A 2018
scientific review presents substantial evidence that high LDL and total
cholesterol are not an indication of heart disease risk, and that statin
treatment is of doubtful benefit as a form of primary prevention for
this reason
Three recent
reviews that supported the cholesterol hypothesis were found to have
misrepresented data and findings of previous studies to support their
own conclusions
Overall, the analysis found the association between total cholesterol and CVD is weak, absent or inverse in many studies
Older people
with high LDL do not die prematurely — they actually live the longest,
outliving both those with untreated low LDL and those on statin
treatment
A 2015
meta-analysis of 11 statin drug studies found statin use postponed death
by a mere 3.2 days in primary prevention trials and 4.1 days in
secondary prevention trials
For the past six decades, the U.S.
dietary advice has warned against eating cholesterol-rich foods,
claiming dietary cholesterol promotes arterial plaque formation that
leads to heart disease. We now have overwhelming evidence to the
contrary, yet dogmatic thinking can be persistent, to say the least.
After decades’ worth of research failed to demonstrate a correlation
between dietary cholesterol and heart disease, the 2015-2020 Dietary
Guidelines for Americans1,2
finally addressed this scientific shortcoming, announcing “cholesterol
is not considered a nutrient of concern for overconsumption.”
To this day, the evidence keeps mounting, showing there’s no link
between the two. Similarly, the evidence supporting the use of cholesterol-lowering statin drugs
to lower your risk of heart disease is slim to none, and is likely
little more than the manufactured work of statin makers — at least
that’s the implied conclusion of a scientific review3 published in the Expert Review of Clinical Pharmacology in 2018.
Cholesterol myth kept alive by statin advocates?
The 2018 review4
identified significant flaws in three recent studies “published by
statin advocates” attempting “to validate the current dogma.” The paper
presents substantial evidence that total cholesterol and low-density
lipoprotein (LDL) cholesterol levels are not an indication of heart
disease risk, and that statin treatment is of “doubtful benefit” as a
form of primary prevention for this reason. According to the authors:5
“According to the British-Austrian philosopher Karl Popper, a
theory in the empirical sciences can never be proven, but it can be
shown to be false. If it cannot be falsified, it is not a scientific
hypothesis. In the following, we have followed Popper’s principle to see
whether it is possible to falsify the cholesterol hypothesis.
We have also assessed whether the conclusions from three recent
reviews by its supporters are based on an accurate and comprehensive
review of the research on lipids and cardiovascular disease (CVD) …
Our search for falsifications of the cholesterol hypothesis
confirms that it is unable to satisfy any of the Bradford Hill criteria
for causality and that the conclusions of the authors of the three
reviews are based on misleading statistics, exclusion of unsuccessful
trials and by ignoring numerous contradictory observations.”
As reported by Reason.com:6
“A comprehensive new study on cholesterol, based on results from
more than a million patients, could help upend decades of government
advice about diet, nutrition, health, prevention, and medication …
The study … centers on statins, a class of drugs used to lower
levels of LDL-C, the so-called ‘bad’ cholesterol, in the human body.
According to the study, statins are pointless for most people …
The study also reports that ‘heart attack patients were shown to
have lower than normal cholesterol levels of LDL-C’ and that older
people with higher levels of bad cholesterol tend to live longer than
those with lower levels.”
No evidence cholesterol influences heart disease risk
Indeed, the authors of the Expert Review of Clinical Pharmacology
analysis point out that were high total cholesterol in fact a major
cause of atherosclerosis, “there should be exposure-response in
cholesterol-lowering drug trials.”7
In other words, patients whose total cholesterol is lowered the most
should also see the greatest benefit. Alas, that’s not the case.
A review of 16 relevant cholesterol-lowering trials (studies in
which exposure-response was actually calculated), showed this kind of
exposure-response was not detected in 15 of them. What’s more, the
researchers point out that the only study8 showing a positive exposure-response to lowered cholesterol used exercise-only as the treatment.
Patients with high total cholesterol should also be at increased
risk of death from CVD, but the researchers found no evidence of this
either, not-so-subtly pointing out that this is “an idea supported by
fraudulent reviews of the literature.” They provide the following
example of how research has been misrepresented:9
“The hypothesis that high TC [total cholesterol] causes CVD was
introduced in the 1960s by the authors of the Framingham Heart Study.
However, in their 30-year follow-up study published in 1987, the
authors reported that ‘For each 1 mg/dl drop in TC per year, there was
an eleven percent increase in coronary and total mortality’.
Three years later, the American Heart Association and the U.S.
National Heart, Lung and Blood Institute published a joint summary
concluding, ‘a one percent reduction in an individual’s TC results in
an approximate two percent reduction in CHD risk’. The authors
fraudulently referred to the Framingham publication to support this
widely quoted false conclusion.”
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Contradictory findings routinely ignored or misrepresented
To determine whether the three reviews under analysis had
misrepresented previous findings, they scoured the three papers for
quotations from 12 studies reporting results “discordant with the
cholesterol hypothesis.” Only one of the three reviews had quoted
articles correctly, and even then, only two of the dozen studies were
quoted correctly.10
“About half of the contradictory articles were ignored. In the
rest, statistically nonsignificant findings in favor of the cholesterol
hypothesis were inflated, and unsupportive results were quoted as if
they were supportive. Only one of the six randomized
cholesterol-lowering trials with a negative outcome was cited and only
in one of the reviews.”
The researchers also highlight a large meta-analysis that simply
ignored “at least a dozen studies” in which no or inverse association
was shown. Overall, the Expert Review of Clinical Pharmacology analysis
found that “the association between total cholesterol and CVD is weak,
absent or inverse in many studies.”
No link between LDL and heart disease either
The Expert Review of Clinical Pharmacology paper11
also tears apart claims that high LDL causes atherosclerosis and/or
CVD. Just as with total cholesterol, if high LDL was in fact
responsible for atherosclerosis, then patients with high LDL would be
diagnosed with atherosclerosis more frequently, yet they’re not, and
those with the highest levels would have the greatest severity of
atherosclerosis, yet they don’t.
The researchers cite studies showing “no association” between LDL
and coronary calcification or degree of atherosclerosis. Ditto for LDL
and CVD. In fact, a study looking at nearly 140,000 patients with acute
myocardial infarction found them to have lower than normal LDL at the time of admission.
Even more telling, another study, which had originally reported
similar findings, still went ahead and lowered the patients’ LDL even
more. At follow-up three years later, they discovered that patients
with an LDL level below 105 mg/dl (2 mmol/L) had double the mortality
rate of those with higher LDL.12
Interestingly, the authors suggest this inverse relationship may be
due to low LDL increasing your risk for infectious diseases and cancer,
both of which are common killers.
They also review evidence showing older people with high LDL do not
die prematurely — they actually live the longest, outliving both those
with untreated low LDL and those on statin treatment. One such study13,14 — a meta-analysis of 19 studies — found 92% of individuals with high cholesterol lived longer.
Benefits of statin treatment are overblown
Lastly, the Expert Review of Clinical Pharmacology paper analyzes
statin claims, showing how studies exaggerate benefits through a
variety of different tactics. Again, in some cases, by simply excluding
unsuccessful trials.
“Furthermore, the most important outcome — an increase of life
expectancy — has never been mentioned in any cholesterol-lowering
trial, but as calculated recently by Kristensen et al.,15 statin treatment does not prolong lifespan by more than an average of a few days,” the authors state.16
Indeed, the study they’re referring to, published in BMJ Open in
2015, which looked at 11 studies with a follow-up between two and 6.1
years, found “Death was postponed between -5 and 19 days in primary
prevention trials and between -10 and 27 days in secondary prevention
trials.” The median postponement of death in primary prevention trials
was 3.2 days, and in secondary prevention trials 4.1 days!
Considering the well-documented health risks associated with
statins, this is a mind-bending finding that really should upend the
dogma. And yet, the dogma remains, and may even strengthen in coming
days.
JAMA editorial calls for end to ‘fake news’ about statins
The cholesterol myth
has been a boon to the pharmaceutical industry, as
cholesterol-lowering statins — often prescribed as a primary prevention
against heart attack and stroke — have become one of the most
frequently used drugs on the market. In 2012-2013, 27.8% of American
adults over the age of 40 reported using a statin, up from 17.9% a
decade earlier.17,18 But that was six years ago, I suspect over a third of adults over the age of 40 are now using statins.
In addition to the BMJ Open study cited above, an evidence report19
by the U.S. Preventive Services Task Force, published November 2016 in
JAMA, found 250 people need to take a statin for one to six years to
prevent a single death from any cause; 233 had to take a statin for two
to six years to prevent a single cardiovascular death specifically. To
prevent a single cardiovascular event in people younger than 70, 94
individuals would have to take a statin.
As noted in a 2015 report,20
“statistical deception created the appearance that statins are safe and
effective in primary and secondary prevention of cardiovascular
disease.” The paper points out that by using a statistical tool known
as relative risk reduction, the trivial benefits of statins appear
greatly amplified.
Scientific findings such as these are the core reason why statins
are given negative press. However, we may soon see a reversal in the
news cycle, with negative statin articles being tagged as “fake news.”
According to a June 2019 editorial21 in JAMA Cardiology, written by cardiologist Ann Marie Navar,22
statins are the victim of “fear-based medical information,” just like
vaccines, and this is what’s driving patient nonadherence.
Cardiovascular Business reported:23
“We know that what people read influences their actions, Navar
said, and indeed, one 2016 study in the European Heart Journal found
that on a population level, statin discontinuation increased after
negative news stories about statins surfaced in those communities.
In another study, more than one in three heart patients said
they declined a statin prescription solely for fears of adverse
effects. ‘Measles outbreaks are highly visible: a rash appears, public
health agencies respond, headlines are made and the medical community
responds vocally,’ Navar wrote.
‘In contrast, when a patient who has refused a statin because of
concerns stoked by false information has an MI, the result is less
visible. Nevertheless, cardiologists and primary care physicians observe
the smoldering outbreak of statin refusal daily.’”
Cardiovascular Business summarizes Navar’s suggestions for how
doctors can fight back against false information about statins and
build adherence, such as handing out yearlong prescriptions with
automatic refills.24
When I first wrote about the censorship of anti-vaccine material
occurring on every single online platform, I warned that this censorship
would not stop at vaccines. And here we’re already seeing the call for
censoring anti-statin information by glibly labeling it all “fake
news.”
Chances are, the censoring of anti-statin information is already
underway. A quick Google search for “statin side effects” garnered pages
worth of links talking about minor risks, the benefits of statins,
comparison articles, looking at two different brands — in other words,
mostly positive news.
The scientific fact is, aside from being a “waste of time” and not
doing anything to reduce mortality, statins also come with a long list
of potential side effects and clinical challenges, including:
Nutrient depletions — Including CoQ10 and vitamin K2, both of which are important for cardiovascular and heart health
Impaired fertility — Importantly, statins are a Category X medication,26 meaning they cause serious birth defects,27 so they should never be used by a pregnant woman or women planning a pregnancy
Increased risk of cancer — Long-term statin
use (10 years or longer) more than doubles women's risk of two major
types of breast cancer: invasive ductal carcinoma and invasive
lobular carcinoma28
Nerve damage — Research has shown statin
treatment lasting longer than two years causes “definite damage to
peripheral nerves”29
How to assess your heart disease risk
As a general rule, cholesterol-lowering drugs are not required or
prudent for the majority of people — especially if both high
cholesterol and longevity run in your family. Remember, the evidence
overwhelmingly suggests your overall cholesterol level has little to
nothing to do with your risk for heart disease.
For more information about cholesterol and what the different levels
mean, take a look at the infographic above. You can also learn more
about the benefits of cholesterol, and why you don’t want your level to
be too low, in “Cholesterol Plays Key Role in Cell Signaling.” As for evaluating your heart disease risk, the following tests will provide you with a more accurate picture of your risk:
HDL/Cholesterol ratio — HDL
percentage is a very potent heart disease risk factor. Just divide your
HDL level by your total cholesterol. That percentage should ideally
be above 24%.
Triglyceride/HDL ratio — You can also do the same thing with your triglycerides and HDL ratio. That percentage should be below 2.
NMR LipoProfile —
Large LDL particles do not appear to be harmful. Only small dense
LDL particles can potentially be a problem, as they can squeeze
through the lining of your arteries. If they oxidize, they can cause
damage and inflammation.
Some groups, such as the National Lipid Association, are now
starting to shift the focus toward LDL particle number instead of
total and LDL cholesterol to better assess your heart disease risk.
Once you know your particle size numbers, you and your doctor can
develop a more customized program to help manage your risk.
Your fasting insulin level — Heart disease is primarily rooted in insulin resistance,30 which is the result of a high-sugar diet. Sugar, not cholesterol or saturated fat, is the primary driver. Clinical trials have shown high fructose corn syrup can trigger risk factors for cardiovascular disease within as little as two weeks.31
Any meal or snack high in carbohydrates like fructose and refined
grains generates a rapid rise in blood glucose and then insulin to
compensate for the rise in blood sugar.
The insulin released from eating too many carbs promotes fat
accumulation and makes it more difficult for your body to shed excess
weight. Excess fat, particularly around your belly, is one of the
major contributors to heart disease.
Your fasting blood sugar level —
Research has shown people with a fasting blood sugar level of 100 to
125 mg/dl have a nearly 300% increased higher risk of coronary heart
disease than people with a level below 79 mg/dl.32,33
Your iron level — Iron can be a
very potent oxidative stress, so if you have excess iron levels you
can damage your blood vessels and increase your risk of heart
disease. Ideally, you should monitor your ferritin levels and make
sure they are not much above 80 ng/ml.
The simplest way to lower them if they are elevated is to donate
your blood. If that is not possible you can have a therapeutic
phlebotomy and that will effectively eliminate the excess iron from
your body.
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