Target organ damage occurs through multiple mechanisms in metabolic syndrome. The individual diseases leading to metabolic syndrome produce adverse clinical consequences. For example, hypertension in metabolic syndrome causes left ventricular hypertrophy, progressive peripheral arterial disease, and renal dysfunction. [12] However, the cumulative risk for metabolic syndrome appears to cause microvascular dysfunction, which further amplifies insulin resistance and promotes hypertension. [13]
^ Jump up to: a b Acierno, Mark J.; Brown, Scott; Coleman, Amanda E.; Jepson, Rosanne E.; Papich, Mark; Stepien, Rebecca L.; Syme, Harriet M. (2018-10-24). "ACVIM consensus statement: Guidelines for the identification, evaluation, and management of systemic hypertension in dogs and cats". Journal of Veterinary Internal Medicine. 32 (6): 1803–1822. doi:10.1111/jvim.15331. ISSN 1939-1676. PMC 6271319. PMID 30353952.
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]
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.
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).
 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!

In addition, metabolic syndrome has been implicated in the pathophysiology of several other diseases, including obstructive sleep apnea. Breast cancer has also been linked to metabolic syndrome, possibly through dysregulation of the plasminogen activator inhibitor-1 (PAI-1) cycle. [64] Additional studies have linked metabolic syndrome with cancers of the colon, gallbladder, kidney, and, possibly, prostate gland. [65] Evidence is emerging of an association with psoriasis. [66, 67]

You can take additional magnesium if you do not think you’re getting enough in the diet. Dr. Weil recommends magnesium citrate, chelate, or glycinate. Avoid magnesium oxide, which can be irritating, and take half the amount of magnesium as the calcium you take in supplemental form. If you do not take any supplemental calcium, watch out for taking large amounts of magnesium, which can cause diarrhea.
According to guidelines from the American Heart Association (AHA) and the American College of Cardiology (ACC), a reading below 120/80 mm Hg is classified as normal blood pressure. Those with a blood pressure reading anywhere from 120/80 up to 129/80 are classified within a category called elevated blood pressure. Hypertension is defined as a reading of 130/80 or higher.

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]

Type 2 diabetes, which is often diagnosed when a person has an A1C of at least 7 on two separate occasions, can lead to potentially serious issues, like neuropathy, or nerve damage; vision problems; an increased risk of heart disease; and other diabetes complications. A person’s A1C is the two- to three-month average of his or her blood sugar levels.
Okay, you've suffered through the particulars and are sufficiently MRT-educated. Let's get to the good stuff: three tried-and-true MRT strategies guaranteed to help strip away stubborn fat and heighten acid-buffering ability. You can stick with one strategy for a given timeframe or periodize strategies from one week to the next. Regardless of what you decide to do, it's best to insert an "unloading microcycle" (one week of light weight) every fourth week or so to avoid the potential for overtraining. During the unloading cycle, reduce the effort expended so you're not substantially challenging your muscles on the last few reps of each set (aim for about a 7 on an RPE scale of 1-10). As a general rule, limit metabolic training cycles to a maximum of about 8 weeks. Any longer and you risk compromising muscular gains.
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).[27] 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.[23]

Your current healthcare provider may not end up being your future provider, but your current body is yours forever. If you undergo any blood tests or exams, ask for copies of the results so that you can keep them filed away at home. It’s essential that you know your baseline numbers and keep track of the evolution of your health throughout the course of your life.

Polycystic ovarian syndrome. Thought to be related to insulin resistance, this disorder involves the release of extra male hormones by the ovaries, which can lead to abnormal menstrual bleeding, excessive hair growth, acne, and fertility problems. It is also associated with an increased risk for obesity, hypertension, and — in the long-term — diabetes, heart disease, and cancer.
The classic oral glucose tolerance test measures blood glucose levels five times over a period of three hours. Some physicians simply get a baseline blood sample followed by a sample two hours after drinking the glucose solution. In a person without diabetes, the glucose levels rise and then fall quickly. In someone with diabetes, glucose levels rise higher than normal and fail to come back down as fast.
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).
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.
Exogenous administration of the other steroids used for therapeutic purposes also increases blood pressure (BP), especially in susceptible individuals, mainly by volume expansion. Nonsteroidal anti-inflammatory drugs (NSAIDs) may also have adverse effects on BP. NSAIDs block both cyclooxygenase-1 (COX-1) and COX-2 enzymes. The inhibition of COX-2 can inhibit its natriuretic effect, which, in turn, increases sodium retention. NSAIDs also inhibit the vasodilating effects of prostaglandins and the production of vasoconstricting factors—namely, endothelin-1. These effects can contribute to the induction of hypertension in a normotensive or controlled hypertensive patient.
In addition, metabolic syndrome has been implicated in the pathophysiology of several other diseases, including obstructive sleep apnea. Breast cancer has also been linked to metabolic syndrome, possibly through dysregulation of the plasminogen activator inhibitor-1 (PAI-1) cycle. [64] Additional studies have linked metabolic syndrome with cancers of the colon, gallbladder, kidney, and, possibly, prostate gland. [65] Evidence is emerging of an association with psoriasis. [66, 67]
Potassium – as part of the electrolyte panel, which also includes sodium, chloride, and carbon dioxide (CO2); to evaluate and monitor the balance of the body's electrolytes. For example, low potassium can be seen in Cushing syndrome and Conn syndrome, two causes of secondary hypertension. Some high blood pressure medications can upset electrolyte balance by causing excessive loss of potassium or potassium retention.
^ 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.

Creatinine is a chemical waste molecule that is generated from muscle metabolism. Creatinine is produced from creatine, a molecule of major importance for energy production in muscles. Creatinine has been found to be a fairly reliable indicator of kidney function. As the kidneys become impaired the creatinine level in the blood will rise. Normal levels of creatinine in the blood vary from gender and age of the individual.
^ Sacks, F. M.; Svetkey, L. P.; Vollmer, W. M.; Appel, L. J.; Bray, G. A.; Harsha, D.; Obarzanek, E.; Conlin, P. R.; Miller, E. R. (2001-01-04). "Effects on blood pressure of reduced dietary sodium and the Dietary Approaches to Stop Hypertension (DASH) diet. DASH-Sodium Collaborative Research Group". The New England Journal of Medicine. 344 (1): 3–10. doi:10.1056/NEJM200101043440101. ISSN 0028-4793. PMID 11136953.

It has not been contested that cardiovascular risk factors tend to cluster together; the matter of contention has been the assertion that the metabolic syndrome is anything more than the sum of its constituent parts. Phenotypic heterogeneity (for example, represented by variation in metabolic syndrome factor combinations among individuals with metabolic syndrome) has fueled that debate. However, more recent evidence suggests that common triggers (for example, excessive sugar-intake in the environment of overabundant food) can contribute to the development of multiple metabolic abnormalities at the same time, supporting the commonality of the energy utilization and storage pathways in metabolic syndrome.

Findings from the Diabetes Control and Complications Trial (DCCT) and the United Kingdom Prospective Diabetes Study (UKPDS) have clearly shown that aggressive and intensive control of elevated levels of blood sugar in patients with type 1 and type 2 diabetes decreases the complications of nephropathy, neuropathy, retinopathy, and may reduce the occurrence and severity of large blood vessel diseases. Aggressive control with intensive therapy means achieving fasting glucose levels between 70-120 mg/dl; glucose levels of less than 160 mg/dl after meals; and a near normal hemoglobin A1c levels (see below).

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]

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]
Hypertension (HTN or HT), also known as high blood pressure (HBP), is a long-term medical condition in which the blood pressure in the arteries is persistently elevated.[10] High blood pressure typically does not cause symptoms.[1] Long-term high blood pressure, however, is a major risk factor for coronary artery disease, stroke, heart failure, atrial fibrillation, peripheral vascular disease, vision loss, chronic kidney disease, and dementia.[2][3][4][11]
From another perspective, hypertension may be categorized as either essential or secondary. Primary (essential) hypertension is diagnosed in the absence of an identifiable secondary cause. Approximately 90-95% of adults with hypertension have primary hypertension, whereas secondary hypertension accounts for around 5-10% of the cases. [9] However, secondary forms of hypertension, such as primary hyperaldosteronism, account for 20% of resistant hypertension (hypertension in which BP is >140/90 mm Hg despite the use of medications from 3 or more drug classes, 1 of which is a thiazide diuretic).
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]
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

The 1989 "St. Vincent Declaration"[117][118] 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.