levels?
The question is hardly academic. In 1992, forty-four years after the Framingham project began, study director William Castelli, M.D., wrote the following in an editorial in the
Archives of Internal Medicine
:
“In Framingham, Mass., the
more
saturated fat one ate, the
more
cholesterol one ate, the
more
calories one ate, the
lower
the person’s serum cholesterol . . . we found that people who ate the
most
cholesterol, ate the
most
saturated fat, [and] ate the
most
calories weighed the least and were the most physically active [italics ours].” 15
Okay, cholesterol goes down, heart disease drops by a thimble, and the researchers conclude that lowering cholesterol lowers the risk of heart disease. But remember, this was a
drug
trial, not a
diet
trial. The researchers made a huge leap of faith by assuming that if lowering cholesterol is “good” (i.e., it reduces the risk of heart disease), it shouldn’t much matter
how
you lower it. Lowering it through diet should get you the same “good” result (if you can call the miniscule drop in heart disease that may or may not be related to the drop in cholesterol a “good” result). Their leap of faith was that we should recommend low-fat diets because they will achieve the same result as the drug—cholesterol will go down and everyone will live happily ever after.
But drugs often have many effects in addition to their main purpose. (Remember, Viagra was originally designed as a blood pressure medication!) The drug used in the LRC-CPPT might also have had some good effects, such as lowering inflammation, for example. Assuming that lowering cholesterol with a low-fat diet was identical to lowering it with a multifaceted medication that could in fact have had unintended benefits was a complete leap of faith and led to the wholesale recommendation of a low-fat diet for the prevention of heart disease.
That same year, the NIH held what’s called a “consensus conference” to basically justify the LRC-CPPT and the dietary recommendations that came out of it, yet it was anything but a consensus. Several experts pointed to significant defects in the studies and even called into question their accuracy. But you’d never know it from the final report, which made it seem like everyone had unquestioningly hitched their collective stars to the low-fat bandwagon.
Well, not exactly everyone.
CHAPTER 3
INFLAMMATION: THE TRUE CAUSE OF HEART DISEASE
SO IF CHOLESTEROL
ISN’T
THE CAUSE OF HEART DISEASE, what is?
We know you don’t want to wait any longer, so here’s the short answer: The primary cause of heart disease is
inflammation
.
The subject of inflammation will be a running theme throughout this book for reasons that will soon be made clear, but the first thing you need to know about inflammation is this: It comes in two flavors. You’re probably already familiar with one of them, but it’s the one you’re
less
familiar with that’s at the core of heart disease.
Let us explain.
Almost all of us have experience with
acute
inflammation. It happens every time you stub your toe, bang your knee, or get a splinter in your finger. When you complain about your aching back, an abscess in your mouth, or a rash on your skin, that’s acute inflammation. It’s visible and uncomfortable, if not downright painful. The redness on your skin is a result of blood that’s rushed to the affected area. The swelling you experience is the result of an army of specialized cells (with names like
phagocytes
and
lymphocytes)
dispatched by the immune system to mend the injured area. (The job of these immune system cells is to surround the site of the injury andneutralize nasty invaders such as microbes, preventing the spread of potential infection.) The swelling, redness, and soreness you experience as a result of acute inflammation are all natural accompaniments to the healing process.
So we all know about acute inflammation, most of us from personal experience. But
The question is hardly academic. In 1992, forty-four years after the Framingham project began, study director William Castelli, M.D., wrote the following in an editorial in the
Archives of Internal Medicine
:
“In Framingham, Mass., the
more
saturated fat one ate, the
more
cholesterol one ate, the
more
calories one ate, the
lower
the person’s serum cholesterol . . . we found that people who ate the
most
cholesterol, ate the
most
saturated fat, [and] ate the
most
calories weighed the least and were the most physically active [italics ours].” 15
Okay, cholesterol goes down, heart disease drops by a thimble, and the researchers conclude that lowering cholesterol lowers the risk of heart disease. But remember, this was a
drug
trial, not a
diet
trial. The researchers made a huge leap of faith by assuming that if lowering cholesterol is “good” (i.e., it reduces the risk of heart disease), it shouldn’t much matter
how
you lower it. Lowering it through diet should get you the same “good” result (if you can call the miniscule drop in heart disease that may or may not be related to the drop in cholesterol a “good” result). Their leap of faith was that we should recommend low-fat diets because they will achieve the same result as the drug—cholesterol will go down and everyone will live happily ever after.
But drugs often have many effects in addition to their main purpose. (Remember, Viagra was originally designed as a blood pressure medication!) The drug used in the LRC-CPPT might also have had some good effects, such as lowering inflammation, for example. Assuming that lowering cholesterol with a low-fat diet was identical to lowering it with a multifaceted medication that could in fact have had unintended benefits was a complete leap of faith and led to the wholesale recommendation of a low-fat diet for the prevention of heart disease.
That same year, the NIH held what’s called a “consensus conference” to basically justify the LRC-CPPT and the dietary recommendations that came out of it, yet it was anything but a consensus. Several experts pointed to significant defects in the studies and even called into question their accuracy. But you’d never know it from the final report, which made it seem like everyone had unquestioningly hitched their collective stars to the low-fat bandwagon.
Well, not exactly everyone.
CHAPTER 3
INFLAMMATION: THE TRUE CAUSE OF HEART DISEASE
SO IF CHOLESTEROL
ISN’T
THE CAUSE OF HEART DISEASE, what is?
We know you don’t want to wait any longer, so here’s the short answer: The primary cause of heart disease is
inflammation
.
The subject of inflammation will be a running theme throughout this book for reasons that will soon be made clear, but the first thing you need to know about inflammation is this: It comes in two flavors. You’re probably already familiar with one of them, but it’s the one you’re
less
familiar with that’s at the core of heart disease.
Let us explain.
Almost all of us have experience with
acute
inflammation. It happens every time you stub your toe, bang your knee, or get a splinter in your finger. When you complain about your aching back, an abscess in your mouth, or a rash on your skin, that’s acute inflammation. It’s visible and uncomfortable, if not downright painful. The redness on your skin is a result of blood that’s rushed to the affected area. The swelling you experience is the result of an army of specialized cells (with names like
phagocytes
and
lymphocytes)
dispatched by the immune system to mend the injured area. (The job of these immune system cells is to surround the site of the injury andneutralize nasty invaders such as microbes, preventing the spread of potential infection.) The swelling, redness, and soreness you experience as a result of acute inflammation are all natural accompaniments to the healing process.
So we all know about acute inflammation, most of us from personal experience. But
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