30.3 million people have diabetes (9.4% of the US population), in one type or another. 84.1 million adults aged 18 years or older have prediabetes (33.9% of the adult US population. But what exactly is Diabetes? There are a lot of myths and misunderstandings surrounding the disease, particularly when it comes to type 1 versus type 2.

So let’s start with the basics.

The two main types of diabetes are type 1 and type 2. In type 1 diabetes (which used to be called juvenile-onset or insulin-dependent diabetes), the body completely stops making insulin. People with type 1 diabetes must take daily insulin injections (or use an insulin pump) to survive. This form of diabetes usually develops in children or young adults, but can occur at any age.

In type 2 diabetes (which used to be called adult-onset or non-insulin-dependent diabetes) the body produces insulin, but the cells don’t respond to insulin the way they should. This is called insulin resistance. In response to this insulin resistance, the pancreas should make more insulin, but in the case of type 2 diabetes, this does not happen. Because of these two problems, insulin resistance and trouble making extra insulin, there is not enough of an insulin effect to move the glucose from the blood into the cells. Type 2 diabetes is more likely to occur in people who are over the age of 40, overweight, and have a family history of diabetes, although more and more younger people, including adolescents, are developing type 2 diabetes.

It’s important to know a few things about how your body works before you can take the best care of your diabetes.

Blood sugar, or glucose, is the body’s main source of energy. This glucose comes from food—mostly carbohydrates, but occasionally from proteins, too.

In a healthy body, carbs are all broken down into glucose.  That glucose leaves the intestine, travels through the liver, and eventually makes its way into the blood stream. Its final destination is the body’s cells, where it is used to create energy. Insulin comes into play here, at the cells’ entrance. The hormone acts as a doorman, allowing glucose to come inside.

Insulin is produced in the pancreas by little clusters of cells, known as beta cells. Beta cells sense when there is an excess of glucose in the blood stream, such as just after a meal, and they send insulin out to meet the glucose at the cell’s doors. When working properly, this interplay between glucose, insulin, and beta cells maintains glucose levels between 70 and 140 milligrams per deciliter of blood. In both types of diabetes, this balance gets interrupted in some way.

Diabetes is a disease that occurs when the body is unable to properly use and store glucose.
When you have diabetes, glucose builds up in the bloodstream, causing your blood glucose to rise too high, which, if not treated and managed, can cause damage to various parts of the body over time.

In type 1, the body’s immune system starts attacking and destroying parts of itself—specifically, its own beta cells. Fewer beta cells means less insulin secreted into the body. And less insulin means that glucose is locked out of cells, and stays in the blood stream. As type 1 diabetes progresses, it’s thought that beta cells are completely wiped out (though some early research suggests there may still be some faint activity of beta cells in some people with type 1).

Most people with type 1 diabetes need to start injecting insulin as soon as they are diagnosed. They do need to be careful of what they eat, so to avoid causing spikes in their blood glucose, but type 1 cannot be controlled solely with diet. The necessity for treatment with insulin is why type 1 is classified as insulin-dependent.

In type 2, some insulin is released but the locks on the cells are damaged. Insulin’s keys no longer fit, and the cells refuse to unlock. Because the door isn’t opened, glucose can’t enter, also resulting in heightened blood glucose levels. This is called insulin resistance—since the cells are resistant to the influences of insulin.

Genetics certainly affect susceptibility to insulin resistance, but another major factor is obesity. The greater your BMI, the harder your body has to work to make insulin effective. So it’s no coincidence that the global epidemic of type 2 diabetes coincides with rising rates of obesity.

In early stages, it’s possible to control type 2 with diet and exercise. Losing just 7 to 10 percent of your body weight can make the insulin your body produces more effective; meal planning helps you eat according to the amount of insulin available in your body, and exercise helps to increase insulin sensitivity.

And for a while the body can overcome the cells’ resistance. But over the course of type 2, particularly when it’s poorly managed, the body stops being able to make enough insulin to force its way into the cells. When this happens, people with type 2 also need to start insulin injections.

Type 1 and type 2 are different in their root causes, but the effects are eventually the same. Problems with insulin interrupt the finely honed system and glucose in the blood rises, which, if left untreated, may result in complications like nerve and eye damage.

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