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),[6] genetics,[7][8][9][10] aging, sedentary behavior[11] or low physical activity,[12][13] disrupted chronobiology/sleep,[14] mood disorders/psychotropic medication use,[15][16] and excessive alcohol use.[17]
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.
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. [18] Both adipose cell enlargement and infiltration of macrophages into adipose tissue result in the release of proinflammatory cytokines and promote insulin resistance. [19]
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]

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]

If someone has already had a heart attack, their LDL ("bad") cholesterol should be reduced below 70mg/dl. A person who has diabetes has a heart attack risk equivalent to that of someone who has already one and so should be treated in the same way. If you have metabolic syndrome, a detailed discussion about lipid therapy is needed between you and your doctor, as each individual is unique.
Blood pressure was traditionally measured using a stethoscope and a blood pressure cuff (called a sphygmomanometer), a device that includes a cuff, a bulb, and a pressure dial that reads the pressure in millimeters of mercury (mm Hg). This is still considered the best method but, more commonly, devices that combine a blood pressure cuff with electronic sensors are used to measure blood pressure. http://4.bp.blogspot.com/-du4BiwBwloo/UbfEdfaxaSI/AAAAAAAABa4/ikJjD8ruIkw/s1600/claire-kerslake-graphic-for-renew-promo-post-with-logo-final.jpg

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.


Moreover, it is estimated that 1 death is prevented per 11 patients treated for stage 1 hypertension and other cardiovascular risk factors when a sustained reduction of 12 mm Hg in systolic BP over 10 years is achieved. [2] However, for the same reduction is systolic BP reduction, it is estimated that 1 death is prevented per 9 patients treated when cardiovascular disease or end-organ damage is present. [2]
Diabetes mellitus is a chronic disease, for which there is no known cure except in very specific situations.[75] Management concentrates on keeping blood sugar levels as close to normal, without causing low blood sugar. This can usually be accomplished with a healthy diet, exercise, weight loss, and use of appropriate medications (insulin in the case of type 1 diabetes; oral medications, as well as possibly insulin, in type 2 diabetes).
Instead of an arbitrary goal to “lose weight,” talk with your doctor about a healthy weight for you. The Centers for Disease Control and Prevention (CDC) recommends a weight loss goal of one to two pounds a week. That means starting off eating 500 calories less per day than what you normally eat. Then decide on what physical activity you can start in order to reach that goal. If exercising five nights a week is too hard to work into your schedule, aim for one more night than what you’re doing right now. When that fits comfortably into your schedule, add another night.
The Mediterranean diet is palatable and easily sustained. In addition, recent studies have shown that when compared to a low fat diet, people on the Mediterranean diet have a greater decrease in body weight, and also had greater improvements in blood pressure, cholesterol levels, and other markers of heart disease -- all of which are important in evaluating and treating metabolic syndrome.
Menopause is the time in a woman's life when menstrual periods permanently stop, also called the "change of life." Menopause symptoms include hot flashes, night sweats, irregular vaginal bleeding, vaginal dryness, painful intercourse, urinary incontinence, weight gain, and emotional symptoms such as mood swings. Treatment of menopausal symptoms varies, and should be discussed with your physician.
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).
Hypertension results from a complex interaction of genes and environmental factors. Numerous common genetic variants with small effects on blood pressure have been identified[34] as well as some rare genetic variants with large effects on blood pressure.[35] 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.[36] 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.[36]

When a blood pressure reading is taken, the higher number represents the systolic pressure and the lower number represents the diastolic pressure. For example: 120/80 (120 over 80) in an adult means that the systolic pressure is 120 and the diastolic pressure is 80. As kids grow, their blood pressure increases from a systolic pressure of about 70–90 (as babies) to adult values (when they're teens).
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]

But, the metabolism compensates. This person starts feeling hungry all the time. Their energy begins to suffer, and they feel cravings for sweet, salty, and fatty foods. This makes it harder for them to comply. But worse than that, depending on their individual response to the law of metabolic compensation, their metabolism has now put on the brakes, slowing their daily calorie burn rate by between 200 and 800 calories per day.

The prognosis of diabetes is related to the extent to which the condition is kept under control to prevent the development of the complications described in the preceding sections. Some of the more serious complications of diabetes such as kidney failure and cardiovascular disease, can be life-threatening. Acute complications such as diabetic ketoacidosis can also be life-threatening. As mentioned above, aggressive control of blood sugar levels can prevent or delay the onset of complications, and many people with diabetes lead long and full lives.
Cortisol reactivity, an index of hypothalamic-pituitary-adrenal function, may be another mechanism by which psychosocial stress is associated with future hypertension. [20] 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. [20]
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