Some cases of diabetes are caused by the body's tissue receptors not responding to insulin (even when insulin levels are normal, which is what separates it from type 2 diabetes); this form is very uncommon. Genetic mutations (autosomal or mitochondrial) can lead to defects in beta cell function. Abnormal insulin action may also have been genetically determined in some cases. Any disease that causes extensive damage to the pancreas may lead to diabetes (for example, chronic pancreatitis and cystic fibrosis). Diseases associated with excessive secretion of insulin-antagonistic hormones can cause diabetes (which is typically resolved once the hormone excess is removed). Many drugs impair insulin secretion and some toxins damage pancreatic beta cells. The ICD-10 (1992) diagnostic entity, malnutrition-related diabetes mellitus (MRDM or MMDM, ICD-10 code E12), was deprecated by the World Health Organization (WHO) when the current taxonomy was introduced in 1999.[53]
Diabetes mellitus is classified into four broad categories: type 1, type 2, gestational diabetes, and "other specific types".[11] The "other specific types" are a collection of a few dozen individual causes.[11] Diabetes is a more variable disease than once thought and people may have combinations of forms.[37] The term "diabetes", without qualification, usually refers to diabetes mellitus.
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.
Recent research indicates prolonged chronic stress can contribute to metabolic syndrome by disrupting the hormonal balance of the hypothalamic-pituitary-adrenal axis (HPA-axis).[23] A dysfunctional HPA-axis causes high cortisol levels to circulate, which results in raising glucose and insulin levels, which in turn cause insulin-mediated effects on adipose tissue, ultimately promoting visceral adiposity, insulin resistance, dyslipidemia and hypertension, with direct effects on the bone, causing "low turnover" osteoporosis.[24] HPA-axis dysfunction may explain the reported risk indication of abdominal obesity to cardiovascular disease (CVD), type 2 diabetes and stroke.[25] Psychosocial stress is also linked to heart disease.[26]
Dietary changes: The health care provider might recommend a diet that includes more vegetables (especially leafy green vegetables), fruits, low-fat dairy products, and fiber-rich foods, and fewer carbohydrates, fats, processed foods, and sugary drinks. He or she also might recommend preparing low-sodium dishes and not adding salt to foods. Watch out for foods with lots of hidden salt (like bread, sandwiches, pizza, and many restaurant and fast-food options).
Type 2 diabetes was also previously referred to as non-insulin dependent diabetes mellitus (NIDDM), or adult-onset diabetes mellitus (AODM). In type 2 diabetes, patients can still produce insulin, but do so relatively inadequately for their body's needs, particularly in the face of insulin resistance as discussed above. In many cases this actually means the pancreas produces larger than normal quantities of insulin. A major feature of type 2 diabetes is a lack of sensitivity to insulin by the cells of the body (particularly fat and muscle cells). http://www.clairekerslake.com/wp-content/uploads/2014/03/ipad_new.png

Physical changes: If something in your body changes, you may begin experiencing issues throughout your body. High blood pressure may be one of those issues. For example, it’s thought that changes in your kidney function due to aging may upset the body’s natural balance of salts and fluid. This change may cause your body’s blood pressure to increase.
Recent research indicates prolonged chronic stress can contribute to metabolic syndrome by disrupting the hormonal balance of the hypothalamic-pituitary-adrenal axis (HPA-axis).[23] A dysfunctional HPA-axis causes high cortisol levels to circulate, which results in raising glucose and insulin levels, which in turn cause insulin-mediated effects on adipose tissue, ultimately promoting visceral adiposity, insulin resistance, dyslipidemia and hypertension, with direct effects on the bone, causing "low turnover" osteoporosis.[24] HPA-axis dysfunction may explain the reported risk indication of abdominal obesity to cardiovascular disease (CVD), type 2 diabetes and stroke.[25] Psychosocial stress is also linked to heart disease.[26] http://www.sandysidhumedia.com/wp-content/uploads/2012/12/nailahquote.png
Various strategies have been proposed to prevent the development of metabolic syndrome. These include increased physical activity (such as walking 30 minutes every day),[48] and a healthy, reduced calorie diet.[49] 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.[12] The International Obesity Taskforce states that interventions on a sociopolitical level are required to reduce development of the metabolic syndrome in populations.[50]

The goal of treating metabolic syndrome is to prevent the development of diabetes, heart disease, and stroke. Your doctor will first suggest lifestyle modifications such as exercising for 30 minutes most days of the week. One study showed that individuals who are physically active (30 minutes of activity at least once per week) have half the risk of developing metabolic syndrome than those who are inactive. Your doctor may also suggest eating a healthy diet to promote weight loss and normal blood cholesterol and fat levels.
Nerve damage from diabetes is called diabetic neuropathy and is also caused by disease of small blood vessels. In essence, the blood flow to the nerves is limited, leaving the nerves without blood flow, and they get damaged or die as a result (a term known as ischemia). Symptoms of diabetic nerve damage include numbness, burning, and aching of the feet and lower extremities. When the nerve disease causes a complete loss of sensation in the feet, patients may not be aware of injuries to the feet, and fail to properly protect them. Shoes or other protection should be worn as much as possible. Seemingly minor skin injuries should be attended to promptly to avoid serious infections. Because of poor blood circulation, diabetic foot injuries may not heal. Sometimes, minor foot injuries can lead to serious infection, ulcers, and even gangrene, necessitating surgical amputation of toes, feet, and other infected parts.
Health care providers measure blood pressure with a sphygmomanometer (sfig-mo-muh-NAH-muh-ter), which has a cuff that's wrapped around the upper arm and pumped up to create pressure. When the cuff is inflated, it squeezes a large artery in the arm, stopping the blood flow for a moment. Blood pressure is measured as air is gradually let out of the cuff, which allows blood to flow through the artery again.
Hypertension occurs in around 0.2 to 3% of newborns; however, blood pressure is not measured routinely in healthy newborns.[33] Hypertension is more common in high risk newborns. A variety of factors, such as gestational age, postconceptional age and birth weight needs to be taken into account when deciding if a blood pressure is normal in a newborn.[33]

^ Jump up to: a b Go, AS; Bauman, M; King, SM; Fonarow, GC; Lawrence, W; Williams, KA; Sanchez, E (15 November 2013). "An Effective Approach to High Blood Pressure Control: A Science Advisory From the American Heart Association, the American College of Cardiology, and the Centers for Disease Control and Prevention". Hypertension. 63 (4): 878–85. doi:10.1161/HYP.0000000000000003. PMID 24243703. Archived from the original on 20 November 2013. Retrieved 20 November 2013.

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