Good Calories, Bad Calories

twist: the principal fat in red meat, eggs, and bacon is not saturated fat, but the very same monounsaturated fat as in olive oil. The implications are almost impossible to believe after three decades of public-health recommendations suggesting that any red meat consumed should at least be lean, with any excess fat removed.

Consider a porterhouse steak with a quarter-inch layer of fat. After broiling, this steak will reduce to almost equal parts fat and protein.^*48 Fifty-one percent of the fat is monounsaturated, of which 90 percent is oleic acid. Saturated fat constitutes 45 percent of the total fat, but a third of that is stearic acid, which will increase HDL cholesterol while having no effect on LDL. (Stearic acid is metabolized in the body to oleic acid, according to Grundy’s research.) The remaining 4 percent of the fat is polyunsaturated, which lowers LDL cholesterol but has no meaningful effect on HDL. In sum, perhaps as much as 70 percent of the fat content of a porterhouse steak will improve the relative levels of LDL and HDL cholesterol, compared with what they would be if carbohydrates such as bread, potatoes, or pasta were consumed. The remaining 30 percent will raise LDL cholesterol but will also raise HDL cholesterol and will have an insignificant effect, if any, on the ratio of total cholesterol to HDL. All of this suggests that eating a porterhouse steak in lieu of bread or potatoes would actually reduce heart-disease risk, although virtually no nutritional authority will say so publicly. The same is true for lard and bacon.

“Everything should be made as simple as possible,” Albert Einstein once supposedly said, “but no simpler.” Our understanding of the nutritional causes of heart disease started with Keys’s original oversimplification that heart disease is caused by the effect of all dietary fat on total serum cholesterol. Total cholesterol gave way to HDL and LDL cholesterol and even triglycerides. All fat gave way to animal and vegetable fat, which gave way to saturated, monounsaturated, and polyunsaturated fat, and then polyunsaturated fats branched into omega-three and omega- six polyunsaturated fats. By the mid-1980s, these new levels of complexity had still not deterred the AHA and NIH from promoting carbohydrates as effectively the antidote to heart disease, and either all fats or just saturated fats as the dietary cause.

What would now become apparent was that LDL cholesterol is little more than an arbitrary concept that oversimplifies its own complex diversity. The fact that LDL and LDL cholesterol are not synonymous complicates the science. Just as Gofman had reported in 1950 that cholesterol itself was divided up among different lipoproteins, and those lipoproteins had different atherogenic properties and responded differently to diet, a lipid metabolism specialist named Ronald Krauss, using Gofman’s ultracentrifuge, began reporting in 1980 that low-density lipoproteins were in turn composed of different, distinct subclasses, each containing differing amounts of cholesterol, and each, once again, with different atherogenic properties and different behavior in response to the carbohydrates and fats in our diet. Although Krauss has long been considered one of the most thoughtful researchers in nutrition and heart disease—the American Heart Association has treated him as such—it’s worth noting in advance that his dietary research has been almost universally ignored, precisely because of its ultimate implications for what constitutes a healthy diet and what does not.

LDL cholesterol is only a “marginal risk factor,” Tavia Gordon and his colleagues had observed in 1977. In other words, little difference can be observed between the average LDL cholesterol of those with and without heart disease. Only by comparing the LDL-cholesterol and heart-disease rates between nations (with all the attendant complications of such comparisons) can conspicuous differences be seen. In the analysis from Framingham, San Francisco, Albany, Honolulu, and Puerto Rico published by Gordon and his collaborators, the average LDL cholesterol of heart-disease sufferers was only a few percentage points higher than the average of those who remained healthy. “If you look in the literature and just look at the average coronary patients,” Krauss says, “their LDL- cholesterol levels are often barely discernibly elevated compared to patients who do not have coronary disease.”

In the late 1940s, Gofman and his collaborators began asking why the same level of LDL cholesterol will cause heart disease in some people but not in others. Krauss and his collaborators began asking this question again, thirty years later.

Krauss himself is an idiosyncratic figure in this world. He has produced a dozen years of research suggesting that high-carbohydrate diets, for the great proportion of the population, are the nutritional cause of heart disease, and yet he has also chaired the nutrition committee of the American Heart Association and was the primary author of the 1996 and 2000 AHA nutrition guidelines. In the process, he eased the AHA away from its thirty-year-old position that the maximum fat content of a heart-healthy diet should be 30 percent of calories. Or, as Krauss remarked, he managed to put the “30-percent-fat recommendation in small print.” Krauss trained as a physician in the late 1960s and then worked with Fredrickson and Levy at the NIH, where he discovered a protein known as hepatic lipase that regulates how the liver metabolizes lipoproteins. He then moved to Berkeley to practice internal medicine, and it was there, in 1976, that he began working with Gofman’s ultracentrifuge and with Alex Nichols and Frank Lindgren, both of whom had collaborated with Gofman in the 1950s.

When Krauss began his research at Berkeley, he had what he calls “this conventional notion, which many people still have, that LDL is just one thing, a single entity.” But that turned out not to be the case. Using data from the ultracentrifuge dating back to the early 1960s, Krauss discovered that LDL actually comes in distinct subspecies, all characterized by still finer gradations in density and size. “It was blazingly obvious. Unignorable,” says Krauss.^*49 Eventually, Krauss identified seven discrete subclasses of LDL. He also noted that the smallest and densest of the low-density lipoproteins had two significant properties: it had a strong negative correlation with HDL, and it was the subspecies that was elevated in patients with heart disease.

In the early 1980s, Krauss published three papers on what he calls the “remarkable heterogeneity of LDL,” all of which, he says, were met with indifference mixed with occasional hostility. Acceptance of Krauss’s research was also constrained by the fact that Gofman’s ultracentrifuge had been necessary to differentiate these LDL subclasses, which meant that this, too, was not the kind of measurement that could be ordered up easily by physicians. In his later publications, Krauss described a simpler, inexpensive measurement technique, but the research was still perceived as an esoteric endeavor.

To understand the implications of this association between small, dense LDL and heart disease, it helps to picture the configuration of the low-density lipoprotein itself. Imagine it as a balloon. It has a single protein—known as apo B, for short—that serves as the structural foundation of the balloon and holds it together. It has an outer membrane that is composed of cholesterol and fats of yet another type, called phospholipids. And then, inside the balloon, inflating it, are triglycerides and more cholesterol. The size of the LDL balloon itself can vary, depending on the amount of triglycerides and cholesterol it contains. Thus, as Krauss reported, some people have mostly large, fluffy LDL, with a lot of cholesterol and triglycerides inflating the balloon, and some people have mostly smaller, denser LDL particles, with less cholesterol and triglycerides.

In the 1970s, investigators had developed yet another way to quantify the concentration of these circulating lipoproteins, in this case by counting only the number of apo B proteins that provide the structural foundation to the LDL balloon. Because there’s only one protein per LDL particle, and because VLDL is also composed of identical apo B proteins, this technique measured the number of LDL and VLDL particles in a blood sample, rather than the cholesterol or triglycerides they contained. As it turned out, the number of apo B proteins, and so the total number of LDL and VLDL particles combined, is also abnormally elevated in heart-disease patients. This was first reported in 1980 by Peter Kwiterovich, a lipid-metabolism specialist from Johns Hopkins, together with Allan Sniderman, a cardiologist from McGill University. Kwiterovich and Sniderman then collaborated with Krauss on the last of his three papers on the heterogeneity of LDL. In 1983, they reported that the disproportionate elevation in the apo B protein in heart-disease patients was due to a disproportionate elevation in the amount of the smallest and densest of the low-density lipoproteins.