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.
Jackson Bloore is a nationally published fitness model, certified personal trainer, and owner of Action Jackson Fitness. He was named by San Francisco Magazine as “Best Personal Trainer for Abs” in 2015 and has been featured on the cover of six fitness products for Perfect Fitness and has modeled for Nike, ESPN, Men's Health, and Men's Fitness among others.
In addition to the problems with an increase in insulin resistance, the release of insulin by the pancreas may also be defective and suboptimal. In fact, there is a known steady decline in beta cell production of insulin in type 2 diabetes that contributes to worsening glucose control. (This is a major factor for many patients with type 2 diabetes who ultimately require insulin therapy.) Finally, the liver in these patients continues to produce glucose through a process called gluconeogenesis despite elevated glucose levels. The control of gluconeogenesis becomes compromised.
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.
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.
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]
Most people who have metabolic syndrome have insulin resistance. The body makes insulin to move glucose (sugar) into cells for use as energy. Obesity, commonly found in people with metabolic syndrome, makes it more difficult for cells in the body to respond to insulin. If the body can’t make enough insulin to override the resistance, the blood sugar level increases, causing type 2 diabetes. Metabolic syndrome may be a start of the development of type 2 diabetes.
Family or personal history. Your risk increases if you have prediabetes — a precursor to type 2 diabetes — or if a close family member, such as a parent or sibling, has type 2 diabetes. You're also at greater risk if you had gestational diabetes during a previous pregnancy, if you delivered a very large baby or if you had an unexplained stillbirth.
If you're short on time but still want to fit in an effective training session—especially if your goal is fat burn—metabolic resistance training (MRT) is tough to beat. With this training style, the goal is to maximize caloric expenditure while also increasing your metabolic rate. There are many different ways to structure an MRT session, but generally speaking, circuit training lends itself well to this approach.

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.
Stress reduction techniques such as biofeedback or transcendental meditation may be considered as an add-on to other treatments to reduce hypertension, but do not have evidence for preventing cardiovascular disease on their own.[125][126][127] Self-monitoring and appointment reminders might support the use of other strategies to improve blood pressure control, but need further evaluation.[128]
Exposure to certain viral infections (mumps and Coxsackie viruses) or other environmental toxins may serve to trigger abnormal antibody responses that cause damage to the pancreas cells where insulin is made. Some of the antibodies seen in type 1 diabetes include anti-islet cell antibodies, anti-insulin antibodies and anti-glutamic decarboxylase antibodies. These antibodies can be detected in the majority of patients, and may help determine which individuals are at risk for developing type 1 diabetes.
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]
“Individual responses to different diets–from low fat and vegan to low carb and paleo–vary enormously. “Some people on a diet program lose 60 lb. and keep it off for two years, and other people follow the same program religiously, and they gain 5 lb.,” says Frank Sacks, a leading weight-loss researcher and professor of cardiovascular disease prevention at the Harvard T.H. Chan School of Public Health. “If we can figure out why, the potential to help people will be huge.”

Some people may ask: Why not just have liposuction of the abdomen and remove the large amount of abdominal fat that is a big part of the problem? Data thus far shows no benefit in liposuction on insulin sensitivity, blood pressure, or cholesterol. As the saying goes, "If it's too good to be true, it probably is." Diet and exercise are still the preferred primary treatment of metabolic syndrome.
At present, the American Diabetes Association does not recommend general screening of the population for type 1 diabetes, though screening of high risk individuals, such as those with a first degree relative (sibling or parent) with type 1 diabetes should be encouraged. Type 1 diabetes tends to occur in young, lean individuals, usually before 30 years of age; however, older patients do present with this form of diabetes on occasion. This subgroup is referred to as latent autoimmune diabetes in adults (LADA). LADA is a slow, progressive form of type 1 diabetes. Of all the people with diabetes, only approximately 10% have type 1 diabetes and the remaining 90% have type 2 diabetes. https://www.healthshare.com.au/storage/avatars/34690.png.60x60_q85_box-0,0,256,256.jpg

"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]
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. https://i.ytimg.com/vi/KjIf146TsFM/hqdefault.jpg?sqp

The pathogenesis of essential hypertension is multifactorial and complex. [13] Multiple factors modulate the blood pressure (BP) including humoral mediators, vascular reactivity, circulating blood volume, vascular caliber, blood viscosity, cardiac output, blood vessel elasticity, and neural stimulation. A possible pathogenesis of essential hypertension has been proposed in which multiple factors, including genetic predisposition, excess dietary salt intake, and adrenergic tone, may interact to produce hypertension. Although genetics appears to contribute, the exact mechanisms underlying essential hypertension have not been established.


^ 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 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. 
The earliest surviving work with a detailed reference to diabetes is that of Aretaeus of Cappadocia (2nd or early 3rd century CE). He described the symptoms and the course of the disease, which he attributed to the moisture and coldness, reflecting the beliefs of the "Pneumatic School". He hypothesized a correlation of diabetes with other diseases, and he discussed differential diagnosis from the snakebite which also provokes excessive thirst. His work remained unknown in the West until 1552, when the first Latin edition was published in Venice.[110]

Have you ever eaten a salad with low fat dressing, hold the nuts with a swap for lean protein? Did you leave feeling hungry, unsatisfied and searching for something else to fill you up? When this happens and you end up snacking throughout the day you never have the opportunity to burn fat as fuel because your metabolic hormones are increased and you never enter the fasting stage. No Bueno!


Current strategies for controlling cardiovascular disease (CVD) risk factors, such as high blood pressure and high cholesterol, are not widely used as standard practice. CDC developed this guide to provide health professionals with evidence-based strategies for effective and sustainable CVD prevention, including health and economic impact and potential for reducing health disparities.
Insulin is vital to patients with type 1 diabetes - they cannot live without a source of exogenous insulin. Without insulin, patients with type 1 diabetes develop severely elevated blood sugar levels. This leads to increased urine glucose, which in turn leads to excessive loss of fluid and electrolytes in the urine. Lack of insulin also causes the inability to store fat and protein along with breakdown of existing fat and protein stores. This dysregulation, results in the process of ketosis and the release of ketones into the blood. Ketones turn the blood acidic, a condition called diabetic ketoacidosis (DKA). Symptoms of diabetic ketoacidosis include nausea, vomiting, and abdominal pain. Without prompt medical treatment, patients with diabetic ketoacidosis can rapidly go into shock, coma, and even death may result.
^ Grundy SM, Cleeman JI, Daniels SR, Donato KA, Eckel RH, Franklin BA, Gordon DJ, Krauss RM, Savage PJ, Smith SC, Spertus JA, Costa F (October 2005). "Diagnosis and management of the metabolic syndrome: an American Heart Association/National Heart, Lung, and Blood Institute Scientific Statement". Circulation. 112 (17): 2735–52. doi:10.1161/CIRCULATIONAHA.105.169404. PMID 16157765.
MRT should be a total-body routine that works all the major muscles each session. Since the metabolic cost of an exercise relates directly to the amount of muscle worked, incorporate multi-joint exercises whenever possible.[3] Involve more muscle, and you expend more energy. Opt for compound movements: squats, rows and presses will work the muscles of the torso and thighs. Reserve single-joint movements for the arms and calves. Train three, non-consecutive days per week (i.e. Monday, Wednesday, Friday) to allow for adequate recuperation.

Measuring BP takes into account two pressures, measured in millimeters of mercury (mm Hg). The first, systolic pressure, is the force exerted on the blood vessel walls when the heart is pumping blood. Diastolic pressure reflects the force present when the heart relaxes between beats. They are written as systolic over diastolic pressure. For instance, a blood pressure of 120/80 mm Hg or 120 over 80 corresponds to a systolic pressure of 120 and a diastolic pressure of 80.
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).
In an attempt to elucidate the genetic components of hypertension, multiple genome wide association studies (GWAS) have been conducted, revealing multiple gene loci in known pathways of hypertension as well as some novel genes with no known link to hypertension as of yet. [25] Further research into these novel genes, some of which are immune-related, will likely increase the understanding of hypertension's pathophysiology, allowing for increased risk stratification and individualized treatment.
Most conventional practitioners recommend that patients follow a healthy eating plan like the American Dietary Association (ADA) diet, the Dietary Approaches to Stop Hypertension (DASH) diet or the Mediterranean Diet. All of these emphasize fruits, vegetables, and whole grains, while limiting unhealthy fats and promoting leaner protein foods like low-fat dairy and lean meats like chicken and fish.
Metabolic syndrome promotes coronary heart disease through several mechanisms. It increases the thrombogenicity of circulating blood, in part by raising plasminogen activator type 1 and adipokine levels, and it causes endothelial dysfunction. [14] Metabolic syndrome may also increase cardiovascular risks by increasing arterial stiffness. [15] Additional mechanisms include oxidative stress, [16] which has been associated with numerous components of metabolic syndrome. [17]

If you're short on time but still want to fit in an effective training session—especially if your goal is fat burn—metabolic resistance training (MRT) is tough to beat. With this training style, the goal is to maximize caloric expenditure while also increasing your metabolic rate. There are many different ways to structure an MRT session, but generally speaking, circuit training lends itself well to this approach.
Measuring BP takes into account two pressures, measured in millimeters of mercury (mm Hg). The first, systolic pressure, is the force exerted on the blood vessel walls when the heart is pumping blood. Diastolic pressure reflects the force present when the heart relaxes between beats. They are written as systolic over diastolic pressure. For instance, a blood pressure of 120/80 mm Hg or 120 over 80 corresponds to a systolic pressure of 120 and a diastolic pressure of 80.
How many calories should I eat a day? A calorie is an amount of energy that a particular food provides. Consuming more calories than needed will result in weight gain, consuming too few will result in weight loss. How many calories a person should eat each day depends on a variety of factors, such as age, size, sex, activity levels, and general health. Read now
Lifestyle changes and medications can lower blood pressure and decrease the risk of health complications.[8] Lifestyle changes include weight loss, physical exercise, decreased salt intake, reducing alcohol intake, and a healthy diet.[5] If lifestyle changes are not sufficient then blood pressure medications are used.[8] Up to three medications can control blood pressure in 90% of people.[5] The treatment of moderately high arterial blood pressure (defined as >160/100 mmHg) with medications is associated with an improved life expectancy.[14] The effect of treatment of blood pressure between 130/80 mmHg and 160/100 mmHg is less clear, with some reviews finding benefit[7][15][16] and others finding unclear benefit.[17][18][19] High blood pressure affects between 16 and 37% of the population globally.[5] In 2010 hypertension was believed to have been a factor in 18% of all deaths (9.4 million globally).[9]

Lipase inhibitors can play a role. These are foods that have action in decreasing the digestion of fats so they move out of the body instead of getting absorbed. Since the digestive tract is the major place where POPs are both removed from the body and taken into the body, doing what is possible to NOT allow fat soluble compounds reentry is important. Some common lipase inhibitors include green tea, oolong tea, mate tea, and ginger root.
When the glucose concentration in the blood remains high over time, the kidneys will reach a threshold of reabsorption, and glucose will be excreted in the urine (glycosuria).[62] This increases the osmotic pressure of the urine and inhibits reabsorption of water by the kidney, resulting in increased urine production (polyuria) and increased fluid loss. Lost blood volume will be replaced osmotically from water held in body cells and other body compartments, causing dehydration and increased thirst (polydipsia).[60]
This is true for two reasons. Not only are many fad diets low fat, but they are also low calorie. Your body is not stupid! It can see that you are not taking in enough energy to support your basal metabolic rate. Your basal metabolic rate is the number of calories that your body requires to run your heart, brain, liver, digestive system, lungs etc. This critical number is very responsive to the environment because back in the good old days food wasn’t widely available. If you weren’t able to find food for a few days then your whole system slowed down to require less calories and protect you from dying.
Regarding age, data shows that for each decade after 40 years of age regardless of weight there is an increase in incidence of diabetes. The prevalence of diabetes in persons 65 years of age and older is around 25%. Type 2 diabetes is also more common in certain ethnic groups. Compared with a 7% prevalence in non-Hispanic Caucasians, the prevalence in Asian Americans is estimated to be 8.0%, in Hispanics 13%, in blacks around 12.3%, and in certain Native American communities 20% to 50%. Finally, diabetes occurs much more frequently in women with a prior history of diabetes that develops during pregnancy (gestational diabetes).
Now for the big surprise cause. There is another set of signaling molecules that have a huge impact on metabolic compensations during dieting. These compounds are present in your fat cells, and when fat is burned, they are released in significant concentrations. The shocking thing about these compounds is they did not come from your body. They are man made chemicals that you eat, put on your skin, drink in your water, and inhale through the air.

In patients with type 2 diabetes, stress, infection, and medications (such as corticosteroids) can also lead to severely elevated blood sugar levels. Accompanied by dehydration, severe blood sugar elevation in patients with type 2 diabetes can lead to an increase in blood osmolality (hyperosmolar state). This condition can worsen and lead to coma (hyperosmolar coma). A hyperosmolar coma usually occurs in elderly patients with type 2 diabetes. Like diabetic ketoacidosis, a hyperosmolar coma is a medical emergency. Immediate treatment with intravenous fluid and insulin is important in reversing the hyperosmolar state. Unlike patients with type 1 diabetes, patients with type 2 diabetes do not generally develop ketoacidosis solely on the basis of their diabetes. Since in general, type 2 diabetes occurs in an older population, concomitant medical conditions are more likely to be present, and these patients may actually be sicker overall. The complication and death rates from hyperosmolar coma is thus higher than in diabetic ketoacidosis.
Fasting glucose test This test involves giving a blood sample after you have fasted for eight hours. (18) If you have a fasting blood sugar level of less than 100 milligrams per deciliter (mg/dl), your blood sugar levels are normal. But if you have one from 100 to 125 mg/dl, you have prediabetes, and if you have 126 mg/dl on two separate occasions, you have diabetes. (17)

Bhasin et al, as part of the Framingham Heart Study, found that sex hormone-binding globulin is independently associated with the risk of metabolic syndrome, whereas testosterone is not. Age, body mass index (BMI), and insulin sensitivity independently affect sex hormone-binding globulin and testosterone levels. [48] More recent studies have raised the possibility of an association between testosterone deficiency and metabolic syndrome. [49]
In most people with established essential hypertension, increased resistance to blood flow (total peripheral resistance) accounts for the high pressure while cardiac output remains normal.[52] There is evidence that some younger people with prehypertension or 'borderline hypertension' have high cardiac output, an elevated heart rate and normal peripheral resistance, termed hyperkinetic borderline hypertension.[53] These individuals develop the typical features of established essential hypertension in later life as their cardiac output falls and peripheral resistance rises with age.[53] Whether this pattern is typical of all people who ultimately develop hypertension is disputed.[54] The increased peripheral resistance in established hypertension is mainly attributable to structural narrowing of small arteries and arterioles,[55] although a reduction in the number or density of capillaries may also contribute.[56]
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