(March 2014) The word insulin has its roots in the Latin word for island (insula); named so because it is produced in the pancreas, an island-like organ. The related word, insulation, refers to keeping something apart or isolated. However, insulin is no island and cannot stand alone. It depends on a number of factors to make metabolism run efficiently. Many of today’s health issues, in fact, are tied to insulin health. Yet, most people know insulin mainly as some drug that diabetics inject to control blood sugar after a meal. Those who inject insulin no longer produce enough of their own. The rest of us produce our own insulin after meals. It is essential for utilizing nutrients like sugar and protein from food, helping to transport these nutrients into every cell in our body. So, we might say that insulin’s job is to help feed our bodies. That’s why insulin is not only the “master metabolic hormone” but it is also called the “storage hormone” because it helps store excess energy in our cells. If insulin is absent, or not doing its job right, there’s a build-up of sugars and fats in the blood that can inflame and clog our blood vessels. Insulin dysfunction is the central problem that links many chronic diseases, including diabetes, heart disease, kidney problems, Alzheimer’s disease and depression. When insulin malfunctions, the result is high blood sugar, which leads to a cascade of problems. Sugar has a tendency to stick to things, including proteins, cells and blood vessels. This destructive process is called “glycation,” which comes from the Greek word for sweet. However, it is anything but, since glycated proteins are no longer functional. The damage is measured routinely by the HbA1c test, which measures the percent of glycated hemoglobin in our blood (hemoglobin is the iron-containing protein that makes our blood cells red). The HbA1c is one of the more accurate measures of blood sugar. While the body’s defense system toils to remove glycation products from the body, these compounds cause considerable damage and inflammation. Glycation from high blood sugar and diabetes can lead to kidney damage, blindness and limb amputation. Experts are now equating these effects to the aging process itself. Appropriately, the acronym for these “Advanced Glycation End-products” is AGEs. So, a sedentary lifestyle and poor diet promote the “AGEing” process, largely due to insulin dysfunction. So, how does elevated blood sugar arise? Well, of course, it’s diet-related. It’s in the bread, cereal, crackers, pasta, pastries, rice, potatoes, soft drinks, fruit juices, table sugar and other sweet or starchy foods we eat. High fructose corn syrup, for example, is dripping from nearly every processed food on the shelf. Even “healthy” whole grains can elevate blood sugar. Excessive carbohydrate intake causes insulin to spike and stresses the insulin-making machinery in the pancreas. After years of this kind of stress, the body may stop responding to insulin, which causes further carb cravings and promotes obesity. Restricting carbohydrates can correct some of the metabolic problems related to insulin. The problem is that sweet and starchy foods are too comforting to let go of, and they are typically the predominant foods in the pantry. Another source of blood sugar is from the liver, which makes its own sugar (mostly from protein) when our cells are hungry. In health, this process kicks in when blood sugar levels drop. However, when insulin is malfunctioning, the liver pours sugar into the blood even though sugar levels are already elevated. That only adds fuel to the fire. Insulin Resistance Insulin’s job is simple enough. Yet, for some odd reason, the body can stop responding to insulin, a condition called insulin resistance (IR). Dr. David Katz of the Yale Prevention Research Center defines insulin resistance as a condition in which insulin no longer can promote glucose uptake into the body’s cells for fuel. Rather than feeding the body, sugars and fats build up to dangerous levels in the blood, and contribute to chronic and debilitating disease. Insulin resistance is on the rise, with more than 60 million Americans at risk, especially among the obese population. An even higher proportion of critically ill patients have IR. A poor diet and lack of certain micronutrients can contribute to insulin resistance. Why would your cells want to become resistant to insulin? Cells become insulin resistant because they are protecting themselves from the toxic effects of high insulin (basically too much sugar inside cells). They basically close their doors so as not to be stimulated constantly, and they are already overloaded with fat derived from all the carbs in the diet. Our bodies are all different in how we respond to this challenge, some of us being more capable of balancing energy needs than are others. Yet, generally speaking, the more obese we become, the more our cells resist storing more energy. For most, insulin resistance starts in the muscles. Excess energy from food is stored as fat in muscle, liver and other organs. With energy overload, our muscles become marbled, like fatty cuts of steak. Fat and its breakdown products, or metabolites, directly interfere with insulin action. When insulin is not working, blood sugar rises to dangerous levels, prompting more insulin production to bring it back down. Rising blood insulin also prevents fat burning, so there’s no place for the fat to go. As this vicious cycle proceeds, fat accumulates as insulin becomes less effective, despite higher levels in the blood. As obesity progresses, fat ends up in all the wrong places, like in the liver. When the liver becomes insulin resistant, all hell breaks loose. A malfunctioning liver starts spitting out sugar and fat into the blood on top of already dangerous levels. An increasing demand for insulin eventually short-circuits the pancreas. Then insulin begins to drop and blood sugar is out of control. This is type 2 diabetes. In diabetes, high blood sugar reflects a dual defect: first, not enough insulin is being made by a failing pancreas (insulin deficiency); second, the body is not responding to the insulin present (IR). Insulin resistance usually precedes insulin deficiency by decades. In other words, people may spend years in a pre-diabetic state. After the onset of diabetes, insulin resistance continues. Indeed, even injected insulin may not function properly then. Weight gain and IR—to the point of breakdown—is classic type 2 diabetes. This is different from diabetes in children (type 1 diabetes), which usually starts with insulin deficiency (pancreatic destruction). Insulin resistance, however, can also be present in type 1 diabetes. More frightening is the rising incidence (over a tenfold increase in the last decade) of type 2 diabetes in children. We already know that many of our children are overweight or obese. In fact, over 18 percent of U.S. youth are overweight and more likely to develop diabetes than were children of previous generations. Type 2 diabetes, once a disease of old age, is now occurring regularly in younger adults and children. Our children are not starting out with the same vitality as did youngsters a few decades ago; this is particularly apparent in low-income populations. Apparently, our lifestyle sins are being passed on to future generations.