What’s that grout? Cholesterol, but not just any ol’ cholesterol.
Your handyman—let’s call him Lester—carries two things: a bucket of grout and a spatula. The grout can come in the form of lousy cholesterol, which is carried by low-density lipoprotein (LDL). It’s big and puffy, and prone to breaking up and scattering bits of cholesterol when it hits the walls of the artery. When your LDL levels are too high to begin with (maybe from your diet or from your heredity), and then you nick the inner lining of one of your arteries, Lester goes crazy and slaps on more and more and more grout. He starts covering up the damage with the bad cholesterol—loads and loads of bad cholesterol.
But look inside Lester’s tool belt. He’s got a spatula that takes premium-grade grout in the form of cholesterol carried on high-density lipoprotein (it’s the healthy HDL cholesterol). Compact and powerful, the spatula works with this slick stuff to take the extra gunk away.
Now, if you have too much of that LDL grout (this can be familial but is primarily a result of eating the wrong kinds of foods—simple sugars and fats—and especially too much food) and not enough premium-version HDL grout (from not eating enough of the right kinds of foods and fats, not getting enough physical activity, or not having enough female hormones—yes, even men have them), it can lead to a chain of events that has potentially heart-stopping outcomes. We’ll call it fat’s domino effect.
Domino 1: Having too much bad cholesterol not only means you’ll have too much junk (plaque) in your arteries. It also means that LDL cholesterol will get into the middle layer of your artery. That cholesterol in the middle layer acts like a drunk fan with courtside seats, making the environment much more hostile than it’s used to being. The presence of LDL cholesterol in that middle layer stimulates the immune system to attract white-cell protectors to try to smooth out and calm down the rotten cholesterol.
Domino 2: Those white blood cells, in turn, spill some of their toxic contents that normally attack infections—and that causes generalized inflammation.
Domino 3: The toxic contents and cholesterol are soaked up by scavenger cells, building up blister-sized spaces in the walls of your arteries. They’re called foam cells—and they increase the size of the plaque, or grout, even more to make the artery surface rougher.
Domino 4: Sensing something’s wrong, your body responds with more inflammation, creating bulges and potholes in the wall, often in the area of weakness, where the initial nick was and a scar was trying to form over the dangerous plaque. If that plaque ruptures into the middle of your blood vessel, the next domino falls.
Domino 5: These rough patches in the wall then attract sticky blood platelets to form clots in your arteries. Normally, platelets are good (they help form scabs to heal wounds). But when they hit that rough patch in your arterial wall, they grab the lining and form a big clot on top of irritated, inflamed plaque. And this brings in more clotting proteins to the area that act to cement the platelets in place.
Domino 6: All of this gunk piles up faster and faster, and the inside of the arteries becomes so inflamed that the platelets and clots fill the entire artery. YOU-reka! This ruptured plaque process take minutes rather than decades, so you can influence its likelihood today by making the right choices about food.
Domino 7: The blood can’t get through the artery, and nourishment to the heart is shut off.
Game Over: The chain reaction triggers a heart attack (or, depending where the process happens, causes a stroke, memory loss, impotence, wrinkled skin, or any number of health problems that happen when blood flow malfunctions).
As you can see, it’s not the cholesterol by itself that’s so bad; it’s not having high enough levels of healthy and/or low enough lousy cholesterol to thwart the process before it even begins. And it’s not doing things like normalizing your blood pressure and blood sugar to help decrease the chance of developing nicks in the first place.
While genetics dictates some of your cholesterol level, your physical activity levels and poor foods choices—trans and saturated fats, simple sugar, and too many calories—really dictate whether Lester carries the right amount and kind of grout or moves the spatula fast enough to make for a nice, clean wall.
Blood Sugar: Yep, we know how it is. You don’t have diabetes, so you’re going to blow off thinking about blood sugar faster than a flight attendant blows off a flirty coach passenger. And that would be a mistake. Blood sugar is another substance that can nick your arteries if levels are too high. You may think your level is normal, but most blood sugar levels are recorded when you’ve fasted. Having “normal” levels for fasting (under 100 milligrams per deciliter, abbreviated 100 mg/dl) and for after meals (under 140 mg/dl) is important. Why? Because there’s a good chance that even with normal blood sugar levels, your blood sugar may rise significantly throughout the day as you eat. Studies show that men with a waist of 40 inches or more have twelve times the risk of getting diabetes compared with men with a waist smaller than 35 inches. For women, having a 37-inch waist is that much riskier than having a 32½-incher. (The most sensitive way to diagnose diabetes is to measure the blood sugar fasting, and again two hours after taking 75 grams of sugar—to see how your body can deal with the sugar.)
Many people think that diabetes is a purely genetic disease, and of course, it sure would be nice to blame Aunt Mabel for the medical condition, but it doesn’t quite work that way. For type 2 diabetes (type 1 is the juvenile form), your environment (that is, your lifestyle, your behaviors, your macaroons) is a much more dominant trait than genetics.
Yes, type 2 diabetes is a genetic disease. That is, if you are a twin and have an identical twin who gets type 2 diabetes, you have the genetics for it. And it’s a tough disease, too: Diabetes ages you one and a half years for every year you live. For example, if you get it at age thirty and live to sixty, you’re not really sixty. You have the energy and disability risks of a seventy-five-year-old.
Here’s how it works (see Figure 5.5): Insulin in your blood normally takes sugar and puts it into the cells, but in people with type 2 diabetes, the transfer of sugar into your muscle and fat cells is inhibited. While nice in coffee, that sugar in your blood chips away at your arterial wall by weakening the junctions between cells that form the surface lining of your arteries. Ultimately it allows holes to form in these junctions. By causing your insulin levels to go haywire and making proteins in your body less effective, sugar really behaves like nutritional cocaine.
Omentum fat (belly fat) contributes to type 2 diabetes by making it difficult to get glucose inside the cell and let insulin do what it does best: deliver glucose. Simply being overweight, especially having a waist greater than 37 inches (85 centimeters) for women and 40 inches (100 centimeters) for men, makes your body less sensitive to insulin; the insulin receptors on the cells don’t allow insulin to transmit the message enabling glucose transport into the cells, leaving the glucose to float around in your blood. That omentum fat is also selfish; it uses up the insulin so it can’t do its job (one study shows omentum fat sucks up a quarter of the insulin that passes through the blood supply).
Figure 5.5 Carried Away Resistance to the normal effects of insulin makes cells resistant to taking in glucose (sugar). This forces excess glucose to stay in the blood vessels, where it acts like debris to damage the Teflon-like surface of our inner roads. Cholesterol trucks bounce around and spill junk that ruins our blood highways.
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