Statins, Undoctored, and Me
Statins, Undoctored, and Me
UIC member note 2019-12-08: this thread has 2 pages of comments. Here’s
a link to a reply well down on page 2.
This article was written as a link target,
so that I don’t have to re-state my position on statins
every time I post to a thread on that includes that topic.
For the official Undoctored position, skip down to
Excerpts: Undoctored on Statins
Ad hominem: I have had a physician suggest that I take statin, and declined.
My basic position is that, for people who have embraced the
Undoctored or 2014+ Wheat Belly lifestyle, statins may have some net benefit
in narrow situations, but everyone facing the choice needs to do
their own double-checking of the science, and of the countermeasures
needed to mitigate statin hazards. If I were a middle-aged
male who had just had an MI,
I might consider it. I’m not, and never
have been in that situation. If I had a difficult lipidemia, I’d
give it a hard skeptical look.
For those still on typical (SAD)
or USDA/AMA/AHA official diets,
statins may have net benefit in more scenarios, but my bet is that
most if not all of that benefit vanishes, or even goes negative,
once diet and various nutrient and micronutrient deficiencies are corrected.
Those who have corrected diet, including getting ample Omega 3
DHA&EPA, from supplements or food, need to contemplate what
appears to be a material interference between statins and ω3
Blog post by Dr. Davis, cited 2013
paper; newer 2015 paper).
Where are statins useful?
During 2016, Dr. Peter Attia spoke in several places about
when to consider a statin. If I can find this posted anywhere,
I’ll link to it, but the following is from taking notes during
his segment of the 2016 Fat Summit 2.
The presentation must be: elevated ApoB or LDL Particle Number
(particle size matters too).
He identifies 4 drivers:
- excessive cholesterol synthesis (check desmosterol)
- recycled cholesterol in the gut (he identified a role
for genetics here and a phytosterol test is
used to explore this, but there wasn’t any discussion
about a role for microbiome)
- elevated TG, which may be amenable to dietary
intervention, particularly if IR is present
- defective LDL receptors (and here is where further FH
issues arise, including ApoE, Lp(a) and other SNPs)
His posture is that if an MD is prescribing you a statin, and
they can’t explain the four mechanisms by which apoB is
elevated, they should not be treating it.”.
Plus, typical MDs are
understanding ‘residual risk’
and therefore not knowing how to customize the
Where the situation responds to nutritional and lifestyle
interventions, obviously statins
are not needed. Peter does encounter cases where SFAs need to
be dialed-down, and replaced with MUFAs.
Statins are one pharmaceutical in his tool box, but he points
out that statins interfere with cholesterol synthesis,
cholesterol cannot cross the BBB, so
reducing that synth
in the brain is a long term neurological hazard.
As you might imagine, the percentage of patients that are
run through this protocol, and might benefit from a statin,
is tiny compared to rate at which they are actually prescribed.
But there are some who need to weigh the comparative hazards
of statin side effects vs. consequences of raging untreated
Back to my view
There is precious little non-industry science on all-cause
mortality for statin use. There’s
a particular problem for
trials prior to 2004.
The most prominent non-industry trials
(ALLHAT-LLT, and more recently,
showed no net benefit for statins per se. I have a separate
article on HOPE-3.
ALLHAT had material confounding factors.
Raw data from published industry trials is generally not available
for independent analysis (see the email exchange in this article
about the ABC Catalyst scandal). Then there is the question of
studies left entirely unpublished; what were the results, why they were
left unpublished - not even a paper full of industry spin.
However, even if the industry-funded data is otherwise credible,
it’s all seriously confounded
as well, due to diet.
When researchers do conduct deep dives in the lit., they may come
up with conclusions like:
stimulate atherosclerosis and heart failure: pharmacological mechanisms
In contrast to the current belief that cholesterol reduction with
statins decreases atherosclerosis, we present a perspective that statins
may be causative in coronary artery calcification and can function as
mitochondrial toxins that impair muscle function in the heart and blood
vessels through the depletion of coenzyme Q10 and ‘heme A’, and thereby
ATP generation. Statins inhibit the synthesis of vitamin K2, the
cofactor for matrix Gla-protein activation, which in turn protects
arteries from calcification. Statins inhibit the biosynthesis of
selenium containing proteins, one of which is glutathione peroxidase
serving to suppress peroxidative stress. An impairment of selenoprotein
biosynthesis may be a factor in congestive heart failure, reminiscent
of the dilated cardiomyopathies seen with selenium deficiency. Thus,
the epidemic of heart failure and atherosclerosis that plagues the
modern world may paradoxically be aggravated by the pervasive use
of statin drugs. We propose that current statin treatment
guidelines be critically reevaluated.
Statin skepticism is not unique to the present program:
of statins needed
There is of course no data (outside of what a few rogue doctors
might have in their case files) on all-cause outcomes for statin use
on an enlightened ancestral diet: a whole food, low net carb, grain-free, low-inflammatory,
optimized microbiome lifestyle. We will probably never get formal papers
on that (due to obstructive IRBs),
which leaves everyone on their own.
You are your own case manager.
Do statins drive down certain common lipid lab numbers?
There’s little doubt of that, but:
It’s clear that statins shove around the mythical LDL-C number, but
that apparently does not translate to leverage over all-cause
mortality for unspecified phenotypes. The HOPE-3 trial,
reported in April 2016 showed ~30% reduction in LDL, but only
¼% reduction in mortality (over 7 years).
CETP inhibitors also drive ’LDL-C’ down, and raise HDL, and they
are being abandoned by the drug industry as failures.
Statin evangelists have characterized this outcome as a
“paradox”, but only because they are utterly blind to black swans.
Put another way, these drugs might have benefit, but that benefit
does not amount to a US$30 billion market, which is what it is today.
Statins are being pushed to all and sundry (including children),
based on the scientifically unsupported Lipid Hypothesis.
money is a huge problem.
A lot of it gets kicked back to doctors, both above
and below the table.
A lot of it is used to fund "independent" consultants who champion
the defective dogma at every opportunity.
The money is of course also used to lobby
for wider use of these drugs.
The other, more serious problem with statins is how
they are being pushed. Many of the readers on Undoctored are in
unusual situations, are carefully considering their options,
and monitoring their health using tests that are actually
informative. That’s not the case for most people.
The more usual clinical scenario is that:
- No CAC
scan is run to non-invasively image whether calcified
plaque is actually present (and is perhaps instead actively discouraged).
- No tests are run for familial risk factors, such as
Apo E2 or E4, and perhaps not even Lp(a).
- Advanced lipoprotein testing is not offered
(and is perhaps instead actively discouraged),
and the doctor may even admit to not knowing
how to read such results (mine did).
- Your doctor then orders a routine lipid panel,
perhaps not even done fasting (which can materially
distort the actually useful TG number).
- The almost useless TC and completely useless
come back greater
than some vague threshold of ideal.
- A statin is prescribed. Dosing is not based
on material genetic factors.
- No all-cause outcome data is provided
for someone with your presentation.
- No warnings are given on side effects,
many serious, some irreversible.
- No advice is provided on how to counter
some of those effects.
- No caution is provided on losing the benefits
of intentional Omega 3 DHA&EPA intake.
- If anything is said about diet, it is apt
to be advocacy of the very USDA/AMA/AHA diet
that caused the vascular pathology
(assuming any is actually present).
- Future side effects reported by you are
deprecated or ignored, particularly any not
officially listed for the statin. You may
even be given an antidepressant, which can
aggravate any microbiome contribution to
The above bullet list is the Standard of Care for statins.
I have another description for it: malpractice.
I have no problem with a fully-informed patient electing to take a statin.
The fully informed scenario is exceptionally, depressingly, rare.
Who might be a candidate for statins? For temporary use:
♦ a middle-aged male who has just had a heart attack.
For extended use, when the key metrics don’t respond to
diet, such as in some
forms of familial hypercholesterolemia.
Anyone then choosing to take a statin needs to seriously look
at the known side effects. One of the most vocal statin skeptics,
Dr. Duane Graveline
(spacedoc), died in 2016 from peripheral neuropathy
caused by statins.
Insofar as I have considered the matter, CoQ10 and Vitamin K
supplementation would be the minimum countermeasures.
ConsumerLab has separately reported that statins interfere
with Vitamin D, so monitoring titer is important for
dialing-in daily supplementation.
The statin producers, by the way, are very
far from ignorant about CoQ10.
The whole statin industry may be a huge house of cards, with too much
money and liability at stake for anyone making or pushing these drugs to
dare question the dogma. Tom Naughton’s Older Brother put it this way:
are this generation’s thalidomide.” That may be over-stating the
case, but not by a lot, particularly if statins are in fact being
prescribed to children. And not just children - consider this
proposal to extend statins to expectant mothers.
The future looks equally grim. Official deadly diets have yet to shift.
The Lipid Hypothesis is still at large. Statins are now almost all
off patent (despite gaming of the patent system to extend them, such as
use by children). PCSK9
inhibitors were approved with ZERO outcome data (not
even questionable industry data), based on the dogma (drives
LDL-C lab result down, therefore
must be beneficial). PCSK9i’s are astonishingly expensive,
so the industry and their
professional association lackeys are already lobbying to re-define
FH in order
to dramatically expand the pool of patients that simply must have them,
whether or not they provide net benefit.
Forcing insurance to cover them is expected to
raise everyone’s insurance premiums by US$124 per year.
My view of PCSK9i’s is that they may be beneficial, possibly
in more scenarios than statins, but as Peter at
Hyperlipid put it: “We’ll
have to wait to see the body counts.”
In late 2016, one of the first PCSK9 inhibitors
abandoned. As of 2019, the outcome data is still inconclusive, because the
trials have not had arms on PCSK9i alone. Statins are always used.
More ominously, a PCSK9 inhibitor vaccine is being developed.
Vaccines for infectious diseases are already mandatory in many places.
Ponder that: the principle of mandatory vaccination is in place.
With healthcare costs spinning out of control (growing faster than GDP), it is easy to
predict that the economics will give rise to proposals
to mandate vaccines that purport to contain costs, even if the vaccine
is just countering some of the consequences of the
catastrophic consensus diets (and has horrible effects for people on sane
diets, and that’s entirely aside from whatever issues are inherent to vaccines).
You can stop taking an oral statin. A vaccine may be irreversible.
While I was originally composing this article, this MPT article arrived:
2014 Saw Spike in Healthcare Spending
“Policy needs to be focused on trying to keep heath [sic]
spending from growing faster than it needs to...”, Guterman stated.
Is your CAC score under 100?
There is no case for statin benefit, and that’s according to the JACC,
although they managed to avoid reaching that conclusion. See my
remarks on Statins
and CAC: What is This Paper, Really?
OK, a final look at ALLHAT-LLT
MedPageToday (2017-05-23): Analysis:
No Statin Primary Prevention Seen for Seniors
hoc analysis turns up no benefit at ages 65-74
Seniors don’t get a cardiovascular or mortality
benefit from taking a moderate-dose statin for primary
prevention, according to a post hoc subgroup analysis of ALLHAT-LLT.
In the 65- to 74-year-olds, the mortality rate was
15.5% on pravastatin and 14.2% with usual care (HR 1.08, P=0.55).
For adults 75 years and older, the trend actually neared
significance in the wrong direction (24.5% pravastatin vs
18.5%, HR 1.34, P=0.07).
Open-access full-text at JAMA Network:
of Statin Treatment vs Usual Care on Primary Cardiovascular
Prevention Among Older Adults
For some odd reason, those all-cause outcome numbers in the
MPT article were reported as “no benefit”
instead of as the usual “relative risk”
(RR) numbers. Perhaps this is because, using RR, the MPT headline
would have to have been:
9% or 32% greater chance of dying
for seniors on statins.
The Undoctored Position on Statins
Dr. Davis’ most recent statement (2017-09-18) on statins might be this
one, from the UIC forum (members
can view it here):
“If [person’s initials and list of standard program strategies collapsed]
Given the above, is there any incremental benefit to taking a statin over
and above these strategies? Note that these efforts without statins typically
yield FAR superior values to that achieved with statin alone.
We do not have a large clinical trial conducted over many years to
demonstrate reduction in cardiovascular events. But, judging by our surrogates
for risk, such as small LDL, LDL particle number, hsCRP, coronary calcium score,
etc. this program is magnificently effective as it stands without statins.…”
Kendrick on why we’ll never get objective trials.
Undoctored blog posts on statins
Statin Drug Tragedy
To Get Off Statins
Four Dangers of Stopping a Statin Drug
ways to reduce or eliminate heart disease risk
you should have a CT heart scan
is better than a CT heart scan?
statin drugs slow or stop the increase in heart scan scores?