The primary complications of diabetes due to damage in small blood vessels include damage to the eyes, kidneys, and nerves. Damage to the eyes, known as diabetic retinopathy, is caused by damage to the blood vessels in the retina of the eye, and can result in gradual vision loss and eventual blindness. Diabetes also increases the risk of having glaucoma, cataracts, and other eye problems. It is recommended that diabetics visit an eye doctor once a year. Damage to the kidneys, known as diabetic nephropathy, can lead to tissue scarring, urine protein loss, and eventually chronic kidney disease, sometimes requiring dialysis or kidney transplantation. Damage to the nerves of the body, known as diabetic neuropathy, is the most common complication of diabetes. The symptoms can include numbness, tingling, pain, and altered pain sensation, which can lead to damage to the skin. Diabetes-related foot problems (such as diabetic foot ulcers) may occur, and can be difficult to treat, occasionally requiring amputation. Additionally, proximal diabetic neuropathy causes painful muscle atrophy and weakness.
The body obtains glucose from three main sources: the intestinal absorption of food; the breakdown of glycogen (glycogenolysis), the storage form of glucose found in the liver; and gluconeogenesis, the generation of glucose from non-carbohydrate substrates in the body. Insulin plays a critical role in balancing glucose levels in the body. Insulin can inhibit the breakdown of glycogen or the process of gluconeogenesis, it can stimulate the transport of glucose into fat and muscle cells, and it can stimulate the storage of glucose in the form of glycogen.
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Formal guidelines for measuring blood pressure state that it should be measured in a quiet, warm environment after you have been sitting restfully for at least five minutes. You should not have had coffee or used tobacco for at least 30 minutes. At least two blood pressure measurements should be taken under these conditions at least five minutes apart. This should be repeated until the measurements agree to within 5 mmHg.
Modern understanding of the cardiovascular system began with the work of physician William Harvey (1578–1657), who described the circulation of blood in his book "De motu cordis". The English clergyman Stephen Hales made the first published measurement of blood pressure in 1733. However, hypertension as a clinical entity came into its own with the invention of the cuff-based sphygmomanometer by Scipione Riva-Rocci in 1896. This allowed easy measurement of systolic pressure in the clinic. In 1905, Nikolai Korotkoff improved the technique by describing the Korotkoff sounds that are heard when the artery is ausculated with a stethoscope while the sphygmomanometer cuff is deflated. This permitted systolic and diastolic pressure to be measured.
A positive result, in the absence of unequivocal high blood sugar, should be confirmed by a repeat of any of the above methods on a different day. It is preferable to measure a fasting glucose level because of the ease of measurement and the considerable time commitment of formal glucose tolerance testing, which takes two hours to complete and offers no prognostic advantage over the fasting test. According to the current definition, two fasting glucose measurements above 7.0 mmol/l (126 mg/dl) is considered diagnostic for diabetes mellitus.
In autoimmune diseases, such as type 1 diabetes, the immune system mistakenly manufactures antibodies and inflammatory cells that are directed against and cause damage to patients' own body tissues. In persons with type 1 diabetes, the beta cells of the pancreas, which are responsible for insulin production, are attacked by the misdirected immune system. It is believed that the tendency to develop abnormal antibodies in type 1 diabetes is, in part, genetically inherited, though the details are not fully understood.
This last one is going to really bother the primal crowd, but the number one way to avoid POPs is to avoid high fat animal products. This means that a lower carb and higher fat diet may not be the best option as a fat loss diet. Making non-starchy vegetables and lean protein sources the priority may be best to deal with the POP effect above. If you have been doing well on a low carb high fat diet, don’t stop, just realize that this POP issue may become an issue in slowing the rate of your weight loss or be a factor in weight regain. If this has been something you deal with, you may want to try something closer to a 30:40:30 diet.
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.
According to the Centers for Disease Control and Prevention, more than 50% of people age 50 and older have high blood pressure. Women are about as likely as men to develop high blood pressure, though this varies somewhat by age. For people younger than age 45, more men than women are affected, while for those age 65 and older, more women than men are affected. Americans of African descent develop high blood pressure more often and at an earlier age than those of European and Hispanic descent.
The best way to prevent metabolic syndrom is to adopt heart-healthy lifestyle changes. Make sure to schedule routine doctor visits to keep track of your cholesterol, blood pressure, and blood sugar levels. Speak with your doctor about a blood test called a lipoprotein panel, which shows your levels of total cholesterol, LDL cholesterol, HDL cholesterol, and triglycerides.
Emerging data suggest an important correlation between metabolic syndrome and risk of stroke.  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.  Metabolic syndrome may also be linked to neuropathy beyond hyperglycemic mechanisms through inflammatory mediators.