If you haven’t heard the word “epidemic” linked to the word “diabetes,” then you’ve clearly chosen to avoid TV news, the newspaper, or even the Internet. For few health stories have gotten so much coverage in the recent years – and validly so – than the growing menace of type 2, or “adult-onset” diabetes.
As the World Health Organization puts it, “Diabetes is a common condition and its frequency is dramatically rising all over the world.” Today at least 171 million people worldwide have the disease, a figure likely to more than double by 2030 as populations age. And just who are these people? Primarily, those “above the age of retirement” according to the World Health Organization. In other words, older people . In fact, one out of five people age 75 and older have diabetes.
But let’s be clear: Diabetes is not merely a side effect of aging. Yes, it’s true that as we age, our bodies become less efficient at producing and using glucose and insulin – the two key factors in type 2 diabetes. But this natural decline isn’t enough to cause the disease. Instead, look at the other major lifestyle issues of our time.
But how do you “get” diabetes? By eating too many candy corn? Eating a plateful of Halloween sugar cookies? How does your body get so messed up?
Not too long ago, many people – and doctors – blamed a diet high in sugar as the cause of type 2 diabetes. Today, we know that’s not the real issue (though, yes, eating lots of refined sugar and refined carbohydrates does cause troublesome peaks and valleys in your blood sugar amounts that makes diabetes problems worse). More recently doctors have shown that being overweight is a major risk factor for the disease.
But here’s the breakthrough news, based on an increasing body of evidence: The amount you exercise – not just how much you eat – in large part determines your risk of developing diabetes or its precursor, insulin resistance. Put simply sedentary living, coupled with excess body weight, are the real culprits. And you control both!
To prevent diabetes, then, you need to take action. And the first step is to become educated about the disease.
Understanding Insulin Resistance
To start, there are two types of diabetes. Type 1 starts in childhood and is usually related to a malfunctioning pancreas. It requires a lifetime of careful management, and often, daily insulin injections. Type 2 is far more common, and is the form of diabetes that is rising in epidemic proportions, due in large part to the growing unhealthiness of our daily lives.
Type 2 diabetes usually progresses along a predictable pattern. Before there is diabetes, there is insulin resistance. It works like this. Every time you eat, your body signals “beta” cells in your pancreas that it’s time to pump out the hormone insulin. Insulin’s job is to shepherd the energy extracted from your food – in the form of glucose, commonly called blood sugar – into each living cell of your body.
Insulin does this in a kind of lock-and-key process by fitting into molecules on the surface of cells called insulin receptors. Once “unlocked” the cell does its energy exchange, either pulling in glucose from the bloodstream to use or store, or sending out stored energy – in the form of either fat or glycogen (the stored form of glucose) – to be used by other parts of your body when they have depleted their own energy stores.
Once a cell if filled with fat or glycogen, or if the cell has been inactive for a long time, it moves the insulin receptors deep within, effectively making it impossible for insulin to reach them. But as the cell uses up its energy stores, it becomes thinner, and those insulin receptors move to the cell’s surface again. And the cycle resumes, with the receptors ready to bond with insulin and usher in more glucose to the cell.
But if you’re overweight and/or sedentary, more of those insulin receptors stay hidden within the cell. The result? Glucose and insulin build up in the bloodstream. Those high levels of glucose signal the beta cells in your pancreas to pump out more and more insulin, vainly trying to move that glucose into cells. Eventually, thanks to sheer numbers, some insulin links up with insulin receptors and some glucose gets in. But this process gets more difficult every year, until, finally, your beta cells wear out like an overworked engine. Next thing you know, your body lacks the capacity to make enough insulin to carry energy to all your cells. And that is why many people with diabetes need insulin shots.
The relatively simply relationship between glucose and insulin becomes more complex as you age because of the presence of a second hormone called glucagon. While pancreatic beta cells react to high glucose levels by issuing insulin, their neighbors, alpha cells, react to low glucose levels by issuing glucagon. This hormone gloms onto receptors in the liver, telling it to release glucose into the bloodstream to provide energy for the rest of the body.
The thing is, alpha cells only learn about the state of the blood glucose levels from signals they received from beta cells. In older people with type 2 diabetes and insulin resistance, communication breaks downs between alpha and beta cells in the pancreas. So even while beta cells are releasing insulin in response to high blood glucose levels, alpha cells are releasing glucagon, stimulating even more glucose to be release into the bloodstream. You can see where this would become a real mess. And this mess is called diabetes.
Whew! That was a long, but important, explanation of how diabetes happens. In my next blog I will return with some strategies to prevent Diabetes so you can prevent this explained “mess” above from happening to you.
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