While this can produce different types of complications, good blood sugar control efforts can help to prevent them. This relies heavily on lifestyle modifications such as weight loss, dietary changes, exercise and, in some cases, medication. But, depending on your age, weight, blood sugar level, and how long you've had diabetes, you may not need a prescription right away. Treatment must be tailored to you and, though finding the perfect combination may take a little time, it can help you live a healthy, normal life with diabetes.
Type 1 diabetes occurs when your immune system, the body’s system for fighting infection, attacks and destroys the insulin-producing beta cells of the pancreas. Scientists think type 1 diabetes is caused by genes and environmental factors, such as viruses, that might trigger the disease. Studies such as TrialNet are working to pinpoint causes of type 1 diabetes and possible ways to prevent or slow the disease.
Large, population-based studies in China, Finland and USA have recently demonstrated the feasibility of preventing, or delaying, the onset of diabetes in overweight subjects with mild glucose intolerance (IGT). The studies suggest that even moderate reduction in weight and only half an hour of walking each day reduced the incidence of diabetes by more than one half.
The above tips are important for you. But it's also crucial to allow yourself time to cope with the diagnosis and commit to making lifestyle changes that will benefit you forever. The good news is the diabetes is a manageable disease; the tough part is that you must think about it daily. Consider finding support—someone that you can talk to about your struggles—be that a friend, another person with diabetes, or a loved one. This may seem trivial, but it truly can help you take control of diabetes so that it doesn't control you. Some next steps that may help you to get on the right track at this early stage in your journey:

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.


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.[66] According to the current definition, two fasting glucose measurements above 7.0 mmol/l (126 mg/dl) is considered diagnostic for diabetes mellitus.
Arlan L Rosenbloom, MD is a member of the following medical societies: American Academy of Pediatrics, American College of Epidemiology, American Pediatric Society, Endocrine Society, Pediatric Endocrine Society, Society for Pediatric Research, Florida Chapter of The American Academy of Pediatrics, Florida Pediatric Society, International Society for Pediatric and Adolescent Diabetes
A 2018 study suggested that three types should be abandoned as too simplistic.[57] It classified diabetes into five subgroups, with what is typically described as type 1 and autoimmune late-onset diabetes categorized as one group, whereas type 2 encompasses four categories. This is hoped to improve diabetes treatment by tailoring it more specifically to the subgroups.[58]

While poor vision is hardly uncommon—more than 60 percent of the American population wears glasses or contacts, after all—sudden changes in your vision, especially blurriness, need to be addressed by your doctor. Blurry vision is often a symptom of diabetes, as high blood sugar levels can cause swelling in the lenses of your eye, distorting your sight in the process. Fortunately, for many people, the effect is temporary and goes away when their blood sugar is being managed.

Damage to small blood vessels can affect the eyes, kidneys, and nerves. Damage to eyes, specifically the retina, is called diabetic retinopathy and is the leading cause of blindness. Damage to the kidneys, called diabetic nephropathy, can lead to kidney failure and the need for dialysis. Damage to the nerves that supply the legs and arms and gastrointestinal tract is called diabetic neuropathy. Some people with diabetes who develop peripheral neuropathy (damage to the nerves in the legs) and have poor blood flow to the legs may eventually need an amputation.
People with type 2 diabetes have insulin resistance, which means the body cannot use insulin properly to help glucose get into the cells. In people with type 2 diabetes, insulin doesn’t work well in muscle, fat, and other tissues, so your pancreas (the organ that makes insulin) starts to put out a lot more of it to try and compensate. "This results in high insulin levels in the body,” says Fernando Ovalle, MD, director of the multidisciplinary diabetes clinic at the University of Alabama in Birmingham. This insulin level sends signals to the brain that your body is hungry.
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