From Dr. Joseph Mercola's website -
www.mercola.com
By Sally
Fallon and Mary G. Enig, PhD
Originally printed at
Weston A.
Price
Hypercholesterolemia is the
health issue of the 21st century. It is actually an
invented disease, a "problem" that emerged when health
professionals learned how to measure cholesterol levels in
the blood. High cholesterol exhibits no outward
signs--unlike other conditions of the blood, such as
diabetes or anemia, diseases that manifest telltale
symptoms like thirst or weakness--hypercholesterolemia
requires the services of a physician to detect its
presence. Many people who feel perfectly healthy suffer
from high cholesterol--in fact, feeling good is actually a
symptom of high cholesterol!
Doctors who treat this new disease must first convince
their patients that they are sick and need to take one or
more expensive drugs for the rest of their lives, drugs
that require regular checkups and blood tests. But such
doctors do not work in a vacuum--their efforts to convert
healthy people into patients are bolstered by the full
weight of the U.S. government, the media and the medical
establishment, agencies that have worked in concert to
disseminate the cholesterol dogma and convince the
population that high cholesterol is the forerunner of heart
disease and possibly other diseases as well.
Who suffers from hypercholesterolemia? Peruse the medical
literature of 25 or 30 years ago and you'll get the
following answer: any middle-aged man whose cholesterol is
over 240 with other risk factors, such as smoking or
overweight.
After the Cholesterol Consensus Conference in 1984, the
parameters changed; anyone (male or female) with
cholesterol over 200 could receive the dreaded diagnosis
and a prescription for pills. Recently that number has been
moved down to 180. If you have had a heart attack, you get
to take cholesterol-lowering medicines even if your
cholesterol is already very low--after all, you have
committed the sin of having a heart attack so your
cholesterol must therefore be too high. The penance is a
lifetime of cholesterol-lowering medications along with a
boring low-fat diet. But why wait until you have a heart
attack? Since we all labor under the stigma of original
sin, we are all candidates for treatment. Current edicts
stipulate cholesterol testing and treatment for young
adults and even children.
The drugs that doctors use to treat the new disease are
called statins--sold under a variety of names including:
• Lipitor (atorvastatin)
• Zocor (simvastatin)
• Mevacor (lovastatin)
• Pravachol (pravastatin)
How
Statins Work
The
process begins with acetyl-CoA, a two-carbon molecule
sometimes referred to as the "building block of life."
Three acetyl-CoA molecules combine to form six-carbon
hydroxymethyl glutaric acid (HMG). The step from HMG to
mevalonate requires an enzyme, HMG-CoA reductase. Statin
drugs work by inhibiting this enzyme--hence the formal name
of HMG-CoA reductase inhibitors. Herein lies the potential
for numerous side effects, because statin drugs inhibit not
just the production of cholesterol, but a whole family of
intermediary substances, many if not all of which have
important biochemical functions in their own right.
Consider the findings of pediatricians at the University of
California, San Diego who published a description of a
child with a hereditary defect of mevalonic kinase, the
enzyme that facilitates the next step beyond HMG-CoA
reductase.1 The child was mentally
retarded, microcephalic (very small head), small for his
age, profoundly anemic, acidotic and febrile. He also had
cataracts. Predictably, his cholesterol was consistently
low--70-79 mg/dl. He died at the age of 24 months. The
child represents an extreme example of cholesterol
inhibition, but his case illuminates the possible
consequences of taking statins in strong doses or for a
lengthy period of time:
• Depression of mental
acuity
• Anemia
• Acidosis
• Frequent fevers
• Cataracts
Cholesterol is one of three end
products in the mevalonate chain. The two others are
ubiquinone and dilochol. Ubiquinone or Co-Enzyme Q10 is a
critical cellular nutrient biosynthesized in the
mitochondria. It plays a role in ATP production in the
cells and functions as an electron carrier to cytochrome
oxidase, our main respiratory enzyme. The heart requires
high levels of Co-Q10. A form of Co-Q10 called ubiquinone
is found in all cell membranes where it plays a role in
maintaining membrane integrity so critical to nerve
conduction and muscle integrity. Co-Q10 is also vital to
the formation of elastin and collagen. Side effects of
Co-Q10 deficiency include muscle wasting leading to
weakness and severe back pain, heart failure (the heart is
a muscle!), neuropathy and inflammation of the tendons and
ligaments, often leading to rupture.
Dolichols also play a role of immense importance. In the
cells they direct various proteins manufactured in response
to DNA directives to their proper targets, ensuring that
the cells respond correctly to genetically programmed
instruction. Thus statin drugs can lead to unpredictable
chaos on the cellular level, much like a computer virus
that wipes out certain pathways or files.
Squalene, the immediate precursor to cholesterol, has
anti-cancer effects, according to research.
The fact that some studies have shown that statins can
prevent heart disease, at least in the short term, is most
likely explained not by the inhibition of cholesterol
production but because they block the creation of
mevalonate. Reduced amounts of mevalonate seem to make
smooth muscle cells less active, and platelets less able to
produce thromboxane. Atherosclerosis begins with the growth
of smooth muscle cells in side artery walls and thromboxane
is necessary for blood clotting.
Cholesterol
Of
course, statins inhibit the production of cholesterol--they
do this very well. Nowhere is the failing of our medical
system more evident than in the wholesale acceptance of
cholesterol reduction as a way to prevent disease--have all
these doctors forgotten what they learned in biochemistry
101 about the many roles of cholesterol in the human
biochemistry?
Every cell membrane in our body contains cholesterol
because cholesterol is what makes our cells
waterproof--without cholesterol we could not have a
different biochemistry on the inside and the outside of the
cell. When cholesterol levels are not adequate, the cell
membrane becomes leaky or porous, a situation the body
interprets as an emergency, releasing a flood of corticoid
hormones that work by sequestering cholesterol from one
part of the body and transporting it to areas where it is
lacking. Cholesterol is the body's repair substance: scar
tissue contains high levels of cholesterol, including scar
tissue in the arteries.
Cholesterol is the precursor to vitamin D, necessary for
numerous biochemical processes including mineral
metabolism. The bile salts, required for the digestion of
fat, are made of cholesterol. Those who suffer from low
cholesterol often have trouble digesting fats. Cholesterol
also functions as a powerful antioxidant, thus protecting
us against cancer and aging.
Cholesterol is vital to proper neurological function. It
plays a key role in the formation of memory and the uptake
of hormones in the brain, including serotonin, the body's
feel-good chemical. When cholesterol levels drop too low,
the serotonin receptors cannot work. Cholesterol is the
main organic molecule in the brain, constituting over half
the dry weight of the cerebral cortex.
Finally, cholesterol is the precursor to all the hormones
produced in the adrenal cortex including glucocorticoids,
which regulate blood sugar levels, and mineralocorticoids,
which regulate mineral balance. Corticoids are the
cholesterol-based adrenal hormones that the body uses in
response to stress of various types; it promotes healing
and balances the tendency to inflammation. The adrenal
cortex also produces sex hormones, including testosterone,
estrogen and progesterone, out of cholesterol. Thus, low
cholesterol--whether due to an innate error of metabolism
or induced by cholesterol-lowering diets and drugs--can be
expected to disrupt the production of adrenal hormones and
lead to:
• Blood sugar problems
• Edema
• Mineral deficiencies
• Chronic inflammation
• Difficulty in healing
• Allergies
• Asthma
• Reduced libido
• Infertility
• Various reproductive problems
Enter
the Statins
Statin
drugs entered the market with great promise. They replaced
a class of pharmaceuticals that lowered cholesterol by
preventing its absorption from the gut. These drugs often
had immediate and unpleasant side effects, including
nausea, indigestion and constipation, and in the typical
patient they lowered cholesterol levels only slightly.
Patient compliance was low: the benefit did not seem worth
the side effects and the potential for use very limited. By
contrast, statin drugs had no immediate side effects: they
did not cause nausea or indigestion and they were
consistently effective, often lowering cholesterol levels
by 50 points or more.
During the last 20 years, the industry has mounted an
incredible promotional campaign--enlisting scientists,
advertising agencies, the media and the medical profession
in a blitz that turned the statins into one of the
bestselling pharmaceuticals of all time. Sixteen million
Americans now take Lipitor, the most popular statin, and
drug company officials claim that 36 million Americans are
candidates for statin drug therapy.
What bedevils the industry is growing reports of side
effects that manifest many months after the commencement of
therapy; the November 2003 issue of Smart Money magazine
reports on a 1999 study at St. Thomas' Hospital in London
(apparently unpublished), which found that 36 percent of
patients on Lipitor's highest dose reported side effects;
even at the lowest dose, 10 percent reported side
effects.2
Muscle
Pain and Weakness
The
most common side effect is muscle pain and weakness, a
condition called rhabdomyolysis, most likely due to the
depletion of Co-Q10, a nutrient that supports muscle
function. Dr. Beatrice Golomb of San Diego, California is
currently conducting a series of studies on statin side
effects. The industry insists that only 2-3 percent of
patients get muscle aches and cramps but in one study,
Golomb found that 98 percent of patients taking Lipitor and
one-third of the patients taking Mevachor (a lower-dose
statin) suffered from muscle problems.3 A message board devoted to
Lipitor at forum.ditonline.com
contains more than
800 posts, many detailing severe side effects. The Lipitor
board at www.rxlist.com
contains more than
2,600 posts.
The test for muscle wasting or rhabdomyolysis is elevated
levels of a chemical called creatine kinase (CK). But many
people experience pain and fatigue even though they have
normal CK levels.4
Tahoe
City resident Doug Peterson developed slurred speech,
balance problems and severe fatigue after three years on
Lipitor--for two and a half years, he had no side effects
at all.5 It began with restless sleep
patterns--twitching and flailing his arms. Loss of balance
followed and the beginning of what Doug calls the "statin
shuffle"--a slow, wobbly walk across the room. Fine motor
skills suffered next. It took him five minutes to write
four words, much of which was illegible. Cognitive function
also declined. It was hard to convince his doctors that
Lipitor could be the culprit, but when he finally stopped
taking it, his coordination and memory improved.
John Altrocchi took Mevacor for three years without side
effects; then he developed calf pain so severe he could
hardly walk. He also experienced episodes of temporary
memory loss.
For some, however, muscle problems show up shortly after
treatment begins. Ed Ontiveros began having muscle problems
within 30 days of taking Lipitor. He fell in the bathroom
and had trouble getting up. The weakness subsided when he
went off Lipitor. In another case, reported in the medical
journal Heart, a patient developed rhabdomyolysis after a
single dose of a statin.6 Heel pain from plantar fascitis
(heel spurs) is another common complaint among those taking
statin drugs. One correspondent reported the onset of pain
in the feet shortly after beginning statin treatment. She
had visited an evangelist, requesting that he pray for her
sore feet. He enquired whether she was taking Lipitor. When
she said yes, he told her that his feet had also hurt when
he took Lipitor.7
Active
people are much more likely to develop problems from statin
use than those who are sedentary. In a study carried out in
Austria, only six out of 22 athletes with familial
hypercholesterolemia were able to endure statin
treatment.8 The others discontinued
treatment because of muscle pain.
By the way, other cholesterol-lowering agents besides
statin drugs can cause joint pain and muscle weakness. A
report in Southern Medical Journal described muscle pains
and weakness in a man who took Chinese red rice, an herbal
preparation that lowers cholesterol.9 Anyone suffering from myopathy,
fibromyalgia, coordination problems and fatigue needs to
look at low cholesterol plus Co-Q10 deficiency as a
possible cause.
Neuropathy
Polyneuropathy, also known as peripheral neuropathy, is
characterized by weakness, tingling and pain in the hands
and feet as well as difficulty walking. Researchers who
studied 500,000 residents of Denmark, about 9 percent of
that country's population, found that people who took
statins were more likely to develop
polyneuropathy.10
Taking statins for one year raised the risk of nerve damage
by about 15 percent--about one case for every 2,200
patients. For those who took statins for two or more years,
the additional risk rose to 26 percent.
According to the research of Dr. Golomb, nerve problems are
a common side effect from statin use; patients who use
statins for two or more years are at a four to 14-fold
increased risk of developing idiopathic polyneuropathy
compared to controls.11
She reports that in many cases, patients told her they had
complained to their doctors about neurological problems,
only to be assured that their symptoms could not be related
to cholesterol-lowering medications.
The damage is often irreversible. People who take large
doses for a long time may be left with permanent nerve
damage, even after they stop taking the drug.
The question is, does widespread statin-induced neuropathy
make our elderly drivers (and even not-so-elderly drivers)
more accident prone? In July 2003, an 86-year-old driver
with an excellent driving record plowed into a farmers'
market in Santa Monica, California, killing 10 people.
Several days later, a most interesting letter from a Lake
Oswego, Oregon woman appeared in the Washington
Post:12
"My
husband, at age 68, backed into the garage and stepped on
the gas, wrecking a lot of stuff. He said his foot slipped
off the brake. He had health problems and is on medication,
including a cholesterol drug, which is now known to cause
problems with feeling in one's legs.
"In my little community, older drivers have missed a turn
and taken out the end of a music store, the double doors of
the post office and the front of a bakery. In Portland, a
bank had to do without its drive-up window for some time.
"It is easy to say that one's foot slipped, but the problem
could be lack of sensation. My husband's sister-in-law
thought her car was malfunctioning when it refused to go
when a light turned green, until she looked down and saw
that her foot was on the brake. I have another friend who
mentioned having no feeling in her lower extremities. She
thought about having her car retrofitted with hand controls
but opted for the handicapped bus instead."
Heart
Failure
We are currently in the midst of a congestive heart failure
epidemic in the United States--while the incidence of heart
attack has declined slightly, an increase in the number of
heart failure cases has outpaced these gains. Deaths
attributed to heart failure more than doubled from 1989 to
1997.13
(Statins were first given pre-market approval in 1987.)
Interference with production of Co-Q10 by statin drugs is
the most likely explanation. The heart is a muscle and it
cannot work when deprived of Co-Q10.
Cardiologist Peter Langsjoen studied 20 patients with
completely normal heart function. After six months on a low
dose of 20 mg of Lipitor a day, two-thirds of the patients
had abnormalities in the heart's filling phase, when the
muscle fills with blood. According to Langsjoen, this
malfunction is due to Co-Q10 depletion.
Without Co-Q10, the cell's mitochondria are inhibited from
producing energy, leading to muscle pain and weakness. The
heart is especially susceptible because it uses so much
energy.14
Co-Q10
depletion becomes more and more of a problem as the
pharmaceutical industry encourages doctors to lower
cholesterol levels in their patients by greater and greater
amounts. Fifteen animal studies in six different animal
species have documented statin-induced Co-Q10 depletion
leading to decreased ATP production, increased injury from
heart failure, skeletal muscle injury and increased
mortality. Of the nine controlled trials on statin-induced
Co-Q10 depletion in humans, eight showed significant Co-Q10
depletion leading to decline in left ventricular function
and biochemical imbalances.15
Yet virtually all patients with heart failure are put on
statin drugs, even if their cholesterol is already low. Of
interest is a recent study indicating that patients with
chronic heart failure benefit from having high levels of
cholesterol rather than low. Researchers in Hull, UK
followed 114 heart failure patients for at least 12
months.16
Survival was 78 percent at 12 months and 56 percent at 36
months.
They found that for every point of decrease in serum
cholesterol, there was a 36 percent increase in the risk of
death within three years.
Dizziness
Dizziness is commonly associated with statin use, possibly
due to pressure-lowering effects. One woman reported
dizziness one half hour after taking
Pravachol.17
When she stopped taking it, the dizziness cleared up. Blood
pressure lowering has been reported with several statins in
published studies. According to Dr. Golumb, who notes that
dizziness is a common adverse effect, the elderly may be
particularly sensitive to drops in blood
pressure.18
Cognitive
Impairment
The November 2003 issue of Smart Money19
describes the case of Mike Hope, owner of a successful
ophthalmologic supply company:
"There's an awkward silence when you ask Mike Hope his age.
He doesn't change the subject or stammer, or make a silly
joke about how he stopped counting at 21. He simply doesn't
remember. Ten seconds pass. Then 20. Finally an answer
comes to him. 'I'm 56,' he says. Close, but not quite. 'I
will be 56 this year.' Later, if you happen to ask him
about the book he's reading, you'll hit another roadblock.
He can't recall the title, the author or the plot."
Statin use since 1998 has caused his speech and memory to
fade. He was forced to close his business and went on
Social Security 10 years early. Things improved when he
discontinued Lipitor in 2002, but he is far from complete
recovery--he still cannot sustain a conversation. What
Lipitor did was turn Mike Hope into an old man when he was
in the prime of life.
Cases like Mike's have shown up in the medical literature
as well. An article in Pharmacotherapy, December 2003, for
example, reports two cases of cognitive impairment
associated with Lipitor and Zocor.20
Both patients suffered progressive cognitive decline that
reversed completely within a month after discontinuation of
the statins. A study conducted at the University of
Pittsburgh showed that patients treated with statins for
six months compared poorly with patients on a placebo in
solving complex mazes, psychomotor skills and memory
tests.21
Dr.
Golomb has found that 15 percent of statin patients develop
some cognitive side effects.22
The most harrowing involve global transient
amnesia--complete memory loss for a brief or lengthy
period--described by former astronaut Duane Graveline in
his book Lipitor: Thief of Memory.23
Sufferers report baffling incidents involving complete loss
of memory--arriving at a store and not remembering why they
are there, unable to remember their name or the names of
their loved ones, unable to find their way home in the car.
These episodes occur suddenly and disappear just as
suddenly. Graveline points out that we are all at risk when
the general public is taking statins--do you want to be in
an airplane when your pilot develops statin-induced
amnesia?
While the pharmaceutical industry denies that statins can
cause amnesia, memory loss has shown up in several statin
trials. In a trial involving 2,502 subjects, amnesia
occurred in seven receiving Lipitor; amnesia also occurred
in two of 742 subjects during comparative trials with other
statins. In addition, "abnormal thinking" was reported in
four of the 2,502 clinical trial
subjects.24
The total recorded side effects was therefore 0.5 percent;
a figure that likely under-represents the true frequency
since memory loss was not specifically studied in these
trials.
Cancer
In every study with rodents to date, statins have caused
cancer.25
Why have we not seen such a dramatic correlation in human
studies? Because cancer takes a long time to develop and
most of the statin trials do not go on longer than two or
three years. Still, in one trial, the CARE trial, breast
cancer rates of those taking a statin went up 1500
percent.26
In the Heart Protection Study, non-melanoma skin cancer
occurred in 243 patients treated with simvastatin compared
with 202 cases in the control group.27
Manufacturers
of statin drugs have recognized the fact that statins
depress the immune system, an effect that can lead to
cancer and infectious disease, recommending statin use for
inflammatory arthritis and as an immune suppressor for
transplant patients.28
Pancreatic
Rot
The medical literature contains several reports of
pancreatitis in patients taking statins. One paper
describes the case of a 49-year-old woman who was admitted
to the hospital with diarrhea and septic shock one month
after beginning treatment with
lovastatin.29
She
died after prolonged hospitalization; the cause of death
was necrotizing pancreatitis. Her doctors noted that the
patient had no evidence of common risk factors for acute
pancreatitis, such as biliary tract disease or alcohol use.
"Prescribers of statins (particularly simvastatin and
lovastatin) should take into account the possibility of
acute pancreatitis in patients who develop abdominal pain
within the first weeks of treatment with these drugs," they
warned.
Depression
Numerous studies have linked low cholesterol with
depression. One of the most recent found that women with
low cholesterol are twice as likely to suffer from
depression and anxiety. Researchers from Duke University
Medical Center carried out personality trait measurements
on 121 young women aged 18 to 27.30
They found that 39 percent of the women with low
cholesterol levels scored high on personality traits that
signaled proneness to depression, compared to 19 percent of
women with normal or high levels of cholesterol.
In addition, one in three of the women with low cholesterol
levels scored high on anxiety indicators, compared to 21
percent with normal levels. Yet the author of the study,
Dr. Edward Suarez, cautioned women with low cholesterol
against eating "foods such as cream cakes" to raise
cholesterol, warning that these types of food "can cause
heart disease." In previous studies on men, Dr. Suarez
found that men who lower their cholesterol levels with
medication have increased rates of suicide and violent
death, leading the researchers to theorize "that low
cholesterol levels were causing mood disturbances."
How many elderly statin-takers eke through their golden
years feeling miserable and depressed, when they should be
enjoying their grandchildren and looking back with pride on
their accomplishments? But that is the new dogma--you may
have a long life as long as it is experienced as a vale of
tears.
Any
Benefits?
Most doctors are convinced--and seek to convince their
patients--that the benefits of statin drugs far outweigh
the side effects. They can cite a number of studies in
which statin use has lowered the number of coronary deaths
compared to controls. But as Dr. Ravnskov has pointed out
in his book
The Cholesterol Myths,31
the results of the major studies up to the year 2000--the
4S, WOSCOPS, CARE, AFCAPS and LIPID studies--generally
showed only small differences and these differences were
often statistically insignificant and independent of the
amount of cholesterol lowering achieved.
In two studies, EXCEL, and FACAPT/TexCAPS, more deaths
occurred in the treatment group compared to controls. Dr.
Ravnskov's 1992 meta-analysis of 26 controlled
cholesterol-lowering trials found an equal number of
cardiovascular deaths in the treatment and control groups
and a greater number of total deaths in the treatment
groups.32
An analysis of all the big controlled trials reported
before 2000 found that long-term use of statins for primary
prevention of heart disase produced a 1 percent greater
risk of death over 10 years compared to a
placebo.33
Recently
published studies do not provide any more justification for
the current campaign to put as many people as possible on
statin drugs.
Honolulu
Hearth Program (2001)
This
report, part of an ongoing study, looked at cholesterol
lowering in the elderly. Researchers compared changes in
cholesterol concentrations over 20 years with all-cause
mortality.34 To quote:
"Our data accords with previous findings of increased
mortality in elderly people with low serum cholesterol, and
show that long-term persistence of low cholesterol
concentration actually increases risk of death. Thus, the
earlier that patients start to have lower cholesterol
concentrations, the greater the risk of death ... The most
striking findings were related to changes in cholesterol
between examination three (1971-74) and examination four
(1991-93).
There are few studies that have cholesterol concentrations
from the same patients at both middle age and old age.
Although our results lend support to previous findings that
low serum cholesterol imparts a poor outlook when compared
with higher concentrations of cholesterol in elderly
people, our data also suggest that those individuals with a
low serum cholesterol maintained over a 20-year period will
have the worst outlook for all-cause mortality [emphasis
ours]."
MIRACL
(2001)
The
MIRACL study looked at the effects of a high dose of
Lipitor on 3,086 patients in the hospital after angina or
nonfatal MI and followed them for 16
weeks.35 According to the abstract: "For
patients with acute coronary syndrome, lipid-lowering
therapy with atorvastatin, 80 mg/day, reduced recurrent
ischemic events in the first 16 weeks, mostly recurrent
symptomatic ischemia requiring rehospitalization." What the
abstract did not mention was that there was no change in
death rate compared to controls and no significant change
in re-infarction rate or need for resuscitation from
cardiac arrest. The only change was a significant drop in
chest pain requiring rehospitalization.
ALLHAT
(2002)
ALLHAT
(Antihypertensive and Lipid-Lowering Treatment to Prevent
Heart Attack Trial), the largest North American
cholesterol-lowering trial ever and the largest trial in
the world using Lipitor, showed mortality of the treatment
group and controls after three or six years was
identical.36
Researchers used data from more than 10,000 participants
and followed them over a period of four years, comparing
the use of a statin drug to "usual care," namely
maintaining proper body weight, no smoking, regular
exercise, etc., in treating subjects with moderately high
levels of LDL cholesterol. Of the 5170 subjects in the
group that received statin drugs, 28 percent lowered their
LDL cholesterol significantly. And of the 5,185 usual-care
subjects, about 11 percent had a similar drop in LDL. But
both groups showed the same rates of death, heart attack
and heart disease.
Heart
Protection Study (2002)
Carried out at Oxford
University,37 this study received widespread
press coverage; researchers claimed "massive benefits" from
cholesterol-lowering,38 leading one commentator to
predict that statin drugs were "the new
aspirin."39 But as Dr. Ravnskov points
out,40 the benefits were far from
massive. Those who took simvastatin had an 87.1 percent
survival rate after five years compared to an 85.4 percent
survival rate for the controls and these results were
independent of the amount of cholesterol lowering. The
authors of the Heart Protection Study never published
cumulative mortality data, even though they received many
requests to do so and even though they received funding and
carried out a study to look at cumulative data.
According to the authors, providing year-by-year mortality
data would be an "inappropriate" way of publishing their
study results.41
PROSPER
(2002)
PROSPER (Prospective Study of
Pravastatin in the Elderly at Risk) studied the effect of
pravastatin compared to placebo in two older populations of
patients of which 56 percent were primary prevention cases
(no past or symptomatic cardiovascular disease) and 44
percent were secondary prevention cases (past or
symptomatic cardiovascular disease).42
Pravastatin did not reduce total myocardial infarction or
total stroke in the primary prevention population but did
so in the secondary. However, measures of overall health
impact in the combined populations, total mortality and
total serious adverse events were unchanged by pravastatin
as compared to the placebo and those in the treatment group
had increased cancer. In other words: not one life saved.
J-LIT
(2002)
Japanese Lipid Intervention
Trial was a six-year study of 47,294 patients treated with
the same dose of simvastatin.43 Patients were grouped by the
amount of cholesterol lowering. Some patient had no
reduction in LDL levels, some had a moderate fall in LDL
and some had very large LDL reductions. The results: no
correlation between the amount of LDL lowering and death
rate at five years. Those with LDL cholesterol lower than
80 had a death rate of just over 3.5 at five years; those
whose LDL was over 200 had a death rate of just over 3.5 at
five years.
Meta-Analysis
(2003)
In a
meta-analysis of 44 trials involving almost 10,000
patients, the death rate was identical at 1 percent of
patients in each of the three groups--those taking
atorvastatin (Lipitor), those taking other statins and
those taking nothing.44 Furthermore, 65 percent of
those on treatment versus 45 percent of the controls
experienced an adverse event. Researchers claimed that the
incidence of adverse effects was the same in all three
groups, but 3 percent of the atorvastatin-treated patients
and 4 percent of those receiving other statins withdrew due
to treatment-associated adverse events, compared with 1
percent of patients on the placebo.
Statins
and Plaque (2003)
A
study published in the American Journal of Cardiology casts
serious doubts on the commonly held belief that lowering
your LDL-cholesterol, the so-called bad cholesterol, is the
most effective way to reduced arterial
plaque.45 Researchers at Beth Israel
Medical Center in New York City examined the coronary
plaque buildup in 182 subjects who took statin drugs to
lower cholesterol levels. One group of subjects used the
drug aggressively (more than 80 mg per day) while the
balance of the subjects took less than 80 mg per day.
Using electron beam tomography, the researchers measured
plaque in all of the subjects before and after a study
period of more than one year. The subjects were generally
successful in lowering their cholesterol, but in the end
there was no statistical difference in the two groups in
the progression of arterial calcified plaque. On average,
subjects in both groups showed a 9.2 percent increase in
plaque buildup.
Statins
and Women (2003)
No
study has shown a significant reduction in mortality in
women treated with statins. The University of British
Columbia Therapeutics Initiative came to the same
conclusion, with the finding that statins offer no benefit
to women for prevention of heart
disease.46
Yet in February
2004, Circulation published an article in which more than
20 organizations endorsed cardiovascular disease prevention
guidelines for women with several mentions of "preferably a
statin."47
ASCOT-LLA
(2003)
ASCOT-LLA (Anglo-Scandinavian
Cardiac Outcomes Trial -- Lipid Lowering Arm) was designed
to assess the benefits of atorvastatin (Lipitor) versus a
placebo in patients who had high blood pressure with
average or lower-than-average cholesterol concentrations
and at least three other cardiovascular risk
factors.48 The trial was originally
planned for five years but was stopped after a median
follow-up of 3.3 years because of a significant reduction
in cardiac events. Lipitor did reduce total myocardial
infarction and total stroke; however, total mortality was
not significantly reduced. In fact, women were worse off
with treatment. The trial report stated that total serious
adverse events "did not differ between patients assigned
atorvastatin or placebo," but did not supply the actual
numbers of serious events.
Cholesterol
Levels in Dialysis Patients (2004)
In a
study of dialysis patients, those with higher cholesterol
levels had lower mortality than those with low
cholesterol.49 Yet the authors claimed that
the "inverse association of total cholesterol level with
mortality in dialysis patients is likely due to the
cholesterol-lowering effect of systemic inflammation and
malnutrition, not to a protective effect of high
cholesterol concentrations." Keeping an eye on further
funding opportunities, the authors concluded: "These
findings support treatment of hypercholesterolemia in this
population."
References
1.
Hoffman G. N Engl J Med 1986;314:1610-24
2. Eleanor Laise. The Lipitor Dilemma, Smart Money: The
Wall Street Journal Magazine of Personal Business, November
2003.
3. Eleanor Laise. The Lipitor Dilemma, Smart Money: The
Wall Street Journal Magazine of Personal Business, November
2003.
4. Beatrice A. Golomb, MD, PhD on Statin Drugs, March 7,
2002.
www.coloradohealthsite.org/topics/interviews/golomb.html
5. Melissa Siig. Life After Lipitor: Is Pfizer product a
quick fix or dangerous drug? Residents experience adverse
reactions. Tahoe World, January 29, 2004.
6. Jamil S, Iqbal P. Heart 2004 Jan;90(1):e3.
7. Personal communication, Laura Cooper, May 1, 2003.
8. Sinzinger H, O'Grady J. Br J Clin Pharmacol. 2004
Apr;57(4):525-8.
9. Smith DJ and Olive KE. Southern Medical Journal
96(12):1265-1267, December 2003.
10. Gaist D and others. Neurology 2002 May 14;58(9):1321-2.
11. Statins and the Risk of Polyneuropathy.
www.coloradohealthsite.org/CHNReports/statins_polyneuropathy.html.
12. The Struggles of Older Drivers, letter by Elizabeth
Scherdt. Washington Post, June 21, 2003.
13. Langsjoen PH. The clinical use of HMG Co-A reductase
inhibitors (statins) and the associated depletion of the
essential co-factor coenzyme Q10: a review of pertinent
human and animal data.
http://www.fda.gov/ohrms/dockets/dailys/02/May02/052902/02p-0244-cp00001-02-Exhibit_A-vol1.pdf
14. Eleanor Laise. The Lipitor Dilemma, Smart Money: The
Wall Street Journal Magazine of Personal Business, November
2003.
15. Langsjoen PH. The clinical use of HMG Co-A reductase
inhibitors (statins) and the associated depletion of the
essential co-factor coenzyme Q10: a review of pertinent
human and animal data.
http://www.fda.gov/ohrms/dockets/dailys/02/May02/052902/02p-0244-cp00001-02-Exhibit_A-vol1.pdf
16. Clark AL and others. J Am Coll Cardiol
2003;42:1933-1943.
17. Personal communication, Jason DuPont, MD, July 7, 2003
18. Sandra G Boodman. Statins' Nerve Problems. Washington
Post, September 3, 2002.
19. Eleanor Laise. The Lipitor Dilemma, Smart Money: The
Wall Street Journal Magazine of Personal Business, November
2003,
20. King, DS. Pharmacotherapy 25(12):1663-7, Dec, 2003.
21. Muldoon MF and others. Am J Med 2000 May;108(7):538-46.
22. Email communication, Beatrice Golomb, July 10, 2003.
23. Duane Graveline, MD. Lipitor: Thief of Memory, 2004.
24. Lopena OF. Pharm D, Pfizer, Inc., written
communication, 2002. Quoted in an email communication from
Duane Graveline, spacedoc@webtv.net
25. Newman TB, Hulley SB. JAMA 1996;27:55-60
26. Sacks FM and others. N Eng J Med 1996;385;1001-1009.
27. Heart Protection Study Collaborative Group. Lancet
2002;360:7-22.
28. Leung BP and others. J Immunol. Feb 2003
170(3);1524-30; Palinski W. Nature Medicine Dec 2000
6;1311-1312.
29. J Pharm Technol 2003;19:283-286.
30. Low Cholesterol Linked to Depression. BBC Online
Network, May 25,1999.
31. Uffe Ravnskov, MD, PhD. The Cholesterol
Myths.
NewTrends Publishing, 2000.
32. Ravnskov U. BMJ. 1992;305:15-19.
33. Jackson PR. Br J Clin Pharmacol 2001;52:439-46.
34. Schatz IJ and others. Lancet 2001 Aug 4;358:351-355.
35. Schwartz GG and others. J Am Med Assoc.
2001;285:1711-8.
36. The ALLHAT Officers and Coordinators for the ALLHAT
Collaborative Research Group. JAMA 2002;288:2998-3007.
37. Heart Protection Study Collaborative Group. Lancet
2002;360:7-22.
38. Medical Research Council/British Heart Foundation Heart
Protection Study.Press release. Life-saver: World's largest
cholesterol-lowering trial reveals massive benefits for
high-risk patients. Available at
www.ctsu.ox.ac.uk/~hps/pr.shtml.
39. Kmietowicz A. BMJ 2001;323:1145
40. Ravnskov U. BMJ 2002;324:789
41. Email communication, Eddie Vos, February 13, 2004 and
posted at www.health-heart.org/comments.htm#PetoCollins.
42. Shepherd J and others. Lancet 2002;360:1623-1630.
43. Matsuzaki M and others. Circ J. 2002
Dec;66(12):1087-95.
44. Hecht HS, Harmon SM. Am J Cardiol 2003; 92:670-676
45. Hecht HS and others. Am J Cardiol 2003;92:334-336
46. Jenkins AJ. BMJ 2003 Oct 18;327(7420):933.
47. Circulation, 2004 Feb 17;109(6):714-21.
48. Sever PS and others. Lancet 2003;361:1149-1158.
49. Liu Y and others. JAMA 2004;291:451-459.
50. Cannon CP and others. N Engl J Med 2004 Apr
8;350(15):1495-504. Epub 2004 Mar 08.
51. Gina Kolata. Study of Two Cholesterol Drugs Finds One
Halts Heart Disease. The New York Times, November 13, 2003.
52. Extra-Low Cholesterol, The New York Times, March 10,
2003
53. Rob Stein. Striking Benefits Found in Ultra-Low
Cholesterol, The Washington Post, March 9, 2004
54. Dr. Malcolm Kendrick. PROVE IT- PROVE WHAT?
http://www.redflagsweekly.com/applications/ui/login.php?Next=/kendrick/2004_mar10.php&e=4
55. Health Sciences Institute e-alert,
www.hsibaltimore.com, March 11, 2004
56. Email communication, Joel Kauffman, April 15, 2004.
57. Nissen SE and others. JAMA 2004 Mar 3;291(9):1071-80.
58. Dr. Malcolm Kendrick. PROVE IT- PROVE WHAT?
http://www.redflagsweekly.com/applications/ui/login.php?Next=/kendrick/2004_mar10.php&e=4
59. Scott Hensley. The Statin Dilemma: How Sluggish Sales
Hurt Merck, Pfizer. The Wall Street Journal, July 25, 2003.
60. Ravnskov, U. Unpublished letter. ravnskov@tele2.se .
61. Cholesterol -- And Beyond: Statin Drugs Have Cut Heart
Disease. Now They Show Promise Against Alzheimer's,
Multiple Sclerosis & Osteoporosis. Newsweek, July 14.
2003.
62. John O'Neil. Treatments: Statins and Diabetes: New
Advice. New York Times, April 20, 2004.
63. Peter Jaret. Statins' Burst of Benefits. Los Angeles
Times, July 2. 2003.
64. Behind the 'Boomer Coalition,' A Heart Message from
Pfizer, Wall Street Journal, March 10, 2004
65. Paul J. Fallon, personal communication, March, 2004.
66. Uffe Ravnskov, MD, PhD. The Cholesterol Myths.
NewTrends Publishing, 2000, pp 208-210.