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Member Forum >> Heart Health Forum >> Statins, Undoctored, and Me
 Statins, Undoctored, and Me
Bob Niland

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Posted: 12/4/2015 10:37:29 AM
Edited: 7/3/2017 11:03:10 AM (32)
 
Statins, Undoctored, and Me

Statins, Undoctored, and Me

Edition: 2017-07-02

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 and Cureality 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, Cureality or 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 benefits (2013 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:

  1. excessive cholesterol synthesis (check desmosterol)
  2. 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)
  3. elevated TG, which may be amenable to dietary intervention, particularly if IR is present
  4. 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
If they can’t explain the four mechanisms by which apoB is elevated, they should not be treating it.”.
Plus, typical MDs are
…not understanding ‘residual risk’ and therefore not knowing how to customize the LDL-P target.

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 hyperlipidemia.

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, HOPE-3) 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:
ERCP: Statins 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.

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 a low net carb, grain-free low-inflammatory, ancestral nutrient, optimized microbiome lifestyle. We will probably never get formal papers on that, 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:

  • Are the two main numbers (LDL-C & TC) actually meaningful?
  • Does driving these numbers down actually extend lifespan by more than a few days, for someone with your presentation?
  • Was the patient tested for genetic factors that mediate statin effect, such as CYP450 or SLCO1B1 c.521CC variant genotype, before dosing?
  • Are the side effects worth it?
  • Was the patient even advised about the side effects?
  • Was the patient counseled on how to avoid some of them?
  • If the patient is female, was it pointed out that there is no data supporting net benefit for statin use?

It’s clear that statins drive down 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. The 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 Cureality are in unusual situations, are carefully considering their options, supplementing intelligently, 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.
  • 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 largely useless LDL-C 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 adverse lipids.

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, the following cases might look into it:
♦ elevated Lp(a),
♦ ApoE2 and E4 carriers,
♦ other 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), recently died 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: “Statins 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 have just been 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.
(Update: in late 2016, one of the first PCSK9 inhibitors was abandoned.)

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:
CMS: 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.

OK, a final look at ALLHAT-LLT

MedPageToday (2017-05-23): Analysis: No Statin Primary Prevention Seen for Seniors
 Post 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:
Effect 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 & Cureality Position on Statins

Dr. Davis’ most recent statement (2017-03-12) on statins might be this one, from the UIC forum:
“I now view statins as drugs of last resort when nothing else remains to reduce the atherogenicity of an abnormal lipoprotein profile.”

Here’s a remark by Dr. Davis on his personal statin experience:
Soon after Mevacor, the first statin cholesterol drug, was approved by the FDA and released, I took it. Within 72 hours, I became acutely ill, thought I was going to die and couldn’t get out of bed for 48 hours. Likewise, simvastatin, Lipitor, and Crestor made me sore all over, made me think I had aged 30 years overnight. Needless to say, I stopped playing with them both personally and, over time, learned how to help patients control the situation with almost no reliance on this deeply flawed group of drugs.

Cureality Program Guide on Statins

Page numbers are the printed page number. Add 10 for PDF page number.

Page 10: The Cureality nutrition principles maximize the health benefits of diet, minimizing, often eliminating, the need for treatments including statin drugs, drugs for hypertension, acid reflux, and arthritis, and helps you achieve other health goals, including reduction in waist size and weight loss, often dramatic.

Page 79: The conventional response to high LDL particle number or Apo B are statin cholesterol drugs. But there are plenty of other strategies to consider before resorting to these drugs:
… Red yeast rice: The statin-like monacolins in red yeast rice reduce LDL particle number … However, note that, like prescription statin drugs, there is still potential for muscle aches and muscle damage with red yeast rice, though less commonly than with the drugs.

Page 82: The presence of IDL and remnant lipoproteins can predict progression of carotid and coronary plaque, even when treatment is administered, e.g., statin drug (Hodis 1997; Krauss 1987).

Page 83 (as last remark on options for VLDL & TG): Niacin, as well as prescription agents like statin drugs and fibrates (gemfibrozil, fenofibrate) also reduce triglycerides.

Page 85: The conventional solution to increased CRP is to take a statin cholesterol drug, a solution that we do not endorse in Cureality.

Wheat Belly (Blog) on Statins (&LDL-C)

“Treat” cholesterol, exorcise the bogeyman (2016-08-22)

Statin scare (2016-05-23)

Statin cholesterol drugs are for bread-eaters (2016-02-20)

Leprechauns, nymphs, high cholesterol, and other fanciful notions (2015-09-17)

Cureality Health Tracks on Statins

  • Cureality Diet Basics:
    The Cureality nutrition principles maximize the health benefits of diet, minimizing, often eliminating, the need for treatments including statin drugs, drugs for hypertension, acid reflux, and arthritis, and helps you achieve other health goals, including reduction in waist size and weight loss, often dramatic.
  • Heart Health Basics:
    (”statin” not found)
  • LDL Particles:
    The conventional response to high LDL particle number or Apo B are statin cholesterol drugs. But there are plenty of other strategies to consider before resorting to these drugs:
  • HDL Particles:
    (”statin” not found)
  • IDL VLDL, Triglycerides:
    The presence of IDL and remnant lipoproteins can predict progression of carotid and coronary plaque, even when treatment is administered, e.g., statin drug. …
    Then, as the last suggestion for VLDL & TG, and not exactly an endorsement:
    Niacin, as well as prescription agents like statin drugs and fibrates (gemfibrozil, fenofibrate) also reduce triglycerides.
  • Advanced Topics:
    The conventional solution to increased CRP is to take a statin cholesterol drug, a solution that we do not endorse in Cureality.

This older TYP document (2011) discusses statins for Apo E2 & E4:
A Track Your Plaque practical guide to Apoprotein E

This even older Heart Scan Blog article (2011) has more detail on the potential situations in which statins might be useful:
When MIGHT statins be helpful?

__________
Bob Niland [disclosures] [topics]

Tags: ,fish oil,Omega 3,Statins




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Bob, could not have said it better.  Good job.




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Posted: 5/24/2016 10:44:18 AM
 
APO3/3 Pthuet. 
Nevertheless, i am not at this point willing to go off statins. If they reduce inflammation, i'd rather be on them.
I need to ask Dr about oxLDL test, considering my high MPO issue, at next visit in July


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Posted: 5/24/2016 8:24:56 PM
 
statins do not reduce inflammation.  PERIOD.  oxLDL and MPO is "hocus pokus".  

statins induce CoQ10 issues which are far worst than the perceived "inflammation" issues.  

time for a beer 




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Posted: 5/25/2016 6:48:16 AM
 
Just an FYI, Crestor has just been approved as a generic in the US, manufactured by Watson Pharmaceuticals. So I'm guessing whatever advertising Eli Lilly is doing is about to end.


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Posted: 5/25/2016 10:19:56 AM
 
Crestor is owned by a Japanese company




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Posted: 5/25/2016 12:38:36 PM
 
Astra zeneca, my bad, i think i was thinking about Effient when i mentioned Eli Lilly


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Posted: 5/25/2016 9:25:10 PM
 
Abigall:  your Lp(a) is reduced or drops when you take Vitamin C.  




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Posted: 5/26/2016 1:48:36 PM
 
Pat 
thanks for explanation that E4 , s clear fat soluable vitamins at twice rate E2 and E 3 with priority of getting K.Coq10 , C , D and a levels correct - will check out 


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Posted: 4/21/2017 6:11:51 AM
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Posted: 5/22/2017 7:05:53 AM
 
But isn't it the soft plaque that is the real danger? While the calcified plaque is stable and poses much less risk? Meaning statins can prevent heart attacks in people with heart disease, if those results are correct.




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Posted: 5/23/2017 9:28:05 AM
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Posted: 5/24/2017 12:16:22 AM
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Posted: 7/3/2017 9:54:06 AM
 
Steve:  yup, more CAD and T2D




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Posted: 7/14/2017 7:15:24 AM
 
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Posted: 7/17/2017 1:04:47 PM
 
Hypostases?

Is that hypothesis with a lisp?


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