Why We Get Fat: And What to Do About It (26 page)

This logic, though, has critical flaws. For starters, what drugs do and diets do are two entirely different things. Changing the nutrient content of our diets has many effects throughout our bodies, and many effects on different risk factors for heart disease, as do cholesterol-lowering drugs. That a particular fat in the diet raises LDL cholesterol, compared with, say, other fats or carbohydrates, does not mean it increases our risk of heart disease or is otherwise deleterious to our health.

Another flaw in the logic concerns the implication of causality: the fact that the drugs known as statins lower LDL cholesterol
and
prevent heart disease does not necessarily imply that they prevent heart disease
because
they lower LDL. Consider aspirin: it cures headaches
and
prevents heart disease, but no one would ever suggest that aspirin prevents heart disease
because
it cures headaches. It does other things as well, as statins do, and any one of these other things could be the reason why either drug prevents heart attacks.

•   •   •

When we consider all of the effects of the fats and carbohydrates in our diet, and all of the risk factors for heart disease that have become clear as the science has evolved since the 1970s, an entirely different picture emerges.

Let’s start with triglycerides. These are also a risk factor for heart disease. The higher your level of circulating triglycerides (which are transported in the same lipoprotein particles that carry cholesterol), the greater the likelihood that you’ll have a heart attack. This is not controversial. But it’s the carbohydrates we eat that elevate triglyceride levels; fat, saturated or not, has nothing to do with them.

If you replace the saturated fat in your diet with carbohydrates—replace eggs and bacon for breakfast, say, with cornflakes, skim milk, and bananas—your LDL cholesterol may go down, but your triglycerides will go up. What
might
be a good thing, lowering LDL cholesterol (and I’ll explain the “might” shortly), will be compensated for by a bad thing, raising triglycerides. This has been recognized since the early 1960s.

Low HDL cholesterol (aka the “good cholesterol”) is also a risk factor for heart disease. Those of us with low HDL cholesterol are at far greater risk of having a heart attack than those of us with high total or LDL cholesterol. For women, HDL levels are so good at predicting future heart disease that they are, effectively, the only predictors of risk that matter. (When researchers look for genes that predispose individuals to living an exceedingly lengthy life—more than ninety-five or a hundred years—one of the few genes that stand out is a gene for a naturally high HDL cholesterol level.)

When you replace fat in your diet, even saturated fat, with carbohydrates, you lower your HDL, which means you make it more likely that you’ll have a heart attack, at least by this predictor of risk. Once again, if you give up scrambled eggs and bacon for breakfast and replace them with cornflakes, skim milk, and bananas, your HDL cholesterol, your “good” cholesterol, will go
down
, and your heart-attack risk will go
up
. If you’re currently eating
cereal, skim milk, and bananas and switch instead to eggs and bacon, your HDL cholesterol will go up, and your heart-attack risk will go down. This has been known since the 1970s.

The advice we’ve been given to lower our total and LDL cholesterol
and
our body weight—eat less saturated fat and more carbohydrates—simply contradicts the advice we could have been given instead to raise our HDL, and HDL, again, is a far better predictor of heart disease. We’ve been told that we can increase our HDL by exercise, by losing weight, and even by moderate alcohol consumption, but we will rarely, if ever, be told that we can accomplish the same thing by replacing the carbohydrates in our diet with fat. (The reason why weight loss probably works so well to raise HDL is that the weight is lost—even on a low-calorie diet—because we eat fewer carbohydrates and less of the really fattening carbohydrates in particular. We lower our insulin levels, lose weight,
and
raise our HDL all because of the change in carbohydrate consumption.)

Nutritionists and public-health authorities who are resolute in their insistence that we eat low-fat, carbohydrate-rich diets to avoid heart disease will acknowledge in other contexts that carbohydrate-rich diets not only lower HDL cholesterol, and so increase our heart-disease risk, but do this so reliably that researchers have lately taken to using HDL as a way to determine the amount of carbohydrates that their clinical-trial subjects eat. HDL cholesterol, as a recent
New England Journal of Medicine
article explained, is “a biomarker for dietary carbohydrate.”
^*
In other words, if your HDL is high, it’s a good bet that you’re eating few carbohydrates. If your HDL cholesterol is low, then you’re very likely eating a lot of carbohydrates.

When we pay attention to how HDL tracks with heart disease—not just LDL and total cholesterol—we learn something about the purported risks and benefits of the foods we might choose to eat instead of fattening carbohydrates: red meat, say, or eggs and bacon, even lard and butter. It’s important to understand that the fat in these foods is not all saturated. Rather, these animal fats are mixtures of saturated and unsaturated fats, just as vegetable fats are, and these fats all have different effects on our LDL and HDL cholesterol.

Take lard, for example, which has long been considered the archetypal example of a killer fat. It was lard that bakeries and fast-food restaurants used in large quantities before they were pressured to replace it with the artificial trans fats that nutritionists have now decided might be a cause of heart disease after all. You can find the fat composition of lard easily enough, as you can for most foods, by going to a U.S. Department of Agriculture website called the National Nutrient Database for Standard Reference. You’ll find that nearly half the fat in lard (47 percent) is monounsaturated, which is almost universally considered a “good” fat. Monounsaturated fat raises HDL cholesterol
and
lowers LDL cholesterol (both good things, according to our doctors). Ninety percent of that monounsaturated fat is the same oleic acid that’s in the olive oil so highly touted by champions of the Mediterranean diet. Slightly more than 40 percent of the fat in lard is indeed saturated, but a third of that is the same stearic acid that’s in chocolate and is now also considered a “good fat,” because it will raise our HDL levels but have no effect on LDL (a good thing and a neutral thing). The remaining fat (about 12 percent of the total) is polyunsaturated, which actually lowers LDL cholesterol but has no effect on HDL (also a good thing and a neutral thing).

In total, more than 70 percent of the fat in lard will improve your cholesterol profile compared with what would happen if you replaced that lard with carbohydrates. The remaining 30 percent will raise LDL cholesterol (bad) but also raise HDL (good). In other words, and hard as this may be to believe, if you replace the carbohydrates in your diet with an equal quantity of lard, it will
actually reduce your risk of having a heart attack. It will make you healthier. The same is true for red meat, bacon and eggs, and virtually any other animal product we might choose to eat instead of the carbohydrates that make us fat. (Butter is a slight exception, because only half the fat will definitively improve your cholesterol profile; the other half will raise LDL but also raise HDL.)

Now let’s look at what has happened in clinical trials in which subjects were instructed to do just what I’ve been proposing—replace the fattening carbohydrates they’d been eating with animal products high in fat and even high in saturated fat.

In the last ten years, researchers have carried out quite a few trials to compare diets that are very low in carbohydrates but high in fat and protein—typically, the Atkins diet, made famous by Dr. Robert Atkins in his 1972 best-seller,
Dr. Atkins’ Diet Revolution—
with the kind of low-fat, low-calorie diet recommended by the American Heart Association or the British Heart Foundation.

These trials are the best studies ever done on the effect of eating high-fat, high-saturated-fat diets on weight and on risk factors for both heart disease and diabetes. The results have been remarkably consistent. In these trials, subjects would be instructed to eat as much fat and protein as they wanted—as much meat, fish, and fowl—but to avoid carbohydrates (eat fewer than fifty or sixty grams a day—200 to 240 calories’ worth), and they would be compared with subjects who had been instructed not only to eat fewer total calories but particularly to avoid fat and saturated fat. This is what happened to those who ate mostly fat and protein:

Let’s look at one of these studies in detail. This one cost two million dollars, was government-funded, and was done by researchers at Stanford University. The results were published in
The Journal of the American Medical Association
in 2007. It was known as the A TO Z Weight Loss Study and compared four diets:

Here are the results for weight and for risk factors for heart disease, a year after the subjects embarked on their diets:

Even though the subjects on the Atkins diet were counseled to eat as much food as they wanted, to eat copious amounts of red meat and thus the saturated fat that goes with it, they lost more weight, their triglycerides dropped further (a good thing), their HDL went up further (a good thing), and their blood pressure down further (a good thing) than those on any of the other diets.
^*

Here’s how the Stanford researchers described the results:

The point man on this trial was Christopher Gardner, director of Nutrition Studies at the Stanford Prevention Research Center. Gardner presented the results of the trial in a lecture that’s now viewable on YouTube—“The Battle of Weight Loss Diets: Is Anyone Winning (at Losing)?” He begins the lecture by acknowledging that he’s been a vegetarian for twenty-five years. He did the study, he explains, because he was concerned that a diet like the Atkins diet, rich in meat and saturated fat, could be dangerous. When he described the triumph of the very low-carbohydrate, meat-rich Atkins diet, he called it “a bitter pill to swallow.”

These clinical trials alone should put your mind to rest about the idea that eating high-fat or high-saturated-fat diets will give you heart disease. But there are a few other factors worth discussing that most of these trials didn’t address. The first involves LDL. It speaks again to how the science of heart disease has evolved since the 1970s.

When we first started hearing about the evils of LDL and physicians and health reporters began to refer to LDL as the “bad cholesterol,” they did so because they thought it was the cholesterol that caused the buildup of plaque in our arteries. LDL, though, actually isn’t cholesterol; it’s the particle (the low-density lipoprotein—i.e., LDL) that contains the cholesterol and shuttles it (and triglycerides) around the bloodstream. The “bad cholesterol” terminology is a problem only because the researchers who study these things now say that it’s not the cholesterol carried by the LDL that is to blame for heart disease but, rather, the LDL particle itself and other similar particles. The cholesterol seems to be an innocent bystander.

To complicate matters, not all LDL particles appear to be equally harmful, or “atherogenic,” which is the term used by the experts to describe something that causes atherosclerosis or makes it worse. Some of the LDL in our circulation is large and buoyant, and some is small and dense, and there are gradations in between. The small and dense LDL particles appear to be the atherogenic ones, the ones we want to avoid. They work themselves into the walls of our arteries and begin the process of forming plaques. The large, buoyant LDL particles appear to be harmless.