Here’s how it works: Each time you hit the gym, you work your whole body with circuits or pairs of multijoint, free-weight exercises that put the body through a full range of basic functional movements such as squatting, deadlifting, lunging, pulling, pushing and twisting. Because you exercise your entire body every workout, your metabolism has to work overtime for many hours afterward to help you recover. This leads to an intense, round-the-clock fat burn that you can’t get from programs that isolate muscle groups.
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.  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. 
MRUT is just about the best acronym I've heard in awhile. Have to check it out, but I can already say I like it. The other point of note is that I'm putting together a Jenn Sinkler incidence table. By my early estimates I can't get through three hours of my day without running into Jenn's name or mention of her new book. Add that one to the reading list too. At this rate, with all of this content, my workouts are suffering. I'm going to recommend these books move to MP3 formats with good background tunes so we can all listen while we lift. Problem solved. Thanks John. Good stuff.
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). https://i.ytimg.com/vi/03Ar9vo6VbM/hqdefault.jpg?sqp
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.
Many mechanisms have been proposed to account for the rise in peripheral resistance in hypertension. Most evidence implicates either disturbances in the kidneys' salt and water handling (particularly abnormalities in the intrarenal renin–angiotensin system) or abnormalities of the sympathetic nervous system. These mechanisms are not mutually exclusive and it is likely that both contribute to some extent in most cases of essential hypertension. It has also been suggested that endothelial dysfunction and vascular inflammation may also contribute to increased peripheral resistance and vascular damage in hypertension. Interleukin 17 has garnered interest for its role in increasing the production of several other immune system chemical signals thought to be involved in hypertension such as tumor necrosis factor alpha, interleukin 1, interleukin 6, and interleukin 8.
The exact mechanisms of the complex pathways of metabolic syndrome are under investigation. The pathophysiology is very complex and has been only partially elucidated. Most patients are older, obese, sedentary, and have a degree of insulin resistance. Stress can also be a contributing factor. The most important risk factors are diet (particularly sugar-sweetened beverage consumption), genetics, aging, sedentary behavior or low physical activity, disrupted chronobiology/sleep, mood disorders/psychotropic medication use, and excessive alcohol use.
As of 2016, 422 million people have diabetes worldwide, up from an estimated 382 million people in 2013 and from 108 million in 1980. Accounting for the shifting age structure of the global population, the prevalence of diabetes is 8.5% among adults, nearly double the rate of 4.7% in 1980. Type 2 makes up about 90% of the cases. Some data indicate rates are roughly equal in women and men, but male excess in diabetes has been found in many populations with higher type 2 incidence, possibly due to sex-related differences in insulin sensitivity, consequences of obesity and regional body fat deposition, and other contributing factors such as high blood pressure, tobacco smoking, and alcohol intake.
Metformin is generally recommended as a first line treatment for type 2 diabetes, as there is good evidence that it decreases mortality. It works by decreasing the liver's production of glucose. Several other groups of drugs, mostly given by mouth, may also decrease blood sugar in type II DM. These include agents that increase insulin release, agents that decrease absorption of sugar from the intestines, and agents that make the body more sensitive to insulin. When insulin is used in type 2 diabetes, a long-acting formulation is usually added initially, while continuing oral medications. Doses of insulin are then increased to effect.
Metabolic syndrome is quite common. Approximately 32% of the population in the U.S. has metabolic syndrome, and about 85% of those with type 2 diabetes have metabolic syndrome. Around 25% of adults in Europe and Latin America are estimated to have the condition, and rates are rising in developing East Asian countries. Within the US, Mexican Americans have the highest prevalence of metabolic syndrome. The prevalence of metabolic syndrome increases with age, and about 40% of people over 60 are affected.
Hypertension is one of the most common worldwide diseases afflicting humans and is a major risk factor for stroke, myocardial infarction, vascular disease, and chronic kidney disease. Despite extensive research over the past several decades, the etiology of most cases of adult hypertension is still unknown, and control of blood pressure is suboptimal in the general population. Due to the associated morbidity and mortality and cost to society, preventing and treating hypertension is an important public health challenge. Fortunately, recent advances and trials in hypertension research are leading to an increased understanding of the pathophysiology of hypertension and the promise for novel pharmacologic and interventional treatments for this widespread disease.
The pressure generated by the beating heart forces the blood forward and stretches the elastic walls of the arteries. In between heartbeats, as the heart muscle relaxes, the arterial walls snap back to their original shape, moving the blood forward to the body’s tissues. With hypertension, the pressure in the arteries is high enough to eventually produce damage to the blood vessels.
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. 
Cortisol reactivity, an index of hypothalamic-pituitary-adrenal function, may be another mechanism by which psychosocial stress is associated with future hypertension.  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. 
Between 2006 and 2011, there was a 25% increase in the number of people visiting US emergency rooms for essential hypertension, according to an analysis of data from the Nationwide Emergency Department Sample in 2014.  The reason for the increase, however, remained uncertain. The rate of emergency department visits also increased significantly, according to the study, rising from 190.1 visits per 100,000 population in 2006 to 238.5 visits per 100,000 population in 2011. Over the same period, however, admission rates decreased, from 10.47% in 2006 to 8.85% in 2011. 
Hypertension results from a complex interaction of genes and environmental factors. Numerous common genetic variants with small effects on blood pressure have been identified as well as some rare genetic variants with large effects on blood pressure. Also, genome-wide association studies (GWAS) have identified 35 genetic loci related to blood pressure; 12 of these genetic loci influencing blood pressure were newly found. Sentinel SNP for each new genetic locus identified has shown an association with DNA methylation at multiple nearby CpG sites. These sentinel SNP are located within genes related to vascular smooth muscle and renal function. DNA methylation might affect in some way linking common genetic variation to multiple phenotypes even though mechanisms underlying these associations are not understood. Single variant test performed in this study for the 35 sentinel SNP (known and new) showed that genetic variants singly or in aggregate contribute to risk of clinical phenotypes related to high blood pressure.