Wednesday, March 20, 2013

Sta'ins, CoQ, diabetes and Dr Andreas Eenfeldt's link

I'm not very conscientious about reading many blogs as I don't really have time to look after my own blog properly, but I will occasionally flick through the links from Stan's site and I felt that Dr Andreas Eenfeldt's link to the official Swedish data sheet for simvastatin was rather excellent. Via Google translation:

"Diabetes is a possible side effect. This is more likely if you have high blood sugar and high blood fat levels, are overweight and have high blood pressure. Your doctor will monitor you while you are taking this medicine."

Statins deplete CoQ. This means that for every electron carried from any input, NADH or FADH2, down the ETC there will be less CoQ available in the redox couple and the CoQH2 levels will be relatively high. An highly reduced CoQ couple (ie low CoQ per unit CoQH2) will drive reverse electron flow through complex I and generate superoxide. Insulin resistance. Diabetes.

I suspect that EVERYONE on a statin will step their insulin resistance up by an amount proportional to the CoQ depletion. Everyone. Just a few will cross the arbitrary boundaries between "normality", "impaired glucose tolerance" and "diabetes".

Hyperglycaemia doesn't care about labels or boundaries. You get it, you suffer.

Obviously this rather nasty side effect can be COMPLETELY avoided by putting the statin script in the bin.

If you are going to take simvastatin anyway then some coenzyme Q10 might ameliorate some of the damage you have chosen to do to yourself.

Peter

21 comments:

Tyler said...

I can't help but read "An highly" with a cockney accent.

An 'ighly reduced what, now?

blackdog said...

Perfect analysis, and so succint.

Manythings said...

I think "Stains" in the title should probably read "Statins" (it's a good name for them, though).

Chris Tunstall said...

Sta'ins. Cockney.

ItsTheWooo said...

Smart doctors that care put their patients on coq10 with statins.

With that said, I see this occurring about 10% of the time a patient is prescribed a statin.

Sounds about right.

Roger Cauvin said...

Do we have any evidence confirming that supplementation compensates at all for the depletion caused by stains?

Peter said...

Apostrophe added, excellent typo!

Peter

Jane said...

You know why people take statins? Because their doctors have no idea that statins do what magnesium should be doing.

'Since Mg(2+)-ATP is the controlling factor for the rate-limiting enzyme in the cholesterol biosynthesis sequence that is targeted by the statin pharmaceutical drugs, comparison of the effects of Mg(2+) on lipoproteins with those of the statin drugs is warranted. ...The rate-limiting reaction of this pathway is the enzymatic conversion of HMG CoA to mevalonate via HMG CoA reductase. The statins and Mg inhibit that enzyme. ...statins lower [LDL-C] blood levels ...They also reduce the incidence of heart attacks, angina and other nonfatal cardiac events, as well as cardiac, stroke, and total mortality. These effects of statins derive less from their lowering of LDL-C than from their reduction of mevalonate formation which improves endothelial function, inhibits proliferation and migration of vascular smooth muscle cells and macrophages, promotes plaque stabilization and regression, and reduces inflammation. Mg has effects that parallel those of statins. ..'
http://www.ncbi.nlm.nih.gov/pubmed/15466951

Nigel Kinbrum said...

Would anybody like to comment on the following paragraph from Why cells go bad: a new appreciation and understanding of ATP opens up an untapped avenue for fighting diabetes, cancer, aging, etc.
"The structure of ubiquinone resembles that of vitamins K and E, so it’s conceivable that in the absence of ubiquinone, vitamins K and E could stand in its place."

Purposelessness said...

Nigel, Wooo or Peter would have to give me IV ondensatron to enable me finishing the blogpost you linked.

The second source he cites talks about intranasal insulin and cognition, which he uses to say that sugar and insulin makes us smart, and suggests that ketosis makes us dumb. I'm very sorry, but I can't read stuff like that. There are arguments to be made against ketosis, for sure, but come on..

Regarding vitamin k and e, I seem to remember a recent paper that suggested that vitamin k can act as an electron carrier, but I can't find the paper I am thinking of at the moment. I also remember from microbiology II that some of the more obscure bacteria use vitamin k1 and all sorts of stuff as electron carriers. No idea what the practical implication is, if there is one at all.

Nigel Kinbrum said...

Andrew Kim is rather pro-carbohydrate, lol! I read the blogs of people that I don't agree with as there is useful information in them.

donny said...

That's an interesting blog Nigel. You'd think if you wanted to decrease lactic acid metabolism, a fairly low carb diet would make sense, though...


The idea of interchangeable antioxidants bugs me. Sort of like the acid/alkaline thing--vitamin e, c, etc, just like magnesium, sodium, etc. don't just have "class" attributes, they have very specific functions in the body as well. It seems as logical to suppose that vitamin e and k, if they were similar enough to Q10 (but not identical) might exacerbate a CoQ10 deficiency.

IcedCoffee said...

I'll second donny. Even minute changes in chemical structure effect huge changes in function. Absent some actual indication they are interchangeable, I wouldn't even consider it.

john said...

Andrew Kim basically pulls Ray Peat arguments from his articles, books, interviews and spits them out into his own blog posts...same as that Cliff guy...same as Danny Roddy. Apparently Andrew isn't as worried about iodine supplementation as Peat though.

Agreeing with a person is fine, but to me it's silly to have a blog entirely composed of someone else's work--or sell a book that summarizes it.

Robert Andrew Brown said...

Purposelessness is likely right in suggesting there is a paper looking at Vit K having some capacity to act as an electron transporter - I too remember reading such a paper.

karl said...

@Jane

I don't think Stalins work via Cholesterol levels - low LDL is probably just a side effect. They do block LOX-1 which is probably how they do their good stuff - but the question is if the trade offs are worth it.

LOX-1 is the receptor that takes oxLDL ( not LDL) into the macrophages in the artery walls. There are many ways to lower oxLDL instead - they lack patent protection for the most part, so not a lot of money will go that way for research.

Jane said...

Hi Karl
That's interesting. I just looked up LOX-1 and it's in membrane rafts, which are high in cholesterol, meaning that statins would inhibit it by lowering cholesterol.

It seems statins also lower ROS, and increase nitric oxide by upregulating eNOS.

'By inhibiting l-mevalonic acid synthesis, statins also prevent the synthesis of other isoprenoid intermediates of the cholesterol biosynthetic pathway such as geranylgeranylpyrophosphate (GGPP). These intermediates serve as important lipid attachments for the post-translational modification of a variety of proteins, including small GTP-binding proteins. Because Rho proteins are major targets of geranylgeranylation, their inhibition is a likely mechanism mediating some of the pleiotropic effects of statins [1]. Rho family members play an important role in the organization of the actin cytoskeleton and cell signaling. In endothelial cells, inhibition of RhoA leads to upregulation of eNOS via prolongation of its mRNA stability [1]. In vascular smooth muscle cells as well as in cardiac myocytes, statin treatment inhibits the activity of Rho family member Rac1 GTPase. An important function of Rac1 is the regulation of the NADPH oxidase, the major source of reactive oxygen species (ROS) production both in the vessel wall and in the myocardium [10]. ROS not only participate in ischemia–reperfusion induced injury but may be important mediators of cardiac hypertrophy and the development of contractile dysfunction. Indeed, in patients with chronic heart failure, increased oxidative stress is associated with reduced left ventricular function and correlates with the severity of the disease. Inhibition of Rac1 by statins has been shown to decrease NADPH oxidase-related ROS production in vascular smooth muscle cells and cardiac myocytes.'
http://cardiovascres.oxfordjournals.org/content/66/3/427.full

karl said...

@Jane said...

..."meaning that statins would inhibit it by lowering cholesterol."

I don't think that is true.

If you dig through the literature, I don't think you will find any evidence that can show that oxLDL is held constant, that LDL is a risk factor by itself.

Jane said...

Sorry Karl, I didn't explain myself properly. The point about LOX-1 is that it's located in membrane rafts, which are enriched in cholesterol. Enzymes located in rafts can be inactivated by dispersing or decreasing the cholesterol. I didn't mean to say anything about cholesterol in the blood.

'Cholesterol-lowering drugs inhibit LOX-1 receptor function by membrane raft disruption'
http://www.atgcchecker.com/pubmed/22570368

JoAnn Lennon said...

Great Post..

George Henderson said...

@ Nigel, vit K does act as co-Q supporter in some bacteria, but this has not been found in mammals. PQQ and maybe fulvic acids do seem to support CoQ in mammals, that is to say they can probably catch and pass on electrons to CoQ like extra fielders.
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2212345/

@ Roger Cauvin, none of the case studies of serious reactions to statins on David Evans' website
http://healthydietsandscience.blogspot.co.nz/
have mentioned the use of Co-Q10 so far as I know. So there is negative evidence that it's protective to some extent.

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2042680/

Lipid-lowering drugs and mitochondrial function: effects of HMG-CoA reductase inhibitors on serum ubiquinone and blood lactate/pyruvate ratio