What Is Type 1 Diabetes?
Learn the major characteristics of type 1 diabetes.
So what makes type 1 diabetes different than type 2? First, type 1 is much rarer, accounting for only 5 to 10 percent of all diagnosed cases of diabetes. With type 1 diabetes, the body’s immune system destroys special cells in the pancreas that manufacture insulin. These cells, called beta cells, are the only places in the body where insulin is produced. Without them, the body lacks the insulin it needs to move glucose out of circulation and control high blood sugar.
Other major characteristics of type 1:
[step-list-wrapper title=”” time=””] [step-item number=”1. ” image_url=”” title=”Needles are necessary.” ] Because the body can’t produce insulin, type 1 patients need an outside supply of the hormone, self-administered by daily injections. That’s why type 1 is sometimes called insulin dependent diabetes mellitus, or IDDM. This term is used less frequently today, however, because people with type 2 diabetes sometimes need to take insulin as well. But the fact that injections are an inevitable part of daily life for all type 1 diabetes patients remains one of the key characteristics of this form of the disease.[/step-item]
[step-item number=”2. ” image_url=”” title=”It strikes early.” ] Type 1 diabetes often sets in during childhood, with about half of all cases developing before age 20. Most other cases begin in people up to age 30. It’s very unusual to see a case of type 1 diabetes crop up in anyone over age 40. Because it’s widely seen as a disease of the young (although you continue to have it your entire life), type 1 is sometimes called juvenile-onset diabetes. This term, too, has fallen out of favor, both because adults can get type 1 diabetes and because rates of type 2 diabetes in children are exploding.[/step-item]
[step-item number=”3. ” image_url=”” title=”It strikes fast.” ] The onset of type 1 diabetes is rapid compared with type 2, which can take years to develop. If you (or your child) have type 1, such classic symptoms as fatigue, excessive thirst, and frequent urination will probably become worse over a period of just weeks or months.[/step-item]
[step-item number=”4. ” image_url=”” title=”There is a ‘honeymoon’ period.” ] In the first several months after type 1 is diagnosed and treatment begins, 20 percent of patients seem to improve as the pancreas temporarily begins to increase insulin production once again. This period of remission may last for as long as a year, during which blood-sugar levels become more stable and insulin injections may not even be necessary. While all honeymoons must come to an end, researchers see this period as a potential window of opportunity. One day it may allow yet-to-be-perfected therapies to preserve beta cell function before it’s too late.[/step-item]
[step-item number=”5. ” image_url=”” title=”Blood sugar jumps wildly.” ] With type 1, the pancreas loses its ability to monitor and control blood sugar. As a result, blood-sugar levels tend to spike and crash with greater volatility than in people who have type 2 diabetes, since their pancreatic function is usually less severely impaired. With type 1, the job of the pancreas essentially falls to you. You control your blood-sugar level with the timing and dosage of your insulin injections. This makes monitoring your blood sugar critically important.[/step-item][/step-list-wrapper]
Type 1 diabetes seems to appear out of nowhere and, as far as anyone knows, is not easily preventable — something that is definitely not true of type 2. So why does type 1 occur?
The bottom line is that researchers don’t know yet. But clues can be found in the nature of the disease. Type 1 diabetes is thought to involve a misguided attack by the immune system on the body’s own tissue — specifically, the beta cells of the pancreas. This type of attack is known as an autoimmune response. Other autoimmune diseases include lupus, multiple sclerosis, rheumatoid arthritis, and Graves disease.
Scientists are studying the different players involved with helping the body distinguish its own cells from foreign cells. Eventually they may be able to develop new therapies to prevent and treat type 1 diabetes. Meanwhile, the question still lingers as to why an autoimmune attack occurs in the first place. There appear to be a number of factors at work in type 1:
Genetics. Having a family history of type 1 diabetes may be the single most important risk factor in determining who will get the disease. Even so, the genetic connection is weak. It’s actually uncommon to find two people in any given family who have type 1 diabetes. If you already have the disease, your children or siblings have only about a 5 percent chance of developing it. (For reasons that aren’t well understood, men with type 1 diabetes have a slightly higher chance of transmitting it to their children than women with type 1 do.) Among identical twins, there’s only a 30 to 50 percent chance that the second twin will develop the disease if the first one has it.
Genetics does make certain ethnic groups more susceptible than others to type 1 diabetes. Caucasians are at the highest risk, as evidenced by studies showing that whites living in Hawaii get type 1 diabetes more than nonwhite Hawaiians who share the same island environment.
Even though genetics doesn’t completely predict the disease, scientists are working to better understand the genes involved with type 1 diabetes, and they may someday be able to develop genetic therapies for people most at risk.
Viruses. Could type 1 be caused by an infection? It’s possible. One reason researchers think so is that the onset of the disease appears to follow a seasonal pattern, with the fewest new cases in summer and the most in winter — when many viral illnesses are more common. A number of viruses have been implicated as suspects, particularly coxsackievirus, mumps, and rubella. Some studies have found that a high percentage of people newly diagnosed with type 1 have coxsackievirus antibodies in their blood, suggesting that the body has been fighting this viral infection. In the lab, a cousin of the coxsackievirus has been shown to produce type 1-like symptoms in animals.
Some researchers question whether the virus idea has any merit, but a number of theories explain how it might work. One hypothesis is that the immune system may have trouble telling the difference between certain viruses and the insulin producing beta cells in the pancreas. After fighting off the virus, this premise goes, the immune system continues the battle by attacking the pancreas. Other theories suggest that viruses may change the beta cells in ways that make them appear foreign to the immune system. Or they may destroy proteins in the pancreas that manufacture insulin.
Cow’s milk. This idea is mostly speculation and far from proven, but some research has suggested a link between feeding children cow’s milk before three or four months of age and the risk of developing type 1 diabetes. People with type 1 sometimes have higher levels of antibodies that bind to both a protein found in milk and a protein sometimes found on beta cells, but the significance of this isn’t clear. Other studies have failed to find any connection between cow’s milk and type 1 diabetes. Still, the concern offers more reason not to wean a baby from breast milk or formula before 12 months of age, as recommended by the American Academy of Pediatrics.
Free radicals. These unstable molecules are formed as a byproduct of natural bodily functions (such as breathing) that involve the use of oxygen. Free radicals have a single, unpaired electron instead of the usual pair, making them unstable. As they circulate around the body, they try to latch onto other molecules, inflicting damage on healthy cells in the process.
Normally, enzymes in the body neutralize free radicals and keep this damage to a minimum. But toxins, such as air pollution and tobacco smoke, can boost their numbers to levels the body can’t adequately handle. Studies suggest that the insulin-producing cells of the pancreas may be particularly vulnerable to free-radical damage because they are less well guarded by protective enzymes than other parts of the body are.
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