), but not over 11.1 mmol/l (200 mg/dl), two hours after a 75 gram oral glucose load are considered to have impaired glucose tolerance. Of these two prediabetic states, the latter in particular is a major risk factor for progression to full-blown diabetes mellitus, as well as cardiovascular disease.[68] The American Diabetes Association (ADA) since 2003 uses a slightly different range for impaired fasting glucose of 5.6 to 6.9 mmol/l (100 to 125 mg/dl).[69]
What causes high cholesterol? High cholesterol is a risk factor for heart attacks and coronary heart disease, because it builds up in the arteries, narrowing them. It does not usually have any symptoms, and many people do not know they have it. We look at healthy levels and ranges of cholesterol, at ways to prevent it, and medications to treat it. Read now
The second hormone that becomes involved when you begin to lose weight is a hormone known as leptin. Leptin is a hormone that is released from the fat cells to signal to the brain about how much fat we have in storage. To our body this is kind of like the indicator on a car telling us how much fuel we have in the tank. Leptin is also a messenger that is involved with controlling your metabolic rate AND your appetite.
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]
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.
The clinical value of using "metabolic syndrome" as a diagnosis has previously been debated due to different sets of conflicting and incomplete diagnostic criteria. These concerns have led the American Diabetes Association and the European Association for the Study of Diabetes to issue a joint statement identifying eight major concerns on the clinical utility of the metabolic syndrome diagnosis.[69] The principal argument has been that when confounding factors such as obesity are accounted for, diagnosis of the metabolic syndrome has a negligible association with the risk of heart disease.[70] http://media-cache-ec5.pinterest.com/upload/21110691974453216_0I4oS4Zs_c.jpg
Although treatment of sleep apnea with continuous airway positive pressure (CPAP) would logically seem to improve CV outcomes and hypertension, studies evaluating this mode of therapy have been disappointing. A 2016 review of several studies indicated that CPAP either had no effect or a modest BP-lowering effect. [29] Findings from the SAVE study showed no effect of CPAP therapy on BP above usual care. [30] It is likely that patients with sleep apnea have other etiologies of hypertension, including obesity, hyperaldosteronism, increased sympathetic drive, and activation of the renin/angiotensin system that contribute to their hypertension. Although CPAP remains an effective therapy for other aspects of sleep apnea, it should not be expected to normalize BP in the majority of patients.
Cortisol reactivity, an index of hypothalamic-pituitary-adrenal function, may be another mechanism by which psychosocial stress is associated with future hypertension. [20] In a prospective sub-study of the Whitehall II cohort, with 3 years follow-up of an occupational cohort in previously healthy patients, investigators reported 15.9% of the patient sample developed hypertension in response to laboratory-induced mental stressors and found an association between cortisol stress reactivity and incident hypertension. [20]
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