Reply to anthony's paper
http://www.jpands.org/vol11no1/correspondence.pdf
The recent paper by Anthony Colpo is
critically flawed from a scientific
standpoint.
The author states: “The belief that lowdensity
lipoprotein (LDL) cholesterol causes
atherosclerosis and subsequent heart disease is
a fundamental precept of modern medicine.”
Generally, normal levels of LDLcholesterol,
in and of themselves, do not
cause atherosclerosis; rather it is important
for normal physiological functions. There
is no disputing that hypercholesterolemia,
most commonly associated with an
elevation of plasma LDL, is an important
contributing factor in atherogenesis; its
correction can reduce the risk of coronary
heart disease (CHD).
Colpo states that “proliferation of
[atherosclerotic] plaques may occur, not
because of simple elevations in blood
cholesterol, but because of unfavorable
physiological conditions that damage or
weaken the structure of the arterial wall,” a
statement that is illogical and unscientific
because a high blood level of cholesterol
itself is one of the most unfavorable
physiological conditions that can lead to
damaging the structure of the arterial wall.
He then goes on to conclude that “all of
these factors have been shown to exert an
atherogenic effect unrelated to serum
cholesterol elevation.” Reaching such a
conclusion suggests a basic misunderstanding
of the pathogenesis of cardiovascular
diseases. The earliest recognizable
lesion of atherosclerosis is the fatty streaks
within the innermost layer of the artery
wall. They precede the development of
intermediate lesions, and develop into the
more complex occlusive lesions that may
impede blood flow by projecting into the
arterial lumen. The occlusive lesions of
atherosclerosis can be clinically reversed in
many cases after aggressive treatment with
various lipid-lowering drugs.
Colpo realized that “the number of
deaths from CHD has indeed decreased
since the late 1960s,” but argued that “total
incidence of CHD has not declined.” He
further blamed the medical community,
since it has “failed to help people avoid
CHD in the first place.” Strangely, Colpo
has ignored the fact that the world’s
population has doubled since 1960 and is
aging. The risk for CHD increases steeply
with advancing age. The claim that the
“war on cholesterol” has “delivered no
benefit to public health” is not only
irresponsible, but false.
Of further concern, Colpo has
repeatedly mixed up the terms LDL, highdensity
lipoprotein (HDL), and cholesterol.
He states that, “the concept that LDL is
‘bad’ cholesterol is a simplistic and
scientifically untenable hypothesis.” LDL
is not cholesterol. He also states that, “HDL
cholesterol, on the other hand, is the ‘heartfriendly
’lipoprotein.”
Cholesterol is not a lipoprotein.
Cholesterol is a lipid present in cell
membrane and travels in the blood in
distinct particles containing both lipid and
lipoproteins. LDL provides cholesterol to
cells through LDLreceptors, whereas HDL
removes excess cholesterol through reverse
cholesterol transport, thus maintaining
cholesterol homeostasis.
The link between lipids and CHD has
been firmly established by epidemiologic
studies and long-term outcomes trials.
Despite the emergence of new markers of CHD such as C-reactive protein, LDL
cholesterol currently should remain the
primary target for reduction of risk of CHD