I’m involved in a debate over diet and health over at Dean’s and in the course of that debate, was encouraged to read a paper by Corr et al. that suggests low-fat diets are essentially useless for reducing heart disease. This post started out as a comment but it grew enough to warrant a post in it’s own right. So, let’s look at what the Corr paper is actually saying, shall we?
The international bodies which developed the current recommendations based them on the best available evidence[1-3]. Numerous epidemiological surveys confirmed beyond doubt the seminal observation of Keys in the Seven Countries Study of a positive correlation between intake of dietary fat and the prevalence of coronary heart disease[4] although recently a cohort study of more than 43,000 men followed for 6 years has shown that this is not independent of fiber intake[5] or risk factors. The prevalence of coronary heart disease has been shown to be correlated with the level of serum total and low density lipoprotein cholesterol (LDL) as well as inversely with high density lipoprotein.
So, high intake of dietary fat indeed has a positive correlation for coronary heart disease. Corr is conceding this at the very start!
Further, coronary heart disease is also indeed associated with high LDL and low HDL. So far I am not seeing any Cholesterol Conspiracy here… the ADA seems to be right on the ball.
So, we’ve already established that CHD is associated with high fat, high LDL, and low HDL. So, what’s left to argue about?
As a consequence of these studies, it was assumed that the reverse would hold true: reduction in dietary total and especially saturated fat would lead to a fall in serum cholesterol and a reduction in the incidence of coronary heart disease. The evidence from clinical trials does not support this hypothesis.
Hmm. Two sentences here. one about a reasonable inference from the conceded association between fat and LDL with CHD. But ok, let’s call the question of whether teh reverse is true, Question A – “does reducing fat and LDL in the diet reduce CHD?”
And then another sentence, about evidence from clinical trials not supporting that inference. What about those clinical trials, exactly?
It can be argued that it is virtually impossible to design and conduct an adequate dietary trial. The alteration of any one component of a diet will lead to alterations in others and often to further changes in lifestyle so it is extremely difficult to determine which, if any, of these produce an effect. Dietary trials cannot generally be blinded and changes in the diet of the ‘control’ population are frequently seen: they may be so marked as to render the study irrevocably flawed. It is also recognized that adherence to dietary advice over many years by large population samples, as for most people in real life, is poor and that the stricter the diet, the worse the compliance.
Ah. so the available evidence from clinical trials is fundamentally suspect to systematic error. Fair enough. So, any conclusions we make from them should be tempered with that, right?
(long analysis of clinical trials in literature follows)
The message from these trials is that dietary advice to reduce saturated fat and cholesterol intake, even combined with intervention to reduce other risk factors, appears to be relatively ineffective for the primary prevention of coronary heart disease and has not been shown to reduce mortality.
OK, so the trials focusing on low-fat diets alone didn’t show any primary prevention benefit. Well, see caveat above, right? (and Corr’s noted exception about the MRFIT study…)
However, what about secondary prevention?
well, good! But still, is there some reason that maybe we aren’t seeing better results here? Is diet necessary, or sufficient? Let’s look at studies that not only remove fat, but also add HDL:
The first successful dietary study to show reduction in overall mortality in patients with coronary heart disease was the DART study reported in 1989[20]. The three-way design of this ‘open’ trial compared a low saturated fat diet plus increased polyunsaturated fats, similar to the trials above, with a diet including at least two portions of fatty fish or fish oil supplements per week, and a high cereal fibre diet. No benefit in death or reinfarctions was seen in the low fat or the high fibre groups. In the group given fish advise there was a significant reduction in coronary heart disease deaths and overall mortality was reduced by about 29% after 2 years, although there was a non-significant increase in myocardial infarction rates. The reduction in saturated fats in the fish advice group was less than in the low fat diet group and there was no significant change in their serum cholesterol.
Finally, the more recent Lyon trial[21] used a Mediterranean-type of diet with a modest reduction in total and saturated fat, a decrease in polyunsaturated fat and an increase in omega-3 fatty acids from vegetables and fish. As in the DART study there was little change in cholesterol or body weight, but the trial was stopped early following a 70% reduction in myocardial infarction, coronary mortality and total mortality after 2 years.
In other words, adding HDL to your diet helps a lot, whereas reducing polyunsaturated fat (or just increasing fiber) still doesn’t seem to do anything. We’ve established that a modest increase in HDL can help. But have we established that a modest reduction in LDL will not help?
Unfortunately, the design and conduct of these trials are insufficient to permit conclusions about which polyunsaturates and other elements of these diets are the most beneficial. The long term effects of these trials[20,21] and the compliance with the dietary regimes remain to be seen.
So, we don’t really know if these studies answer that question. It’s possible that lowering LDL has a longer-timescale benefit than increasing HDL. These studies don’t answer the question either way, because of the limitations Corr concedes – certainly we haven’t proven that lowered LDL is not genuinely helpful yet.
Anyway, how much LDL was really reduced anyway?
An important aspect of the lipid-lowering dietary trials is that on average they were only able to achieve about a 10% reduction in total cholesterol. The results of recent drug trials have demonstrated that there is a linear relation between the extent of the cholesterol, or LDL, reduction and the decrease in coronary heart disease mortality and morbidity, and a significant effect seen only when these lipids are lowered by more than 25%[23].
Ahhhh. Corr goes on to quote a bunch of studies that show frankly awesome improvements in mortality using drugs to lower LDL by 25% or more.
(in other words, definitively proving that lower LDL does indeed reduce heart disease. We just answered Question A from above).
So, let’s summarize:
conceded by Corr at the outset:
– increased HDL reduces CHD.
– increased fat increases CHD.
– increased LDL increases CHD.
dietary trials:
– somewhat lowered LDL does not reduce CHD.
drug trials:
– significantly reduced LDL does reduce CHD.
caveats:
– dietary trials have systematic errors.
– long-term trials on reducing LDL have not been performed.
special note: The MRFIT trial follow up focused on reducing LDL diet alone, and did show reduced myocardial infarctions over a longer term.
My conclusion from this would be that a. increase HDL now for immediate benefit, and b. reduce fat and LDL in my diet for long term benefit. Seems obvious enough, and fully in accord with what the ADA recommends.
Corr’s conclusion?
diets focused exclusively on reduction of saturated fats and cholesterol are relatively ineffective for secondary prevention and should be abandoned.
umm.. what?!?!
This is where they cross over into vaccines-autism and flouridated water territory, frankly.
What would have made the Corr paper immeasurably stronger would have been for them to devise an experiment that would answer these questions and fill the gaps. That’s always my challenge to these self-styled “skeptics” of the scientific consensus. What’s the experiment you propose? What would you do to make your case?
That’s how science works. Theory drives experiment, experiment refines theory, and back again. If your claim is that available evidence (in this case, clinical trials) don’t support the contention, that’s not enough. You need to come up with an experiment that actually refutes the contention. Formulate your hypothesis and test it! Anything else is just nitpicking from the sidelines, which is how most of these agenda-driven meta-analyses end up reading.
Frankly, I am very much eager to be able to dispense with the low-fat, low-cholesterol crap. Here’s why in a nutshell.
So please, Dr Corr and anyone other “cholesterol skeptics” out there. Show me the proposal for your experiment, and I guarantee you the fast food industry will show you the money.
Oh, good grief. “The International Network of Cholesterol Skeptics”
http://www.thincs.org/
I dispensed with it a while ago. I eat a lot of whole foods. I also eat a strength training diet, so I’m taking in tons of eggs and whole milk. I go looking for saturated fat, because it boosts testosterone production.
Was tested last week. LDL? Slightly elevated. HDL? High, 3.5 ratio. Triglycerides were plenty low enough to be healthy.
I honestly believe that there’s much more to worry about the processed foods that people switch to in order to eat “low fat” and “cholesterol friendly” than boogeyman stories about whole foods. Eggs, milk, cream, butter and (naturally raised) red meat are better for you than margarine, food additives and hormone addled boneless skinless chicken.
you’re strength training. That right there says it all, man. My triglycerides are pretty low, and my HDL is 44, because i workout three times a week (moderate, 20-30min on an ellitptical) and take Omega 3 supplements. So i coudl probably eat more cheese curds if I wanted to.
Of course the entire debate is about CHD – but eating fatty foods does increase obesity, which leads to diabetes, of which CHD is an outcome. The timescale is the thing, of course.
I doubt you will have an issue there because your’e clearly working out aggressively. So the diabetes/obesity route is not a concern. But the average joe doesn’t workout as much as even I (barely) do, let alone what you’re doing.
these are issues of public health policy. The guidelines are vague – reduce fat and LDL, increase HDL. The outcomes are vague too, due to variability in lifestyle, genetics, etc. (you are a case in point). But in teh aggregate, it helps.
When I was diagnosed diabetic, the doctor started on the big speech about cholesterol and blood pressure, and then looked at my test results and said, “never mind, just lose some weight and eat more eggs” (LDL 56, HDL 39).
The ADA’s diabetes guidebook is quite well-written and science-based, by the way. It avoids all the trendy nonsense that tends to dominate “news” on the subject.
-j
I’m not surprised he advised you to eat eggs – the specific type of fat that increases LDL is saturated (ie, animal) fat. Eggs have cholesterol in them but that cholesterol is a different type that doesn’t convert to cholesterol in theblood the way saturated fats do. The real advice in your doctor’s wisdom was probably teh lose weight part – which is really the key I think to overall health.
I should update the post with this link, but it’s too long, so i’ll leave it in comments – here’s a fantastic interview with Dr. Ron Krause, who basically was the first researcher to identify the difference in HDL vs LDL, and who now is exploring teh different types of LDL (basically, LDL Bad is oversimplifying; actually, small LDL bad and large LDL less bad). There’s tremendous insights in this interview – the man is a real data-driven expert.
J, I’m curious what you make of the Krause interview in particular since much of what he says has direct bearing on diabetic diet. You are out there in the trenches, so to speak, whereas he is up on the hill. How would you grade him?
(as an interesting aside, my present research is in quantifying fat using MRI. We are aiming at metabolic syndrome. So this is useful for me to write about and blog about! That’s why I let myself get drawn into the debate over there.)
My short response to the interview is that his answers made me want to find other things he’s written that are not chopped up into sound bites by an artificial Q&A format, and that the questions made me want to reach through the screen and slap the interviewer. I just stopped reading the questions about a third of the way through.
My own unscientific experience leads me to believe that blood sugar, including Hemoglobin A1C testing, is an inadequate proxy for the status of the underlying condition. Basically, the few physical symptoms I can effectively correlate to high blood sugar were present at roughly the same level for more than 16 years before I was diagnosed diabetic, a period where my sugar consumption was very high. So, either I was an undiagnosed type 2 diabetic for 16 years who suffered no damage that can be detected by any of the standard tests, or else I just ate so much sugar that a perfectly healthy system couldn’t flush it all out.
I’m definitely diabetic now, though. Five years with modest carbs and almost no sugar still leave me with an A1C outside the “safe” range, unless I burn it off with regular exercise. Obviously, if my body still has trouble processing sugar when I’m not eating it like candy any more (heh), then I’m diabetic, but I think my late-Twenties A1C would have been off the charts.
It will be interesting to see how my body responds to my upcoming trip to Kyoto. Last time I went to Japan, I ate everything in sight and walked at least 10 miles a day (with lots of hills and stairs), never saw a fasting blood sugar reading above 120, and came home 7 pounds lighter.
-j
Cholesterol conspiracy? What? Where do Corr & Oliver talk about any such thing?
You seem to be confusing serum cholesterol with dietary cholesterol, and also injecting things into Corr & Oliver’s paper that aren’t there. Are you even familiar with the dietary interventions they’re talking about, which tend to focus exclusively on reduction of fat and cholesterol in the diet? I also wonder: do you just have a problem in general with people doing literature reviews and meta-analysis and concluding that there’s something wrong with a paradigm? Does this have no use in science? It seems like you object any time someone does this and expect them to instantly provide extensive new studies, even if all they’re calling for is a re-evaluation by the research community.
Despite your own skepticism, since the publication of the Corr paper, whole boatloads of research have come out to vindicate their view. Indeed, the paper seems to have touched off a whole slew of research (it was dietary researchers, real ones, who turned me on to this paper) looking at things other than merely reducing dietary fat and cholesterol; this paper is historically significant because it signaled a shift in the dietary research community. Most researchers (unlike many doctors) now concede that simply reducing fat and cholesterol intake wasn’t making a big difference, and, as we’re seeing now in a whole lot of research, there’s good reason to believe that the simple “eat less fat and cholesterol” advice wasn’t just of little value, it gave negative results.
Also, you recommend in the discussion on my site this interview with Ron Krause. But everything Dr. Krause is saying here is -completely- in line with Corr & Oliver. In fact, much of what he says, if it is correct, would explain perfectly why the low-fat/low-cholesterol diet paradigm was and is such a failure–in fact, he goes much further, suggesting that such a dietary pattern isn’t just worthless, but potentially highly unhealthy for a good portion of the population. I don’t think I’m quoting him out of context here to note the following statements:
“People think that blood cholesterol comes from dietary cholesterol. That’s definitely not true. Dietary cholesterol coming in eggs and shellfish has modest effects on cholesterol. It’s much more effected by the type of fat and carbohydrate.” (Emphasis mine)
That all by itself would explain the failure of the low fat/low cholesterol diet paradigm. Because by focusing entirely on lowering fat and cholesterol intake, we assumed cholesterol intake is of high importance (it isn’t), and that just reducing fat would improve things (it often didn’t). Probably worst of all, we paid almost no attention to carbohydrate intake, even recommended increasing it (which is the usual pattern by default if you strictly reduce fat anyway).
Further by Krause:
In certain subgroups, well over half the population is overweight and has metabolic disturbances. For those people carbohydrate is a far more important metabolic determinant than saturated fat.
So Dr. Krause explains here why diets focusing simply on reducing fat and cholesterol intake have been worthless, even counterproductive, for much of the population.
Krause yet again validating Corr & Oliver:
We’ve been studying over the years, a lot of my research has focused on looking at various dietary changes and how they affect the blood cholesterol profile and heart disease rick in general, and we’ve moved now to something closer to 35 to 40 percent of carbs being more optimal, for people particularly at risk because of obesity or metabolic syndrome, as opposed to 55 percent or higher, as is often recommended.
In other words, these people are eating too much carbohydrate, not too much fat.
The fat that causes LDL to go up is saturated fat. Animal fat. We’ve shown that it tends to affect the larger LDL, interestingly. What we tend to think of as bad fat primarily affects the less bad form of LDL, whereas carbohydrates, in a somewhat counterintuitive way, it’s starches and sugars that raise the bad form of LDL. (Emphasis still mine.)
In other words, animal fats aren’t great, but they drive up what he says is the less-bad form of low-density lipoproteins, whereas starches and sugars drive up the much more damaging smaller LDL. Score another one for those who said the low-fat/low-cholesterol diet paradigm wasn’t working.
In fact, probably the biggest, most challenging statement of all from Krause:
A high fat, low carb diet can be extremely helpful. One of the things one has to say about high fat diets, particularly In the populations that tend to have healthy lives, it often involves fat coming from things like fish. So called healthy fats. We’ve shown If you have some animal fats along the way, it doesn’t seem to be a serious impediment to health.
I bolded the whole thing. This goes massively further than Corr & Oliver, who only noted the fact that study on diets that focused simply on reducing fat and cholesterol was ineffective; here is Krause stating point-blank that in some cases, the exact opposite, a HIGH fat diet can be a healthy choice and some animal fats (the saturated, cholesterol-y type) may actually be just fine.
Dude. Read the Corr paper again, and focus: this was about a reigning dietary paradigm of the 1980s and 1990s, which focused exclusively on cutting fat and cholesterol from the diet. A paradigm which is still being recommended by many physicians, despite the boatload of research suggesting it’s ineffective and possibly even unhealthy for many patients.
I should point out that there’s a significant difference between what someone like Krause calls “low-carb” and what Atkins-ish fad diets have proposed. Extreme low-carb diets have some serious risks; do some reading on ketoacidosis and gout. Bottom line, don’t go really-low-carb without frequent ketone testing, especially if you’re diabetic. The cure is worse than the disease.
-j
Dean, this is a strange conversation. You say that there’s this paradign that low0fat diets are supposedly good for you, but then point to Corr and now also to Krause who both acknowledge that high fat diets are bad. The statement from Krause you found most interesting , he is talking about so-called healthy fats. The distinctions between animal fat vsnon animal, LDL and HDL, cholesterol in food versus cholesterol in serum, etc are obviously complex enough that perhaps I am just not getting it. But the Corr paper, on its own, contradicted itself as far as I can tell, because it presented no evidence that abandoning the lowfat paradigm was justified.
And it’s odd that you and i both read Krause and come away certain he’s confirming our point. Since both of us have etter than average writing and reading skill, perhaps our points arent as divergent as they seem.
Fundamentally, what IS your point? that you can eat as many eggs as you want? (I’d agree, if the eggs are boiled. Fried, not so much, depending on what oil you use.) What specific foods do you think we can eat wiothout any fear whatsoever, but which ost people avoid now due to the prevailin paradigm?
Thanks, folks, for linking to my little website, meandmydiabetes, and the interview with Ron Krauss. Very intriguing discussion you’ve been having. Very lively, and lots of food for thought. I’m just catching up because I noticed yet another ping today based on your discussions here. If you like Ron Krauss, I’m wondering what you’d think of what Loren Cordain has to say in his interview about Saturated Fats and Grains, and also Binx Selby’s “Balance Point” program. And Steve Phinney and Ron Rosedale. Very intriguing thoughts from both of them. Dariush Mozzafarrian’s been doing some mind-bending looks at just what it is about meat that’s made it be a bad guy, and he’s saying from close looking at the data, saturated fat’s neutral and the biggest concern that he’s got is with the loads of salt in processed foods (he’s a Harvard Public Health cardiology epidemiologist). But then, Steve Phinney says on a low carb diet, more salt’s okay! And wildly, if you listen to the reasoning of each of these experts, it all sort of makes sense. And then . . . there’s a scientist I got to interview recently who is recommending lots of eggs a day to build muscle better AND because, while you’re working on building muscle, he says serum cholesterol levels are lower if you’re eating ENOUGH cholesterol. It’s an elegant argument. Especially if you like eggs. It’s a phone tape interview. Still . . . do you want me to get it cleaned up and post it?
Or is this too much stuff and don’t bother?
Last but not least, wouldn’t it be nice if, with just one tube of blood, any one of us could get data about 1,000 different circulating proteins in our bloodstream that indicate what’s going on with our genetic expression? All from just one test? I don’t know what the ethics would be of consumers getting that much information, but I’m curious about it, and we’re on the verge of it being doable, technically.
Well, that’s enough for now. — Shelley