Diabetes mellitus is a public health problem around the world. In 1980, 108 million adults worldwide had diabetes (4.7% of the global population). By 2014 this had risen to 422 million adults (8.5% of the global population). By 2040, the number is expected to be 642 million adults. In the UK, there is estimated to be between 3 and 4 million people with diabetes. Type 2 diabetes accounts for more than 90% of all patients with diabetes.
Type 2 (formerly called 'adult-onset' or 'non insulin-dependent') diabetes results when the body doesn’t produce enough insulin and/or is unable to use insulin properly (this is also referred to as ‘insulin resistance’). This form of diabetes usually occurs in people who are over 40 years of age, overweight, and have a family history of diabetes, although today it is increasingly found in younger people.
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.
As of 2016, 422 million people have diabetes worldwide, up from an estimated 382 million people in 2013 and from 108 million in 1980. Accounting for the shifting age structure of the global population, the prevalence of diabetes is 8.5% among adults, nearly double the rate of 4.7% in 1980. Type 2 makes up about 90% of the cases. Some data indicate rates are roughly equal in women and men, but male excess in diabetes has been found in many populations with higher type 2 incidence, possibly due to sex-related differences in insulin sensitivity, consequences of obesity and regional body fat deposition, and other contributing factors such as high blood pressure, tobacco smoking, and alcohol intake.
Diabetes is a chronic condition, and it can last an entire lifetime. The goal of treating diabetes is to keep blood glucose levels as close to a normal range as possible. This prevents the symptoms of diabetes and the long-term complications of the condition. If you've been diagnosed with diabetes, your doctor – working with the members of your diabetes care team – will help you find your target blood glucose levels.
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.
Whether you’re dealing with frequent UTIs or skin infections, undiagnosed diabetes may be to blame. The high blood sugar associated with diabetes can weaken a person’s immune system, making them more susceptible to infection. In more advanced cases of the disease, nerve damage and tissue death can open people up to further infections, often in the skin, and could be a precursor to amputation.
2.Retinopathy - Diabetes may cause blood vessels in the retina (the light sensitive lining of the eye) to become leaky, blocked, or grow abnormally [Figure 1]. Retinopathy is rare before the age of 10 and the risk increases with the length of time a person has diabetes. Treatments such as laser, injections in the eye, or other procedures may be helpful to prevent visual loss or restore sight. The longer a patient has diabetes, the greater chance of developing an eye problem. All patients with diabetes are at risk for developing retinopathy, but the risk is higher for patients with worse blood sugar control. Early retinopathy may have no symptoms, but early treatment is essential to prevent any loss of vision.
There is no single gene that “causes” type 1 diabetes. Instead, there are a large number of inherited factors that may increase an individual’s likelihood of developing diabetes. This is known as multifactorial inheritance. The genes implicated in the development of type 1 diabetes mellitus control the human leukocyte antigen (HLA) system. This system is involved in the complex process of identifying cells which are a normal part of the body, and distinguishing them from foreign cells, such as those of bacteria or viruses. In an autoimmune disease such as diabetes mellitus, this system makes a mistake in identifying the normal ‘self’ cells as ‘foreign’, and attacks the body.
Apart from severe DKA or hypoglycemia, type 1 diabetes mellitus has little immediate morbidity. The risk of complications relates to diabetic control. With good management, patients can expect to lead full, normal, and healthy lives. Nevertheless, the average life expectancy of a child diagnosed with type 1 diabetes mellitus has been variously suggested to be reduced by 13-19 years, compared with their nondiabetic peers. 
Doctors can also measure the level of a protein, hemoglobin A1C (also called glycosylated or glycolated hemoglobin), in the blood. Hemoglobin is the red, oxygen-carrying substance in red blood cells. When blood is exposed to high blood glucose levels over a period of time, glucose attaches to the hemoglobin and forms glycosylated hemoglobin. The hemoglobin A1C level (reported as the percentage of hemoglobin that is A1C) reflects long-term trends in blood glucose levels rather than rapid changes.
A third notion is that changes in how babies are fed may be stoking the spread of type 1. In the 1980s, researchers noticed a decreased risk of type 1 in children who had been breast-fed. This could mean that there is a component of breast milk that is particularly protective for diabetes. But it has also led to a hypothesis that proteins in cow's milk, a component of infant formula, somehow aggravate the immune system and cause type 1 in genetically susceptible people. If true, it might be possible to remove that risk by chopping those proteins up into little innocuous chunks through a process called hydrolyzation. A large-scale clinical trial, called TRIGR, is testing this hypothesis and scheduled for completion in 2017.
Accelerated atherosclerosis is the main underlying factor contributing to the high risk of atherothrombotic events in DM patients. CAD, peripheral vascular disease, stroke, and increased intima-media thickness are the main macrovascular complications. Diabetics are 2–4 times more likely to develop stroke than people without DM.2 CVD, particularly CAD, is the leading cause of morbidity and mortality in patients with DM.4 Patients with T2DM have a 2- to 4-fold increase in the risk of CAD, and patients with DM but without previous myocardial infarction (MI) carry the same level of risk for subsequent acute coronary events as nondiabetic patients with previous MI.5 Furthermore, people with diabetes have a poorer long-term prognosis after MI, including an increased risk for congestive heart failure and death.
Although some people with this type of diabetes are thin, the majority of people (90%) are overweight. Losing weight, even 2 kg to 5 kg (5 lbs to 10 lbs) can help lower blood glucose levels. For many people, following a healthy diet and an exercise program may be all that is needed to help control glucose levels. For others, healthy eating and exercise alone aren't enough to lower blood glucose levels.
Is it your fault for getting type 2 diabetes? No – type 2 diabetes is not a personal failing. It develops through a combination of factors that are still being uncovered and better understood. Lifestyle (food, exercise, stress, sleep) certainly plays a major role, but genetics play a significant role as well. Type 2 diabetes is often described in the media as a result of being overweight, but the relationship is not that simple. Many overweight individuals never get type 2, and some people with type 2 were never overweight, (although obesity is probably an underlying cause of insulin resistance). To make matters worse, when someone gains weight (for whatever reason), the body makes it extremely difficult to lose the new weight and keep it off. If it were just a matter of choice or a bit of willpower, we would probably all be skinny. At its core, type 2 involves two physiological issues: resistance to the insulin made by the person’s beta cells and too little insulin production relative to the amount one needs.
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).
In type 1 diabetes, other symptoms to watch for include unexplained weight loss, lethargy, drowsiness, and hunger. Symptoms sometimes occur after a viral illness. In some cases, a person may reach the point of diabetic ketoacidosis (DKA) before a type 1 diagnosis is made. DKA occurs when blood glucose is dangerously high and the body can't get nutrients into the cells because of the absence of insulin. The body then breaks down muscle and fat for energy, causing an accumulation of ketones in the blood and urine. Symptoms of DKA include a fruity odor on the breath; heavy, taxed breathing; and vomiting. If left untreated, DKA can result in stupor, unconsciousness, and even death.
The treatment of low blood sugar consists of administering a quickly absorbed glucose source. These include glucose containing drinks, such as orange juice, soft drinks (not sugar-free), or glucose tablets in doses of 15-20 grams at a time (for example, the equivalent of half a glass of juice). Even cake frosting applied inside the cheeks can work in a pinch if patient cooperation is difficult. If the individual becomes unconscious, glucagon can be given by intramuscular injection.
Because both yeast and bacteria multiply more quickly when blood sugar levels are elevated, women with diabetes are overall at a higher risk of feminine health issues, such as bacterial infections, yeast infections, and vaginal thrush, especially when blood sugar isn't well controlled. And a lack of awareness about having prediabetes or diabetes can make managing blood sugar impossible.