urged to avoid eating fat, to quit smoking, to exercise, and to lower their blood pressure.
After seven years of follow-up, the intervention group had slightly lower blood pressure and cholesterol than the control group, but there was
no difference
in either cardiovascular mortality or all-cause mortality (scientific lingo for “total number of deaths no matter what the reason”). The intervention group had 17.9 deaths per one thousand men from cardio-vascular disease, and the control group had 19.3 deaths per one thousand men, a variation that did not amount to what researchers call
statistical significance
, meaning it was likely due to chance. 12
In addition, the data on overall mortality—death from any cause—was troubling. There were actually
more
deaths in the intervention group—from any cause—than there were in the control group! Remember, the real reason we want to avoid heart disease is so we can live longer; avoiding heart disease isn’t much of a victory if it means you die early from some other disease!
The researchers themselves described the results as “disappointing.” The only
real
reduction in overall mortality was seen with the people who stopped smoking, regardless of the group they were in. 13
Leaping to the Wrong Conclusion
The sixth of the NIH-funded trials, the Lipid Research Clinics Coronary Primary Prevention Trial (LRC-CPPT), which was initiated in 1973, is worth mentioning because of an interesting leap of faith made by the investigators based on virtually no evidence. But this leap of faith became the cornerstone of anti-fat policy for decades to come. Here’s what happened.
Researchers from the National Heart, Lung, and Blood Institute measured cholesterol in almost one-third of a million middle-aged men and chose only those with the highest cholesterol levels for the study (about 4,000 men). They gave half of them a new cholesterol–lowering drug (cholestyramine), while the other half got a placebo. The medicine did indeed lower cholesterol levels in the men who had abnormally high levels to begin with, and it modestly reduced heart disease rates in the process. (The probability of suffering a heart attack during the seven to eight years of the study went from 8.6 percent in the placebo group to 7 percent in the group treated with cholestyramine, while the probability of dying from a heart attack dropped from 2 to 1.6 percent, not exactly jaw-dropping numbers. 16 )
WHAT THE FRAMINGHAM HEART STUDY FOUND
One study mentioned most often by the defenders of the cholesterol theory is the Framingham Heart Study. This long-running research study started back in 1948 and monitored heart disease in more than 5,000 residents of Framingham, Massachusetts. After following up for sixteen years, the researchers claimed to find a direct correlation between heart disease and cholesterol levels.
But God is in the details. As it turned out, the group of Framingham residents who developed heart disease and the group of Framingham residents who didn’t had similar ranges of cholesterol levels. In fact, the
average
cholesterol level of the heart disease group was only 11 percent higher than that of the group
without
heart disease. Cardiovascular disease struck people with cholesterol levels as low as 150 mg/dL. Low cholesterol, according to this study, was hardly a guarantee of a healthy heart.
It gets better (or worse, depending on your position). When researchers went back and looked at the Framingham data thirty years after the project started, they found that once men passed the age of forty-seven, it didn’t make a whit of difference whether their cholesterol was low or high. 14 Those with high cholesterol at age forty-eight lived just as long as, or
longer
than, those who have had low cholesterol. So if cholesterol is important only for the relatively few who have had a heart attack before the age of forty-eight, why are the rest of us worried about high-fat food and cholesterol
After seven years of follow-up, the intervention group had slightly lower blood pressure and cholesterol than the control group, but there was
no difference
in either cardiovascular mortality or all-cause mortality (scientific lingo for “total number of deaths no matter what the reason”). The intervention group had 17.9 deaths per one thousand men from cardio-vascular disease, and the control group had 19.3 deaths per one thousand men, a variation that did not amount to what researchers call
statistical significance
, meaning it was likely due to chance. 12
In addition, the data on overall mortality—death from any cause—was troubling. There were actually
more
deaths in the intervention group—from any cause—than there were in the control group! Remember, the real reason we want to avoid heart disease is so we can live longer; avoiding heart disease isn’t much of a victory if it means you die early from some other disease!
The researchers themselves described the results as “disappointing.” The only
real
reduction in overall mortality was seen with the people who stopped smoking, regardless of the group they were in. 13
Leaping to the Wrong Conclusion
The sixth of the NIH-funded trials, the Lipid Research Clinics Coronary Primary Prevention Trial (LRC-CPPT), which was initiated in 1973, is worth mentioning because of an interesting leap of faith made by the investigators based on virtually no evidence. But this leap of faith became the cornerstone of anti-fat policy for decades to come. Here’s what happened.
Researchers from the National Heart, Lung, and Blood Institute measured cholesterol in almost one-third of a million middle-aged men and chose only those with the highest cholesterol levels for the study (about 4,000 men). They gave half of them a new cholesterol–lowering drug (cholestyramine), while the other half got a placebo. The medicine did indeed lower cholesterol levels in the men who had abnormally high levels to begin with, and it modestly reduced heart disease rates in the process. (The probability of suffering a heart attack during the seven to eight years of the study went from 8.6 percent in the placebo group to 7 percent in the group treated with cholestyramine, while the probability of dying from a heart attack dropped from 2 to 1.6 percent, not exactly jaw-dropping numbers. 16 )
WHAT THE FRAMINGHAM HEART STUDY FOUND
One study mentioned most often by the defenders of the cholesterol theory is the Framingham Heart Study. This long-running research study started back in 1948 and monitored heart disease in more than 5,000 residents of Framingham, Massachusetts. After following up for sixteen years, the researchers claimed to find a direct correlation between heart disease and cholesterol levels.
But God is in the details. As it turned out, the group of Framingham residents who developed heart disease and the group of Framingham residents who didn’t had similar ranges of cholesterol levels. In fact, the
average
cholesterol level of the heart disease group was only 11 percent higher than that of the group
without
heart disease. Cardiovascular disease struck people with cholesterol levels as low as 150 mg/dL. Low cholesterol, according to this study, was hardly a guarantee of a healthy heart.
It gets better (or worse, depending on your position). When researchers went back and looked at the Framingham data thirty years after the project started, they found that once men passed the age of forty-seven, it didn’t make a whit of difference whether their cholesterol was low or high. 14 Those with high cholesterol at age forty-eight lived just as long as, or
longer
than, those who have had low cholesterol. So if cholesterol is important only for the relatively few who have had a heart attack before the age of forty-eight, why are the rest of us worried about high-fat food and cholesterol
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