Blood pressure rises with aging and the risk of becoming hypertensive in later life is considerable. Several environmental factors influence blood pressure. High salt intake raises the blood pressure in salt sensitive individuals; lack of exercise, obesity, and depression can play a role in individual cases. The possible roles of other factors such as caffeine consumption, and vitamin D deficiency are less clear. Insulin resistance, which is common in obesity and is a component of syndrome X (or the metabolic syndrome), is also thought to contribute to hypertension. One review suggests that sugar may play an important role in hypertension and salt is just an innocent bystander.
Now for the big surprise cause. There is another set of signaling molecules that have a huge impact on metabolic compensations during dieting. These compounds are present in your fat cells, and when fat is burned, they are released in significant concentrations. The shocking thing about these compounds is they did not come from your body. They are man made chemicals that you eat, put on your skin, drink in your water, and inhale through the air.
^ Piwernetz K, Home PD, Snorgaard O, Antsiferov M, Staehr-Johansen K, Krans M (May 1993). "Monitoring the targets of the St Vincent Declaration and the implementation of quality management in diabetes care: the DIABCARE initiative. The DIABCARE Monitoring Group of the St Vincent Declaration Steering Committee". Diabetic Medicine. 10 (4): 371–77. doi:10.1111/j.1464-5491.1993.tb00083.x. PMID 8508624.
The good news is that with changes to diet and exercise, you can prevent, control, or even reverse metabolic syndrome. If you don’t, you could develop significant health risks related to the diabetes, heart disease, and stroke as part of the condition. Your risk for metabolic syndrome increases with age, so it’s important to start adjusting your health habits early on.
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  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.  It also increases risk of stroke, fatty liver disease, and cancer.  (See Prognosis.)
Prevention and treatment involve maintaining a healthy diet, regular physical exercise, a normal body weight, and avoiding use of tobacco. Control of blood pressure and maintaining proper foot care are important for people with the disease. Type 1 DM must be managed with insulin injections. Type 2 DM may be treated with medications with or without insulin. Insulin and some oral medications can cause low blood sugar. Weight loss surgery in those with obesity is sometimes an effective measure in those with type 2 DM. Gestational diabetes usually resolves after the birth of the baby.
Various strategies have been proposed to prevent the development of metabolic syndrome. These include increased physical activity (such as walking 30 minutes every day), and a healthy, reduced calorie diet. Many studies support the value of a healthy lifestyle as above. However, one study stated these potentially beneficial measures are effective in only a minority of people, primarily due to a lack of compliance with lifestyle and diet changes. The International Obesity Taskforce states that interventions on a sociopolitical level are required to reduce development of the metabolic syndrome in populations.
Insulin resistance also may increase your risk for metabolic syndrome. Insulin resistance is a condition in which the body can’t use its insulin properly. Insulin is a hormone that helps move blood sugar into cells where it’s used for energy. Insulin resistance can lead to high blood sugar levels, and it’s closely linked to overweight and obesity. Genetics (ethnicity and family history) and older age are other factors that may play a role in causing metabolic syndrome.
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).
Another method is to have the individual wear a device that monitors and records the blood pressure at regular intervals during the day to evaluate blood pressure over time. This is especially helpful during the diagnostic process and can help rule out "white coat" hypertension, the high measurements that are sometimes present only when the person is in the doctor's office and not at other times. (See High Blood Pressure: Using an Ambulatory Blood Pressure Monitor on FamilyDoctor.org.)
Rates of high blood pressure in children and adolescents have increased in the last 20 years in the United States. Childhood hypertension, particularly in pre-adolescents, is more often secondary to an underlying disorder than in adults. Kidney disease is the most common secondary cause of hypertension in children and adolescents. Nevertheless, primary or essential hypertension accounts for most cases.
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).
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.
Diabetes mellitus occurs throughout the world but is more common (especially type 2) in more developed countries. The greatest increase in rates has however been seen in low- and middle-income countries, where more than 80% of diabetic deaths occur. The fastest prevalence increase is expected to occur in Asia and Africa, where most people with diabetes will probably live in 2030. The increase in rates in developing countries follows the trend of urbanization and lifestyle changes, including increasingly sedentary lifestyles, less physically demanding work and the global nutrition transition, marked by increased intake of foods that are high energy-dense but nutrient-poor (often high in sugar and saturated fats, sometimes referred to as the "Western-style" diet). The global prevalence of diabetes might increase by 55% between 2013 and 2035. https://www.pickthebrain.com/blog/wp-content/uploads/2013/03/meditation.png
Hypertension develops secondary to environmental factors, as well as multiple genes, whose inheritance appears to be complex. [12, 21] Furthermore, obesity, diabetes, and heart disease also have genetic components and contribute to hypertension. Epidemiological studies using twin data and data from Framingham Heart Study families reveal that BP has a substantial heritable component, ranging from 33-57%. [22, 23, 24]
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.
Doctors may also prescribe medications to lower blood pressure, control cholesterol or help you lose weight. Insulin sensitizers like Glucophage (Metformin) may be prescribed to help your body use insulin more effectively. It lowers blood sugar, which also seems to help lower cholesterol and triglycerides as well as decreasing appetite. The side effects of Metformin (often temporary) include nausea, stomach pain, bloating and diarrhea. A more serious side effect, lactic acidosis, can affect those with kidney or liver disease, severe heart failure or a history of alcohol abuse and is potentially, though rarely, fatal. Aspirin therapy is often given to help reduce risk of heart attack and stroke.
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.
Another common endocrine cause is oral contraceptive use. Activation of the renin-angiotensin-aldosterone system (RAAS) is the likely mechanism, because hepatic synthesis of angiotensinogen is induced by the estrogen component of oral contraceptives. Approximately 5% of women taking oral contraceptives may develop hypertension, which abates within 6 months after discontinuation. The risk factors for oral contraceptive–associated hypertension include mild renal disease, familial history of essential hypertension, age older than 35 years, and obesity. It would be better to group oral contraceptives and steroids with drug-induced hypertension (see Table 1, below).
I hate to burst anyone's bubble, but doing 5-10s intervals probably isn't going to do much for you – unless you're doing a ton of them, or using really short rest intervals. Essentially, you have to get to the point where you shift over from the ATP-PC to the glycolitic (anaerobic) system. This is a sweet spot where intensity of exercise is high while volume remains up – and that's how you create the "metabolic debt" that makes interval training so beneficial.
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).
Gary Edward Sander, MD, PhD, FACC, FAHA, FACP, FASH is a member of the following medical societies: Alpha Omega Alpha, American Chemical Society, American College of Cardiology, American College of Chest Physicians, American College of Physicians, American Federation for Clinical Research, American Federation for Medical Research, American Heart Association, American Society for Pharmacology and Experimental Therapeutics, American Society of Hypertension, American Thoracic Society, Heart Failure Society of America, National Lipid Association, Southern Society for Clinical Investigation
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).
Naturally, since the metabolic syndrome is a disorder of energy distribution and storage, fat accumulation explains for a significant proportion of cardiovascular risk. However, obesity without metabolic syndrome does not confer a significant cardiovascular risk, whereas metabolic syndrome without obesity is associated with a significant risk of diabetes and cardiovascular disease. This association of metabolic syndrome with diabetes can be illustrated by generalized lipodystrophy (near complete absence of adipose tissue). The animals and humans with generalized lipodystrophy develop signs of metabolic syndrome in the absence of adipose tissue; and the metabolic syndrome progresses to type 2 diabetes. Adipose tissue transplantation in transgenic mice with lipodystrophy can cure the type 2 diabetes.
Diabetes mellitus is a group of metabolic diseases characterized by high blood sugar (glucose) levels that result from defects in insulin secretion, or its action, or both. Diabetes mellitus, commonly referred to as diabetes (as it will be in this article) was first identified as a disease associated with "sweet urine," and excessive muscle loss in the ancient world. Elevated levels of blood glucose (hyperglycemia) lead to spillage of glucose into the urine, hence the term sweet urine.
Gestational diabetes mellitus (GDM) resembles type 2 DM in several respects, involving a combination of relatively inadequate insulin secretion and responsiveness. It occurs in about 2–10% of all pregnancies and may improve or disappear after delivery. However, after pregnancy approximately 5–10% of women with GDM are found to have DM, most commonly type 2. GDM is fully treatable, but requires careful medical supervision throughout the pregnancy. Management may include dietary changes, blood glucose monitoring, and in some cases, insulin may be required.