Hypertension is the most important preventable risk factor for premature death worldwide.[149] It increases the risk of ischemic heart disease,[150] strokes,[23] peripheral vascular disease,[151] and other cardiovascular diseases, including heart failure, aortic aneurysms, diffuse atherosclerosis, chronic kidney disease, atrial fibrillation, and pulmonary embolism.[11][23] Hypertension is also a risk factor for cognitive impairment and dementia.[23] Other complications include hypertensive retinopathy and hypertensive nephropathy.[27]
Optimally, the management approach results in weight loss based on a healthy diet and regular physical activity, which includes a combination of aerobic activity and resistance training, reinforced with behavioral therapy. Metformin, an insulin sensitizer, or a thiazolidinedione (eg, rosiglitazone, pioglitazone) may be useful. Weight loss of ≈ 7% may be sufficient to reverse the syndrome, but if not, each feature of the syndrome should be managed to achieve recommended targets; available drug treatment is very effective.

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]
After reading a recent Time article entitled “The Weight loss trap” I quite literally jumped off of my office chair, frustrated, angry and delighted. (I also lit up my husband’s phone with a thousand messages). I am so over misinformation in the weight loss space, but even more, it kills me that people are made to feel out of control and hopeless in their own bodies. Why delighted? Well, I was not quite ready to announce my upcoming book but I just could not give up this opportunity to share with you all of the reasons why Time has great points, but doesn’t tell the whole story. You can finally overcome weight loss resistance!
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.
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.
As waistlines expand, so does the epidemic of metabolic syndrome. It’s estimated that nearly one of every four American adults has this condition(1). If you’re one of them, it puts you on the track to developing type 2 diabetes and triples your risk for heart disease down the road. The identification of metabolic syndrome two decades ago(2) is now recognized as a turning point in our understanding of how metabolism can go awry, resulting in obesity, diabetes and cardiovascular disease.
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).
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]
^ Jump up to: a b Petzold A, Solimena M, Knoch KP (October 2015). "Mechanisms of Beta Cell Dysfunction Associated With Viral Infection". Current Diabetes Reports (Review). 15 (10): 73. doi:10.1007/s11892-015-0654-x. PMC 4539350. PMID 26280364. So far, none of the hypotheses accounting for virus-induced beta cell autoimmunity has been supported by stringent evidence in humans, and the involvement of several mechanisms rather than just one is also plausible.

^ Brunner EJ, Hemingway H, Walker BR, Page M, Clarke P, Juneja M, Shipley MJ, Kumari M, Andrew R, Seckl JR, Papadopoulos A, Checkley S, Rumley A, Lowe GD, Stansfeld SA, Marmot MG (November 2002). "Adrenocortical, autonomic, and inflammatory causes of the metabolic syndrome: nested case-control study". Circulation. 106 (21): 2659–65. doi:10.1161/01.cir.0000038364.26310.bd. PMID 12438290.


Emerging data suggest an important correlation between metabolic syndrome and risk of stroke. [58] Each of the components of metabolic syndrome has been associated with elevated stroke risk, and evidence demonstrates a relationship between the collective metabolic syndrome and risk of ischemic stroke. [59] Metabolic syndrome may also be linked to neuropathy beyond hyperglycemic mechanisms through inflammatory mediators. [60]
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