Bolding mine.
Well, do they? At statistically significant numbers, I mean? I’m not trying to be snarky here, I really can’t figure it out. Even the ads for some cholesterol lowering drugs (I can’t recall which ones, nor if they’re statins) show fine print at the bottom of the screen saying something to the effect of “this drug has not been shown to prevent heart attacks” while seriously implying that they do. I’m just confuddled on this one.
Stains reliably lower total cholesterol. But there’s very little evidence to suggest that lowering total cholesterol with statins prevents heart attacks in more than a teeny, tiny handful of individuals.
KarlGauss, I guess you haven’t heard about the chewable Lipitor tablets recently approved in the EU for ‘treating’ children 10-17 who have elevated cholesterol and triglycerides… your levels of triglycerides are affected almost entirely by dietary carbohydrate, FWIW.
I’ve heard the ‘statins in the water’ from doctors before.
My dad died of atherosclerotic heart disease. (That was the cause listed on the autopsy report.) He wasn’t a smoker, but he was overweight and had high cholesterol. High cholesterol seems to run in the family, as all three of my siblings have it. My cholesterol was at 200 a few years ago–my doctor said it was “higher than * would like to see it, but not high enough to treat with statins.” I work out like a fiend, eat a healthy (but that includes those infamous whole grains) diet, and have brought it down to 164.
So this thread has obvious importance to me. And I have questions!
Are heart attack rates really lower in countries where people follow a “Mediterranean diet”? They consume a fair amount of wheat. If memory serves, they also have a higher percentage of smokers. They also drink more red wine, at least in France and Italy, and wine has a fairly high sugar content.
If the inflammation theory is valid, why are the drug companies not jumping on this? Why aren’t there commercials touting Motrin and other anti-inflammatory drugs as good for heart health? Or does this type of inflammation not respond to OTC anti-inflammatory drugs?
So does diet matter or not? I’m reading here that the food we eat has no or minimal impact on probability of heart attacks and that starches (particularly wheat) and sugar are the Foods of the Devil. Which is it?
Finally, lots of doubts expressed here about food, but I’m assuming we’re all on the same page about exercise, right? For one thing, it definitely relieves stress–or does stress not play a role in heart attacks either?
This is not my area, so what I say certainly shouldn’t be taken as the last word on the subject. That being said, I believe that all commercially available statin drugs* have now been shown to prevent heart attacks and death from heart disease. This is true for both men and women. Not all of the statins, though, have been shown to reduce overall death rates (but, in my mind, reducing heart attacks alone is more than enough to justify their use)
I am not quite as confident that it’s the case that each specific statin drug has been shown to prevent heart attacks when used for both ‘primary’ and ‘secondary’ prevention (with primary prevention referring to people who’ve never had a heart attack, and secondary prevention referring to people who’ve already had at least one). In other words, although each specific statin drug has been shown to prevent heart attacks in a research study looking at either primary or secondary prevention, I just don’t know if each member of the class has been proven to be of benefit for both primary and secondary prevention purposes. This is a minor point and I hope by mentioning it I am not appearing to cast doubt on any of the statins. Again, they’ve all been shown to prevent heart attacks (just maybe not in both a primary and a secondary preventative way).
However, there are other types of cholesterol and lipid lowering medicines and not all of them have been shown to prevent heart attacks. Specifically, to the best of my knowledge ezetimibe (Zetia and Ezetrol) has not been shown to prevent heart attacks or have other clincally beneficial effects. I never prescribe it. And, the class of drugs known as fibrates (used primarily to lower triglycerides and raise levels of HDL-cholesterol) have not had as many trials as statins examining their effect on things like heart attacks. As I understand it, they have been shown IN MEN to prevent heart attacks in individuals with no history of them. They have also been found to prevent heart attacks in diabetic MEN. I am unaware of data about the use of fibrates used as monotherapy to prevent recurrent heart attacks (secondary prevention) or that show benefit for women in either primary or secondary prevention.
Well,
Diabetes alone has a prevalence of somewhere between 5 and 10 percent, and the number of people who’ve had a heart attack or have other evidence of established atherosclerosis covers huge numbers of the North American adult population. Then, when you add in the “high risk” individuals (as defined above), you’ve got to be talking about more than a small minority, or as you sensationalized it, “a teeny, tiny handful”.
Hey, I’m not saying that statins are a panacea or even that cholesterol is the major cause of coronary disease (only half of heart attack survivors have even modestly elevated cholesterol). Like everything else, atherosclerosis is a complex issue. But in your zeal to attack statins and the “cholesterol hypothesis”, you are throwing out a very substantial baby with the bath water.
I should have simply noted that 2 in 5 North American people will die from some form of atherosclerosis. At face value, that means that 2 in 5 people might benefit from a statin, and maybe more if you want to include non-fatal atherosclerotic illnesses and events (like a stroke or heart failure due to previous MIs). Hardly trivial.
I agree that statins *might * be beneficial for that 2 in 5 people. But how many of the people in that risk group do they actually benefit?
THAT is the question! And, I agree with the implication - only a minority. Still, as time goes on, even a 1 or 2 percent per annum reduction, really builds up.
But, if statins are safe, and I believe they are in the vast majority of people, then there is only an expectation of gain with no loss (aside from the cost and “labeling” of the person, I agree).
It also behooves us to note that most interventions in medicine achieve only small gains. Needing to treat 100 people with intervention X for one year to prevent one bad outcome, is a pretty typical occurrence. That’s the current situation for much of heart disease.
I don’t have anything substantial to add at this point, but I want to thank you, KarlGauss, for sharing your medical knowledge with us. Looks like I have some more reading to do!
As I read the points presented above, it seems to me that there are some logical inconsistencies in the whole blood cholesterol/heart attacks/statins argument.
Assuming these data items are true, it seems to me that the logical deductions from these are that the blood level of cholesterol is immaterial to heart attacks, and statins serve no useful purpose.
My logic is as follows:
prevent on heart attack out of 300 people: suggests that the observed effect is indistinguishable from random chance.
blood cholesterol levels follow a normal distribution: suggests that there is no clinical significance to blood levels of cholesterol, except at the outlying extremes; ie: what is “high”, what is “low”, what is “normal”?
different cholesterol lowering drugs have different effects on the rate of “prevention” of heart attacks: suggests that there is a hidden underlying mechanism involved, and this mechanism is independent of cholesterol. Some statins affect this underlying mechanism, some don’t; their effect on cholesterol levels seems coincidental and peripheral.
The observed result seems to be the consequence of the effect of the drugs on the underlying mechanism; it is not a consequence of the reduction in the cholesterol levels.
On another point: in my travels through the Mediterranean, I have observed that there is no such thing as “The Mediterranean Diet”.
I have observed that the diet in any particular area in the Mediterranean is dependent on the local availability of produce and the financial capacity of the locals to pay for food. Therefore, poorer regions subsist on pasta and olives, the richer areas thrive on meat and potatoes.
I’m not a doctor and I have only heard here and there about the statins and their ineffectiveness. I have read of studies that showed overwhelmingly the link(s) between diet and longevity (in general): for example, the China Study, a much larger study than 100 patients a year, showed a clear (inverse) relation between eating meat/meat products and longevity. The study and similar studies are reviewed by Dean Ornish and presumably in his later books as well.
So maybe we are asking the wrong question about the food: while we’re asking whether we should be cutting down on the potatoes or pasta, maybe we should be looking at the burgers instead.
Here is a video of Gary Taubes giving a talk on his book.
IMO the book The China Study (which has little relation to the actual data of the China Study) has been shown to be a total fraud. I have abundant links if you’d like to see them.
I also think Dean Ornish is dangerously deluded.
I speak as a former vegan/vegetarian for health reasons, BTW. In the last 4 years I’ve done a 180 in my beliefs about what’s good for people to eat; because I’ve read much of the available (conflicting) information.
I certainly don’t subscribe to the notion that heart attacks are genetic and diet has nothing to do with it.
Heart attacks are essentially nonexistent among populations who have not yet adopted the typical Western diet. For example, one study that looked at over 4,000 hearts of Ugandans at autopsy found exactly 1 instance of myocardial infarction (MI). If they had conducted the same study here in the U.S., they probably would have found thousands of MIs.
So it’s evident that heart disease is yet another Disease of Civilization, and is therefore nearly completely preventable. But since there’s no money in preventing disease, the American Heart Association makes absolutely no attempt to get Americans to consume fewer processed foods/refined carbohydrates that cause disease.
In fact, the AHA actively encourages it. At one point, they actually endorsed Cookie Crisp, Count Chocula, and Cocoa Puffs cereals, presumably because they are low in fat (fat consumption has been shown to have absolutely no relationship to cardiovascular disease). But refined carbohydrates in the AHA’s beloved Count Chocula are known to increase triglycerides, decrease HDL, increases LDL (particularly the small, dense, easily oxidized LDL particles that are thought to be the most atherogenic).
That’s absolutely incorrect. If you do a study with a large enough sample size, you can easily distinguish an effect of that magnitude from random chance.
Here’s what the AHA has to say:
More whole grain foods, less sodium… sort of seems like they’re advising against refined carbohydrates and processed foods, doesn’t it?
Do you have any idea what the AHA diet (low fat, plenty of fruits & vegetables, and, of course, “healthy” whole grains) does to the cholesterol of healthy people?
See for yourself:
So it not only increases oxidized LDL (this is what’s thought to actually cause MIs) as well as Lp(a). Doesn’t sound like a diet I’d want to follow.
Exactly where is the evidence to support this?
Take a look at this:
http://www.nature.com/ejcn/journal/v64/n6/abs/ejcn201045a.html
So if you follow the AHA’s advice and consume low-fat dairy products instead of the full-fat varieties, you’ll be more THREE TIMES more likely to drop dead from heart disease.
Great advice! Better pour some skim milk on your Cocoa Puffs…
I couldn’t help but notice that the dietary recommendations from the AMA quoted above say in all of their recommendations: “… may help you…”
The operative word is: “may”.
Does this mean that they are just making it up as they go along, or is there some kind of scientific basis for their recommendations?
Also “Shmendrik”, thank you for your comment regarding the validity of statistical analysis (noted above).
Do you have any further information on this specific issue? Ie: how big a sample was involved in this specific drug study, and does their study produce a valid and credible result? And does that result have any real world clinical significance?
Anybody who’s interested in the (purported) effect of various diets and dietary constituents on the risk of coronary disease would do well to look at this free, full-text article published last year in the decent Archives of Internal Medicine. A huge amount of work must have gone into it, but more importantly the authors are part of the group that quite literally invented “evidence-based medicine”. Indeed, one can’t help but be impressed with the quality of the analyses they performed.
I won’t spoil the surprises to be found therein, except I can’t resist noting that dietary fat intake, including total, saturated, and polyunsaturated, could not be shown to be associated, positively or inversely, with coronary disease. If nothing else, look at tables 3 and 5 (and 4 if you’ve got the time).