Type 2 diabetes is a preventable disease that affects more than 9 percent of the U.S. population, or about 29 million people. According to the Centers for Disease Control and Prevention, more than a quarter — some 8 million people — remain undiagnosed. With complications including nerve damage, kidney damage, poor blood circulation, and even death, it’s important for us all to know the early signs of type 2 diabetes.
Although this newfound knowledge on sugar, and specifically added sugar, may prompt you to ditch the soda, juice, and processed foods, be mindful of the other factors that can similarly influence your risk for type 2 diabetes. Obesity, a family history of diabetes, a personal history of heart disease, and depression, for instance, are other predictors for the disease, according to the NIH.
Jump up ^ Haw, JS; Galaviz, KI; Straus, AN; Kowalski, AJ; Magee, MJ; Weber, MB; Wei, J; Narayan, KMV; Ali, MK (6 November 2017). "Long-term Sustainability of Diabetes Prevention Approaches: A Systematic Review and Meta-analysis of Randomized Clinical Trials". JAMA Internal Medicine. 177 (12): 1808–17. doi:10.1001/jamainternmed.2017.6040. PMID 29114778.
With type 1, a disease that often seems to strike suddenly and unexpectedly, the effects of environment and lifestyle are far less clear. But several theories attempt to explain why cases of type 1 have increased so dramatically in recent decades, by around 5 percent per year since 1980. The three main suspects now are too little sun, too good hygiene, and too much cow's milk.
Type 2 diabetes, a form of diabetes mellitus, is likely one of the better-known chronic diseases in the world — and that's no surprise. Data from the Centers for Disease Control and Prevention suggest in the United States alone, 30.3 million people, or 9.4 percent of the U.S. population, has diabetes, and the majority of these people have type 2. (1)
Type 2 diabetes is usually associated with being overweight (BMI greater than 25), and is harder to control when food choices are not adjusted, and you get no physical activity. And while it’s true that too much body fat and physical inactivity (being sedentary) does increase the likelihood of developing type 2, even people who are fit and trim can develop this type of diabetes.2,3
Kidney disease: According to the Centers for Disease Control and Prevention (CDC), an estimated 33 percent of people with diabetes have chronic kidney disease. Diabetes can also damage blood vessels in the kidneys, impairing function. The kidneys play a vital role in balancing fluid levels and removing waste from the body. Kidney health is therefore vital for preserving overall health.
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Most pediatric patients with diabetes have type 1 diabetes mellitus (T1DM) and a lifetime dependence on exogenous insulin. Diabetes mellitus (DM) is a chronic metabolic disorder caused by an absolute or relative deficiency of insulin, an anabolic hormone. Insulin is produced by the beta cells of the islets of Langerhans located in the pancreas, and the absence, destruction, or other loss of these cells results in type 1 diabetes (insulin-dependent diabetes mellitus [IDDM]). A possible mechanism for the development of type 1 diabetes is shown in the image below. (See Etiology.)
All types of diabetes mellitus have something in common. Normally, your body breaks down the sugars and carbohydrates you eat into a special sugar called glucose. Glucose fuels the cells in your body. But the cells need insulin, a hormone, in your bloodstream in order to take in the glucose and use it for energy. With diabetes mellitus, either your body doesn't make enough insulin, it can't use the insulin it does produce, or a combination of both.
Diabetes has been coined the “silent killer” because the symptoms are so easy to miss. Over 24 million people in America have diabetes, so this is no tiny issue. Kids years ago hardly ever knew another child with diabetes, but such is no longer the case. Approximately 1.25 million children in the United States living with diabetes, which is very telling for state of health in America in 2016 when children are having to endure a medical lifestyle at such a young age.
In 2013, of the estimated 382 million people with diabetes globally, more than 80 per cent lived in LMIC. It was estimated that India had 65.1 million adults with diabetes in 2013, and had the 2nd position among the top 10 countries with the largest number of diabetes. This number is predicted to increase to 109 million by 2035 unless steps are taken to prevent new cases of diabetes1. Primary prevention of diabetes is feasible and strategies such as lifestyle modification are shown to be effective in populations of varied ethnicity2,3. However, for implementation of the strategies at the population level, national programmes which are culturally and socially acceptable and practical have to be formulated which are currently lacking in most of the developed and developing countries. Early diagnosis and institution of appropriate therapeutic measures yield the desired glycaemic outcomes and prevent the vascular complications4.
In Japan, China, and other Asian countries, the transition from traditional carbohydrate-rich (e.g., rice-based) diets to lower-carbohydrate Westernized eating habits emphasizing meats, dairy products, and fried foods has been accompanied by a major increase in diabetes prevalence. Similarly, in the United States, a meat-based (omnivorous) diet is associated with a high prevalence of diabetes, compared with dietary patterns emphasizing plant-derived foods. In the Adventist Health Study-2, after adjusting for differences in body weight, physical activity, and other factors, an omnivorous diet was associated with roughly double the risk of diabetes, compared with a diet omitting animal products.5
Every cell in the human body needs energy in order to function. The body's primary energy source is glucose, a simple sugar resulting from the digestion of foods containing carbohydrates (sugars and starches). Glucose from the digested food circulates in the blood as a ready energy source for any cells that need it. Insulin is a hormone or chemical produced by cells in the pancreas, an organ located behind the stomach. Insulin bonds to a receptor site on the outside of cell and acts like a key to open a doorway into the cell through which glucose can enter. Some of the glucose can be converted to concentrated energy sources like glycogen or fatty acids and saved for later use. When there is not enough insulin produced or when the doorway no longer recognizes the insulin key, glucose stays in the blood rather entering the cells.
FIGURE 19-1 ■. This figure shows the hyperbolic relationship of insulin resistance and beta cell function. On the y-axis is beta cell function as reflected in the first-phase insulin response during intravenous (IV) glucose infusion; on the x-axis is insulin sensitivity and its mirror image resistance. In a subject with normal glucose tolerance (NGT) and beta-cell reserve, an increase in insulin resistance results in increased insulin release and normal glucose tolerance. In an individual for whom the capacity to increase insulin release is compromised, increasing insulin resistance with partial or no beta-cell compensation results in progression from normal glucose tolerance, to impaired glucose tolerance (IGT), and finally to diabetes (T2D). Differences between these categories are small at high insulin sensitivity, which may be maintained by weight reduction, exercise, and certain drugs. At a critical degree of insulin resistance, due to obesity or other listed factors, only a further small increment in resistance requires a large increase in insulin output. Those that can increase insulin secretion to this extent retain normal glucose tolerance; those who cannot achieve this degree of insulin secretion (e.g., due to a mild defect in genes regulating insulin synthesis, insulin secretion, insulin action, or an ongoing immune destruction of beta cells) now unmask varying degrees of carbohydrate intolerance. The product of insulin sensitivity (the reciprocal of insulin resistance) and acute insulin response (a measurement beta-cell function) has been called the “disposition index.” This index remains constant in an individual with normal beta cell compensation in response to changes in insulin resistance. IGT, impaired glucose tolerance; NGT, normal glucose tolerance; T2D, type 2 diabetes.
The word diabetes (/ˌdaɪ.əˈbiːtiːz/ or /ˌdaɪ.əˈbiːtɪs/) comes from Latin diabētēs, which in turn comes from Ancient Greek διαβήτης (diabētēs), which literally means "a passer through; a siphon".[111] Ancient Greek physician Aretaeus of Cappadocia (fl. 1st century CE) used that word, with the intended meaning "excessive discharge of urine", as the name for the disease.[112][113] Ultimately, the word comes from Greek διαβαίνειν (diabainein), meaning "to pass through,"[111] which is composed of δια- (dia-), meaning "through" and βαίνειν (bainein), meaning "to go".[112] The word "diabetes" is first recorded in English, in the form diabete, in a medical text written around 1425.

In this health topic, we discuss hyperglycemic hyperosmolar nonketotic syndrome (HHNS), an extremely serious complication that can lead to diabetic coma and even death in type 2 diabetes. This serious condition occurs when the blood sugar gets too high and the body becomes severely dehydrated. To prevent HHNS and diabetic coma in type 2 diabetes, check your blood sugar regularly as recommended by your health care provider; check your blood sugar more frequently when you are sick, drink plenty of fluids, and watch for signs of dehydration.
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