Why We Get Fat: And What to Do About It (27 page)

This is important because carbohydrate-rich diets not only lower HDL and raise triglycerides, they also make LDL small and dense. These three effects all increase our risk of heart disease. When we eat high-fat diets and avoid carbohydrates, the
opposite happens: HDL goes up, triglycerides go down, and the LDL in the circulation becomes larger and fluffier. Individually and together, these changes
decrease
our risk of having a heart attack. So what appears to be a bad thing, circa 1970 science (the effect of saturated fat on LDL cholesterol), is again a good thing, circa 2010 science (the effect of saturated fat on the LDL particle itself).

The health officials hesitate to discuss this science publicly, because it contradicts much of what we’ve been told for the past thirty to fifty years. Occasionally, though, researchers will let the facts break through, as did Chris Gardner and his Stanford colleagues when they wrote up the results of their A TO Z study. Their language is on the technical side, but it’s not so technical that you shouldn’t be able to follow it:

These findings may indeed be a bitter pill for some to swallow, but they confirm that the diet we have to eat to lose weight—the one restricted in fattening carbohydrates—is also the diet that will best prevent heart disease.

What I’ve tried to make clear in this chapter is that the fear of fat—saturated, in particular—is based on the state of the science in the 1960s and 1970s, and it simply doesn’t hold up in the light of more recent research and the state of the science today. But one more very important point has to be made.

Earlier I discussed what happens when we become what’s technically known as insulin-resistant—when muscle and liver cells, in particular, become resistant to the effect of the hormone insulin. Not only do we secrete more insulin in response, and so tend to get fatter, especially around the waist (where the fat cells are most sensitive to insulin), but we begin to manifest a host of other, related metabolic disturbances as well: blood pressure goes up; triglycerides go up; HDL cholesterol goes down. What I didn’t mention earlier is that LDL particles become small and dense. We become glucose-intolerant, which means we have trouble controlling our blood sugar. We might even develop type 2 diabetes, which happens when the pancreas can no longer secrete enough insulin to compensate for the insulin resistance.

This combination of heart-disease risk factors is now known as “metabolic syndrome,” and it is, in effect, the intermediate step on the way to heart disease. More than a quarter of the adult population in the United States now suffers from metabolic syndrome, according to the official estimates, and the reason why this number is so high is that metabolic syndrome includes diabetes and obesity among its symptoms, and we’re experiencing epidemics of both. As you get fatter, as your waistline expands, you tend to lose control of your blood sugar; you are more likely to get hypertension, atherosclerosis, heart disease, and strokes. All these conditions are associated with the same cluster of what the experts call “lipid” abnormalities—low HDL, high triglycerides, and small, dense LDL. And all of these are triggered by the insulin resistance and the elevated insulin secretion that accompanies it,
by the carbohydrates in our diet, and maybe the sugars (sucrose and high-fructose corn syrup) in particular.

The science of metabolic syndrome has been evolving since the late 1950s, when researchers first linked carbohydrate consumption to high triglycerides and then high triglycerides to heart disease. It went virtually unnoticed for decades because the heart-disease experts and the nutritionists were focused so obsessively on saturated fat and cholesterol. They didn’t see a need to entertain alternative explanations for why we have heart attacks, and so they didn’t. The driving force in the science of metabolic syndrome was a Stanford University physician named Gerald Reaven, who recognized early that excessive insulin secretion and insulin resistance are the root causes of this entire suite of metabolic disturbances.

When the authorities began paying attention to Reaven’s work, in the mid-1980s, they had trouble embracing it, because his research implicated carbohydrates, not fat, as the dietary causes of both heart disease and diabetes. “Anyone who consumes more carbohydrates has to dispose of the load by secreting more insulin,” as Reaven explained at a National Institutes of Health diabetes conference in 1986. Then he presented the evidence linking insulin to heart disease. The chair of the conference, Harvard’s George Cahill, said Reaven’s results “speak for themselves,” which they did. But that was the problem. “Sometimes we wish it would go away, because nobody knows how to deal with it,” said one NIH administrator of Reaven’s work.

Today the science of metabolic syndrome represents probably the single greatest advance of the last half-century in our understanding of what causes heart disease and its intimate association with hypertension, obesity, and diabetes. It explains why those three conditions all increase dramatically our risk of heart disease, and why, if we have one of these conditions, we’re likely to have the others as well. What metabolic syndrome tells us is that heart disease and diabetes are not caused by individual risk factors—low HDL, for instance, or high triglycerides, or small, dense
LDL—but by insulin resistance and elevated levels of insulin and blood sugar playing havoc with cells everywhere.

The insulin works on the fat cells to make us accumulate fat, and the expanding fat cells then release what are called “inflammatory molecules” (“cytokines,” in the technical lingo) that have adverse effects throughout the body. It works on the liver to convert carbohydrates into fat, and this fat (triglycerides) is sent off into the bloodstream on the particles that eventually become small, dense LDL. It works on the kidney to raise blood pressure by reabsorbing sodium (and so has the same effect as eating extreme amounts of salt) and by impairing the secretion of uric acid, which also accumulates to unhealthy levels in the blood stream. (High uric-acid levels cause gout, which is also associated with obesity and diabetes, and the incidence of gout, too, is increasing in Western societies.) The insulin also works on the artery walls to stiffen them and cause the accumulation of triglycerides and cholesterol in the budding atherosclerotic plaques.

While this is happening, the chronically elevated blood sugar level that goes along with insulin resistance creates a host of problems on its own. It causes
oxidative stress
throughout the body. (The reason we’re always told to consume foods rich with antioxidants is to combat or prevent this oxidative stress.) And it leads to the creation of
advanced glycation end products
, which seem to cause everything from the stiffening of our arteries to the aging of our skin and the premature aging that is part and parcel of diabetes.

To diagnose metabolic syndrome, doctors are told to look first for an expanding waistline, because metabolic syndrome is so closely tied to obesity. And because saying someone has metabolic syndrome is equivalent to saying someone is insulin-resistant, the experts blame both conditions on sedentary behavior and overeating. Why? Because they believe overeating and sedentary behavior make people fat. They then offer the familiar advice about low-fat diets (because they worry about the increased risk of heart disease that accompanies metabolic syndrome)
and about eating less and exercising, because they think these are required for weight loss.

Here a little common sense is in order. As Reaven said a quarter-century ago, it’s the carbohydrates that drive up insulin levels. We know now that carbohydrates make us fat, and it’s been demonstrated in numerous clinical trials that low-carbohydrate, high-fat diets improve each and every one of the metabolic and hormonal abnormalities of metabolic syndrome—the low HDL, the high triglycerides, the small, dense LDL, the high blood pressure, and the insulin resistance and chronically elevated levels of insulin. This suggests the obvious: that the same carbohydrates that make us fat are the ones that cause metabolic syndrome. And it tells us that the best and perhaps only way to treat the condition, as with obesity and overweight, is to avoid carbohydrate-rich foods, particularly the ones we digest easily, and sugars.

Just a few more points need to be made about the importance of understanding the relationship between carbohydrates and metabolic syndrome. As it turns out, both Alzheimer’s disease and most cancers—including breast cancer and colon cancer—are associated with metabolic syndrome, obesity, and diabetes. This means that, the fatter we are, the more likely we are to get cancer and the more likely we are to become demented as we age.
^*
Researchers have begun to work out mechanisms through which insulin and high blood sugar might cause the brain deterioration
symptomatic of Alzheimer’s (some researchers have even taken to referring to Alzheimer’s as “type 3 diabetes”) and how high blood sugar, insulin, and the related hormone, insulin-like growth factor, spur tumor growth and cause tumors to metastasize.

The link between cancer and metabolic syndrome is sufficiently well accepted that public-health recommendations have already been made based on this research. In 2007, the World Cancer Research Fund and the American Institute of Cancer Research jointly published a five-hundred-page report entitled
Food, Nutrition, Physical Activity and the Prevention of Cancer
. The report, co-authored by two dozen experts, discussed the evidence linking diet to cancer and found that the most convincing link ran from diet through “greater body fatness” to “cancers of the colorectum, esophagus (adenocarcinoma), pancreas, kidney and breast (postmenopause),” and probably gallbladder cancer as well.

The report then provided recommendations on how we might remain cancer free. The first is to “be as lean as possible” and “to avoid weight gain and increased waist circumference through adulthood.” The second recommendation is to “be physically active as part of everyday life,” because the experts who wrote this report believe that “physical activity protects against weight gain, overweight and obesity” and by doing so protects against cancer. And the third recommendation is to “limit consumption of energy-dense foods [and] avoid sugary drinks,” because this is also thought “to prevent and control weight gain, overweight and obesity.”

The first recommendation is now virtually indisputable. If you’re lean, you will be less likely to get cancer than if you’re obese. (Although this does
not
mean that body fatness causes cancers, as the report says.) The second and third recommendations are based on the belief that we get fat because we consume more calories than we expend. If the expert authors of the report had paid attention to the science of fat accumulation to Adiposity 101—nowhere to be found in the report’s five hundred pages—they
would have concluded the obvious: that the same carbohydrates that make us fat are the ones that ultimately cause these cancers.

The simplest way to look at all these associations, between obesity, heart disease, type 2 diabetes, metabolic syndrome, cancer, and Alzheimer’s (not to mention the other conditions that also associate with obesity and diabetes, such as gout, asthma, and fatty liver disease), is that what makes us fat—the quality and quantity of carbohydrates we consume—also makes us sick.