Although there are dozens of known type 1 genes, about half of the risk attributable to heredity comes from a handful that coordinate a part of the immune system called HLA, which helps the body recognize nefarious foreign invaders, such as viruses, bacteria, and parasites. Type 1 diabetes is an autoimmune disease, in which the body's own immune system destroys the cells in the pancreas that produce insulin, so perhaps it is no surprise that immunity genes are involved. Other autoimmune diseases share the HLA gene link, which may be why people with type 1 are more likely to develop additional autoimmune disorders.
Diabetic neuropathy is probably the most common complication of diabetes. Studies suggest that up to 50% of people with diabetes are affected to some degree. Major risk factors of this condition are the level and duration of elevated blood glucose. Neuropathy can lead to sensory loss and damage to the limbs. It is also a major cause of impotence in diabetic men.
Can type 2 diabetes be prevented? It is possible to reduce the risk of developing type 2 diabetes, although the underlying risk of type 2 diabetes depends strongly on genetic factors. But there was less type 2 diabetes around some years ago when people had a more active life and didn’t eat a modern Western diet. So it is fair to say that risk of getting type 2 diabetes is based on a genetic predisposition that is aggravated by lifestyle. Type 2 diabetes is associated with obesity, as well as a variety of environmental factors. To lower the risk of developing type 2 diabetes (as well as other diseases), it is highly recommended to exercise often, eat healthily, and maintain a healthy weight.
In type 2 diabetes, there also is a steady decline of beta cells that adds to the process of elevated blood sugars. Essentially, if someone is resistant to insulin, the body can, to some degree, increase production of insulin and overcome the level of resistance. After time, if production decreases and insulin cannot be released as vigorously, hyperglycemia develops.
Keep your immunizations up to date. High blood sugar can weaken your immune system. Get a flu shot every year, and your doctor will likely recommend the pneumonia vaccine, as well. The Centers for Disease Control and Prevention (CDC) also recommends the hepatitis B vaccination if you haven't previously received this vaccine and you're an adult age 19 to 59 with type 1 or type 2 diabetes. The CDC advises vaccination as soon as possible after diagnosis with type 1 or type 2 diabetes. If you are age 60 or older, have diabetes and haven't previously received the vaccine, talk to your doctor about whether it's right for you.
Good metabolic control can delay the onset and progression of diabetic retinopathy. Loss of vision and blindness in persons with diabetes can be prevented by early detection and treatment of vision-threatening retinopathy: regular eye examinations and timely intervention with laser treatment, or through surgery in cases of advanced retinopathy. There is evidence that, even in developed countries, a large proportion of those in need is not receiving such care due to lack of public and professional awareness, as well as an absence of treatment facilities. In developing countries, in many of which diabetes is now common, such care is inaccessible to the majority of the population.
The problem with sweetened drinks is that, due to their liquid form, they’re among the fastest simple carbs to be digested in the body, causing blood sugar levels to spike even more than a simple carb in solid-food form would. Research supports this idea: A review published in November 2010 in the journal Diabetes Care suggested adding only one serving of a sweetened beverage to your diet may increase your risk for type 2 diabetes by 15 percent.
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.
Visual impairment and blindness are common sequelae of uncontrolled diabetes. The three most frequently occurring problems involving the eye are diabetic retinopathy, cataracts, and glaucoma. photocoagulation of destructive lesions of the retina with laser beams can be used to delay further progress of pathologic changes and thereby preserve sight in the affected eye.
Jump up ^ Zheng, Sean L.; Roddick, Alistair J.; Aghar-Jaffar, Rochan; Shun-Shin, Matthew J.; Francis, Darrel; Oliver, Nick; Meeran, Karim (17 April 2018). "Association Between Use of Sodium-Glucose Cotransporter 2 Inhibitors, Glucagon-like Peptide 1 Agonists, and Dipeptidyl Peptidase 4 Inhibitors With All-Cause Mortality in Patients With Type 2 Diabetes". JAMA. 319 (15): 1580. doi:10.1001/jama.2018.3024.
To explain what hemoglobin A1c is, think in simple terms. Sugar sticks, and when it's around for a long time, it's harder to get it off. In the body, sugar sticks too, particularly to proteins. The red blood cells that circulate in the body live for about three months before they die off. When sugar sticks to these hemoglobin proteins in these cells, it is known as glycosylated hemoglobin or hemoglobin A1c (HBA1c). Measurement of HBA1c gives us an idea of how much sugar is present in the bloodstream for the preceding three months. In most labs, the normal range is 4%-5.9 %. In poorly controlled diabetes, its 8.0% or above, and in well controlled patients it's less than 7.0% (optimal is <6.5%). The benefits of measuring A1c is that is gives a more reasonable and stable view of what's happening over the course of time (three months), and the value does not vary as much as finger stick blood sugar measurements. There is a direct correlation between A1c levels and average blood sugar levels as follows.
Type 2 diabetes typically starts with insulin resistance. That is, the cells of the body resist insulin’s efforts to escort glucose into the cells. What causes insulin resistance? It appears to be caused by an accumulation of microscopic fat particles within muscle and liver cells.4 This fat comes mainly from the diet—chicken fat, beef fat, cheese fat, fish fat, and even vegetable fat. To try to overcome insulin resistance, the pancreas produces extra insulin. When the pancreas can no longer keep up, blood sugar rises. The combination of insulin resistance and pancreatic cell failure leads to type 2 diabetes.
What you need to know about borderline diabetes Borderline diabetes, known as prediabetes, is a condition where blood sugar levels are higher than normal but not yet high enough to be type 2 diabetes. This MNT Knowledge Center article explains the signs to look out for, how to monitor the disease, and ways to prevent it becoming full diabetes. Read now
Low testosterone (low-T) can be caused by conditions such as type 2 diabetes, obesity, liver or kidney disease, hormonal disorders, certain infections, and hypogonadism. Signs and symptoms that a person may have low-T include insomnia, increased body fat, weight gain, reduced muscle, infertility, decreased sex drive, depression, and worsening of congestive heart failure or sleep apnea.
Another dipstick test can determine the presence of protein or albumin in the urine. Protein in the urine can indicate problems with kidney function and can be used to track the development of renal failure. A more sensitive test for urine protein uses radioactively tagged chemicals to detect microalbuminuria, small amounts of protein in the urine, that may not show up on dipstick tests.
Insulin, a hormone released from the pancreas (an organ behind the stomach that also produces digestive enzymes), controls the amount of glucose in the blood. Glucose in the bloodstream stimulates the pancreas to produce insulin. Insulin helps glucose to move from the blood into the cells. Once inside the cells, glucose is converted to energy, which is used immediately, or the glucose is stored as fat or glycogen until it is needed.
Treatment of high blood pressure and high cholesterol levels, which can contribute to circulation problems, can help prevent some of the complications of diabetes as well. A low dose of aspirin taken daily is recommended in people with risk factors for heart disease. All people with diabetes who are between 40 and 75 years are given a statin (a drug to decrease cholesterol levels) regardless of cholesterol levels. Younger people with an elevated risk of heart disease should also take a statin .
Prevention and treatment involve maintaining a healthy diet, regular physical exercise, a normal body weight, and avoiding use of tobacco. Control of blood pressure and maintaining proper foot care are important for people with the disease. Type 1 DM must be managed with insulin injections. Type 2 DM may be treated with medications with or without insulin. Insulin and some oral medications can cause low blood sugar. Weight loss surgery in those with obesity is sometimes an effective measure in those with type 2 DM. Gestational diabetes usually resolves after the birth of the baby.
Insulin-dependent diabetes mellitus is believed to result from autoimmune, environmental, and/or genetic factors. Whatever the cause, the end result is destruction of insulin-producing pancreatic beta cells, a dramatic decrease in the secretion of insulin, and hyperglycemia. Non-insulin-dependent diabetes mellitus is presumably heterogeneous in origin. It is associated with older age, obesity, a family history of diabetes, and ethnicity (genetic components). The vast majority of those with non-insulin-dependent diabetes are overweight Kahn (2003). This form of the disorder has a much slower rate of progression than insulin-dependent diabetes. Over time the ability to respond to insulin decreases, resulting in increased levels of blood glucose. The pancreatic secretion of insulin increases in an attempt to compensate for the elevated levels of glucose. If the condition is untreated, the pancreatic production of insulin decreases and may even cease.
Hyperglycemia (ie, random blood glucose concentration of more than 200 mg/dL or 11 mmol/L) results when insulin deficiency leads to uninhibited gluconeogenesis and prevents the use and storage of circulating glucose. The kidneys cannot reabsorb the excess glucose load, causing glycosuria, osmotic diuresis, thirst, and dehydration. Increased fat and protein breakdown leads to ketone production and weight loss. Without insulin, a child with type 1 diabetes mellitus wastes away and eventually dies due to DKA. The effects of insulin deficiency are shown in the image below.
John P. Cunha, DO, is a U.S. board-certified Emergency Medicine Physician. Dr. Cunha's educational background includes a BS in Biology from Rutgers, the State University of New Jersey, and a DO from the Kansas City University of Medicine and Biosciences in Kansas City, MO. He completed residency training in Emergency Medicine at Newark Beth Israel Medical Center in Newark, New Jersey.
Yet carbs are processed differently in the body based on their type: While simple carbs are digested and metabolized quickly, complex carbs take longer to go through this system, resulting in more stable blood sugar. “It comes down to their chemical forms: A simple carbohydrate has a simpler chemical makeup, so it doesn’t take as much for it to be digested, whereas the complex ones take a little longer,” Grieger explains.
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.
Supporting evidence for Shulman's theory comes from observations about a rare genetic illness called lipodystrophy. People with lipodystrophy can't make fat tissue, which is where fat should properly be stored. These thin people also develop severe insulin resistance and type 2 diabetes. "They have fat stored in places it doesn't belong," like the liver and muscles, says Shulman. "When we treat them . . . we melt the fat away, reversing insulin resistance and type 2 diabetes." Shulman's theory also suggests why some people who carry extra fat don't get type 2. "There are some individuals who store fat [under the skin] who have relatively normal insulin sensitivity, a so-called fit fat individual," he says. Because of the way their bodies store fat, he believes, they don't get diabetes.
nephrogenic diabetes insipidus a rare form caused by failure of the renal tubules to reabsorb water; there is excessive production of antidiuretic hormone but the tubules fail to respond to it. Characteristics include polyuria, extreme thirst, growth retardation, and developmental delay. The condition does not respond to exogenous vasopressin. It may be inherited as an X-linked trait or be acquired as a result of drug therapy or systemic disease.
With gestational diabetes, risks to the unborn baby are even greater than risks to the mother. Risks to the baby include abnormal weight gain before birth, breathing problems at birth, and higher obesity and diabetes risk later in life. Risks to the mother include needing a cesarean section due to an overly large baby, as well as damage to heart, kidney, nerves, and eye.
Although the signs of diabetes can begin to show early, sometimes it takes a person a while to recognize the symptoms. This often makes it seem like signs and symptoms of diabetes appear suddenly. That’s why it’s important to pay attention to your body, rather than simply brushing them off. To that end, here are some type 1 and type 2 diabetes symptoms that you may want to watch out for:
The elderly diabetic person is at increased risk of atrial fibrillation (odds ratio: 1.4 for men and 1.6 for women)232 and at twofold increased risk of thromboembolism from atrial fibrillation.233,234 We can find no subgroup analysis of the major atrial fibrillation trials to examine the benefits of warfarin specifically in older diabetic subjects. It appears that the adverse event rate in diabetic people drops from 8.6 events per 100 patients per year to 2.8 events with warfarin use.234 It is important to check for retinal new vessels when diabetic subjects are placed on warfarin, although the Early Treatment Diabetic Retinopathy Study235 showed no excess vitreous or preretinal hemorrhages in subjects given aspirin for vascular prophylaxis.
Rates of type 2 diabetes have increased markedly since 1960 in parallel with obesity. As of 2015 there were approximately 392 million people diagnosed with the disease compared to around 30 million in 1985. Typically it begins in middle or older age, although rates of type 2 diabetes are increasing in young people. Type 2 diabetes is associated with a ten-year-shorter life expectancy. Diabetes was one of the first diseases described. The importance of insulin in the disease was determined in the 1920s.
The blood vessels and blood are the highways that transport sugar from where it is either taken in (the stomach) or manufactured (in the liver) to the cells where it is used (muscles) or where it is stored (fat). Sugar cannot go into the cells by itself. The pancreas releases insulin into the blood, which serves as the helper, or the "key," that lets sugar into the cells for use as energy.
Research has shown that there are some ways of preventing type 2 diabetes, or at least delaying its onset. Lifestyle changes such as becoming more active (or staying active, if you already engage in regular physical activity) and making sure your weight stays in a healthy range are two ways to help ward off type 2 diabetes, but talk to your doctor about what else you can do to prevent or manage the disease.
Diabetes mellitus, or as it's more commonly known diabetes, is a disease characterized by an excess of blood glucose, or blood sugar, which builds up in the bloodstream when your body isn't able to adequately process the sugar in food. High blood sugar is an abnormal state for the body and creates specific symptoms and possible long-term health problems if blood sugar is not managed well.
Diabetes mellitus is a serious metabolic disease, affecting people of all geographic, ethnic or racial origin and its prevalence is increasing globally1. Burden from this costly disease is high on the low and middle income countries (LMIC) where the impacts of modernization and urbanization have caused marked adverse changes in lifestyle parameters.