"How Statins Kill You One Cell at a Time"

None of your cites seem to mention anything about 'widow makers', by which I assume you mean the 50% of heart attacks that are 'sudden death'. I suspect the acute cause is a clot, mostly prevented with aspirin, but I don't recall ever reading about decreases in 'widow makers' in any study. More data mining may show that.

Your cites all look like sub sets of patients, probably data mined from the usual "statins = good for some patients so we all ought to be taking them" studies. Yet NNT is 1,000. And since my concern is that I am only ONE, the chances of me gaining anydamnthing from statins are a thousand to one against me. But the medicos HAVE to treat based on those population studies. Why, they have 300 million patients, which means they will 'save' 300,000 lives this year! But the death rate is still ONE, and those 300.000,000 will average a few hours longer lives for all of that.

The big picture as see it is that to treat those 1,000 patients to postpone (not prevent) one death from this year to next year, costs about $50,000 dollars. So using those big numbers, the average stain patient will live 1/1000 year longer, per year of treatment. Or, 20 year of treatment = about one week each. That is the basis for treating large numbers. Now, take a drop of my blood for some testing, (genetic?) and tell me that I am that one guy in 1000, and I'll take the damn drug.

I had dinner last month with 5 gray haired men. All five of us sitting at the table had had statin myopathy. Other readings mention cardiac care clinics where 50% of the doctors' time is spent treating statin side effects. Yet the drug companies claim 'myopathy is rare' and as a for instance, the 4S study had 18,000 patients to begin, and 500 left at five years. 95% drop out rate, how can they claim 'rare' side effects? How can they claim anything? Voodoo math.

In America, we spend $8,000 per year average for health care. We live 76 years, that s $600.000 per person over their lives. We live 10 years longer than we did in 1960. Those ten years cost us $60,000 each. Can we afford that, on an average income of $15,000? (man, woman, child, retiree?) Looks to me like the QALY of our total health car is $60,000. But you want us to spend $50,000 for statins alone? And BP treatment is $40,000 QALY, Guardasil vaccine is $47,000, pretty soon we have to ration, just to afford antibiotics, with a QALY of $12.
 
1) Perhaps I should back-up and define what a "widow maker" is?

It is a plaque rupture in one of the main coronaries, typically the left anterior descending. This presents with a sudden, massive chest pain, ST segment elevation, and usually rapid demise unless this can be averted quickly in the cath lab or by emergency surgery.

Now, I freely admit - and have not changed my position in the past few posts - that there is no direct study that has looked at the rate of this with any specific variable. In the 20+ years I've been involved in the medical field, the past 11 of which as a physician/physician in training, I can tell you - again anecdotally - that the number of these "Tim Russert" type of MI's we are seeing has all but disappeared. Do we still see them? Yes. But, nowhere near the frequency up to the late 80's and early 90's, which was the time I began to get involved in medicine.

The only three major contributing population variables that have significantly changed in that timeframe are (1) people aren't smoking as much as they used to, (2) the widespread use of statins and other cholesterol lowering agents, and (3) more widespread and readily available cardiac catheterization, both diagnostic and interventional, when there is a suspected problem.

However, obesity and type 2 diabetes are on the rise, and we are seeing a greater number of the so-called ACS or subendocardial MI's (non-STEMI) than we did before too. The belief, again backed-up by understanding physiology and pathology, is that microcirculation is being affected in the latter disease category whereas major vessel disease, while maybe not gone, is being ameliorated in no small part due to statins helping to stabilize and reduce plaque burden in larger caliber vessels. This is hard to prove directly because, as I've mentioned to you before, there are so many variables.

Many people want to apply population statistics to some meaningful prediction about what's going to happen to them. I think that this is the most frustrating complaint people have with physicians and medical science. I often describe to my patients that echo similar concerns to me that performing clinical studies is often like trying to redraw the Mona Lisa with crayons. You'll often get an image of what's really happening and be able to tell some details, but it won't be perfect representation. And, no physician worth his salt would ever tell you that he/she can predict exactly what's going to happen in any given patient with any given therapy. Diseases are multi-factorial, and the best strategy is to attack them on many different fronts.

2) Statin side effects

Yes, some people get myalgias. Your point to "five gray-haired dudes" sitting around kibitzing about their cramps is a statistical hotspot in my mind. Of the multitude of patients I see on a daily basis for various reasons, many of whom are on statins, I will occasionally see someone who had a statin-related myalgia. I will ask about whether or not they tried a different statin, and some will say, yes, and the myalgia returned. That is a legitimate side-effect. Some people it is not.

We have to look at dose and population statistics. There is some benefit to low-dose statins, with lower attributed side effects, in significantly lowering cholesterol in some people who don't need a higher dose. This goes to your point about individualization of therapy and my point about crayons and the Mona Lisa. Too often studies look at one dose, and try to draw specific conclusions across that population. What is paramount is what happens with the effect of that drug in a particular patient that is being monitored. Again, a good clinician will use the data to guide the treatment, not dictate it. What I mean is that a medication has a particular physiologic cause that a blunt study tries to elucidate. If 40 mg of a particular statin shows a specific population benefit in a study, perhaps 10 mg in a particular patient will significantly lower the cholesterol without the side effects. Many doctors, unfortunately, follow clinical trials like the bible (for many reasons) and are unwilling to individualize therapy. Yes, this is a real problem as well.

So, Casebro, I get what you are saying and I don't completely disagree with you. But, it appears to me that you are too willing to throw the baby out with the bathwater. I, too, get frustrated that studies are not better at elucidating actual cause-effect relationships. But, they are blunt tools that can't prove everything... which is what I've been saying all along. It is the kernel and underlying truth about what the medication does, directly or indirectly, that is important. Statins, in this case, clearly lower cholesterol and there is enough evidence that this has benefit. What we need more of is common sense application of that technology in individuals, and not just rote prescribing based upon what this-or-that studies supposedly mandates for us to do. No disagreement there. But, "individualization" is a scary word for a lot of doctors who've fully invested themselves in the "evidence-base" movement.

~Dr. Imago
 
My reading gives me doubts that there is any cholesterol connection, or whether it is something else the statins do. Yes, statns lower lipids. Yes, statins lower CAD rate. But commonality is not causality. Some points:

1) In combined therapy studies with aspirin, we could give statins a score of 80. Aspirin would get a score of 60. Yet combined, the total is only 100. Therefor, about 50% of what statins do, is done exactly by aspirin. No lipid connection to aspirin, is there?

2) the mono-un/poly-un/saturated fat comparisons don't make any sense/ Typical fat chains are abotu 20 molecules long. In Saturated fats, they are all 'filled' with hydrogen (? carbon?). In Mono-unsatruated, 19 0f 20 are 'saturated, and in Poly-un-saturated fats, 18 0f 20 are saturated. So why is 19 0f 20 better than 18 of 20, when they each have at least 18? If one 'un' is better, why isn't two? Plus, any study iof a partcular fat shows it to be OK. And the highest source of mono-un-saturated fat in our diets is LARD, but that is a no-no.

3) I went to coconut oil, which is totally saturated. My lipid panel was excellent- when I went to low carb- and lost weight.

4) My HDL came up from 30 to 50, when I started supplementing with vitamin K2, for it's calcium balancing action.

5) Calcium plays a HUGE role in plaque.

6) K2 is made in the intestines by e-coli.

7) Goose liver and fat is the highest source of dietary K2. Lowest CAD rate is where they eat the most goose grease, southern France, where all the Foi Gras is raised. Solves the Mediterranean Paradox, on which the mono-un theory is based? I guess Salmonella also makes K2. Chicken livers are a good source, but the lipid theory tells us to stay away from organ meats.

8) Perhaps the critical activity of statins has to do with digestive activity re: e-coli? Cholesterol being a 'detergent', the lowered production brought about by statins would have some effect on digestive content balance? Maybe aspirin does too- aspirin fer sure does something to stomachs.

Remind me to look for <"k2 level" statins> and <"K2 level" aspirin>, maybe the proof already exists?

(eta this one para: My wheat allergy gives me angina. No new angioplasties in 6 years since quitting wheat. Wheat senstivity causes poor absorption- of K2? )

Anyway, I have CAD, and calcified valves and arteries, and a myopathy as well . Oh, seems calcium probs could be the cause of myopathies too. Anyhow, in my position, I HAVE TO bet my live that cholesterol is not the key, but so far calcium is the horse I'm riding. And I'm leading the pack.
 
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I'm not familiar with "K2", which you've been talking a lot about in this and other recent posts.

Vitamin K, which is a fat-soluble vitamin produced, in part, by bacterial flora in the intestine and also found in green leafy vegetables, is a necessary co-factor in the production of the Vitamin K-dependent factors in the clotting cascade. These are produced in the liver, and are necessary for proper clotting.

Vitamin K supplementation, wherever the source, is dangerous in patients who are on warfarin for chronic atrial fibrillation or deep venous thrombosis as it acts as a "pro-coagulant" reversing the effects, in part or in whole, of the medication.

~Dr. Imago
 
No. K2 is made from the leafy-green K1 by the biota in the intestines.

No, excess of k2 does not clot up blood- no downside for warfarin patients.

The RDA for K is based on minimum for clotting.

The K2- calcium connection has only recently been learned. The Japanese are using 40 mg/day to treat osteoporosis- oops, I didn't mention that Ostioporosis is a major risk factor on CAD? Huge. 40mg/day = 40,000% of rda

The discovery was made by the Rotterdam Study, similar to our Framignham Study. Resluts were published only this year? It has been reinforced by others. More studies have been funded- prospective? see if CAD is prevented by addition of K2? At least ne is open/recruitng now, check the nih site that lists studies? But it will be a couple years before we hear results. Mean time, I'm going for it.
 
Looking at the populations studies angle of any type of health care brings up another notion- Avg lifespan af all of us- 76. Avg life span of heart attack victims, 76. An absolute cure of heart disease will not add anything to our lifespan- on a population study basis. ( maybe months? I dunno, we need data from a big study, Framingham or Harvard, to show live span vs.... )

Therefor, treatment HAS TO BE done on an individual basis. Treat the right patient, add 20 years to his lifespan. Treat the rest of us, add nothing, even if it works.
 
Hey Imago. looking into K2 informed me that Warfarin causes kidneys to clog with calcium. Calcitonin is given for that. Here is a cite that says K2 is good for that. Note no mention that the K2 causes clots, in fact IIRC, it assuredly does not: http://next-level-nutrition.com/?p=5451

I think that same interview is cited elsewhere on the net.

I guess I may take the terms 'skeptic' or 'critical thinker' to much to heart, and I admit that I may be swallowing hook, line, and sinker of another mega-vitamin scam. But a thousand people here on JREF have read my posts, nobody has refuted any. Please dive in.
 
<http://www.lef.org/magazine/mag2008/mar2008_Protecting-Bone-And-Arterial-Health-With-Vitamin-K2_01.htm> is a summation of my current thinking. Please note that it was not my original exposure, but that I found it while looking for a summation-in-toto. One long net page, I'm thinking everybody ought to be interested to take the time to read it. .
 
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