The primary goal of clinical management is to reduce cardiovascular risk factors and prevent type 2 diabetes. The major risk factors for cardiac disease include cigarette smoking, blood lipid abnormalities, elevated blood pressure and glucose, all of which should be reduced to recommended levels. Aggressive lifestyle changes, and in some cases medication, can improve most if not all components of metabolic syndrome.
^ Emadian A, Andrews RC, England CY, Wallace V, Thompson JL (November 2015). "The effect of macronutrients on glycaemic control: a systematic review of dietary randomised controlled trials in overweight and obese adults with type 2 diabetes in which there was no difference in weight loss between treatment groups". The British Journal of Nutrition. 114 (10): 1656–66. doi:10.1017/S0007114515003475. PMC 4657029. PMID 26411958.
Push-ups would be another example.  We've all seen the classic push-up form deterioration under fatigued conditions: a sagging, excessively arched lower back; forward head posture; and elbows flaring out.  It's the classic "panic mode" strategy employed by beginners.  However, you never see it in experienced lifters; they'll simply fail before the technique breaks down.  Part of this comes from technical proficiency, but it's also related to the fact that the limiting factor shifts from anterior core stability to upper body strength/endurance as an individual gets more experienced.
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]
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.

Out of this whole article this quote from a participant was the thing that drove my emotions. For anyone who struggles with weight loss resistance this will stab you in the heart. It is so incredibly true. There is nothing quite like feeling like your body is failing you and that even starving yourself, restricting every delicious food and exercising to the max is not enough.
Mark A Silverberg, MD, MMB, FACEP Assistant Professor, Associate Residency Director, Department of Emergency Medicine, State University of New York Downstate College of Medicine; Consulting Staff, Department of Emergency Medicine, Staten Island University Hospital, Kings County Hospital, University Hospital, State University of New York Downstate Medical Center
Because metabolic syndrome and insulin resistance are closely tied, many healthcare providers believe that insulin resistance may be a cause of metabolic syndrome. But they have not found a direct link between the two conditions. Others believe that hormone changes caused by chronic stress lead to abdominal obesity, insulin resistance, and higher blood lipids (triglycerides and cholesterol).
Abundant data suggest that patients meeting these diagnostic criteria have a greater risk of significant clinical consequences, the 2 most prominent of which are the development of diabetes mellitus [6] and of coronary heart disease. Pooled data from 37 studies involving more than 170,000 patients have shown that metabolic syndrome doubles the risk of coronary artery disease. [7] It also increases risk of stroke, fatty liver disease, and cancer. [8] (See Prognosis.)
Defining abnormally high blood pressure (BP) is extremely difficult and arbitrary. Furthermore, the relationship between systemic arterial pressure and morbidity appears to be quantitative rather than qualitative. A level for high BP must be agreed upon in clinical practice for screening patients with hypertension and for instituting diagnostic evaluation and initiating therapy. Because the risk to an individual patient may correlate with the severity of hypertension, a classification system is essential for making decisions about aggressiveness of treatment or therapeutic interventions. (See Presentation.)

* Some examples of agents that induce hypertension include nonsteroidal anti-inflammatory drugs (NSAIDs) and cyclooxygenase-2 (COX-2) inhibitors; illicit drugs; sympathomimetic agents; oral contraceptive or adrenal steroid hormones; cyclosporine and tacrolimus; licorice; erythropoietin; and certain over-the-counter dietary supplements and medicines, such as ephedra, ma huang, and bitter orange. Drug-related causes of hypertension may be due to nonadherence, inadequate doses, and inappropriate combinations.


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.

The most common side effects of anti-hypertensive medications include hypotension (low blood pressure) and dizziness. These effects are the result of the excessive lowering of blood pressure, and they can be alleviated if your doctor adjusts your medication dose. Each drug and medication category also has its own unique side effects, which you should familiarize yourself with when you begin taking the medication (check patient information provided by your pharmacy, or ask the pharmacist herself).

There are several classes of drugs available to treat hypertension; each works differently, targeting a specific aspect of blood pressure regulation. Frequently, someone will need to take a couple of different medications together to achieve blood pressure control. Your health practitioner will work with you to select the appropriate combinations and dosages. (See How is High Blood Pressure Treated? on the NHLBI website.)


Leptin is considered by many to be THE most important metabolic hormone as far as setting metabolic output and weight regain. If you want to keep your metabolic rate up, you have to make sure leptin levels don’t fall too fast. One way to overcome this appears to be a short period of overeating of between 1 and 3 days. This technique raises leptin levels and has also been shown to substantially raise a depressed metabolic rate. This effect varies substantially from person to person with some people showing no effect from the brief overfeeding and others seeing a jump in resting calorie burn of several hundred calories per day.
Events in early life, such as low birth weight, maternal smoking, and lack of breastfeeding may be risk factors for adult essential hypertension, although the mechanisms linking these exposures to adult hypertension remain unclear.[43] An increased rate of high blood urea has been found in untreated people with hypertension in comparison with people with normal blood pressure, although it is uncertain whether the former plays a causal role or is subsidiary to poor kidney function.[44] Average blood pressure may be higher in the winter than in the summer.[45] Periodontal disease is also associated with high blood pressure.[46]
Metabolic training (MT) is a hybrid of anaerobic strength training and aerobic cardio exercise. In a nutshell, effective MT training ignites your metabolism, allowing for a longer period of calorie burning. Essentially, your body's furnace is lit and on overdrive for up to 48 hours after the workout. The catch? The workout needs to be both intense and dense. Meaning you have to go all out and complete a high volume of work in a short period of time. An hour of weight training or a 30-minute jog around the park will not suffice.
“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.
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).
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.
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.

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.
The first chemical for hypertension, sodium thiocyanate, was used in 1900 but had many side effects and was unpopular.[152] Several other agents were developed after the Second World War, the most popular and reasonably effective of which were tetramethylammonium chloride, hexamethonium, hydralazine, and reserpine (derived from the medicinal plant Rauwolfia serpentina). None of these were well tolerated.[159][160] A major breakthrough was achieved with the discovery of the first well-tolerated orally available agents. The first was chlorothiazide, the first thiazide diuretic and developed from the antibiotic sulfanilamide, which became available in 1958.[152][161] Subsequently, beta blockers, calcium channel blockers, angiotensin converting enzyme (ACE) inhibitors, angiotensin receptor blockers, and renin inhibitors were developed as antihypertensive agents.[158]

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! https://i.ytimg.com/vi/OM263kSxLm4/hqdefault.jpg?sqp
Various expert groups have produced guidelines regarding how low the blood pressure target should be when a person is treated for hypertension. These groups recommend a target below the range 140–160 / 90–100 mmHg for the general population.[13][99][100][101][102] Cochrane reviews recommend similar targets for subgroups such as people with diabetes[103] and people with prior cardiovascular disease.[104]
Various expert groups have produced guidelines regarding how low the blood pressure target should be when a person is treated for hypertension. These groups recommend a target below the range 140–160 / 90–100 mmHg for the general population.[13][99][100][101][102] Cochrane reviews recommend similar targets for subgroups such as people with diabetes[103] and people with prior cardiovascular disease.[104]
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]
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.

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]

The treatment of low blood sugar consists of administering a quickly absorbed glucose source. These include glucose containing drinks, such as orange juice, soft drinks (not sugar-free), or glucose tablets in doses of 15-20 grams at a time (for example, the equivalent of half a glass of juice). Even cake frosting applied inside the cheeks can work in a pinch if patient cooperation is difficult. If the individual becomes unconscious, glucagon can be given by intramuscular injection.
^ Jump up to: a b c Giuseppe, Mancia; Fagard, R; Narkiewicz, K; Redon, J; Zanchetti, A; Bohm, M; Christiaens, T; Cifkova, R; De Backer, G; Dominiczak, A; Galderisi, M; Grobbee, DE; Jaarsma, T; Kirchhof, P; Kjeldsen, SE; Laurent, S; Manolis, AJ; Nilsson, PM; Ruilope, LM; Schmieder, RE; Sirnes, PA; Sleight, P; Viigimaa, M; Waeber, B; Zannad, F; Redon, J; Dominiczak, A; Narkiewicz, K; Nilsson, PM; et al. (July 2013). "2013 ESH/ESC Guidelines for the management of arterial hypertension: The Task Force for the management of arterial hypertension of the European Society of Hypertension (ESH) and of the European Society of Cardiology (ESC)". European Heart Journal. 34 (28): 2159–219. doi:10.1093/eurheartj/eht151. PMID 23771844.
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).
Most drugs take 4–8 weeks for maximum effect. Thus, it is recommended that a minimum period of 6 weeks is trialled before changes to medications are made.Generally treatment starts with a single drug. Recent large studies have shown that cheaper, older drugs, are just as effective as newer drugs. If a single drug fails to achieve blood pressure goals, other agents can be added in.
Metabolic syndrome (also known as metabolic syndrome X) is a grouping of cardiac risk factors that result from insulin resistance (when the body's tissues do not respond normally to insulin). A person with metabolic syndrome has a greatly increased risk of developing type 2 diabetes, cardiovascular disease and premature death. In fact, another name for metabolic syndrome is pre-diabetes. https://www.clairekerslake.com/wp-content/uploads/2011/11/candles.jpg
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.
Cirrhosis of the liver refers to a disease in which normal liver cells are replaced by scar tissue caused by alcohol and viral hepatitis B and C. This disease leads to abnormalities in the liver's ability to handle toxins and blood flow, causing internal bleeding, kidney failure, mental confusion, coma, body fluid accumulation, and frequent infections.
Melissa Conrad Stöppler, MD, is a U.S. board-certified Anatomic Pathologist with subspecialty training in the fields of Experimental and Molecular Pathology. Dr. Stöppler's educational background includes a BA with Highest Distinction from the University of Virginia and an MD from the University of North Carolina. She completed residency training in Anatomic Pathology at Georgetown University followed by subspecialty fellowship training in molecular diagnostics and experimental pathology.
If lifestyle modifications are insufficient to achieve the goal BP, there are several drug options for treating and managing hypertension. Thiazide diuretics, an angiotensin-converting enzyme inhibitor (ACEI) /angiotensin receptor blocker (ARB), or calcium channel blocker (CCB) are the preferred agents in nonblack populations, whereas CCBs or thiazide diuretics are favored in black hypertensive populations. [8] These recommendations do not exclude the use of ACE inhibitors or ARBs in treatment of black patients, or CCBs or diuretics in non-black persons. Often, patients require several antihypertensive agents to achieve adequate BP control.
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.
Metabolic syndrome is increasing in prevalence, paralleling an increasing epidemic of obesity. In the United States, where almost two thirds of the population is overweight or obese, more than one fourth of the population meets diagnostic criteria for metabolic syndrome. [25] In the United States, data from a 1999-2000 survey showed that the age-adjusted prevalence of metabolic syndrome among adults aged 20 years or older had risen from 27% (data from 1988-1994) to 32%. [26]
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.

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]
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).

While the lipid abnormalities seen with metabolic syndrome (low HDL, high LDL, and high triglycerides) respond nicely to weight loss and exercise, drug therapy is often required. Treatment should be aimed primarily at reducing LDL levels according to specific recommendations. Once reduced LDL targets are reached, efforts at reducing triglyceride levels and raising HDL levels should be made. Successful drug treatment usually requires treatment with a statin, a fibrate drug, or a combination of a statin with either niacin or a fibrate.
Central obesity is a key feature of the syndrome, being both a sign and a cause, in that the increasing adiposity often reflected in high waist circumference may both result from and contribute to insulin resistance. However, despite the importance of obesity, patients who are of normal weight may also be insulin-resistant and have the syndrome.[27]

[Guideline] Skyler JS, Bergenstal R, Bonow RO, et al. Intensive glycemic control and the prevention of cardiovascular events: implications of the ACCORD, ADVANCE, and VA Diabetes Trials: a position statement of the American Diabetes Association and a Scientific Statement of the American College of Cardiology Foundation and the American Heart Association. J Am Coll Cardiol. 2009 Jan 20. 53(3):298-304. [Medline].

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