What’s a good cholesterol count these days – and does it really even matter?
Ask the average American what he or she believes is the most common risk associated with heart disease and you’ll likely hear, “high cholesterol.” We’ve heard it from doctors, we’ve read about it in newspapers and magazines, and we’ve seen all the commercials for cholesterol-lowering drugs. With each new study, the accepted safe blood cholesterol numbers are getting lower and lower. It used to be that a total cholesterol count under 300 was acceptable, then 250, and now the American Heart Association recommends it be under 200. This ever-decreasing figure, coupled with evidence suggesting that cholesterol is not the villain it’s been made out to be, has some physicians wondering if we are putting too much emphasis on cholesterol’s role in contributing to heart disease. In fact, some cardiologists and scientists adamantly are campaigning to stop our obsession with cholesterol and look at other factors that they say are being woefully ignored.
CHOLESTEROL DEFINED
Your body needs cholesterol, a soft, waxy substance which it uses to produce hormones, vitamin D, and the bile acids that aid in digestion. Your liver produces about 75 percent of your needed cholesterol, while the remaining 25 percent comes from food containing animal fats. Some people have a genetic predisposition to produce more cholesterol than necessary (each day, the liver produces an average of 600 to 900 milligrams of cholesterol), while eating foods high in saturated fats, trans fats, and dietary cholesterol will also increase your blood levels (for more on fats, see sidebar, “Fats 101”).
Because cholesterol is insoluble in water, it is transported through the blood stream by lipoproteins, which act as carriers for the cholesterol. The two types of carriers are High-Density Lipoproteins (HDL) and Low-Density Lipoproteins (LDL). When you get your “LDL” or “HDL” cholesterol figures checked, it’s the number of these carriers that’s actually being counted in the blood test. The “total cholesterol” figure is derived from the sum of your HDL and LDL counts, plus the triglycerides (another form of fat made in the body), and Lp(a) cholesterol (a genetic variation of LDL).
“THE LIPID HYPOTHESIS”
If cholesterol is so important to the body, why do we fear it so much? The answer goes as far back as 1856, when German pathologist Rudolph Virchow suggested that cholesterol accumulation in the arterial walls causes atherosclerosis, better known as the “hardening” and “clogging” of the arteries (and, of course, the more the arteries are clogged, the greater chance of a heart attack).
Then a study in 1913 by Nikolai Anitschkow demonstrated that feeding rabbits a diet rich in cholesterol led to the rabbits’ development of atherosclerosis. In 1953, scientist Ancel Keys (famous for his “K rations” and Mediterranean diet) claimed a direct causal relationship between the dietary intake of saturated fats and cholesterol and heart disease.
How so? His premise: when excessive amounts of cholesterol circulate in the bloodstream, it can build up in the inner walls of the arteries, which supply blood to the heart and brain. The cholesterol combines with other substances to form hard, plaque-like deposits that narrow and constrict the arteries. When the deposits affect a complete blockage, a heart attack or stroke ensues.
This premise, known as “the lipid hypothesis,” became the focus of further study and research in the last half-century, culminating in a general acceptance of it by the mainstream scientific community. In 1978, 90 percent of 211 prominent researchers in the field agreed that a connection existed between blood cholesterol levels and the development of coronary heart disease (CHD). In 1984, the National Institutes of Health convened a conference on the subject, at which its expert panel unanimously concurred that a causal relationship existed between elevated cholesterol levels and CHD. This assertion was fine-tuned over the years, suggesting that not all cholesterol is alike, and that high levels of LDL—not just cholesterol—was the more precise culprit of heart disease (hence the moniker “bad cholesterol”), while HDL was determined to actually be good at preventing CHD (ergo the “good cholesterol.”) HDL, it turns out, carries cholesterol away from the arteries and other parts of the body back to the liver, where it is disposed of and removed from the body. Some experts believe that HDL actually removes cholesterol from arterial plaque, hindering its buildup. “The name of the game is to try to increase the HDL and at the same time try to lower the LDL,” declares Arthur Fass, MD, chief of cardiology at Phelps Memorial Hospital in Sleepy Hollow.
THE ROLE OF STRESS
However, not everyone in the scientific and medical communities is convinced that cholesterol plays a role in heart disease. They question the studies, arguing that there is no real proof to establish a causal link between lowered cholesterol levels and a decreased risk for atherosclerosis and vice versa. Take, for example, the rabbit study. Skeptics point out that rabbits are herbivorous animals—they don’t eat meat, as humans do.
Many skeptics have joined to form the International Network of Cholesterol Skeptics. Founded in 2003 by Danish physician and researcher Dr. Uffe Ravnskov, the network seeks to collectively dispute the lipid hypothesis. While its members espouse divergent and even conflicting theories on what causes atherosclerosis and coronary heart disease, they remain united in their belief that cholesterol is not the culprit.
In fact, Dr. Ravnskov’s review of LDL studies suggested that LDL, the “bad” cholesterol, may be protective against infections within the body and their resultant inflammation—which Dr. Ravnskov and others believe may be the underlying catalyst in atherosclerosis.
“Most researchers in this field today agree that inflammation of the arterial wall is the start,” declared Dr. Ravnskov in a 2005 interview. “The crucial question is, ‘What starts the inflammation?’ When arteries become inflamed the body immediately starts a repair process to strengthen the vascular wall….atherosclerosis should therefore be considered as scars, remnants from a long life’s combat with [inflammation].”
Dr. Ravnskov claims that LDL, like HDL, may actually protect against atherosclerosis rather than exacerbate it. In a 2005 interview, Dr. Ravnskov was asked for his opinion on the causes of heart disease. His answer, in part: “All studies of dead people have failed to show an association between their intake of saturated fat, or their serum cholesterol, and the degree of atherosclerosis. People who avoid all saturated fat and who have low cholesterol become just as atherosclerotic as people who gorge in animal food and whose cholesterol is high.” Indeed, Malcolm Kendrick, MD, in an article entitled “The Great Cholesterol Myth,” notes that a massive United States study in which more than 350,000 men at high risk of heart disease were recruited and in which a slew cut their cholesterol consumption by 42 percent, saturated fat consumption by 28 percent, and total calories by 21 percent, found…“nothing—no noticeable dent in heart disease.” In fact, Dr. Kendrick wrote, “no clinical trial on reducing saturated-fat intake has ever shown a reduction in heart disease.”
Dr. Ravnskov details a wealth of research to support his assertions that cholesterol is not the culprit in heart disease, both on the network’s website (thincs.org) and on his own (ravnskov.nu/cholesterol.htm). He includes a pair of studies comparing the levels of atherosclerosis in Japan and America. At the time of the first study, the average cholesterol level of the Japanese was 170 versus 220 for Americans, and the incidence of heart attacks among Japanese people was similarly smaller than for Americans. While the level of atherosclerosis observed post-mortem increased in all individuals from age 40 upwards, there was hardly any difference in the degree of atherosclerosis compared within each age group: between ages 40 and 60, Americans were slightly more arteriosclerotic; between ages 60 and 80, both groups were the same; and among individuals older than 80 the Japanese were slightly more arteriosclerotic than the Americans. A second study examined the brain arteries among thousands of Japanese and Americans and found that the Japanese were more arteriosclerotic than the Americans in all age groups.
Dr. Paul J. Rosch, president of the American Institute of Stress in Yonkers and a member of the International Network of Cholesterol Skeptics, and others not only believe that a high cholesterol level may not be bad for you—he says that his own
research finds no evidence of elevated cholesterol levels contributing to coronary heart disease—but that a low cholesterol level may do more harm than good. Dr. Kendrick noted in his
“Cholesterol Myth” article that studies show “after the age of 50, the lower your cholesterol level is, the lower your life expectancy.” And he pointed out that 90 percent of heart attacks occur after the age of 50. Dr. Rosch adds that some studies show that low cholesterol levels increase death from respiratory and digestive diseases and lowers resistance to infection.
So, if high serum cholesterol isn’t a major risk factor for heart disease, what is? Dr. Rosch and company point the finger at the body’s hard-wired fight-or-flight response to stress, which releases a hormonal cascade culminating in an adrenaline (epinephrine) rush. Such a rush taxes the heart and, Dr. Rosch maintains, can lead to heart damage. Studies show that severe or sudden emotional stress can lead to heart damage and even death. Dr. Rosch notes that a National Institutes of Health study found that after 2 years of treatment, the mortality rates of 4,000 heart patients with type-A personalities (i.e., they are highly competitive, driven, ambitious), who were on Inderal, a hypertension medication that also is prescribed for anxiety and stress, were reduced by 26 percent.
An article in the April, 2008 issue of the Journal of American Cardiology, written by Dr. Joel Dimsdale, reports that marital or work stress or care-giving duties can lead to heart attacks. Dr. Dimsdale even writes that minor stresses, such as a math quiz, can cause heart-rhythm abnormalities. He also reports that short, severe stressors, such as earthquakes and floods, are often followed by a rise in heart-disease deaths.
The American Heart Association does acknowledge that stress plays a role in heart disease, although it believes that the culprit isn’t stress, per se. Rather, according to the AHA, “stress may cause people to overeat, start smoking, or smoke more than they otherwise would”—all risk factors for heart disease. Nevertheless, if, as some believe, stress—or some other factor other than cholesterol—is the main cause of heart disease, why is it that cholesterol-lowering drugs show a decrease in the number of heart attacks?
Jonathan Sackner-Bernstein, MD, cardiologist and chief medical officer of Clinilabs in New York City, hasn’t a clue. Neither, it seems, has anyone else. “Do people who are overweight, inactive, smokers with high blood pressure, have more heart attacks?” he says. “Yes, absolutely they do. But where is the evidence that getting exercise and losing weight will reduce these risks for a heart attack? Most people will be upset to learn that there is no such proof either. One cannot say from available scientific evidence that lowering LDL means heart attacks will be prevented.”
As chief of cardiology at Phelps Memorial Hospital, Dr. Fass agrees that no one quite understands how LDL causes “hardening of the arteries.” Nor, he says, how it may prevent heart attacks. “We’re just now beginning to fully understand the biochemical bases of this problem.” But he, like many doctors, contends that cholesterol (specifically LDL) is undeniably bad. “There’s no doubt that high levels of LDL are associated with coronary artery disease,” he says. And he doesn’t particularly care if we don’t know why LDL-lowering statins work. He is just thrilled that they do work. “I treat far fewer heart attacks today than I did when I started in practice more than twenty years ago. The reason, primarily, is the widespread use of statins—and the use of aspirin and, to a degree, the changes in dietary and lifestyle habits.”
The National Heart, Lung, and Blood Institute, a division of the NIH, which spearheads research and public education in diseases of the heart, blood vessels, and lungs strongly advises that people at risk for heart disease keep their LDL numbers below 100, with a target of 70. But, some might note, at that rate, nearly 36 million Americans—or one out of every five—would be considered in the danger zone and in need of medication. Besides, the problem with a total cholesterol number below 200 is, what if the majority of that number is made up of a high HDL? “What do you tell a patient with a cholesterol over six-hundred, most of which is good cholesterol?” Dr. Rosch asks. Can someone have too much good cholesterol?
No matter cholesterol’s role (and LDL’s in particular) in atherosclerosis and heart disease, the mainstream medical community continues to strongly advocate lowering your cholesterol level to 200 or less, exercising regularly, eating a low-fat, high-nutrition diet, and, if need be, the preventive use of statins. “Just measuring the LDL alone may be an oversimplification,” concedes Dr. Fass. “But my point is still valid: the treatments we have arrived at for lowering LDL happen to protect against coronary events. Whether they do so mainly by lowering the LDL or by some other effect, we do not yet know. We can debate that all day long. Much of what we do in medicine is unexplained. For a hundred years we didn’t know how aspirin worked. We shouldn’t necessarily omit an effective treatment just because we’re not certain of its mechanism of action.”
Valerie Brooks is a full-time writer who reports on a variety of topics, including health and wellness. She regularly writes book reviews from her home in Santa Fe, New Mexico, and is a writer and editor for KosmicLife.com.
