Once again the dishonesty or maybe sheer stupidity of scientists bowls me over. I got an email from an old patient a couple of days ago who is following a low-carb diet while under the care of a skeptical (to say the least) cardiologist. The cardiologist sent the patient an email with a link to a Cardiosource (an online resource for cardiologists) commentary on an article in this month’s issue of the Journal of the American College of Cardiology.
The paper compared a standard high-carbohydrate, low-fat diet (HCLF) to a very-low-carbohydrate, high-fat diet (VLCHF) in terms of blood lipid changes. The Cardiosource commentary seized on the last two lines in the abstract of the paper.

…although both diets had similar improvements for a number of metabolic risk markers, the HCLF diet had more favorable effects on the blood lipid profile. This suggests that the potential long-term health effects of high- and low-carbohydrate weight loss diets remain a concern, and that blood lipid levels should be monitored in obese subjects with the metabolic syndrome.

As the commentator put in in his perspective:

The best diet for the metabolic syndrome is neither of these extremes. Rather, the best is a diet restricted in processed flour and simple carbohydrates, increased in complex carbohydrates and soluble fiber, and high in fish and monounsaturated fats. The results also support patient choice, with careful monitoring of the lipids. Of course, aerobic exercise and weight training should improve the outcome of any diet.

Jesus wept. Nothing in this paper leads to the Cardiosource guy’s pinheaded conclusion. In fact, nothing in this paper leads to the conclusion of the authors of the paper, at least not as they wrote it in the abstract.
Let’s take a look at what the data in the paper show and see how, once again, academic bias rears its ugly head.
A group of 88 abdominally obese subjects were randomized into two equal groups. One group went on a low-calorie HCLF diet; the other went on a VLCHF diet of the same number of calories. Both groups remained on their respective diets for 24 weeks. Researchers measured various blood parameters at the start and at the end of the 24 week trial.
Both groups lost a similar amount of weight over the 24 weeks (subjects on the low-carb diet were trending toward a greater weight loss, bt the difference hadn’t reached significance by 24 weeks). You can see in Table 3 below the results of any lipid changes in both groups over the 24 weeks.
Most of us here in the US are used to seeing these numbers listed in units of mg/dl instead of the mmol/l that are appearing more and more commonly in scientific papers. I converted the mmol/l units into the more familiar units and put them in the table below.
Let’s analyze to see what all this means.
First, we can see that total and LDL- cholesterol didn’t do much on the low-carb diet whereas both dropped on the low-fat diet. This is nothing that hasn’t been seen a thousand times before in other studies. It’s been known forever that reducing fat in the diet brings about a reduction in total and LDL- cholesterol. But it does so at a cost. The cost is that although the LDL-cholesterol level falls, the particles themselves convert to the smaller, denser type that are more atherogenic. Nothing new here – this has been known for a decade or more. More about this in a moment.
Second, the HDL-cholesterol went up by almost 20 percent and the triglycerides dropped by over 40 percent on the low-carb diet. These same values changed but slightly in those on the low-fat diet.
In my opinion (and the opinion of many others) the lipid parameters of most value in determining risk for heart disease are triglyceride levels and HDL levels. In fact an important index of risk is the triglyceride to HDL ratio (TGL/HDL): the lower the better. Looking at the data from this study we see that for the VLCHF diet the TGL/HDL dropped from 2.6 to 1.3. It halved. In those subjects following the HCLF diet the TGL/HDL dropped from 3.0 to 2.3, substantially less. (Now, these kinds of things matter if you’re a real believer in the lipid hypothesis, which, as everyone should know by now, I’m not. If you’re not a believer you think that these figures are markers for something else going on that probably causes heart disease, but are not the causative forces themselves.)
So, we’ve got a situation here where the lipid parameters improved more on the low-carb diet as compared to the low-fat diet, yet we’ve got the authors of the article, the generators of this data, telling us that the HCLF diet had “more favorable effects on the blood lipid profile.” Unbelievable.
But wait, it gets worse.
If you look at the first Table 3 above, you’ll see a category called ApoB at the very bottom. You’ll also notice that apoB didn’t change much in either group. But that is significant. Why? Because it means that the LDL-cholesterol particles really did get smaller in the HCLF group. Let me explain.
Cholesterol is a waxy substance that doesn’t dissolve in water or in blood. The waxiness of cholesterol is what makes it so important for providing structural support for the cells membranes and other fatty acid bilayers, but it’s also what keeps it from dissolving. In order for cholesterol to be ‘dissolved’ in the blood it must be attached to a protein, which will dissolve and carry the cholesterol along with it. Depending upon the protein it’s attached to and its density cholesterol becomes LDL or HDL or VLDL. One of the specific proteins making up LDL is called apoB. There is an apoB for each LDL particle (the particle is composed of the protein, some cholesterol and some triglycerides).
If we know the apoB count we can estimate the number of LDL particles. If the apoB number goes up, there are more; if it goes down, there are fewer.
Since the LDL-cholesterol measurement tells us how much LDL-cholesterol we have and the apoB measurement tells us how many particles we have, we can divide the LDL-cholesterol by the apoB number and get a rough estimate of the size of the LDL-cholesterol particles.
If we look at our two groups of subjects in this study, we find that in the VLCHF group the LDL-cholesterol didn’t change much and neither did the apoB. Therefore we can pretty much say that the diet didn’t really affect the LDL-cholesterol particle size. If we look at the HCLF group, however, we see a different picture. In the subjects following the low-fat diet LDL-cholesterol levels fell while apoB numbers stayed the same. This means that there are the same number of particles as before but they became smaller after 24 weeks of low-fat dieting. In other words, the low-fat diet converted the LDL-particles into the more dangerous smaller, denser type.
And these guys have the temerity to tell the world that low-carb dieting makes lipid numbers worse!
We could write it off to ignorance maybe. But not really. If you read the discussion part of the paper you will find the following statement:

It has been suggested [I would say it has been a whole lot more than suggested] that apoB, which represents the actual number of atherogenic lipoprotein particles, may be a more reliable indicator of CVD risk. Although there was some evidence for a reduction compared with baseline, apoB levels did not change significantly by week 24 in either group, suggesting that atherogenicity did not change despite a high or low saturated fat intake and the absence of an expected reduction in LDL-C with weight loss in the VLCHF.

Say what?
We know these folks know about LDL-cholesterol particle size and atherogenicity because they just described it. Then they go on to lay this smoke screen about there not being any change in particle size in those subjects on the low-carb diet. Duh! But they never mention the change in those on the low-fat diet. Unbelievable!
The disinformation presented in this paper goes to the very heart of the peer-review process. This paper wasn’t published in some low-rent journal – it was published in the Journal of the American College of Cardiology. A major journal. One assumes that the peers who reviewed this paper when it was submitted were cardiologists or at least scientists with more than a modicum of training in diseases of the heart. And one would assume that since these reviewers were cardiologists – almost all of whom are lipid-hypothesis moths of the deepest dye – they would be up on apoB and LDL-particle size and the putative atherogenicity of small, dense LDL-cholesterol particles. It beggars belief that a paper such as this one could make it through an intelligent peer-review process and wind up as it did in the pages of a major medical journal read by cardiologists all over the world.
Most of these cardiologists have their doubts about low-carb dieting, and, just as with the one who sent the email to my former patient, most will never read this paper critically, but will immediately use it as padding for their own anti-low-carb bias.
These are the kinds of shenanigans that go on all the time. They are the reason there is so much disinformation out there. And they are the reason that you should always be skeptical to the max whenever you hear this kind of idiocy bantered about. You must read the entire paper – not just the abstract.


  1. I hope you wrote them a letter explaining the error of their ways and the points you just made above.
    It never occurs to me to do that. I probably should. I suspect, however, that they know the error of their ways.

  2. Thanks for debunking another study. My doctor always says “well, I know a lot of cardiologists who would disagree with you.” I always have some facts and some sort of smart @ss reply like what I said to her last time “Do you always believe what those six drug reps I just saw say?” Seriously, my last physical was just over a month ago and between walking into the office and waiting, I saw 6 drug reps. Of course they were all good looking young men and women.
    Of course, she’s quit arguing with me and has stopped asking me if I would reconsider taking my statin again. She said my numbers were perfect last time, which of course I looked at differently than she did. Now if I could just get her to read some of the books I do. She’s not much older than me, maybe she can be saved. I’m 34 and have had the brain transplant.
    Let’s hope she can be saved. But I wouldn’t bet on it. If she’s like most physicians out there, all her new info comes from the drug reps. It will be a long wait for one of them to tell her to quit giving statins to everyone who walks through the door.
    Glad your labs are looking good.

  3. To be fair, a cursory glance of the numbers gave me the same conclusion that the high carb diet gave better results on the conventional parameters. Total cholestrol went down more and indeed was below that MAGIC number of 200 mg/l to 189 and LDL almost reached the OPTIMAL number of 100 mg/l. Both of these numbers remaining essentially unchanged on the high fat diet. The ratios tell a different story. The Total C/ HDL ratio improved from 3.80 to 3.21 for low carb and from 4.05 to 3.44 for low fat, an 15% reduction for both.
    However, the real story is the triglycerides which decreased 40% in low carb versus 20% for low fat. The guidelines only say that it should be below 150, which it was for both groups after the diet.
    Again, there’s the MAGIC number. All thought processes halt below these MAGIC numbers.
    A more reasonable conclusion even for this close minded felow is that conventional risk factors showed a greater improvement on the low fat diet, which may be balanced out or even outweighed by improvements in newer risk factors for the low carb diet, i.e. both diets improved heart health. The dire dark warnings about the need to monitor blood lipids on either diet for obese subjects with metabolic syndrome is just so much BS. EVERY doctor would continue to monitor those patients.
    The rest of the commentary about “a diet restricted in processed flour and simple carbohydrates, increased in complex carbohydrates and soluble fiber, and high in fish and monounsaturated fats” and “Of course, aerobic exercise and weight training should improve the outcome of any diet” is an improvement over the current low fat paradigm, albeit a 3 steps forward 2 steps back improvement in that reducing processed flour and simple carbohydrates is a good thing and that while aerobic exercise has not been shown to improve diet outcomes (see Taubes), there is some evidence that weight training does. He doesn’t even specifically condemn saturated fats. Thanks for the time and space to give my 2 cents.
    P.S. Melvyn Rubenfire in his disclosure statement lists Pfizer, maker of LIpitor, as his funding source. You don’t think that would lead him to emphasize LDL and lowering it, the most significant effect of Statins (and low fat diets).
    P.P.S. Any sarcasm in my comment is intended.
    Hey Mark–
    All sarcasm avidly welcomed here – even that aimed at me. Sometimes.
    I agree with you that the study shows that ‘conventional’ risk factors are improved, with the definition of conventional being those risk factors thought to be risk factors ten years ago and still lodged as such in the minds of those who haven’t kept up with the science since. But, one would suppose that anyone writing a scientific paper for publication in a major journal would at least be current in the literature. And if you read the ‘Discussion’ section of this paper, you find that the authors are indeed up with the current literature, but chose to ignore it. And to emphasize that the apoB levels didn’t change with either diet, leading the great unwashed masses to believe that therefore the particle size didn’t change, which is clearly not the case. Don’t get me started again with this. I get worked up every time I think about it.

  4. I’m seriously thinking about printing out several of your blog posts and binding them together as sort of a “Best of Dr. Eades” book to give to my doctor the next time I see her. It irks me that I am in better health because of doctors whose blogs I read for free on the Internet than from my personal physician who charges me and my insurance company an outrageous amount to tell me if I ate less fat my LDL number would drop, ignoring my high HDL and low triglyceride and fasting blood sugar readings.
    Hi Ethyl–
    I’m sure your doctor would love to get a ‘Best of Dr. Eades’ book. Not!
    Most docs are doing the best they can. I have an advantage in that I’m not in active practice so I don’t have the time constraints of morning rounds, office, hospital, afternoon rounds, and call that many docs do. So I can devote a good portion of my time to the medical literature and to presenting it in layman’s terms. But don’t sell your doc short, just slowly but surely educate her by doing so well yourself.

  5. The sarcasm wasn’t aimed at you. My apologies if you took it that way. It was aimed at those people like the National Cholesterol Education Program and American Heart Association who pick MAGIC even numbers out of the air as per Mary Enig (sorry I can’t find the reference). It was also meant to show some progress has been made since 5 or 10 years ago when comparisons of low carb and high carb diets wouldn’t have been made, let alone published because low carb diet were too dangerous.They were fad diets, they’d leach out your bones, you’d suffer an instant heart attack and drop dead from all the saturated fat and cholesterol, you’d get cancer, etc. There is beginning to be an acceptance that they might be OK or even healthy. Don’t misunderstand me, my workplace is full of educated people, primarily engineers, and to a person they think that fat is bad and saturated fat is worse and whole grains and aerobic exercise are the solution to everything, but progress is being made.
    P.S. Good thing your name isn’t Colpo or I’d be banned for life from your Blog and then only after a withering diatribe.
    Hey Mark–
    Not to worry. I didn’t think you meant it for me. I have the same aggravations you do about all this. Probably more since I’m often thought of as the anti-Christ for presenting such ‘nonsense.’
    And don’t worry about being banned. I’ve never banned anyone for even a day, let alone for life – and that includes Colpo. Anthony is more than welcome on the site any time as long as he minds his manners.

  6. LDL/ApoB = ~particle size? Does it matter much if LDL is a calculated value instead of measured directly? If some IDL gets counted as LDL does it throw off this estimate very much, like when triglycerides are very low? How do you pronounce ApoB?
    I think there are differences between directly measured LDL and that calculated by the Friedwald equation, especially in those with low triglycerides.
    apoB is pronounced Ay Po (rhymes with NATO) Bee.

  7. No mention is made of which diet is easier to stick with, is it?
    Nope. It does say that 10 people withdrew from the VLCHF group and 11 people withdrew from the HCLF group. 2 of the 10 who withdrew from the low-carb group were dissatisfied with the diet, and 1 of the 11 who withdrew from the low-fat diet was “non-compliant with dietary protocol.” Probably not a lot to be concluded from this.
    The fact that these people withdrew from the study brings up an other issue I intended to discuss in the post but didn’t get around to. This data was evaluated with an intention to treat analysis, which, in my mind at least, almost negates any of the findings. I’ll deal with the intention to treat idea in another post.

  8. The vitamin D post rolled off the page, but the word is getting around. Wish the low-carb word spread as fast and easy.
    Here is an item from today’s jsonline:
    Hi John–
    I’ve pulled this paper from Circulation but haven’t had a chance to read it yet. It looks promising. But it’s just one of many papers showing the virtues of vitamin D hitting the medical literature right now.

  9. It is truly unbelievable. How does someone deliberately ignore relevant data, and yet everyone looks the other way (or is too busy to look for themselves, or both).
    Thank you for bringing this up to our awareness, Dr. Mike. It is one of those things that is just plain frustrating. But as per Dr. Malcolm Kendrick, we should not get upset over it.
    Many of these newer tests (particle size, etc) are considered “experimental” and thus are not covered by insurance, unfortunately.

  10. Thanks again Dr. E I love when studies are picked apart. I don’t have the science to do very much of that myself. Regina Wilshire debunks another study in today’s blog entry.
    Hey Rob–
    Problem with this is that Regina and I shouldn’t have to be doing this. The peer-review process should do it instead. It’s a shame that it doesn’t.

  11. Thought this might bring a smile. Bill Maher on Big Pharma, courtesy of PharmaGiles. http://pharmagiles.blogspot.com/ (Jan 7th).
    On the serious side, the situation you write about in this blog piece brings me to this conclusion: a cardiologist (or any other physician for that matter) who is prescribing statin drugs without reviewing papers like this critically and taking the time to penetrate the hogwash and the hidden marketing agenda is in gross violation of the hippocratic oath. How can they practice medicine like that with a clear conscience? Do they care about their patients or their reputations anymore? Truly sickening, in more ways than one.
    Hey Wil–
    Thanks for the Maher link. I’ve seen another of his rants similar to this one.
    Don’t be too hard on the docs out there. Most of them never read the medical literature. They get most of their information from conferences and from throw-away journals – both of which are usually underwritten by the pharmaceutical industry. Doctors are not taught to critically read the medical literature in medical school. I had to teach myself.

  12. You and Dr. Davis both reviewed the same study in your respective blogs on the same day. Bit of different takes but same conclusion. http://heartscanblog.blogspot.com/
    Hi MAC–
    I’m a reader of Dr. Davis’ blog from time to time. I guess today that great minds thought alike. 😉
    His take on the paper was a little more restrained than mine.

  13. Hooray for you!
    A reader of my blog (the Heart Scan Blog at http://theheartscanblog.blogspot.com) advised me that you had also blogged about this study. I was shocked to read your wonderful insights to this study. I am unaccustomed to reading someone else’s writing that actually reveals some true insights into lipoproteins.
    I came to the very same conclusion: small LDL was almost certainly much worsened by the low-fat, high-carbohydrate diet. I suspect that the calorie restriction imposed on the subjects (around 1400 calories per day in each diet arm) also blunted the differences between the diets. Had NO calorie restriction been imposed, there likely would have been a more dramatic divergence in effect between the two diets.
    I don’t know the authors of this study, but I wonder if they were compelled to provide the nonsensical conclusions because of the demands of the journal’s reviewers who, as you know, can hold the promise of publish or no publish, depending on whether you follow their (often lame) advice for modifications in the paper as submitted.
    You sure did a better job of laying out the data from the tables than I did!
    Hey Dr. Davis–
    Good to hear from you. I read your blog from time to time and read your book Track your Plaque over the holidays. I was already pretty much sold on the idea of calcium scores, but your book really convinced me of their merit.
    If the authors of this study were compelled to provide these “nonsensical conclusions” based on the data they came up with, then the peer-review process at the JACC is in pretty sad shape. In fact, simply allowing these conclusions given the data tells me that the peer-review process there needs some work.
    I enjoyed your take on the paper as well. It was a little more restrained than mine. Sometimes I let my disdain for sloppy thinking (or intentional misdirection) override my normally cheery disposition.

  14. Happy New Year Mike,
    You say;
    “We know these folks know about LDL-cholesterol particle size and atherogenicity because they just described it.”
    If you read that last paragraph you quoted again, I’m not so sure. Aren’t they saying that all you need to do is look at the apoB number, which of itself might be a more reliable indicator of the “the actual number of atherogenic lipoprotein particles”? As apoB didn’t change significantly on either diet they then say that atherogenicity didn’t change either.
    OTOH what you (and others) say is that the apoB number needs to be viewed with respect to any change in LDL as a rough marker of any changes in LDL particle size – and it is the result of this calculation which presents a more compelling marker as to changes in atherogenicity.
    And yes, please write a commentary/review and send it in to the Journal of the American College of Cardiology. I’m sure many people would like to see this garbage challenged.
    Happy New Year back, Malcolm.
    Good to hear from you.
    The author’s are assuming that all LDL-cholesterol particles are equally atherogenic, which simply isn’t the case. The smaller ones are more atherogenic than the larger ones (and that’s implying that the larger ones are atherogenic, which I’m not convinced is the case.)
    Clearly if apoB stays the same and LDL-cholesterol levels fall, particle size has to decrease. It was disinginuous of them to try to skate over that by focusing on the fact that the apoB levels were the same in both groups.

  15. I don’t know what’s worse, the glossing over the triglycerides results or the divorcing of apoB from the LDL-C changes. Even if you give them that they didn’t want to go too cutting edge with the triglycerides, the apoB oversight smacks of intentional wordsmithing. Even the layman’s heart books that I have talk about apoB primarily as it relates to particle size. Hard to believe that researchers at this level could accidentally overlook that and discuss apoB levels while ignoring the differing LDL-C readings of the two groups. And shame on the reviewers for not calling them on it! You can’t help but wonder about the funding.
    I couldn’t access the full paper, but from the excerpt you posted, it seemed that they were discussing apoB levels only, and not particle size. Did they actually say in the paper that particle size didn’t change, or do we have to infer that’s their conclusion from their atherogenicity language. Highly misleading, either way.
    This statement raised my eyebrows as well:
    “…the potential long-term health effects of high- and low-carbohydrate weight loss diets remain a concern…”
    Seems to me that both groups should be applauded for losing about a pound a week. Continue that for another 24 weeks or so with either diet and their long-term health effects picture should be improving significantly (more so for the low-carbers, of course). I guess none of this matters, in the conventional wisdom, in the absence of MAGIC cholesterol numbers.
    One final thought on another quote from the commentary:
    “The best diet for the metabolic syndrome is neither of these extremes. Rather, the best is a diet restricted in processed flour and simple carbohydrates, increased in complex carbohydrates and soluble fiber, and high in fish and monounsaturated fats.”
    The restricted simple carb, high complex carb, no read meat, fishy, low sat fat diet wasn’t tested here. So we’re supposed to believe that while the jury was still out on low-carb and low-fat, the case is closed on this diet. Sure.
    Thanks once again making your insight so readily available.
    Hey Steve–
    No, they never discussed particle size beyond what I quoted. They skimmed over it with the smokescreen about the particle number not changing in either group. Very slippery.

  16. Hey Dr. Eades,
    I’m aCipher from my blog at HeartCipher.com I found your blog through Jimmy Moore’s blog and found Jimmy’s blog through Dr. Davis’ blog. I just added your blog here to my blogroll. I like it. I got the cookbook you wrote with MDE and my wife and I have had some success with
    Of course, the lipid results I’ve experienced since going low-carb won’t be any surprise to you but I have been amazed and some docs at my HMO have taken note. Those are here:
    I noticed too that both you and Dr. Davis wrote about the same journal article on the same day. I also thought Dr. D. gave the journal article authors more of a break than they deserved.
    A couple other things…
    Regarding taking documents in or a document list in when seeing a Primary Care Physician about heart health and low carb: I recently did this and described the experience a bit here just last evening here:
    Also, a person named Peter, in a couple of comments at Dr. Davis’ blog, makes an argument about why fasting may work to regress coronary artery plaque. I’m not a scientist or a doctor, but it seems to me that the argument is eminently reasonable. I’m going to explore it with Peter at his blog but I thought you might have thoughts about the argument as well. That Dr. Davis blog post/comment page is here:
    When I first read Peter’s argument, it reminded me more than anything else of the first paragraph of Gary Taubes’ NYT Magazine article a few years back when he described the irony that would be many doctors standing naked in Time Square moment:
    Dr. Fuhrman, a vegan, promotes fasting as a helpful solution for reducing plaque without realizing and surely without understanding that the reason the solution works is because it amounts to increased animal fat consumption.
    It seems to me that Peter’s argument is a profound one that needs to be analyzed and studied. Your thoughts?
    Finally, thanks for your blog. It’s tremendously encouraging to someone with my kind of cardiac history to find support online because getting doctors’ support in person is so hard.
    Hi aCipher–
    Welcome aboard.
    I’m glad you’re enjoying the blog. In my opinion what Peter says is correct. In fact, what he’s describing is a low-carb diet. A low-carb diet is kind of a fast without fasting. A couple of papers have shown pretty clearly that the metabolic improvements brought about by fasting come as a result of the carbohydrate restriction, not simply a restriction of food in general or any other macronutrient. So, you get the fasting benefits without the fast when you restrict carbs.

  17. I’m actually surprised that the VLCHF group didn’t lose more weight than the HCLF group, given the fact that these 2 groups ate the same amount of calories, and they had 24 weeks to show any differences, which I think is pretty long? Does anyone know what the exact macronutrient breakdown was in both groups? A pity no bodyfat percentage measurements were taken since that probably would’ve shown a bigger improvement in the VLCHF group…
    It’s hard to tell because the authors use an Intention to Treat analysis, which makes much of the data worthless in my opinion. I’ll do a post on Intention to Treat sometime soon so that everyone will know what I mean.

  18. For both Gary Taubes and Mike Eades,
    Thank you both for doing what you can to change the world. Thanks. What can we do to help?
    I’ve been asked to have a talk with a friend in my church. He’s diabetic; his feet are literally turning black. He’s an administrative secretary, not a science guy.
    I’m a diabetic who’s lost 60 pounds and kept it off, who keep my A1c at or below 5.3%. I’ll talk to him about low carb, about Bernstein and Eades and Taubes.
    But realistically, who will he believe—me and some non-mainstream writers, or the American Diabetes Association, the Joslin Center, the American Acadamy of Clinical Endocrinologists, the National Cholesterol Education Project, the US Dept of Agriculture, the New England Journal of Medicine, JAMA, the NY Times, the American Dietetic Association, the American Association of Diabetes Educators, Center for Science in the Public Interest, the American College of Sports Medicine and his endocrinologist?
    I’m tired of this. I’m tired of visiting coworkers and friends in the hospital where they’ve had pieces of their feet cut off while following (or trying and failing to follow) bad diet advice. Visiting them in the hospital after heart attacks and seeing them being fed pasta and bread while their bg > 200.
    What can we, the members of the general public, do to change the course of bad advice that flows from these public institutions? What action would be effective?
    Hi David–
    I understand your frustration. I guess all you can do is provide yourself as a good example. All of these groups give people advice that is the nutritional equivalent of telling them to stick their hands in a wood chipper, but the people all seem so willing to follow the advice. It beggars belief.

  19. Hi Dr. Mike! Again a great informative post! Thanks!
    I’m was working on today’s blogging when I came across this:
    Sounds like someone added coincidences together hoping it would equal a fact. Maybe you could give us your take on this sometime?
    Hey Amy–
    Thanks for the link. I hadn’t seen this one. I’ll need to take a look at the data to see what I really think, but on a worst-case scenario basis if it really is true, all one has to do is pop a folic acid supplement that probably costs a nickel to obviate the problem.

  20. One thing weirds me out: since LDL is a calculated result, you appear to be able to test bad LDL because you have good triglycerides. I have really good triglycerides (63!), lowish-but-not-bad HDL (I didn’t exercise for a year because of a car accident, so that’s no surprise) so my LDL is high enough to get me put on a statin. Even if my total cholesterol were within the “guidelines” (it’s just outside), my LDL would be bad bad bad. If I had “normal” TAG, I’d be “fine.” Why are they saying LDL is bad when it’s calculated in part from something worse? (That is a rhetorical question. I know, it sells statins.)
    I’m glad my doctor isn’t an idiot. She said, “I have to call you because these are abnormal. Exercising more would be good, now that you’re healed.”
    You’ve seen the study of first-trimester statin use in women correlating with birth defects, right? I’m not an expert on medical research, but I think I followed the letter. I hope I misread it. I’ve tried to find more recent information, and it seems curiously sparse.
    Hi Daedala–
    The LDL in this study was calculated by use of the Freidwald equation, which is used by most labs. The Friedwald equation was derived back in the old days when everyone was pretty much on higher carb diets and when triglycerides weren’t considered as important as they are today. At that time triglycerides in the 200-300 range were not uncommon. I don’t think the Friedwald equation is accurate with the lower triglyceride levels found in most people on low-carb diets. As a result, I think LDL-cholesterol levels are are often falsely high in those people.
    The birth defects resulting from statins are a real tragedy. When statins first came out the only people who much took them were older women because pre-menopausal women aren’t at much risk for heart disease. Now that statins are being pushed to everyone up to and including kids, women of childbearing age are taking them. And since many women don’t have a clue that they’re pregnant until well into the first trimester it’s easy to see how the incidence of these birth defects will climb. The tragedy is that there is absolutely no evidence whatsoever that statins do anything positive for these women, yet they are prescribed them.

  21. Dr. Eades, many thanks for your work. It was your book, with Dr. MD, that got me into all this. But here’s a worrisome study that I don’t think you’ve covered:
    Ketosis Leads to Increased Methylglyoxal Production on the Atkins Diet
    Any chance you could comment when your schedule allows?
    Hi Gregory–
    I have commented on this study but I did it in the comments section, which is one of the reasons I don’t like to put a lot of time into lengthly comment answers. Most readers of the blog don’t read the comments. I read a dozen or so blogs a day and I never read the comments (neither does MD. In fact, she doesn’t read the comments on my blog, nor do I on hers.) so I’ve got to assume that many other people do the same. The ones who get the posts by RSS (over 1000 people per day) don’t even get the comments I don’t think.
    At any rate, if you go to the this post and look down through the comments to the exchange I had with a reader named Tim Lundeen you can see my take on the study you mentioned. I think there were four or five back and forths.
    The short answer is: don’t worry about it.

  22. A new year brings a new pro-carb campaign:
    Got to love the balanced reporting, too. We’ve got Cynthia Harriman, spokeswoman for the Whole Grain Council in Boston, Wade Moises, chef at Sassi, a high-end Italian eatery in north Scottsdale and Frank Muir, president of the Idaho Potato Commission all chiming in.
    Maybe we should just give up. I mean, is diabetes, heart disease and [put your favorite industrial disease(s) here] really all that bad? After all, somebody has to support the pharmaceutical industry.
    You gotta hand it to them. They never quit. Until they get fat and sick. And then sometimes they still don’t quit.
    Thanks for the link.

  23. If you get a series of comments like the back-and-forth with Lundeen, it might make sense to erase them and combine them into a post of their own.
    Yes, it probably would. Maybe I’ll put it up.

  24. I just finished reading Gary Taubes’ book (couldn’t put it down…read it in 3 days), so this kind of thing seems very normal to me.
    My mother was an Adelle Davis acolyte, so I’ve been in the middle of this kind of controversy for 40+ years. And it’s been frustrating for most of that time. The good thing now is that with the internet, people like you on your blog, Dr. DeVaney, and others can get into the public conversation, decipher some of the bull, and perhaps get the other, correct, side into the argument and the public conversation. That was impossible when Ancel Keys, for instance, first started passing on his bit of misinformation.
    So I think we should be happy for that, and optimistic for the future. Just as in politics, it’s not as easy to get by with shoddy claims and poorly-researched arguments any more.
    Yep, the internet is a wonderful thing that lays waste to all kinds of BS. But it also acts as a vehicle for more BS as well. One has to be able to read and think critically to not be taken it, that’s for sure.

  25. Doc
    just seen this interesting piece that says researchers have found that people with low cholesterol levels find it harder to build muscle!
    The scientist is quoted as saying:
    “Needless to say, these findings caught us totally off guard,”
    Hey Chris–
    I need to pull this paper to see how they came to their conclusions. I’m sure none of the study subjects ate pure cholesterol – they consumed foods high in cholesterol. So how do the authors know it was the cholesterol and not some other component of the food that caused the findings.

  26. Do you have any thoughts on whether low-carbing to the point of ketosis (which is what I do and have done for years precisely because it keeps my triglycerides nice and low, my weight stable and my energy levels high) can increase the body’s production of Advanced Glycation Endproducts (AGEs)? I ask because someone on an IF forum I participate in posted a reference to the study link below regarding the Atkins diet increasing oxoaldehyde methylglyoxal which is an AGE precursor.
    This study was quoted on a derm site — link is below — skip to the question of whether avoiding sugar will help skin:
    I realize you did a terrific post on ketosis not too long ago but this is the first time I’ve read anything about ketosis increasing AGEs. Thoughts?
    Hey Annie–
    Go to this post and scroll down to the comment section. Take a look at the 4-5 comment exchange I had with Tim Lundeen. He asked the same question and I answered there.

  27. It’s only slightly related, because it involves cholesterol, but I thought you might be interested in this report on a study that found that cholesterol plays a role in muscle gain (http://dmc-news.tamu.edu/templates/?a=5549&z=15). It seems that cholesterol is so vilified that even scientists are gobsmacked when it turns out to have benefits.
    Hi Susan–
    Same way they were (and still are) gobsmacked that low-carb diets have therapeutic benefits.

  28. Great post Dr. Mike!
    Just wanted to add a funny anecdote. I’ve been on Protein Power for 18 months and have been exercising a lot and really enjoy it. I’ve had great results.
    After about 12 month on PP I needed to get private medical insurance. They required a blood test, and since I had just had one by my doctor, the results of which were excellent, I had no worries.
    I was shocked to get a rejection letter from the insurer for poor lipids. My LDL was 98, which is optimal, but they flagged my HDL of 112 as ‘high’. How can you have too high of HDL? You can’t as far as I know. Then they added the two numbers together and said my ‘total cholesterol’ of 220 was ‘high’. My triglycerides were 55.
    I thought it was really funny and exasperating, this is a major health insurer, they didn’t know what the different numbers meant. It worked out OK, I wrote them a letter disputing their findings and explaining the numbers, and they eventually wrote the policy. You would think they would understand this stuff without me as a layman having to explain it to them 🙂
    Keep up the great work! Love the blog 🙂
    Truly unbelievable. The depth of their dumbth is sometimes unfathomable.

  29. Dr. Mike, your comment on my TAG is funny, because I haven’t been on a low-carb diet at all. I’m considering starting one and doing all the research I can. (At least I wasn’t trying to eat low-fat. But oh, yes, lots of carbs. Mostly home-made.)
    Can TAG drop too low? Because if it drops on low carb, and it’s already pretty low, maybe I should worry.
    Has it been demonstrated that it’s the statins causing the birth defects? I mean, it seems pretty obvious, but correlation is not causation, even if the correlation is so strong it breaks the heart. From what I can’t tell, they aren’t even trying to research it, but I just tried following up on the papers that cited the 2004 letter.
    Other than a couple of papers I’ve seen, I’m not all that up on the statin-birth defect science. At this point I suspect it’s a correlation, but with these kinds of things it may not get beyond that. Who’s going to do a controlled study?

  30. Hi Dr Mike,
    Another dodgy scientific paper on nutrition. It makes me despair, especially with people like my cousin who is a doctor and married to a very rich property developer. She believes all the mainstream stuff and has no hesitation in prescribing statins. My opinion doesn’t count because I’m not a doctor. (I could have been one, just chose not to.) I mean, she’s actually a very nice person and all, but I thought she had better critical faculties than that. Never mind that before I went low carb, my trigs were through the roof, had an enlarged fatty liver and kidney stones. Why don’t I have these any more?? Couldn’t be the way I eat, could it! The lack of kidney stones alone — passing one is a charming exercise — is enough to keep me on the restricted carb straight and narrow. A couple of months ago said cousin was nonplussed when I said that the way I eat will be mainstream in 5 year’s time. Yes, I am an optimist.
    Now for the actual reason I’m posting this comment: I get RSS feeds via a Firefox toolbar bookmark. When you look up an item you sure do get the comments. It’s probably the reason why I read the comments, being a lazy kind of guy.
    Finally, the usual irrelevant stuff: Am currently on dial-up because the whole family plus my kids’ friends are on summer holidays. Wifeypoos and the kids have been eating junk, junk, junk. I’ve been a bore eating the right stuff. Except that the town we’re staying at has the best oysters in the country, possibly the world, and oysters do have quite a lot of carbs. Mmmmm…..
    I’m on the net now because of beach sunburn and because the seas have been huge, like 4 metre waves. (But fun!!!!) Only been able to make it to the beach the last couple of days due to rain and really rough weather.
    But before we left Sydney, I caught MD’s Messiah excerpts. Fantastic. I bet She Who Must Be Obeyed had fun working up to those high Gs in the Halleluiah Chorus! The American accent seems a bit strange to me in this music, but then I guess Handel’s original performance was with an Irish lilt or brogue.
    Michael Richards
    Hey Michael–
    Enjoy your time at the beach. Sounds like fun.
    You and a couple of others let me know that the comments come through on RSS. I didn’t realize that.
    MD doesn’t mind the high Gs – but the B flats in Beethoven’s 9th nearly killed her.

  31. In one of your comments above you said, “The ones who get the posts by RSS (over 1000 people per day) don’t even get the comments I don’t think.” As well as the RSS for articles, there’s a feed for comments – which I use, and which is how I saw the comments on this post. I find it very helpful, because, as you say, interesting stuff often comes up in the comments, and sometimes it’s long after the original article was posted. I’d never go back over all the old posts looking for new comments. So, thanks for setting up the RSS feed for them, even if you didn’t know you’d done it.
    Hi Janet–
    I certainly didn’t know I had done it, but I guess I’m glad I did.

  32. Hi Dr. Mike,
    I have two questions for you that don’t really fit this post, but hopefully you’ll find interesting enough to be worth your while:
    1) I’ve always been skinnier than I’d like to be. I’ve been low-carbing for about a year, and had up til recently gained a healthy-looking layer of subcutaneous fat for the first time in my life. I’ve recently lost it again (along with almost 10 lbs), and I suspect this may be due to my holiday-season sweet tooth, but I simply can’t make heads or tails of the biology behind what might be happening. Would you be willing to offer any insight into the inner workings of those of us on the opposite end of the metabolic spectrum?
    2) Do you have any opinions on conjugated linoleic acid (CLA), and whether supplementation with it might be a good or bad idea?
    Thanks for your always entertaining blog, and happy new year to the Eades family.
    David Godot
    Hey David–
    Sorry it’s taken me so long to get to your comment, but for some reason you got hung up in my spam filter. I’ve got to apologize, but I’ve just got to say it: Godot has been waiting for me. 🙂
    The problem of inability to gain weight is as frustrating to those who have it as is the inability to lose weight to the rest of us. As I’ve pointed out before, and as Gary Taubes makes much of in his book, the calories in/calories out side of the energy balance equation are not independent variables. When you decrease calories coming in, the calories going out (i.e., energy expenditure) don’t stay the same: they tend to go down as well. Which makes it difficult to lose weight for most people. Overfeeding studies have shown that when calories are greatly increased, so is energy expenditure so that the people consuming the increased number of calories tend to dissipate more of them than expected, and, hence, gain less weight than simply the caloric intake would predict. In your case and in the case of most of those who can’t gain weight, this system works efficiently.
    As to your gaining a nice layer of sub Q fat on the low-carb diet…about 20 years ago Wolfgang Lutz, a German physician, wrote a medical textbook in German (subsequently translated into English) about the use of low-carb diets to treat a multitude of disorders. The book contained a number of photos of patients who had gone from being underweight to being normal weight on low-carb diets. I think a low-carb diet will tend to normalize weight: it reduces excess fat and puts on fat when there are inadequate amounts.
    CLA is not a single fat but a conglomeration of various isomers. Studies have shown many different effects from the administration of CLA. But most CLA supplements contain just one of the many isomers, which leads me to believe that some are probably beneficial while some others are maybe harmful. Until it’s all sorted out, I would prefer to avoid CLA supplements and confine my CLA consumption to that found in meat from animals that are grass fed. Grass feeding increases CLA content of meat and dairy products considerably.

  33. Hi Dr. MRE, Thank you for your blogs — I’ve lost myself 45 lbs on low carb for the last several yrs and really appreciate the info and ideas that share here! the ADA shortly may not be on everyone’s target list b/c their practice guidelines will advise ‘low carb diets’ for wt loss x1yr (not for glucose control, read, wt loss only ). see diabetes.org (under publications) just fyi! I’m a CDE so I counsel many T2DM patients — I’ll tell you this will make the job 400% easier finally.
    I’m glad to see that you’re getting into TYP — I’ve been investigating it since Sept (I wish that I found the light sooner!) and have found studies that back up nearly every strategy (I just haven’t had the time to look e-v-e-r-y-t-h-i-n-g up yet ;-/ ) and have personally seen it work in a secondary CAD individual (ie, cessation of stable angina). I’ve just had another guy tell me yesterday that his ED is ‘TWO TIMES better’ (translation: he stopped using Cialis). DO you see any changes such as this?
    I was curious, how protein power affects CAC scores? I imagine it would improve it significantly but would it dramatically reduce CAC score 10-30% CAC annually as some people are achieving on TYP (conventional TYP *ha* in case you know what that is)?
    Have you been on Oprah yet? How do we get both you and DR. D and MD on that show? (get Oz impeached?)
    guess who is Vit D deficient (which triggered her hypothyroidism, I conjecture)? probably Oprah… wonderful Oz, think u missed that one…
    Hi g–
    You wrote that you were glad to see that I’m getting into TYP…I suppose I would be glad, too, if I only knew what it was. And CAC scores. What are those?
    Haven’t been asked to be on Oprah yet, and I’m not waiting by the phone.

  34. There you go:
    “Statins for all diabetics urged
    People with diabetes should receive cholesterol-busting drugs regardless of whether they have signs of heart disease, UK researchers say.
    Statins cut the risk of heart attack, stroke and death in diabetic people even in those with low cholesterol levels, analysis of 14 trials shows.
    It means hundreds of thousands more people could benefit from treatment, the Lancet report said.
    There are 2.5 million people diagnosed with diabetes in the UK.”
    Jesus wept.
    Bawled his eyes out more like.

  35. Wow, no, certainly no controlled studies (aiee!). But more followups. I’ve hardly found anything. Do they just not want to know?
    No, I don’t think they do.

  36. In response to Janet,
    I, too, get RSS comment feeds. It is the primary way in which I’m alerted to new comments, but also a primary way in which I’m alerted to new posts (by way of comments).
    I completely agree that sometimes comments show up weeks, months, or even years after the original posts, yet they are worth reading (and even commenting on ;)).
    Anyway, wouldn’t it be funny if anthropologists of the future lamented the lameness of Total Cholesterol and LDL particle size?
    Of course, anthropologists of the future would need an adequate brain to do so… uh oh!
    Darwin weeps. And Homo sapien sapien regresses ever more…
    Or, the other scenario: the Darwinian one, suggests that the Ornishes shall become extinct, and the low carbers (the meek) inherit the Earth? 😉
    I’ll settle for just the Ornishes becoming extinct.

  37. Hi,
    You wrote earlier in response to Dr. Davis and his plaque reversal tome “Track Your Plaque”
    ‘Good to hear from you. I read your blog from time to time and read your book Track your Plaque over the holidays. I was already pretty much sold on the idea of calcium scores, but your book really convinced me of their merit.’
    CAC scores are calcium scores on EBT/CT scan (calcium is pathognomic for plaque). What are your experiences and insights on plaque regression with Protein Power? I would imagine that the potential to reduce small dense LDL is there, but does it have any effects on Lp(a) or Homocysteinemia (as Track Your Plaque does)?
    Much respect, g
    Hi g–
    I’ve not worked much on reducing calcium scores because when I left active practice these things were just getting started. I do know that a Protein Power style diet drastically reduces triglycerides and increases LDL particle size because I have measured those directly. And the increased saturated fat in such a diet markedly reduces Lp(a), another phenomenon I’ve seen first hand. The work on homocysteine was also just becoming known – at least to me – when I stopped practicing, and I didn’t have enough patients whom I had checked homocysteine levels on to really get a feel for whether the diet worked for that as well. I would assume that the program as we administered it would have worked because the patients got plenty of vitamin B12 from the diet and plenty of folic acid and vitamin B6 from both the diet and additional supplements.

  38. Hi,
    Today, we had a lecture by one ’eminent’ doctor (who heads the diabetes treatment division in a big hospital at Bangalore-India) on prevention of diabetes through diet and exercise. He appears to have published a lot. When I asked him about low carbing, he had the guts to say that it is irrational and there is no published evidence showing that it works. When I mentioned about my lab values (after an year of LC, that too falling off the wagon every three weeks-for two weeks) the only thing he pointed out was that my Triglycerides are high due to low carbing. I had got it checked two years ago and it was 175. While I know that he was bluffing through his hat (since I have personally read many papers on LC benefits-thanks to your books and blogs) my high! TG and VLDL put me to a great disadvantage in front of the gathering which did not want to believe me anyway. Am I doing something wrong to have those TG numbers?
    My wife is in US (NJ) since one week and we (2 kids with me) will be joining her in March hopefully by the time the 6 Week cure.. gets out. Could we be fortunate to get your signatures on our copies?
    My lab work:
    HBA1C- Jan 2008: 8.5, Jul 2008: 6.9 and Jan 2009: 6.5. I am on 1000 mg Metformin for a year
    Lipids (Jan 09)- TC 189, TG 220, HDL 41, LDL 104, VLDL 44
    Could you please suggest something for staying on LC continuously? I am doing it typically for 3weeks – 2weeks of mindless eating – 3 weeks LC again… pattern.
    The ’eminent’ doctor is an idiot if he thinks your triglycerides are high because of low-carbing. Triglycerides always fall on low-carb diets. I suspect your triglycerides are high because of the two weeks of backsliding you do after every three weeks of low-carbing. I’m planning a post soon on how you can maybe prevent that.

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