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 mellitus (non–insulin-dependent diabetes mellitus [NIDDM]) is a heterogeneous disorder. Most patients with type 2 diabetes mellitus have insulin resistance, and their beta cells lack the ability to overcome this resistance.  Although this form of diabetes was previously uncommon in children, in some countries, 20% or more of new patients with diabetes in childhood and adolescence have type 2 diabetes mellitus, a change associated with increased rates of obesity. Other patients may have inherited disorders of insulin release, leading to maturity onset diabetes of the young (MODY) or congenital diabetes. [7, 8, 9] This topic addresses only type 1 diabetes mellitus. (See Etiology and Epidemiology.)
Diabetes mellitus type 2 (also known as type 2 diabetes) is a long-term metabolic disorder that is characterized by high blood sugar, insulin resistance, and relative lack of insulin. Common symptoms include increased thirst, frequent urination, and unexplained weight loss. Symptoms may also include increased hunger, feeling tired, and sores that do not heal. Often symptoms come on slowly. Long-term complications from high blood sugar include heart disease, strokes, diabetic retinopathy which can result in blindness, kidney failure, and poor blood flow in the limbs which may lead to amputations. The sudden onset of hyperosmolar hyperglycemic state may occur; however, ketoacidosis is uncommon.
The notion is understandable. Blood sugar levels are high in diabetes, so a common idea has held that eating sugar somehow triggers the disease process. However, the major diabetes organizations take a different view. The American Diabetes Association1 and Diabetes UK2 have labelled this notion a “myth,” as has the Joslin Diabetes Center,3 which wrote, “Diabetes is not caused by eating too much sugar.” These and other organizations have worked to educate people about the causes of diabetes and the role that foods play in the disease process.
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.
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.
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.
Weight loss surgery in those who are obese is an effective measure to treat diabetes. Many are able to maintain normal blood sugar levels with little or no medication following surgery and long-term mortality is decreased. There however is some short-term mortality risk of less than 1% from the surgery. The body mass index cutoffs for when surgery is appropriate are not yet clear. It is recommended that this option be considered in those who are unable to get both their weight and blood sugar under control.
Having diabetes requires life-long treatment and follow-up by health professionals. Diabetes can be linked to damage of the eyes, kidneys and feet. It is also associated with increased risk of strokes, heart attacks and poor blood circulation to the legs. Medical care aims to minimise these risks by controlling diabetes, blood pressure and cholesterol and screening for possible complications caused by the diabetes.
There is no known preventive measure for type 1 diabetes. Type 2 diabetes – which accounts for 85–90% of all cases – can often be prevented or delayed by maintaining a normal body weight, engaging in physical activity, and consuming a healthy diet. Higher levels of physical activity (more than 90 minutes per day) reduce the risk of diabetes by 28%. Dietary changes known to be effective in helping to prevent diabetes include maintaining a diet rich in whole grains and fiber, and choosing good fats, such as the polyunsaturated fats found in nuts, vegetable oils, and fish. Limiting sugary beverages and eating less red meat and other sources of saturated fat can also help prevent diabetes. Tobacco smoking is also associated with an increased risk of diabetes and its complications, so smoking cessation can be an important preventive measure as well.
Given the diverse peculiarities involving the issue, studies have shown that Diabetes mellitus has been extensively investigated in its pathophysiological aspects, highlighting the search for strong evidence that can be used in the clinical practice of the Primary Care nurse, with attributions focused on health promotion, prevention of complications, treatment and rehabilitation of the health of individuals and community, carried out in an interdisciplinary and multidisciplinary manner (Matumoto, Fortuna, Kawata, Mishima, & Pereira, 2011; Florianopolis, 2015).
*All medications have both common (generic) and brand names. The brand name is what a specific manufacturer calls the product (e.g., Tylenol®). The common name is the medical name for the medication (e.g., acetaminophen). A medication may have many brand names, but only one common name. This article lists medications by their common names. For information on a given medication, check our Drug Information database. For more information on brand names, speak with your doctor or pharmacist.
In patients with type 2 diabetes, stress, infection, and medications (such as corticosteroids) can also lead to severely elevated blood sugar levels. Accompanied by dehydration, severe blood sugar elevation in patients with type 2 diabetes can lead to an increase in blood osmolality (hyperosmolar state). This condition can worsen and lead to coma (hyperosmolar coma). A hyperosmolar coma usually occurs in elderly patients with type 2 diabetes. Like diabetic ketoacidosis, a hyperosmolar coma is a medical emergency. Immediate treatment with intravenous fluid and insulin is important in reversing the hyperosmolar state. Unlike patients with type 1 diabetes, patients with type 2 diabetes do not generally develop ketoacidosis solely on the basis of their diabetes. Since in general, type 2 diabetes occurs in an older population, concomitant medical conditions are more likely to be present, and these patients may actually be sicker overall. The complication and death rates from hyperosmolar coma is thus higher than in diabetic ketoacidosis.
The body will attempt to dilute the high level of glucose in the blood, a condition called hyperglycemia, by drawing water out of the cells and into the bloodstream in an effort to dilute the sugar and excrete it in the urine. It is not unusual for people with undiagnosed diabetes to be constantly thirsty, drink large quantities of water, and urinate frequently as their bodies try to get rid of the extra glucose. This creates high levels of glucose in the urine.
Unlike many health conditions, diabetes is managed mostly by you, with support from your health care team (including your primary care doctor, foot doctor, dentist, eye doctor, registered dietitian nutritionist, diabetes educator, and pharmacist), family, and other important people in your life. Managing diabetes can be challenging, but everything you do to improve your health is worth it!
Diabetes mellitus is linked with an increased risk of heart attacks, strokes, poor blood circulation to the legs and damage to the eyes, feet and kidneys. Early diagnosis and strict control of blood sugar, blood pressure and cholesterol levels can help to prevent or delay these complications associated with diabetes. Maintaining a healthy lifestyle (regular exercise, eating healthily and maintaining a healthy weight) is important in reducing the risk of developing type 2 diabetes.
Considering that being overweight is a risk factor for diabetes, it sounds counterintuitive that shedding pounds could be one of the silent symptoms of diabetes. “Weight loss comes from two things,” says Dr. Cypess. “One, from the water that you lose [from urinating]. Two, you lose some calories in the urine and you don’t absorb all the calories from the sugar in your blood.” Once people learn they have diabetes and start controlling their blood sugar, they may even experience some weight gain—but “that’s a good thing,” says Dr. Cypess, because it means your blood sugar levels are more balanced.
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.
Sequelae. The long-term consequences of diabetes mellitus can involve both large and small blood vessels throughout the body. That in large vessels is usually seen in the coronary arteries, cerebral arteries, and arteries of the lower extremities and can eventually lead to myocardial infarction, stroke, or gangrene of the feet and legs. atherosclerosis is far more likely to occur in persons of any age who have diabetes than it is in other people. This predisposition is not clearly understood. Some believe that diabetics inherit the tendency to develop severe atherosclerosis as well as an aberration in glucose metabolism, and that the two are not necessarily related. There is strong evidence to substantiate the claim that optimal control will mitigate the effects of diabetes on the microvasculature, particularly in the young and middle-aged who are at greatest risk for developing complications involving the arterioles. Pathologic changes in the small blood vessels serving the kidney lead to nephrosclerosis, pyelonephritis, and other disorders that eventually result in renal failure. Many of the deaths of persons with type 1 diabetes are caused by renal failure.
Diabetic ketoacidosis (DKA) is much less common than hypoglycemia but is potentially far more serious, creating a life-threatening medical emergency.  Ketosis usually does not occur when insulin is present. In the absence of insulin, however, severe hyperglycemia, dehydration, and ketone production contribute to the development of DKA. The most serious complication of DKA is the development of cerebral edema, which increases the risk of death and long-term morbidity. Very young children at the time of first diagnosis are most likely to develop cerebral edema.
Although age of onset and length of the disease process are related to the frequency with which vascular, renal, and neurologic complications develop, there are some patients who remain relatively free of sequelae even into the later years of their lives. Because diabetes mellitus is not a single disease but rather a complex constellation of syndromes, each patient has a unique response to the disease process.
That said, some research does suggest that eating too many sweetened foods can affect type 2 diabetes risk, and with the Centers for Disease Control and Prevention (CDC) estimating that 30.3 million Americans have the disease — and that millions of more individuals are projected to develop it, too — understanding all the risk factors for the disease, including sugar consumption, is essential to help reverse the diabetes epidemic.
Higher levels of sugar in the urine and the vagina can become a breeding ground for the bacteria and yeast that cause these infections. Recurrent infections are particularly worrisome. “Usually when you keep getting infections, doctors will check for diabetes if you don’t already have it,” says Cypress. “Even women who go to the emergency room for urinary tract infections are often checked.” Don’t miss these other silent diabetes complications you need to know about.
Jump up ^ McBrien, K; Rabi, DM; Campbell, N; Barnieh, L; Clement, F; Hemmelgarn, BR; Tonelli, M; Leiter, LA; Klarenbach, SW; Manns, BJ (6 August 2012). "Intensive and Standard Blood Pressure Targets in Patients With Type 2 Diabetes Mellitus: Systematic Review and Meta-analysis". Archives of Internal Medicine. 172 (17): 1–8. doi:10.1001/archinternmed.2012.3147. PMID 22868819.
While it's conceivable that scientists will isolate a single factor as causing type 1 and type 2, the much more likely outcome is that there is more than one cause. Each person seems to take a unique path in developing diabetes. Someday, doctors may be able to assess an individual's genetic risk for diabetes, allowing him or her to dodge the particular environmental factors that would trigger the disease. And perhaps if the baffling question of why a person gets diabetes can be put to rest, the answer will also offer a cure for the disease.
Melissa Conrad Stöppler, MD, is a U.S. board-certified Anatomic Pathologist with subspecialty training in the fields of Experimental and Molecular Pathology. Dr. Stöppler's educational background includes a BA with Highest Distinction from the University of Virginia and an MD from the University of North Carolina. She completed residency training in Anatomic Pathology at Georgetown University followed by subspecialty fellowship training in molecular diagnostics and experimental pathology.