Metabolic syndrome is a burgeoning global problem. Approximately one fourth of the adult European population is estimated to have metabolic syndrome, with a similar prevalence in Latin America. [25] It is also considered an emerging epidemic in developing East Asian countries, including China, Japan, and Korea. The prevalence of metabolic syndrome in East Asia may range from 8-13% in men and from 2-18% in women, depending on the population and definitions used. [29, 30, 31]
Insulin is a fat storage hormone, it works to shuttle the sugar from your blood stream into your fat cells to store for later. Insulin has a number of other reproductive functions and has effects on skin health, cravings and the like. Insulin levels naturally increase after eating a meal that contains carbohydrates, dairy or protein. If you are insulin resistant then you can have an elevated level of insulin when you are fasting, or you can experience too much insulin release in response to those foods. This can trap your body in fat storage mode and inhibit fat loss.
To expand on my previous article about the five most important movement patterns, I've classified each exercise into the appropriate pattern, taking it one step further by dividing the upper-body push and pull into vertical and horizontal. Designing programs this way helps create balance between opposing muscle groups—which often gets overshadowed by more noticeable training goals like fat loss.
“It may sound odd,” says Jo-Ann Heslin, RD, the author of Diabetes Counter, “but sitting or sedentary activities such as watching TV, using the computer, sitting at work or sitting while commuting have been identified as risks for metabolic syndrome even when you incorporate modest amounts of regular activity into your day.” A study published in June 2015 in Diabetologia connected sitting time with a positive risk for diabetes, reporting that for every hour of daily TV viewing, a person’s risk for diabetes increased by 3.4 percent.
High-sensitivity C-reactive protein has been developed and used as a marker to predict coronary vascular diseases in metabolic syndrome, and it was recently used as a predictor for nonalcoholic fatty liver disease (steatohepatitis) in correlation with serum markers that indicated lipid and glucose metabolism.[45] Fatty liver disease and steatohepatitis can be considered as manifestations of metabolic syndrome, indicative of abnormal energy storage as fat in ectopic distribution. Reproductive disorders (such as polycystic ovary syndrome in women of reproductive age), and erectile dysfunction or decreased total testosterone (low testosterone-binding globulin) in men can be attributed to metabolic syndrome.[46]

Insulin resistance. Insulin is a hormone that helps your body use glucose -- a simple sugar made from the food you eat -- as energy. In people with insulin resistance, the insulin doesn't work as well, so your body keeps making more and more of it to cope with the rising level of glucose. Eventually, this can lead to diabetes. Insulin resistance is closely connected to having excess weight in the belly.
Your doctor may also use a device called an ophthalmoscope to look at the blood vessels in your eyes. Doctors can see if these vessels have thickened, narrowed, or burst, which may be a sign of high blood pressure. Your doctor will also use a stethoscope to listen to your heart and the sound of blood flowing through your arteries. In some cases, a chest x-ray and electrocardiogram may be needed.
Approximately half of individuals with hypertension have OSA, and approximately half with OSA have hypertension. Ambulatory BP monitoring normally reveals a "dip" in BP of at least 10% during sleep. However, if a patient is a "nondipper," the chances that the patient has OSA is increased. Nondipping is thought to be caused by frequent apneic/hypopneic episodes that end with arousals associated with marked spikes in BP that last for several seconds. Apneic episodes are associated with striking increases in sympathetic nerve activity and enormous elevations of BP. Individuals with sleep apnea have increased cardiovascular mortality, in part likely related to the high incidence of hypertension. http://www.sandysidhumedia.com/wp-content/uploads/2013/12/SSM_Logo_White.png
Insulin is a fat storage hormone, it works to shuttle the sugar from your blood stream into your fat cells to store for later. Insulin has a number of other reproductive functions and has effects on skin health, cravings and the like. Insulin levels naturally increase after eating a meal that contains carbohydrates, dairy or protein. If you are insulin resistant then you can have an elevated level of insulin when you are fasting, or you can experience too much insulin release in response to those foods. This can trap your body in fat storage mode and inhibit fat loss.

The value of routine screening for hypertension in children over the age of 3 years is debated.[90][91] In 2004 the National High Blood Pressure Education Program recommended that children aged 3 years and older have blood pressure measurement at least once at every health care visit[89] and the National Heart, Lung, and Blood Institute and American Academy of Pediatrics made a similar recommendation.[92] However, the American Academy of Family Physicians[93] supports the view of the U.S. Preventive Services Task Force that the available evidence is insufficient to determine the balance of benefits and harms of screening for hypertension in children and adolescents who do not have symptoms.[94]


Physical changes: If something in your body changes, you may begin experiencing issues throughout your body. High blood pressure may be one of those issues. For example, it’s thought that changes in your kidney function due to aging may upset the body’s natural balance of salts and fluid. This change may cause your body’s blood pressure to increase.

Type 2 DM is characterized by insulin resistance, which may be combined with relatively reduced insulin secretion.[11] The defective responsiveness of body tissues to insulin is believed to involve the insulin receptor. However, the specific defects are not known. Diabetes mellitus cases due to a known defect are classified separately. Type 2 DM is the most common type of diabetes mellitus.[2]

While diet is the most important aspect of achieving fat loss, increasing physical output after the weight is lost is essential and makes up some of the calorie deficit created by the slowed metabolism. This exercise should be something that does not stimulate appetite and can easily be incorporated into any lifestyle. We suggest you start with leisure walking and shoot for 1-2 hours daily (2.5-5miles or 5K to 10K steps).
The fact that the diagnostic criteria for metabolic syndrome vary between ethnic populations is testimony to significant nuances in the manifestation of metabolic syndrome in these groups. The original metabolic syndrome criteria were derived in mostly Caucasian populations, and some have argued for modification of individual criteria for specific ethnic subgroups, as has been done with waist circumference for patients of Asian origin. [39]

A person who weighed 180 pounds who diets down to 150 pounds burns significantly less energy than another person of the same height who also weighs 150 pounds who did not diet. Something about dieting causes an exaggerated slow down in metabolic rate that goes beyond what would be predicted based on tissue loss. And, as pointed out previously, this comes along with strong and unrelenting biological sensations to seek food. That is a recipe for compensatory weight regain.
Just briefly I want to mention something for the more savvy readers out there. Many, who are well versed in metabolism, will immediately point out that if you lose weight, then of course you are going to be burning less calories because you have less body tissue. True. But what research shows, and my clinical experience validates, is that the reduced rate of metabolic output goes far beyond what would be predicted from loss of fat mass or muscle mass.
These diabetes complications are related to blood vessel diseases and are generally classified into small vessel disease, such as those involving the eyes, kidneys and nerves (microvascular disease), and large vessel disease involving the heart and blood vessels (macrovascular disease). Diabetes accelerates hardening of the arteries (atherosclerosis) of the larger blood vessels, leading to coronary heart disease (angina or heart attack), strokes, and pain in the lower extremities because of lack of blood supply (claudication).

^ 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. http://www.sandysidhumedia.com/wp-content/uploads/2012/12/bennyquote.png


Though not routinely used any longer, the oral glucose tolerance test (OGTT) is a gold standard for making the diagnosis of type 2 diabetes. It is still commonly used for diagnosing gestational diabetes and in conditions of pre-diabetes, such as polycystic ovary syndrome. With an oral glucose tolerance test, the person fasts overnight (at least eight but not more than 16 hours). Then first, the fasting plasma glucose is tested. After this test, the person receives an oral dose (75 grams) of glucose. There are several methods employed by obstetricians to do this test, but the one described here is standard. Usually, the glucose is in a sweet-tasting liquid that the person drinks. Blood samples are taken at specific intervals to measure the blood glucose.
Despite these genetic findings, targeted genetic therapy seems to have little impact on hypertension. In the general population, not only does it appear that individual and joint genetic mutations have very small effects on BP levels, but it has not been shown that any of these genetic abnormalities are responsible for any applicable percentage of cases of hypertension in the general population. [27]

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.
Dr Jacomien de Villiers qualified as a specialist physician at the University of Pretoria in 1995. She worked at various clinics at the Department of Internal Medicine, Steve Biko Hospital, these include General Internal Medicine, Hypertension, Diabetes and Cardiology. She has run a private practice since 2001, as well as a consultant post at the Endocrine Clinic of Steve Biko Hospital.
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