Again, the answer to why has already been discovered! We have a 24hr clock in our body, known as the circadian rhythm. This rhythm controls what hormones are released and when, it controls our wake sleep rhythm and when working properly signals what physiological processes happen during the day and at night. When you think about it, it is a pretty simple concept that we should be eating during the day and not eating during our biological night. People who are ‘night owls’ often eat during their biological night and it has been shown that the insulin and glucose response to a meal eaten at night is that of a DIABETIC! I was shocked when I first discovered this! This means that even a ‘healthy’ thin person is predisposed to weight gain and gets stuck in fat storage mode if they eat all night long. This is aggravated in people who are predisposed to insulin resistance and metabolic hormone chaos!
14 November 2018. On World Diabetes Day 2018, WHO joins partners around the world to highlight the impact diabetes has on families and the role of family members in supporting prevention, early diagnosis and good management of diabetes. More than 400 million people live with diabetes worldwide, and the prevalence is predicted to continue rising if current trends prevail. Diabetes is a major cause of premature dying, blindness, kidney failure, heart attack, stroke and lower limb amputation. It was the seventh leading cause of death in 2016.
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.
The depth of this product really blew me away, as there are 138 pages of sample MRT workouts using all sorts of different equipment, or none at all. There are some great ideas in there for fitness professionals and fitness enthusiasts alike, and I'll certainly be implementing some of the techniques Jen describes in our programming at Cressey Performance. It's on sale at a great introductory price this week, so be sure to check it out.
Renovascular hypertension (RVHT) causes 0.2-4% of cases. Since the seminal experiment in 1934 by Goldblatt et al,  RVHT has become increasingly recognized as an important cause of clinically atypical hypertension and chronic kidney disease—the latter by virtue of renal ischemia. The coexistence of renal arterial vascular (ie, renovascular) disease and hypertension roughly defines this type of nonessential hypertension. More specific diagnoses are made retrospectively when hypertension is improved after intravascular intervention.
In 1977 and 1978, Gerald B. Phillips developed the concept that risk factors for myocardial infarction concur to form a "constellation of abnormalities" (i.e., glucose intolerance, hyperinsulinemia, hypercholesterolemia, hypertriglyceridemia, and hypertension) associated not only with heart disease, but also with aging, obesity and other clinical states. He suggested there must be an underlying linking factor, the identification of which could lead to the prevention of cardiovascular disease; he hypothesized that this factor was sex hormones.
The approximate prevalence of the metabolic syndrome in patients with coronary artery disease (CAD) is 50%, with a prevalence of 37% in patients with premature coronary artery disease (age 45), particularly in women. With appropriate cardiac rehabilitation and changes in lifestyle (e.g., nutrition, physical activity, weight reduction, and, in some cases, drugs), the prevalence of the syndrome can be reduced.
Kidney damage from diabetes is called diabetic nephropathy. The onset of kidney disease and its progression is extremely variable. Initially, diseased small blood vessels in the kidneys cause the leakage of protein in the urine. Later on, the kidneys lose their ability to cleanse and filter blood. The accumulation of toxic waste products in the blood leads to the need for dialysis. Dialysis involves using a machine that serves the function of the kidney by filtering and cleaning the blood. In patients who do not want to undergo chronic dialysis, kidney transplantation can be considered.
In hypertensive emergency, there is evidence of direct damage to one or more organs. The most affected organs include the brain, kidney, heart and lungs, producing symptoms which may include confusion, drowsiness, chest pain and breathlessness. In hypertensive emergency, the blood pressure must be reduced more rapidly to stop ongoing organ damage, however, there is a lack of randomized controlled trial evidence for this approach.
Serum creatinine is measured to assess for the presence of kidney disease, which can be either the cause or the result of hypertension. Serum creatinine alone may overestimate glomerular filtration rate and recent guidelines advocate the use of predictive equations such as the Modification of Diet in Renal Disease (MDRD) formula to estimate glomerular filtration rate (eGFR). eGFR can also provide a baseline measurement of kidney function that can be used to monitor for side effects of certain anti-hypertensive drugs on kidney function. Additionally, testing of urine samples for protein is used as a secondary indicator of kidney disease. Electrocardiogram (EKG/ECG) testing is done to check for evidence that the heart is under strain from high blood pressure. It may also show whether there is thickening of the heart muscle (left ventricular hypertrophy) or whether the heart has experienced a prior minor disturbance such as a silent heart attack. A chest X-ray or an echocardiogram may also be performed to look for signs of heart enlargement or damage to the heart.
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.  Metabolic syndrome may also increase cardiovascular risks by increasing arterial stiffness.  Additional mechanisms include oxidative stress,  which has been associated with numerous components of metabolic syndrome. 
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).
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
Energy expenditure over the course of an MRT workout can easily approach or exceed 600 calories, depending on the routine. Better yet, excess post-exercise oxygen consumption (EPOC) increases dramatically. EPOC, often referred to as afterburn, measures the energy expended to return your body to its normal, resting state after a workout. Post-workout, your body uses an immense amount of energy to go from Mr. Huff-and-Puff back to Mr. Breathe-Normal. Considering that intense training can elevate EPOC for 38 hours or more, the total number of calories burned quickly stacks.
What if there was a way that you could combine muscular and cardiovascular benefits of exercise without sacrificing lean muscle tissue or lowering your metabolism as is usually the case? Well, there is, but it takes a special way to organize your workout and to perform it. The days of long slow cardio are GONE! Not only is that ineffective, but it has a high injury rate too. Don't do that to yourself. Read this book and learn how to get the most from you routine without injury.
Health care providers measure blood pressure with a sphygmomanometer (sfig-mo-muh-NAH-muh-ter), which has a cuff that's wrapped around the upper arm and pumped up to create pressure. When the cuff is inflated, it squeezes a large artery in the arm, stopping the blood flow for a moment. Blood pressure is measured as air is gradually let out of the cuff, which allows blood to flow through the artery again.
When it comes to laboratory values, numbers like blood glucose and A1C levels are commonly checked. Less often, doctors order a test for your fasting insulin level; yet this test can help predict your risk of developing prediabetes and metabolic syndrome. Insulin plays a key role in metabolism, and high insulin levels can promote obesity, stimulate hunger, and increase the storage of fat.
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. 
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.
The best way to prevent metabolic syndrom is to adopt heart-healthy lifestyle changes. Make sure to schedule routine doctor visits to keep track of your cholesterol, blood pressure, and blood sugar levels. Speak with your doctor about a blood test called a lipoprotein panel, which shows your levels of total cholesterol, LDL cholesterol, HDL cholesterol, and triglycerides.
The 1989 "St. Vincent Declaration" was the result of international efforts to improve the care accorded to those with diabetes. Doing so is important not only in terms of quality of life and life expectancy but also economically – expenses due to diabetes have been shown to be a major drain on health – and productivity-related resources for healthcare systems and governments.