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162 thoughts on “Eggs and Atherosclerosis

  1. estockly says:

    >>You’re claiming a successful conspiracy of hundreds of thousands of doctors and researchers, and that’s why you’re wrong.

    I am making so such claim.

    But even when people do make that claim, it does not prove them right or wrong. That is a fallacious argument.

    >>>You’re claiming that you’re smarter than all the people who actually work and do research in the area, using objective measures like cardiac events and deaths to indicate success or failure of interventions, based on you losing weight and reading a book by a science journalist. A respected one, but still – I’m ill-inclined to think a journalist is smarter than so many real scientists.

    I am making no such claim. There are hundreds of doctors, researchers and scientists who are doing work in the field and have embraced this alternate theory. After looking at the evidence and, starting with the impressive body of research done by Taubes and others, I have concluded that the scientists, doctors and researchers who agree with the alternate theory are right.

    >>A fallacy is claiming that “just one study” will overturn an entire body of literature. Skeptics, at least here, don’t ask for “just one study”.

    OK, I was not clear on your meaning, and now I am. And I make no such claim.

    My claim is rather the opposite. I posted links to numerous studies which support the alternate theory. I ask for any studies that contradict the argument that LCHF diets are healthier than LF or CR diets.

    >>Not having the time or inclination to do so, I think instead I will defer to the body of knowledge accumulated and interpreted by genuine experts – not someone posting screeds in the comments section of a website.

    Do skeptics here regularly make arguments from authority and ad hominems? Will you take their word for it or will you ask them to show you the links to the studies?

    >>I’m not sure what you’re trying to say about long-term success of diets – that they reduce weight, or cardiac event risk? That they’re hard to stick with? What do you mean by “success”?

    See my post above where I specified the criteria for success. Do you agree?

    >>Pretty much every diet, which is a form of calorie restriction, will lower weight and with it cardiac risk factors.

    LCHF diets are not calorie restricted. No diets are more effective at lowering weight by burning fat and preserving lean tissue or improving risk factors for CVD and other chronic diseases.

    >>>But diets don’t work over the long term, because you can’t keep losing weight or you’ll die of anorexia. What is really needed is a lifestyle change, which can also be hard – but not as hard as maintaining an extreme restriction diet for your entire life.

    I advocate a LCHF lifestyle change. There can be semantic confusion over the word diet. In once definition it’s a weight loss plan. In another it’s one’s eating patterns. I advocate changing one’s eating patterns to LCHF. A well crafted plan, like Atkins, allows for adjustment in macronutrient composition as the dieter nears and achieves their target weight.

    >>Eat less processed food, eat lots fresh fruits and vegetables, exercise.

    That’s not the worst advice, but for the overweight and obese, that’s not very good advice.

    >>>That seems much more reasonable than eliminating an entire type of food, particularly in the absence of scientific consensus.

    Even if that one food is not necessary for health and nutrition?

    ES

  2. estockly says:

    Correction:

    You know, in Sweeden the government now recommends LCHF diets.

    Typo !

  3. estockly says:

    @Harriet Hall
    >>This seems to be a rehashing of Gary Taubes’ ideas.

    With respect, Dr. Hall, that seems to be a common practice here. To lump someone’s ideas into a broad category in order to dismiss them, rather than consider the arguments on their own merits.

    It’s much easier to dismiss someone as a Cholesterol denier or a conspiracy theorist or, in this case, a rehasher of Taubes, than it is to read the studies and consider the arguments.

    In that spirit, I looked at your review and noticed that you dismissed Taubes analysis of the role of insulin in the storage of fat as a “Theory.” So how is that different than creationists who deny the “theory” of evolution?

    Are you a denier of scientific theory?

    ES

  4. @estockly, is Paleo a diet or religion?

  5. estockly says:

    @skepticalHealth

    >> is Paleo a diet or religion?

    I will try to answer that, even though I don’t follow the Paleo diet.

    “Paleo” is a prefix meaning ancient or older. When it’s used in the paleo-diet it refers to the paleolitic period of human history, which lasted, roughly 2.5 million years. It’s more commonly referred to as the “stone age.”

    The diet consumed by humans during this time varied significantly based on climate, geography and region. But throughout the Paleolithic period there were little or no simple carbs in the human diet. Sugar, from fruit, was available seasonally, and bound with fiber. The human diet consisted of mostly fat and protein, mostly from meats and nuts. The carbs available were almost exclusively complex carbs.

    The paleolithic period ended with the advent of agriculture, when more complex carbs, and a some simple carbs, were added to the human diet.

    Significant consumption of simple carbs (processed flours and sugars) began about 600 years ago.

    Over-consumption of simple carbs is a fairly recent development. (100 years).

    Massive toxic over-consumption of sugars, mostly HFCS is even more recent (20 years).

    The Paleo diet is based on the sciences of nutrition, anthropology and biology. The guiding principle is that for 2.5 million years the human species was able to grow and spread without a large component of carbs in the diet. We evolved on a very low or zero carb diet.

    Today carbs make up the bulk of the western diet, and are the root cause of a number of health problems.

    The Paleolithic diet is a diet based on science, and supported by evidence.

    There. I answered your question.

    Fair is fair. Will you answer mine?

    ES

  6. Harriet Hall says:

    @estockly,

    “It’s much easier to dismiss someone as a Cholesterol denier or a conspiracy theorist or, in this case, a rehasher of Taubes, than it is to read the studies and consider the arguments.”

    But what if I have already read the studies and considered the arguments? Why should I waste time looking at those studies and arguments again? Do you deny that your arguments and studies are similar to Taubes’? If they are different, please explain how they are different.

    “you dismissed Taubes analysis of the role of insulin in the storage of fat as a “Theory.” ”

    No I didn’t. Read again. Perhaps you misread the word “thesis.” I described his “thesis” at the beginning of my article, and I didn’t “dismiss” it, I questioned it and found evidence that appeared to contradict it. I didn’t question the role of insulin in the storage of fat. I didn’t even dismiss his thesis (not theory) about which diet was best. I did point out that the evidence for practical clinical benefits wasn’t in yet, which is exactly what Taubes himself admitted in his book. If Taubes’ thesis is correct, we would expect studies to consistently show a strong superiority of low-carb diets for weight loss and for low fat diets to cause worse health outcomes. They don’t. Yet. I’m inclined to wait for more definitive evidence; Taubes (and apparently, you) are not.

    “Are you a denier of scientific theory?”

    I’m insulted that you asked that question. Of course I’m not!

  7. estockly says:

    Dr. Hall, my question wasn’t intended as an insult.

    >>Read again. Perhaps you misread the word “thesis.”

    OK, I think it’s the word “theoretical” that I found dismissive of the role of insulin in fat storage:

    “He supports his thesis with data from the scientific literature and with persuasive theoretical arguments about insulin, blood sugar levels, glycemic index, insulin resistance, fat storage, inflammation, the metabolic syndrome, and other details of metabolism.”

    Perhaps I hastily concluded that you were being dismissive of “theoretical” arguments. Also, on re-reading I realize I may have read a negative connotation into the word “persuasive” that you may not have intended.

    My concern, then, is you reviewed his book, mentioned his thesis (in a way I originally found was dismissive because it was “theoretical”) but did not address his central theory.

    So, if you’re not dismissing his thesis, and not addressing it in a critical way, are you in agreement with him on his main thesis but differing on his conclusions and recommendations?

    ES

  8. Harriet Hall says:

    No, I don’t agree with Taubes. His thesis is that:

    The calories-in/calories-out model is wrong.
    Carbohydrates are the cause of obesity and are also important causes of heart disease, type 2 diabetes, cancer, Alzheimer’s, and most of the so-called diseases of civilization.
    A low-fat diet is not healthy.
    A low-carb diet is essential both for weight loss and for health.
    Dieters can satisfy their hunger pangs and eat as much as they want and still lose weight as long as they restrict carbohydrates.

    I don’t think there is any convincing evidence for any of these points, and in fact there is evidence against them. Taubes tends to latch onto a grain of truth and go way beyond the evidence. His arguments are based on hypothetical extrapolations from basic science rather than based on the results of clinical studies. Based on currently available evidence, I am provisionally rejecting all these points but I’m quite willing to reconsider if credible new evidence appears.

  9. WilliamLawrenceUtridge says:

    Will you take their word for it or will you ask them to show you the links to the studies?

    Yes, I will absolutely take the word of a consensus of thousands of experts based on knowledge built up over decades. Because I am not an expert in the effects of diet on health. I do not wish to be an expert. At my age, I can’t be an expert. So I rely on experts, and when the consensus is clear, I do not question it. You may think suspicion of genuine expert consensus is something to question. I do not. I think genuine experts who come to an evidence-based consensus are worth listening to. You may think this foolish, but you rely on such a consensus a thousand times a day when you drive, cross a bridge, drink water, use unleaded gasoline and fail to fireproof your home with asbestos. It is arrogance to assume the minority absolutely is correct rather than the milder suggestion that the work is not complete and there is still room for interpretation. Like the CAM proponents, you are promoting an absolutism that makes a caricature of real science.

    My statement about your apparent conspiracy beliefs stems from this statement:

    Nothing like a closed consensus meeting! If one were paranoid, you’d think the organizers would invite only people they know agree with them.

    Perhaps I was wrong in my interpretation, but I don’t believe, given the tenor of your posts and the company that you keep, not to mention the argument you implicitly make, that my interpretation was without merit. I can easily see the same statement being made by Area 51 conspiracy theorists at a NASA meeting, or 9/11 Truthers at a meeting of the 9/11 Commission. Some people aren’t worth inviting to meetings, and some self-proclaimed experts are not seen as such by others.

    I’m pretty much done with your tendentious word games. You can argue specific with others, but I see no reason to pretend your opinion is even close to that of a real expert.

  10. estockly says:

    >>No, I don’t agree with Taubes. His thesis is that:

    >>The calories-in/calories-out model is wrong.

    Well, he certainly argues that it’s the wrong approach for diet. It’s not that simple. If you look at diet as caloric balance then any intervention has to change side one or the other or both. That means eating less and/or exercising more. Those are the two things that make people hungrier and more lethargic.

    To change calories out, you need to do the kinds of exercise that you see on “Biggest Loser.” It’s not realistic.

    To change calories in you need to change the human triggers for hunger and satiety or the response to those. That’s not easy.

    Plus, calories in/out does not speak to fat storage. Simple energy and weight. It doesn’t care if you metabolize fat or lean.

    >>Carbohydrates are the cause of obesity and are also important causes of heart disease, type 2 diabetes, cancer, Alzheimer’s, and most of the so-called diseases of civilization.

    Obesity is excess fat storage. Carbs cause obesity via the blood sugar insulin process. A high carb diet, especially high in simple carbs, leads to CVD, metabolic syndrome T2D and some forms of cancer. A ketogenic diet and a LCHF diet seem to be protective against Alzheimers somewhat.

    There’s good science to support all of that.

    >>A low-fat diet is not healthy.

    Compared to a low carb diet? That’s supported by good science.

    >>A low-carb diet is essential both for weight loss and for health.

    I would use the word “optimal” rather than essential, but yes, supported by good science.

    >>Dieters can satisfy their hunger pangs and eat as much as they want and still lose weight as long as they restrict carbohydrates.

    Again, supported by good science.

    >>I don’t think there is any convincing evidence for any of these points, and in fact there is evidence against them.

    I’ve linked to a page with links to studies, including more than a dozen RCT that support those points. (Here it is again. Yes it’s on a paleo diet page, but it’s the articles that are linked to that matter.)

    http://www.dietdoctor.com/science

    >>Based on currently available evidence, I am provisionally rejecting all these points but I’m quite willing to reconsider if credible new evidence appears.

    I believe this evidence exists and you may find it convincing. What would it take to get you to carefully review a number of these studies? Also, I would like to review on the contrary evidence that you refer to. (I could start with the evidence in your review, is there more?)

    I find the evidence so strong I’m puzzled by why others don’t.

    ES

  11. estockly says:

    >>My statement about your apparent conspiracy beliefs stems from this statement:

    “Nothing like a closed consensus meeting! If one were paranoid, you’d think the organizers would invite only people they know agree with them.”

    >>Perhaps I was wrong in my interpretation

    No. Wrong attribution. That wasn’t me.

    >> I don’t believe, given the tenor of your posts and the company that you keep, not to mention the argument you implicitly make, that my interpretation was without merit.

    I try to keep the tenor of my posts civil. I keep no company. I often disagree, but I try not to be disagreeable.

    >>I can easily see the same statement being made by Area 51 conspiracy theorists at a NASA meeting, or 9/11 Truthers at a meeting of the 9/11 Commission. Some people aren’t worth inviting to meetings, and some self-proclaimed experts are not seen as such by others.

    Again, you are confusing me with someone else.

    ES

  12. Harriet Hall says:

    I said what I had to say in my article. If you’re not able or willing to understand the subtleties of my arguments, that’s your problem.

  13. estockly says:

    >>I’m quite willing to reconsider if credible new evidence appears

    >>I said what I had to say in my article. If you’re not able or willing to understand the subtleties of my arguments, that’s your problem.

    Got it.

  14. Boy, I bet cavemen enjoyed alternating lobster with filet mignon every night, and waking up to fresh grilled bacon and eggs every day, and I’m sure they enjoyed their refridgerated butter and whole fat dairy products up until their ripe old age of 25-30 when they died.

    @estockly, as Harriet already said. We’ve all heard the same old and tired arguments by lipid deniers. We are not YouTube commenters. Most of us are medical professionals, researchers, or very well read individuals. You talk about insulin – most of us know almost everything there is to know about insulin. We know the dozens of different types of insulin, we know the numerous effects that insulin has on cells, and we use insulin to save the lives of people on a daily basis (DKA, severe hyperkalemia, etc.) So you will have to understand that your Mickey Mouse explanation of how insulin works doesn’t do anything to support your position.

    The truth is, I simply don’t care what you think, and it’s not worth my time explaining this yet again to someone who is a follower of the Paleo diet, which is largely panned by dieticians. If you want to be convince yourself that you are leading a healthy lifestyle, that’s perfectly fine. Do what you want. I hope you enjoy it and I hope that you can stay healthy, that would be great. But the facts are, with the evidence we have now, a healthy diet does not consist of large amounts of SFAs. (Also, no one here has ever suggested a diet high in carbs.) It’s just dishonest of you to come in here acting like you understand “scientific theory” and then deny all contrary evidence, as if you are in any way, shape, or form qualified to even comment on a paper, and then mutilate and molest other data to try to fit your almost-Paleo dietary beliefs.

  15. willywisp says:

    @estockly,

    Regarding carbohydrates, have you seen this analysis of Taubes’ hypothesis? Even if you have, the obesity researcher behind the blog has continued to update the piece over time, so you might want to take another look if you haven’t seen it in awhile. It’s an excellent deconstruction.

    http://wholehealthsource.blogspot.com/2011/08/carbohydrate-hypothesis-of-obesity.html

    Regarding fat and cholesterol, I used to earnestly believe the cholesterol skeptics, as you do now. The last few comments from Harriet Hall and SkepticalHealth are probably just going to reinforce your beliefs, so I’d like to help you out with this link:

    http://www.plantpositive.com/

    This guy is anonymous, but he is science-based. On the right-column, you will see his 71-sequence critique of the Paleo Diet and (because they often travel together) low-carbohydrate diets. You will be particularly interested in the following sequences:

    34-35. Cholesterol Denialism
    36-39. The Infamous Ancel Keys
    40-41. Playing Games With Your Heart
    43-45. Anything But LDL
    47-48. Low Carb, High Fad
    49-51. Better Than Low Carb
    52-54. The Best Low Carb Research (Money Can Buy)

    He criticizes Harriet Hall’s post on the China Study in sequence 62, but in my opinion those video sequences (62-65) were among the weakest in his entire set.

    1. Harriet Hall says:

      “He criticizes Harriet Hall’s post on the China Study in sequence 62, but in my opinion those video sequences (62-65) were among the weakest in his entire set.”

      Weak is right. He misinterpreted what what I wrote about Bill Clinton’s diet and assumed I am a follower of Taubes and of the Cholesterol Skeptics when in fact I have written articles criticizing both.

  16. WilliamLawrenceUtridge says:

    No. Wrong attribution. That wasn’t me.

    Oops, you are correct, that was Patohaz. My apologies.

  17. DavidRLogan says:

    @willywisp great link from Stephen Guyenet! He really goes into some hardcore reasons to question Taubes.

    I think that’s a great complement to Dr. Hall’s post. I was just going to post it! So I’m taking half the credit from you :)

  18. jhawk says:

    willywisp,

    Thanks for posting those links, excellent information! Especially the Stephan Guyenet page.

  19. estockly says:

    @SkepticHealth
    >>There’s a tragic story of one of the “board members” of the Weston A. Price Foundation (a pro-saturated fats, cholesterol denying group) who died at age 39 of a heart attack.

    I haven’t been able to find any information about this. Can you provide more details? A name would be helpful.

    ES

  20. estockly says:

    @willwisp

    Thanks for the links RE Taubes, I’ll have a look

    >>Regarding fat and cholesterol, I used to earnestly believe the cholesterol skeptics, as you do now.

    I reject your assertion. There seems to be a tendency to lump people into categories here to make it easier to dismiss them and ignore their arguments.

    I do not “earnestly believe the cholesterol skeptics.”

    Here are my beliefs on cholesterol:

    High levels of LDL with small particles increase risks of CVD (and other chronic diseases).
    Low levels of HDL increase risks of CVD, etc.
    High levels of triglycerides increase risks of CVD.

    The combination of those three increases risks of CVD.

    High levels of HDL decrease risks of CVD
    Low levels of triglycerides decrease risks of CVD
    When LDL particle size is large CVD risk does not increase and may decrease.

    The combination of those three decreases risks of CVD.

    In the 1970′s medicine believed total cholesterol was a primary risk factor.

    Since then we have learned to differentiate between good and bad cholesterol (HDL and LDL)

    And since then we have learned to differentiate between LDL particle sizes.

    What part of that do you dispute?

    That is not cholesterol denial.

    ES

  21. His name was Stephen Byrnes. His “about the author” information included:

    ‘Stephen Byrnes… enjoys robust health on a diet that includes butter, cream, eggs, meat, whole milk, dairy products and offal.’

    Offal… sounds awful! In fact, Stephen Byrnes suffered a fatal stroke in June, 2004. According to reports of his death, he had yet to reach his 40th birthday. The WAPF even addresses his death, and notes “he was a high stress individual, and was very reactive to things.” Wow.

    Now, of course people can have strokes and other cardiovascular events following any number of healthy or unhealthy diets, but in the case of Mr. Byrnes, it’s one of those things where we say “damn…” because he was promoting such an unhealthy lifestyle, and it likely bit him in the rear.

  22. @estockly, I refute your information on LDL particle sizes. While there is a lot of research being done on particle size, and it may be important, we do not have enough good information to make any recommendations regarding managing cardiovascular disease based on LDL particle size. For now, LDL numbers are the ultimate measurement.

    Here is a quote from an email I received from Dr. Steven Nissen, who is a cardiologist at the Cleveland Clinic, and author of a (ridiculous) number of important studies on lipids and cardiovascular disease, from when I asked about the very same thing:

    This is broad advice. LDL subfractions have not been shown to enhance outcomes and they are not endorsed by the NCEP guidelines. These tests are very expensive. Actually, if patients have high triglycerides, they almost always have small dense LDL, so the fractionation adds very little, if anything.

  23. willywisp says:

    @estockly,

    Every belief you listed about triglycerides, HDL, LDL, and particle size is addressed in Plant Positive’s videos. The “Anything But LDL” series addresses lipid biomarkers, so you’ll want to check those out at the very least.

    As far as I can tell, you are still mistaken about cholesterol. Not every one of the cholesterol skeptics is in full agreement with each other, but it is your exact set of beliefs that I believed also.

    If you think the large, fluffy pattern is protecting you from a high LDL-C, and that HDL and triglycerides are both individually more important than LDL, then that is what I dispute.

    A low-carb diet is not a necessary or sufficient requirement to achieve a large LDL pattern anyway. Did you know that a low-carb diet high in dairy fat and red meat will produce small dense LDL?
    http://www.meandmydiabetes.com/2012/04/17/ron-krauss-saturated-fat-red-meat-it-depends/

    People with genetically increased HDL levels do not always seem to experience a reduced CVD risk:
    http://www.eurekalert.org/pub_releases/2012-05/biom-rhn051512.php

    But people with genetically lower LDL levels do in fact enjoy risk reduction:
    http://www.plantpositive.com/blog/2012/4/11/another-devastating-blow-to-the-cholesterol-deniers.html

  24. estockly says:

    @SkepticalHealth’

    >> I refute your information on LDL particle sizes. While there is a lot of research being done on particle size, and it may be important, we do not have enough good information to make any recommendations regarding managing cardiovascular disease based on LDL particle size.

    My information is that small dense LDL particle size is a risk factor for CVD and large buyant LDL particle size is not and may be protective.

    You deny this?

    >>For now, LDL numbers are the ultimate measurement.

    This has changed.

    >>Here is a quote from an email I received from Dr. Steven Nissen, who is a cardiologist at the Cleveland Clinic, and author of a (ridiculous) number of important studies on lipids and cardiovascular disease, from when I asked about the very same thing

    First, I kind of doubt you asked about the “very same thing” because his response is about a closely related thing. But not the very same thing.

    >>This is broad advice. LDL subfractions have not been shown to enhance outcomes and they are not endorsed by the NCEP guidelines. These tests are very expensive. Actually, if patients have high triglycerides, they almost always have small dense LDL, so the fractionation adds very little, if anything.

    Here is where I think you are getting what he is saying wrong.

    “LDL subfractions” is a reference to an expensive test that measures LDL particle size. He’s not saying LDL particle size does not indicate a risk factor for CVD. What he’s saying is that if triglycerides are high, that correlates with low particle size, so the expensive test adds little information.

    He’s a little incomplete, because the correlation is high HDL and low TG = Large LDL particles; low HDL and High TG = small LDL particles.

    It’s interesting that someone else (I think Dr. Hall) made the same mistake you just made. Confusing not needing the expensive test (due to that correlation) with particle size doesn’t matter.

    The point Dr. Nissen is making in that partial quote you provided is the expensive subfraction testing is not needed because triglycerides (and HDL) are predictive of LDL particle size.

    ES

  25. estockly says:

    Here is the full quote from Dr. Hall I referred to:

    The path to LDL-P and Lp(a) is not yet clear.

    “Measuring LDL particle numbers (LDL-P) to predict coronary artery disease risk in healthy individuals should not become part of routine practice, the authors of a new case-control study conclude.”

    http://www.medscape.com/viewarticle/551425

    The study she linked to is not saying particle size doesn’t matter or is not clear. The study is saying LDL particle size correlates with HDL and Triglycerides.

    (It took me a while to find it because it was in a comment, not in the actual post.)

    http://www.sciencebasedmedicine.org/index.php/cholesterol-skeptics-strike-again/

    And, just to add, the LCHF diet in clinical studies results in the best cholesterol/lipid profile. (High HDL; low triglycerides; large LDL particle size.) In most LCHF dieters LDL numbers don’t change significantly but particle size improves significantly. In most LCHF dieters whose LDL number changes, particles size improves .

    http://www.ncbi.nlm.nih.gov/pubmed/17276177

    ES

  26. estockly says:

    >>>Regarding carbohydrates, have you seen this analysis of Taubes’ hypothesis?

    Yes I have. Not sure how to respond, he’s so wrong on so many points the response would be longer than his post, certainly not appropriate for a comment on another post.

    >>
    http://www.plantpositive.com/

    So, since you link to a vegan page you must be a vegan, right? You fad dieter, don’t you know that you can’t believe what vegans say because they are vegans? (To be clear that was sarcasm, Sheldon.)

    >>This guy is anonymous, but he is science-based.

    That’s half right, we don’t know who he is, but while he has some references to science I would think that statement is an insult to science-based writers.

    >>On the right-column, you will see his 71-sequence critique

    Again, wrong wrong wrong, but this is not the forum.

    >>Paleo Diet and (because they often travel together) low-carbohydrate diets.

    But there are important differences.

    >>He criticizes Harriet Hall’s post on the China Study in sequence 62, but in my opinion those video sequences (62-65) were among the weakest in his entire set.

    I confess, I didn’t read the entire set, but I found his comments on Hall’s post as week as any.

    In fact, I would say it was filled with the same inaccurate distortions and mis-statements and ad hominems as the rest of his posts.

    Dr. Hall dared to question the value of a vegan/vegetarian diet lifestyle. She got the same distorted and unscientific response he gave to Taubes and the LCHF diet advocates.

    The China Study Revisited: New Analysis of Raw Data Doesn’t Support Vegetarian Ideology

    http://www.sciencebasedmedicine.org/index.php/the-china-study-revisited/

    ES

  27. It has not changed. You are wrong. There are no evidence based guidelines suggesting treating cardiovascular disease based on any LDL particle size test results.

  28. estockly says:

    >>His name was Stephen Byrnes. His “about the author” information included:

    Thanks. Poor guy.

    >>In fact, Stephen Byrnes suffered a fatal stroke in June, 2004.

    So, not a preventable heart attack?

    >>According to reports of his death, he had yet to reach his 40th birthday. The WAPF even addresses his death, and notes “he was a high stress individual, and was very reactive to things.” Wow.

    Did they also mention he had AIDS? Wow, indeed.

    >>Now, of course people can have strokes and other cardiovascular events following any number of healthy or unhealthy diets, but in the case of Mr. Byrnes, it’s one of those things where we say “damn…” because he was promoting such an unhealthy lifestyle, and it likely bit him in the rear.

    I think the reason you say “damn …” in this case is due to bias. Plain old, old fashion everyday bias. If it agrees with your view you accept unquestioned and trumpet it as truth.

    Strokes are not rare for people with AIDS, regardless of what diet they are on or how young they are.

    http://web.archive.org/web/20050209224345/http://www.powerhealth.net/archives/1May2004.htm

    In all honesty, I think I may have bias in this case too. If you had argued he died because he tried his naturalpathic woo to cure aids, I probably wouldn’t have questioned that.

    Maybe we shouldn’t be so quick to leap to conclusions.

    ES

  29. estockly says:

    @SkepticalHealth

    >>It has not changed. You are wrong. There are no evidence based guidelines suggesting treating cardiovascular disease based on any LDL particle size test results.

    I never said there was. Look at the study I linked to. You don’t need to get the expensive particle size test because LDL particle size correlates with HDL and triglycerides.

    If HDL is high and triglycerides are low, LDL is not an issue because LDL particle size is large. That is what has changed.

    If HDL is low and TG is high LDL is a serious risk factor. That hasn’t changed.

    ES

  30. So, you are arguing that LDL, as measured with a traditional fasting lipid panel, is irrelevant if HDL is high and TG is low. Is that what you are arguing?

  31. estockly says:

    >>So, you are arguing that LDL, as measured with a traditional fasting lipid panel, is irrelevant if HDL is high and TG is low. Is that what you are arguing?

    Yes. That indicates large LDL particle size which does not increase CVD risk and may protect.

    Also, if HDL is low and/or TG is high then LDL is a CVD risk factor.

    ES

  32. Thank you for answering that. It sounds exactly like something that someone who advocates a high fat diet would believe, because a diet rich in saturated fats will indeed elevate LDLs, so why not try to find a way to excuse it?

    There are simply no evidence based guidelines that suggest we should not care about LDLs when HDLs are high and TG is low. In fact, guidelines are based almost solely on LDL measurements, because the vast majority of the evidence demonstrates that LDLs are the best predictor of heart disease. There are other lipoproteins and other biomarkers that are also closely associated with progression to heart disease, but by and large they don’t add much if anything to lipid screening. No doctor worth his salt would ignore elevated LDLs because of favorable HDLs and TGs. Your beliefs simply aren’t supported by much, if any, high quality evidence.

  33. mousethatroared says:

    hmmm, had to go to after hours clinic for stomach/back pain. They can’t tell what’s up, yet * could be gallbladder, kidney stone, ulcer, referred back pain, interstellar parasites with pointy teeth…so don’t eat fatty foods, drinks lots of liquids, try prilosec, Motrin, moist heat**, etc

    Which leads me to the part of the comment that is actually relavant. Besides cardiovascular health, how does the Atkins or Paleo diet effect all of those digestive organs? Setting aside the evolutionary arguments we have seen in SBM comments before, is there actual research on the topic?

    *If ever
    **moist heat can cause quick dental decay in this particular variety interstellar parasite and a toothless parasite is an improvement. (sorry folks, I haven’t gone off the deep end, but I presently can’t stand up without this stupid pain, so I’m laying around, not getting anything done and I’m REALLY bored)

  34. estockly says:

    >>Thank you for answering that.

    You are welcome. I’m wondering why you don’t answer direct questions.

    >>It sounds exactly like something that someone who advocates a high fat diet would believe, because a diet rich in saturated fats will indeed elevate LDLs, so why not try to find a way to excuse it?

    It’s something I believe because there is a lot of good evidence to support it. Also, usually a LCHF diet has a minimal impact on LDLs. But it’s a little complicated. A lot of labs don’t actually measure LDL, but estimate it based on a ratio between HDL and total C and TG in some combination. (I can look it up if you like)

    So if the LCHF diet has no impact on LDL, raises HDL (raising total C) and lowers TG, the lab test report may actually indicate high LDL.

    Physicians may be prescribing statins based on inaccurate reports.

    >>There are simply no evidence based guidelines that suggest we should not care about LDLs when HDLs are high and TG is low. In fact, guidelines are based almost solely on LDL measurements, because the vast majority of the evidence demonstrates that LDLs are the best predictor of heart disease.

    I say it’s true because the studies and evidence show it. You say it’s not true because the people who write the guidelines haven’t said it’s true.

    Argument from authority, much?

    Guidelines are not evidence. They may be from the best authorities, but they do not prove true or false. But even so, some authorities who are writing the guidelines have task forces looking at the LDL particle size issue. Maybe in a few years they’ll change the guidelines.

    Here’s a link to some “guidelines” that do support using LCHF diet for healthy weight loss:

    http://en.wikipedia.org/wiki/Evidence-based_medicine

    >>There are other lipoproteins and other biomarkers that are also closely associated with progression to heart disease, but by and large they don’t add much if anything to lipid screening.

    And lipid screening can be further refined to reveal LDL particle size. Large LDL particle size is not a CVD risk and may be protective.

    (Also, blood pressure is a serious risk factor)

    >>No doctor worth his salt would ignore elevated LDLs because of favorable HDLs and TGs.

    So, a doctor has a patient who is obese with high BP, low HDL, high TG and high LDL. Doctor recommends weight loss and statins.

    Patient comes back 6 months later showing significant weight loss, normal BP, high HDL, low TG and LDL unchanged. Reports feeling better and more active, and that diet change was to LCHF.

    Does said doctor, worth his salt, tell them how unsafe LCHF is? Put them on statins? Recommend changing diet to low-fat calorie restricted?

    >>Your beliefs simply aren’t supported by much, if any, high quality evidence.

    I’m always looking for the best evidence, whether it supports my position or not. The LDL particle size evidence is high quality.

    As is much of the evidence supporting the LCHF diet.

    ES

  35. estockly says:

    >>Besides cardiovascular health, how does the Atkins or Paleo diet effect all of those digestive organs? Setting aside the evolutionary arguments we have seen in SBM comments before, is there actual research on the topic?

    Some of the studies I linked to showed improved liver and kidney function on LC.

    If you’re eating a diet high in simple carbs and processed foods that may be having an impact on those organs plus others (especially the liver) and switching to LCHF may help.

    LCHF won’t help with your acute symptoms, though.

    ES

  36. So, a doctor has a patient who is obese with high BP, low HDL, high TG and high LDL. Doctor recommends weight loss and statins.

    Patient comes back 6 months later showing significant weight loss, normal BP, high HDL, low TG and LDL unchanged. Reports feeling better and more active, and that diet change was to LCHF.

    Does said doctor, worth his salt, tell them how unsafe LCHF is? Put them on statins? Recommend changing diet to low-fat calorie restricted?

    Yes. The doctor should recommend that the patient stay away from non evidence-based fad diets, should keep their saturated fat intake to a minimum, exercise, and DEPENDING upon how high their LDLs are a statin would be started. Remember, LDLs are the best predictors and primary treatment target of cardiovascular disease risk. This is backed up by such a huge mountain of evidence that it’s not even funny.

    We absolutely do *not* base our initial decision to give a statin based on the levels of HDLs and TGs (as in your example, if a patient has a favorable lipid panel, but elevated LDLs, the favorable HDL and TG do *not* cancel out the elevated LDL.) This is because the best evidence shows that LDLs are the best predictors. Favorable HDLs and TGs are not as good of predictors as elevated LDLs. And this is going to be maintained in the new ATPIV guidelines, which should be released later this year. In fact, they are likely gunning at lower (stricter) LDL levels, and it’s looking like there are absolutely no recommendations based on LDL-p or other inflammatory biomarkers, that their use is controversial, but that they may have some utility in further stratifying moderate- to high-risk patients.

    The way I see it, based on the diet you pushing, you have two major problems:

    1. Saturated fats. While there may be some health benefits to them, we have found that replacing saturated fats with unsaturated fats in the diet decreases LDLs and cardiovascular disease risk in a dose-response relationship.

    2. LDLs. Because your diet elevates LDLs, you are now forced to discredit the practice of screening for hyperlipidemia, which is largely based upon a persons LDLs.

    So you have to combat science on multiple fronts: you have to convince people that saturated fats are good for you, you must finagle and twist evidence to support the idea that LDLs are inaccurate, poorly calculated, or otherwise of limited clinical utility, at least under certain scenarios.

    You have your work cut out for you. Good luck.

  37. estockly says:

    >>The doctor should recommend that the patient stay away from non evidence-based fad diets, should keep their saturated fat intake to a minimum, exercise, and DEPENDING upon how high their LDLs are a statin would be started.

    Seriously? I’m flabbergasted. Are you saying LDL is such a key indicator that it’s more of a risk factor than:

    Blood pressure
    Triglycerides
    Obesity
    and outweighs the protective HDL levels

    And that an obese patient on a diet that is working to lose weight and improve most risk factors should go off that diet?

    Isn’t that a potentially harmful intervention?

    >>Remember, LDLs are the best predictors and primary treatment target of cardiovascular disease risk. This is backed up by such a huge mountain of evidence that it’s not even funny.

    LDLs were a good predictor. You’re saying they are so good that they are better than all the other risk factors combined. You do not have a molehill of evidence to support that.

    >>1. Saturated fats. While there may be some health benefits to them, we have found that replacing saturated fats with unsaturated fats in the diet decreases LDLs and cardiovascular disease risk in a dose-response relationship.

    The recommendations had been to replace SF with carbs. Now UF.

    There is no evidence that on a low-carb diet UF are healthier than SF. There is significant evidence that a diet high in SF and low in carbs with moderate protein improves risks for CVD and other chronic conditions.

    Can you explain why the Women’s Health Initiative found no CVD risk benefit to limiting dietary fat?

    >>2. LDLs. Because your diet elevates LDLs, you are now forced to discredit the practice of screening for hyperlipidemia, which is largely based upon a persons LDLs.

    The LCHF diet, per se, does not elevate LDLs. In most cases LDL is not significantly changed. In many cases, lab reports are systematically mis-representing the actual serum LDL (due to the inaccurate ratio mentioned earlier.)

    The science of lipid screening is advancing. So if suggesting that more detailed and better evidence provides a more accurate prediction than current practices is “discrediting” then yes.

    >>So you have to combat science on multiple fronts

    No, I do not combat science. I have a bigger battle to fight.

    Bias. Institutional and other wise. Science is on my side.

    >>You have to convince people that saturated fats are good for you,

    You’re right about that. When I started on this diet that was the hardest obstacle for me. I weighed the risks of continued, and increasing, obesity and a diet higher in saturated fats. It was after I had been on the diet for a few months that I had done enough research and reading to come around on SF.

    >>you must finagle and twist evidence to support the idea that LDLs are inaccurate, poorly calculated, or otherwise of limited clinical utility, at least under certain scenarios.

    I don’t finagle. I point to the studies.

    In terms of finagling evidence, that’s done mostly on the other side, to try to discredit HCLF.

    Seriously. Look at those web pages that were linked to earlier. To “prove” Taubes wrong, they have to argue:

    Insulin doesn’t regulate fat storage
    Insulin doesn’t rise as much with carbs as with Beef
    Blood sugar doesn’t drive insulin
    Eating carbs doesn’t stimulate appetite but suppresses it

    >>You have your work cut out for you. Good luck.

    Thanks, good luck to you too!

    ES

  38. Heh… The hypothetical patient (you…?) lost weight, which helped with their blood pressure. It also had some favorable changes in their lipids, but their LDLs were still elevated. Yes, the standard of care is to keep encouraging weight loss, a healthy diet (one that isn’t heavy in saturated fats), exercise, and if their LDLs are high enough, and depending upon their other cardiac risk factors, a statin may be started.

    You misquoted me when you claimed that I wrote LDLs are the most important thing for everything. We are discussing hyperlipidemia. When treating hyperlipidemia, LDLs are indeed the biomarker used for making treatment decisions. The decision to start a statin or not involves many other factors, you can read about them here:

    http://www.nhlbi.nih.gov/guidelines/cholesterol/atglance.pdf

    You are wrong that it is potentially harmful to encourge a change in diet if a person achieved weightloss through a potentially lethal diet such as your pseudo-Paleo diet. Similarly, if a patient achived weight loss through cocaine abuse, we wouldn’t encourage them to continue using cocaine just because of their weight loss and possible favorable changes in lipids.

    Good luck on “taking down the man!” in your attempt to rationalize eating bacon and steak daily. May the particles be with you.

  39. willywisp says:

    @estockly,

    You ask for the evidence. Then I present some of it to you. Then you say that debating it would be too lengthy and that this is not the forum for it. So what exactly are you expecting to get out of this exchange?

    You say that your views are based on “good science.” Many of us here disagree. Since this forum is not appropriate for us to refute all the science you speak of, what kind of response are you expecting?

    What was the point of accusing me of being a vegan (even if sarcastically), when I am not the one who said you were a paleo dieter?

    I agree that Plant Positive’s anonymity is a downside. But that doesn’t stop you from looking at his arguments and thinking critically about them.

    I’ll even acknowledge that Plant Positive’s videos spend too much time character bashing. But character bashing in and of itself does not qualify as ad hominem — it must also be the sole basis of his argument. Where do you see him committing this fallacy? I didn’t notice any; he always includes other arguments as part of his case.

    As for Stephan Guyenet’s writing, let’s take the four points you mentioned:

    >> Insulin doesn’t regulate fat storage

    Everyone agrees that insulin reduces fat oxidation, even Stephan himself. But insulin also tends to increase glucose oxidation, which is why total energy expenditure is largely unhampered by insulin. This is why long-term body fat regulation is not sufficiently explained by insulin’s effects on LPL and HSL in normal people. Stephan explained this in his article.

    >> Insulin doesn’t rise as much with carbs as with Beef

    Do you disagree with the data from the insulin index? If so, please elaborate why it should be considered faulty.

    >> Blood sugar doesn’t drive insulin

    I don’t recall him (or anyone else) saying this. Can you point out where this claim is being made?

    >> Eating carbs doesn’t stimulate appetite but suppresses it

    Do you disagree with the animal studies suggesting that insulin suppresses appetite in the brain? Do you disagree with the trials that compare carbohydrates against fat, and find that carbohydrates are just as satiating as fat?

  40. estockly says:

    >>Heh… The hypothetical patient (you…?) lost weight, which helped with their blood pressure. It also had some favorable changes in their lipids, but their LDLs were still elevated.

    No. The hypothetical I provided was made up, loosely based on typical patients treated in those studies I linked to (but I’m betting you haven’t read, not even the abstracts.)

    (only discussing my anecdote to answer the question then ask another).

    In my case, my blood pressure was fine; my HDL; LDL; triglycerides were all within the normal ranges. But, when my doctor showed me the trends from the last 5 years, along with my weight, he said I was heading for trouble.

    Blood tests about 18 months later: HDL higher; LDL about the same (actually a little lower, not sig.) triglycerides way down. My doctor and I were very pleased (I gave him a gift of Gary Taubes’ book and heard back from him a few weeks later saying he was reading it). He had recommended the Mediterranean diet and mentioned that he had had patients who had success on Atkins. Since I knew people who had success on Atkins and had learned about the glucose/insulin/fat storage theory, that’s the diet I picked.

    But now I’m curious about my handle my case:

    18 months on Atkins, following it strictly. Healthy HDL; TG; LDL (c and p); good blood pressure; no longer obese, and on the verge of losing weight; burning fat, preserving lean tissue.

    And, before going on LCHF, I had tried low fat; calorie restricted low fat; and low-fat coupled with daily exercise. (None worked). And throughout was fairly active (coached and reffed soccer and other sports).

    Presented with that case history and that lipid panel what would you recommend?

    >>Yes, the standard of care is to keep encouraging weight loss, a healthy diet (one that isn’t heavy in saturated fats), exercise, and if their LDLs are high enough, and depending upon their other cardiac risk factors, a statin may be started.

    So, stop what’s working and go to something that rarely works? That’s kind of like doing harm, isn’t it?

    >>You misquoted me when you claimed that I wrote LDLs are the most important thing for everything.
    >> We are discussing hyperlipidemia.

    I didn’t intend to misquote. And I think what I said stands.

    I also think I understand something better now: The reasons current practice is geared to recognizing and treating elevated LDL are, first, because that’s really all we can do. Statins to lower LDL. Second, because it does reduce stroke and other incidence of CVD. So we have a simple treatment that improves outcomes.

    But we don’t have a good tool for increasing HDL or lowering triglycerides, so everything is focused on LDL first, because we can safely treat that. (We can also safely treat high blood pressure, and we have been for years.)

    Of course, my argument is that a LCHF diet should be the default treatment to improve HDL, TG and LDL particle size. It also lowers blood pressure.

    >>The decision to start a statin or not involves many other factors, you can read about them here:
    http://www.nhlbi.nih.gov/guidelines/cholesterol/atglance.pdf

    Wow, so the guidelines still recommend a diet low in cholesterol. Why is that?

    >>You are wrong that it is potentially harmful to encourge a change in diet if a person achieved weightloss through a potentially lethal diet such as your pseudo-Paleo diet.

    You are wrong that the LCHF diet is potentially lethal. It’s not pseudo-Paleo either. (I don’t eat fruit and do eat Sous Vide meat. Cave men didn’t Sous Vide and they ate fruit seasonally.)

    >>Similarly, if a patient achived weight loss through cocaine abuse, we wouldn’t encourage them to continue using cocaine just because of their weight loss and possible favorable changes in lipids.

    Good. You found something we agree on. I don’t like the analogy, but it’s a clever one, just not valid.

    If LCHF weren’t healthier than the obesity diet people are on now, or the low-fat, low cholesterol calorie restricted diet you’re recommending, it would be a valid analogy.

    >>Good luck on “taking down the man!” in your attempt to rationalize eating bacon and steak daily. May the particles be with you.

    Thanks again for the kind wishes.

    ES

  41. estockly says:

    @ willywisp
    >>You ask for the evidence. Then I present some of it to you.

    First, I wouldn’t say that what you presented was evidence. It was a couple bloggers with axes to grind and a lot of opinion and very little relevant science.

    >>>Then you say that debating it would be too lengthy and that this is not the forum for it. So what exactly are you expecting to get out of this exchange?

    That’s a good question. And I don’t have a good answer. My hope is to convince people that there is an alternative theory to diet and nutrition, which is supported by good science.

    I really don’t hope or expect to persuade anyone in comments on a post to completely change their practice and opinion about LCHF. I’m really hoping they’ll look at the studies I linked to and rethink their positions.

    I think that’s about all I could hope to accomplish. My impression is that most have already made up their minds about LCHF; Atkins and now Paleo, and dismiss them without serious consideration. So may be I’m wasting my time.

    >>You say that your views are based on “good science.” Many of us here disagree. Since this forum is not appropriate for us to refute all the science you speak of, what kind of response are you expecting?

    Actually, I was expecting less in the way of ad hominem and argument from authority and more in the way of serious discussion, since this is a skeptical web site. That said, there is probably less of that crap and vitriol in this discussion than on most internet exchanges.

    >>What was the point of accusing me of being a vegan (even if sarcastically), when I am not the one who said you were a paleo dieter?

    I certainly hope you weren’t offended by that sarcasm, it wasn’t directed at you. I think it made the point, perhaps at your expense, and no, I don’t believe that linking to a vegan’s page in any way suggests you are a vegan. Not that there’s anything wrong with that!

    >>I agree that Plant Positive’s anonymity is a downside. But that doesn’t stop you from looking at his arguments and thinking critically about them.

    I did read a lot of his posts, just not all them.

    >>I’ll even acknowledge that Plant Positive’s videos spend too much time character bashing. But character bashing in and of itself does not qualify as ad hominem — it must also be the sole basis of his argument.

    Didn’t watch the videos. When is character bashing in a discussion about issues, not an ad hominem? Are you saying it’s only an ad hominem if it’s the sole basis of his argument?

    >>Where do you see him committing this fallacy? I didn’t notice any; he always includes other arguments as part of his case.

    Including another argument doesn’t mean he didn’t make an ad hominem argument.

    >>As for Stephan Guyenet’s writing, let’s take the four points you mentioned:
    >> Insulin doesn’t regulate fat storage
    Everyone agrees that insulin reduces fat oxidation, even Stephan himself. But insulin also tends to increase glucose oxidation, which is why total energy expenditure is largely unhampered by insulin. This is why long-term body fat regulation is not sufficiently explained by insulin’s effects on LPL and HSL in normal people. Stephan explained this in his article.

    In his article he said the brain regulates fat storage. Didn’t say how.

    Insuin’s is the hormone that regulates fat storage in adipose tissue in human beings. This is mainstream science. Yes insulin does many other things and there is whole complex side to the equation, but when it comes to fat storage insulin is the key.

    Insulin signaling increases the uptake of fatty acids into fat cells. If fosters the formation of triglycerides inside fat cells. Triglycerides don’t circulate. They have to break down first. Insulin inhibits the breakdown.

    Chronic, high insulin (from high glucose) leads to gradually increased fat storage. The path to obesity usually takes years.

    You’re saying because insulin also manages the uptake of glucose into cells for metabolism that it’s role in fat storage has no effect?

    Fat doesn’t get stored without insulin. Lots of insulin lots of fat storage. Low insulin, fat cells lose fat. Obesity is excess fat storage. Yet your saying insulin has no effect on long term fat storage?

    >>> Insulin doesn’t rise as much with carbs as with Beef
    >>Do you disagree with the data from the insulin index? If so, please elaborate why it should be considered faulty.

    In that particular case, if you look at their methodology they used a lean beef. So, yes a high protein meal will lead to an increase in insulin. But what about regular beef? What about the marbled beef I like so much? If you eat the same number of calories from a marbled steak as the lean beef they used, you’d get a more typical insulin response.

    So he saw the word “beef” in the index, didn’t look up exactly what they were talking about and made an absurd claim based on his bias.

    He also said beef had a similar insulin response as whole grain pastas and bread which he later said was simalr to refined flour.

    Well that’s the same thing I said in one of my earlier comments here. Just cause the label says it’s whole grain doesn’t mean it’s actually whole grain. Look at the FDA definition of whole grain.

    >> Blood sugar doesn’t drive insulin
    >I don’t recall him (or anyone else) saying this. Can you point out where this claim is being made?

    Don’t make me go back there again. Maybe next post

    >> Eating carbs doesn’t stimulate appetite but suppresses it
    >>Do you disagree with the animal studies suggesting that insulin suppresses appetite in the brain?

    No. When you control for all other variables and isolate insulin it may suppress appetite somewhat.

    When people eat, they generally don’t control those other variables and the net effect of people eating high carb, meals is they eat more. (Again, mainstream science, not Taubes, mainstream science.)

    >>Do you disagree with the trials that compare carbohydrates against fat, and find that carbohydrates are just as satiating as fat?

    First I don’t think that’s exactly what those studies found, but it’s close enough.

    Second, there are specific carbs that elicit an addictive response. Sugar and wheat bread to name two. Those two are found to be appetite stimulants.

    Third, if you’re not worried about the calories in/out model, then satiety is not that important.

    On HCLF you can eat all the fat you want, you stop when you’re full, and the result is that you burn stored fat and lose weight.

    Do you disagree with the 15 RCT I linked to that showed that, and also showed the LCHF dieters lost more weight, burned a better proportion of fat to lean and improved risk factors for CVD more when compared to other diets?

    ES

  42. We don’t have a good tool to raise HDLs or lower TGs.

    Not correct. We can give Niacin to raise HDLs, and a fibrate to lower TGs. However, we have found that treating just those numbers do not decrease mortality. So if a patient has good LDLs, but low HDLs, there is no real benefit in treating the low HDLs. The evidence doesn’t find that it improves survival. With TGs, we will usually treat TGs if they are > 500 because that can lead to pancreatitis.

  43. estockly says:

    @ willywisp

    >>>Every belief you listed about triglycerides, HDL, LDL, and particle size is addressed in Plant Positive’s videos.

    Is plant positive the new authority? (Again, sarcasm)

    >>>If you think the large, fluffy pattern is protecting you from a high LDL-C, and that HDL and triglycerides are both individually more important than LDL, then that is what I dispute.

    That’s not how I’d phrase it. I’d say LDL is a risk for CVD when the LDL particles size is small and dense. The large “fluffy” LDL particle size does not increase risk for CVD and may be protective.

    The ratio between Total C; HDL and TG can serve as an accurate indicator of LDL particle size.

    >>A low-carb diet is not a necessary or sufficient requirement to achieve a large LDL pattern anyway.

    Do you know of a more effective way to all of the following: Raise HDL; lower TG; change LDL to large LDL pattern size; reduce blood pressure? Not to mention weight loss achieved through metabolizing more stored fat while preserving lean tissue.

    >>>Did you know that a low-carb diet high in dairy fat and red meat will produce small dense LDL?

    http://www.meandmydiabetes.com/2012/04/17/ron-krauss-saturated-fat-red-meat-it-depends/

    Didn’t know that. It turns out that a diet extremely high in beef, to the exclusion of all other protein, produces a bad lipid profile. Good to know. Not sure if it’s relevant. No one on the LCHF side is advocating this type of eating:

    “…keep in mind, this was a very high beef diet. People were eating beef breakfast lunch and dinner. So this is really way outside of what we would ever consider to be a usual health practice.”

    Did you read the entire interview, he seems to agree with me on LDL particle size and even suggests that’s what most cardiologists think is most important.

    He also suggests the American Heart Association is coming around on this too.

    >>People with genetically increased HDL levels do not always seem to experience a reduced CVD risk:

    That’s a good point, and just to be clear I’ve never said LCHF works for everyone. Also, the studies I linked to show it does not work for everyone.

    That’s why I say it should be the “default” diet rather than the Food pyramid/plate diet based on the USDA guidelines.

    Yes LCHF does not work for everyone but it works better for far more people than our current default diet.

    As to the Plantpositive link, he’s saying because a study shows that drugs that lower HDL don’t improve risks for CVD, LCHF diets don’t work?

    Here’s the thing. The HDL drugs in the study change only HDL. A LCHF diet changes HDL, TG, LDL particle size and lower blood pressure. So, perhaps HDL is a marker rather than the problem. Using a drug to target HDL does not address the underlying metabolic issue. But dramatically changing metabolism through elimination of carbs does.

    Nothing you’ve linked to here convinces me that the large LDL is a risk factor CVD or that the LCHF diet doesn’t offer greater protection for most people than any other diet.

    What am I missing?

    ES

    (I missed this before. With the exception of plantpositive, the articles you linked to here were of much higher quality, and I don’t just mean the one that supported most of my argument on LDL.)

  44. estockly says:

    # SkepticalHealth

    >>>We don’t have a good tool to raise HDLs or lower TGs.
    >Not correct. We can give Niacin to raise HDLs, and a fibrate to lower TGs. However, we have found that treating just those numbers do not decrease mortality. So if a patient has good LDLs, but low HDLs, there is no real benefit in treating the low HDLs. The evidence doesn’t find that it improves survival. With TGs, we will usually treat TGs if they are > 500 because that can lead to pancreatitis.

    That’s a valid point and a good explanation. Thank you

    Let me rephrase:

    The focus is on LDL because we have drugs that lower LDL and work reduce risk for CVD. We don’t have drugs that do both for HDL or TG.

    ES

  45. willywisp says:

    @estockly

    Stephan has actually written a lot about how the brain regulates fat storage, though you’ll need to browse his other posts for it (see “Food Reward”). It’s irrelevant to our discussion, though.

    What you said about insulin upregulating fat storage and downregulating fat release is accurate. But you are missing the big picture. The insulin response is only temporary. Between meals and overnight – when insulin is low – fat burning ramps up again. Over a 24-hour period, body weight remains stable if you are eating to caloric balance. And if you are in caloric deficit, you lose weight. Postprandial insulin does not prevent this from happening.

    I don’t think the claim about beef is “absurd.” I use lean beef in stir-fry. Stephan was using beef to demonstrate that protein generates an insulin response, and it seems like you agree with him on that. Yet high-protein diets cause weight loss, despite the insulin release. That is the paradox that Taubes and others need to address.

    If wheat and sugar are addictive, so what? What does this have to do with rice, beans, corn, potatoes, and other carbohydrates? This is akin to saying all saturated fat is addictive because cheese contains casomorphine.

    > On HCLF you can eat all the fat you want, you stop when you’re full, and the result is that you burn stored fat and lose weight.

    Are you implying that you can be in energy surplus and lose weight on HCLF? Or are you just saying that HCLF works by increasing satiety (which you had just previously said was “not that important”)?

    > Do you disagree with the 15 RCT I linked to

    I agree that LC diets often lead to faster weight loss than LF diets. And this can always explained by a spontaneous reduction in caloric intake.

    But it doesn’t follow that high-carb diets stimulate appetite. Ad-libitum intake of high-carb vegan diets, for example, have also been shown to cause weight loss. The satiating effect just may not be as great as LC. I’m certainly open to that idea.

  46. willywisp says:

    @estockly

    > Did you read the entire interview, he seems to agree with me on LDL particle size

    Yes, I read the interview. Krauss is sympathetic to low-carb, so I’m not saying I agree with every opinion he voices. But his view on LDL particle size is more nuanced than you give him credit for:

    Krauss: “In terms of health, the first order of business is to make sure the total number of particles in a person’s blood is maintained in the healthy range, because that’s what dictates heart disease risk. Beyond that, when the total amount of cholesterol is unusually high, you’ll almost always find that the total number of LDL particles is high.”

    In short, high total cholesterol is almost always atherogenic, regardless of particle size.

    Krauss says that large LDL is preferable to small LDL because it implies a lower LDL particle count. A high number of LDL particles of any size is still atherogenic. You can lower LDL-P by changing the particle size, but you can also do it by lowering LDL-C.

    Small, dense LDL is even decreased when consuming moderate-fat meals compared to high-fat meals:
    http://www.ncbi.nlm.nih.gov/pubmed/21420840

    > As to the Plantpositive link, he’s saying because a study shows that drugs that lower HDL don’t improve risks for CVD, LCHF diets don’t work?

    The Plant Positive link doesn’t even mention HDL. Are you sure you looked at the right one? He talks about LDL.

    > Nothing you’ve linked to here convinces me that the large LDL is a risk factor CVD

    I didn’t say large LDL is a risk factor. I just don’t think it’s as protective as you believe. After all, people with familial hypercholesterolemia have large LDL and they still have a substantially increased risk of coronary artery disease.

    > or that the LCHF diet doesn’t offer greater protection for most people than any other diet.

    There is evidence to suggest that low enough LDL-C might even reverse atherosclerosis, and vegan advocates are touting this as an advantage of their diets. Do any LCHF advocates make a similar claim? I think reversal is a pretty good sign of optimal protection.

  47. estockly says:

    @ willywisp
    >>Stephan has actually written a lot about how the brain regulates fat storage, though you’ll need to browse his other posts for it (see “Food Reward”). It’s irrelevant to our discussion, though.

    Fat storage happens at the cellular level. It is regulated by the hormone insulin. Insulin is not regulated by the brain, it is produced in response to blood sugar. The brain does not regulate blood sugar, that rises following a high carb meal or when the body makes it’s own glucose.

    The brain regulates appetite, but even that is somewhat in response to hormones. (Leptin, for example.). But even when appetite goes up and satiety goes down, the individual can choose to satisfy hunger with low carb foods, and control their blood sugar/insulin/fat storage cycle.

    The brain simply does not regulate fat storage. It responds to signals of hunger and satiety. Fat storage is a chemical process dependent on insulin (and a few other factors).

    >>What you said about insulin upregulating fat storage and downregulating fat release is accurate. But you are missing the big picture. The insulin response is only temporary.

    The insulin response lasts as long as insulin in circulation. That is generally hours. But, fat storage doesn’t go away as soon as insulin drops. Fat is stored rather quickly, breakdown of TG is a slower process, particularly when metabolic requirements have dropped. (overnight). Many overweight and obese have high fasting insulin levels.

    >>Between meals and overnight – when insulin is low – fat burning ramps up again.

    Insulin does not drop between meals and overnight for everyone. Also, many people get in the habit of having high carb snacks (a little hot chocolate, for example) before bed and high carb snacks between meals, further lowering the period of low-blood sugar/low insulin.

    >>Over a 24-hour period, body weight remains stable if you are eating to caloric balance. And if you are in caloric deficit, you lose weight. Postprandial insulin does not prevent this from happening.

    The issue is not weight, it is fat storage. Insulin does not regulate body weight. Insulin regulates fat storage. If insulin is high you will store fat. The FFA will not be available for metabolism. If that puts you at a deficit your brain will seek more food. Your metabolism will slow to conserve energy. If you’re still at a deficit you will metabolize lean tissue, which insulin does not prevent. But insulin does prevent metabolism of stored fat.

    >>I don’t think the claim about beef is “absurd.” I use lean beef in stir-fry. Stephan was using beef to demonstrate that protein generates an insulin response, and it seems like you agree with him on that.

    Maybe “absurd” is not the best word. Perhaps misleading. The implication that “beef” as a food category triggers an insulin response higher than carbs is an inaccurate generalization. They only tested lean beef, which is mostly protein.

    >>Yet high-protein diets cause weight loss, despite the insulin release. That is the paradox that Taubes and others need to address.

    First, it’s not a paradox following the calories in/calories out model. People lose weight on high protein because they ingest fewer calories and/or burn more. (There are a number of issues with high protein diets. LCHF is not high protein.)

    Second, again it’s not the weight, the issue is fat storage. Compared to high protein diets, people on low carb diets burn more fat and preserve or build more lean tissue.

    Third, the process that high protein meals raise insulin is through gluconeogenesis. This is a process that takes time. Much like the breakdown of some complex carbs. So while it will create an insulin response it does not create the kind of insulin spike a meal with simple carbs does. (The II does not account for insulin spikes, but total insulin produced.)

    >>If wheat and sugar are addictive, so what?

    Those two foods are simple carbs which which cause the fastest and highest blood sugar/insulin spikes.

    >>What does this have to do with rice, beans, corn, potatoes, and other carbohydrates?

    Not much, but when the appetite goes up, those come along for the ride.

    >>This is akin to saying all saturated fat is addictive because cheese contains casomorphine.

    I should have said “Some foods highest in simple carbs and consumed in large qualities in the typical western diet are addictive.”

    But, to say that Carbs as a food group don’t stimulate appetite because corn and beans and rice don’t is equally inaccurate.

    >>> On HCLF you can eat all the fat you want, you stop when you’re full, and the result is that you burn stored fat and lose weight.

    >>Are you implying that you can be in energy surplus and lose weight on HCLF?

    No that’s not my implication. On a high carb diet, you have less lethargy. You burn more calories and …

    >>Or are you just saying that HCLF works by increasing satiety (which you had just previously said was “not that important”)?

    and you have less food cravings, you don’t need a blood sugar boost every few hours and the LCHF diet does increase satiety.

    On a calories in/calories out diet satiety is key. On a LCHF diet, satiety is only one component.

    It’s also not important for the dieter. You simply eat when you’re hungry, when you’re full stop. As long as carbs are kept to a minimum and simple carbs are avoided, you will burn fat, preserve lean tissue and lose weight.

    >>> Do you disagree with the 15 RCT I linked to

    >>I agree that LC diets often lead to faster weight loss than LF diets.

    You cut off the rest of my question. Does that mean you disagree with the study findings that LCHF diets lead to improved risk factors for CVD and other chronic diseases and result in burning more fat while preserving lean tissue?

    >>And this can always explained by a spontaneous reduction in caloric intake.

    That’s not always the case. In some of those studies, those on LCHF lost more weight while consuming as many if not more calories.

    In some cases the diets were isocaloric (which makes them modified LCHF, but they still did better.) In other cases they were ad lib fat.

    >>But it doesn’t follow that high-carb diets stimulate appetite.

    I don’t think I said that. If I did, what I should have said that the typical high carb western diet stimulates appetite. And calorie restricted high carb diets leave people hungry.

    >>Ad-libitum intake of high-carb vegan diets, for example, have also been shown to cause weight loss. The satiating effect just may not be as great as LC. I’m certainly open to that idea.

    You know there are LC vegans too. If it’s ad-lib, then then the satiating effect is the same. You eat as much as you want. Vegan diets are generally high carb, but most vegans I know eat mostly complex carbs (whole foods, plants veggies) and less refined sugars and flours. I don’t believe that’s as good of a weight loss diet as LCHF, but I believe it is not as obsegenic as the typical western diet.

    >>>You can lower LDL-P by changing the particle size, but you can also do it by lowering LDL-C.

    Agreed. Probably why statins work.

    >>Small, dense LDL is even decreased when consuming moderate-fat meals compared to high-fat meals

    That’s not relevant to the LCHF discussion. Carbs are the key. They have the biggest influence on the metabolism. So if carbs are high (more then 50% of cal) or moderate (more than 30% of cal) the studies don’t apply to LCHF.

    >>>The Plant Positive link doesn’t even mention HDL. Are you sure you looked at the right one? He talks about LDL.

    Maybe not. He seemed very excited about a study and linked to in the first graph. I am responding to his misinterpretation of that study. I’d much rather read that then his crap. Are you saying that post wasn’t about what he talked about in his lead and the headline?

    >>I didn’t say large LDL is a risk factor. I just don’t think it’s as protective as you believe.

    What I’ve said repeatedly is LDL is not a risk factor and may be protective.

    I haven’t said I believe it is, but there is evidence it may be. I think the jury is still out.

    >>There is evidence to suggest that low enough LDL-C might even reverse atherosclerosis, and vegan advocates are touting this as an advantage of their diets. Do any LCHF advocates make a similar claim? I think reversal is a pretty good sign of optimal protection.

    Yes. High HDL (not induced by drugs) and low TG do lead to halting and reversing atherosclerosis. Plus, the LCHF diet is anti-inflammatory (a ketogenic diet even more so) which also helps.

    ES

  48. Patohaz says:

    I see a lot has happened. Unfortunately I have no time to read through posts in the past two days.

    However, I have some comments on Dr. Hall’s post and to Alia and estockly from before Saturday morning. I am probably breaking blogging protocol, but the consensus committee invited agreed.

    @Alia
    Glad it works. You have very impressive self-discipline. Keep doing what you are doing [my advice is no way intended to take the place of professional medical advice. Consult a physician prior to making any changes in diet].

    @Dr. Hall
    Taubes points out clearly in his book that the USDA dietary guidelines were also adopted before being tested, and there was no consensus at the time. You seem to have no problem with this.

    In your post you state:

    “He [Taubes] says that [restricting carbohydrates]…leads to weight loss and particularly fat loss, independent of the calories we consume from dietary fat and protein. We know that the laws of physics have nothing to do with it.

    This is simply not true. The laws of physics are unavoidable. His demonization of the calories-in/calories-out principle strikes me as a bit of a straw man argument. He says exercising and reducing total calorie intake don’t work; moreover, he says they can’t work. Most of us would argue that they can and do; the problem is not with the principle, but with its implementation. Simple physics requires that to lose weight, we must burn more calories than we ingest: that is indisputable. The devil is in the details. It takes a lot of exercise to burn off a few calories, so exercise is not a practical solution; and it has proved very difficult in practice to get people to reduce their calorie intake significantly over long periods of time. Weight loss is simple, but it is not easy; and those of us who rely on the calories- in/calories-out principle have never suggested that it was. We don’t just berate obese people for lack of will power. We try to understand why most people find it so difficult to lose weight. Perhaps the more intriguing question is why some people maintain a low weight throughout a long lifetime of varying food intake, including people who eat a lot of carbohydrates.”

    The laws of physics are unavoidable, but you leave out all of the details. Thermodynamics is far more complicated and not limited to the first law. A review of why the type of fuel is important is found here:
    Feinman R and Fine E. “A calorie is a calorie” violates the second law of thermodynamics, Nutrition Journal 2004, 3:9 http://www.nutritionj.com/content/3/1/9

    If provoked I will provide more on this point.

    You go on to state that “There are social and cultural influences and practical considerations; but the basic problem is that because of their genetic makeup, some people’s bodies are more efficient at storing calories.”

    Does this not violate calories in/out? Actually it doesn’t, if you accept the second law – that various inefficiencies in chemical loops, or cycles will vary for individuals, but you clearly state a calorie is a calorie. Which is it?

    If you need a more concrete example of calories not balancing in the expected way, refer to the WHI initiative I cited earlier, and that was included as the largest study in the meta-analysis that Dr. Novella cited. You can also look at this study, which maintained a calorific deficit constant, but showed significantly more weight loss for low carbohydrate diets. There are more studies, too.

    JS Volek*, MJ Sharman, AL Gómez, DA Judelson, MR Rubin, G Watson, B Sokmen, R Silvestre, DN French and WJ Kraemer, Comparison of energy-restricted very low-carbohydrate and low-fat diets on weight loss and body composition in overweight men and women, Nutrition & Metabolism 2004, 1:13 http://www.nutritionandmetabolism.com/content/1/1/13

    You cite the following: JAMA. 2003 Apr 9;289(14):1837-50.
    Efficacy and safety of low-carbohydrate diets: a systematic review.
    Bravata DM, Sanders L, Huang J, Krumholz HM, Olkin I, Gardner CD, Bravata DM.

    From the article body (not the abstract!):
    “Of the 34 [references] 21 ,26 ,39 ,42 – 43 ,53 ,67 ,75 – 76 ,78 – 80 ,82 ,84 ,88 – 89 ,95 – 98 ,102 ,106 ,109 ,111 – 112 ,116 – 118 ,121 of 38 lower-carbohydrate diets for which weight change after diet was calculated, these lower-carbohydrate diets were found to produce greater weight loss than higher-carbohydrate diets (absolute summary mean [SD] change, 16.9 [0.2] kg; 95% CI, 16.6-17.3 kg vs 1.9 [0.2] kg; 95% CI, 1.6-2.2 kg) (Table 5). Because the 95% CIs for the lower- and higher-carbohydrate diets do not overlap, it suggests that a difference may exist in weight change between the 2 types of diets. However, the highly heterogeneous nature of the 34 diets is reflected in the significant Q statistic associated with the summary mean changes in weight calculated when all studies were included in the analysis. Given this heterogeneity, little can be concluded about the summary mean change in weight loss when all studies are combined. When only the randomized controlled trials and the randomized crossover trials in the analysis are included, the result of the Q statistic suggests that the studies are homogeneous. From this selected group of relatively similar randomized studies of 7 lower-carbohydrate diets [references 21 ,26 ,39 ,42 - 43 ,53 and 75] higher-carbohydrate diets we found that the absolute summary mean [SD] change decrease in weight for lower-carbohydrate diets was 3.6 (1.2) kg (95% CI, 1.2-6.0 kg) and for higher-carbohydrate diets was 2.1 (0.3) kg (95% CI, 1.6-2.7 kg). This overlap in 95% CIs suggests no difference in weight loss between the lower- and higher-carbohydrate diets.”

    I am not an expert in statistics, however something looks like it needs a bit more explaining. 16.9 kg vs 1.9 kg is a rather big difference favoring low carb diets. And it is fascinating to see the writing style. “Because the 95% confidence intervals do not overlap, it suggests that a difference may exist…”, a basic lesson in stats 101 for dummies followed by discussion of Q statistic without stating it? I am (genuinely!) interested if the Q statistic could completely eliminate the relevance of this difference, and why was it not stated. Or if it would be more appropriate to stated in the article that although there was statistically more weight loss on carbohydrate restricted diets the highly heterogeneous nature of the diets resulted in a high Q statistic suggesting that the result may not be valid”

    You then make a very odd statement:

    “He admits that it is a real challenge to overcome carbohydrate cravings, which amount to an addiction. He admits that high protein diets can be toxic. He also admits that people who restrict carbohydrates tend to eat less, and he says their energy expenditure increases. Wait! This sounds like support for very calories-in/out principle that he rejects.

    That fact that he admits that overcoming carb cravings is difficult – this is why it is hard to lose weight while eating a diet containing significant amounts of carbs, and is part of his argument for eating low carb foods. Protein he already dealt with, based on, if I recall, problems experienced by the Inuit when deprived of enough fat. “He also admits” – you mean he states that people eat less and have more energy on low carb diets. Yes, but you are in the paradigm of the first law and reject the second. Consider that if you are in ketosis, you have ready access to an order of magnitude more stored energy than if you rely on glucose/glycogen and that one is not fighting cyclical crashes in blood sugar. There is more going on that the first law which says nothing about kinetics.

    The 2001 Cochrane review and selective quoting – you mean he actually read the article not just the abstract? How dare he! You go on to selectively quote the abstract. [For those confused, read Dr. Hall’s post and the article.]

    Your 2010 article regarding Swedish men is observational only as is your next citation Nurses’ Health Study and Health Professionals’ Follow-up Study, and the China Study. Why not WHI, a RCT and a big one at that?

    You then cite an article by Sacks et al. which was completely irrelevant. From the article:

    “The nutrient goals for the four diet groups were: 20% fat, 15% protein, and 65% carbohydrates (low-fat, average-protein); 20% fat, 25% protein, and 55% carbohydrates (low-fat, high-protein); 40% fat, 15% protein, and 45% carbohydrates (high-fat, average-protein); and 40% fat, 25% protein, and 35% carbohydrates (high-fat, high-protein).”

    No low carb group in the study at all, and pretty sad results all around. And then you go to cite the editorial on the article. Well, how about this one, [@WLU and SH: note the author, if appeals to authority are your thing]. I am jetlagged and will be leaving you alone for now and end with Uncle Walt:

    “For decades, nutritionists and dietitians have disparaged the very-low-carbohydrate Atkins diet because it is high in saturated fat and because its purported benefits had not been tested in formal studies. According to the conventional wisdom, a diet low in fat and high in starch reduces the risks for heart disease and cancer and promotes weight loss. However, these claims do not have solid evidence to support them.”

    “The primary remaining justification for high-starch diets diets has been weight control, but even this rationale is on shaky ground.”

    “We can no longer dismiss very-low-carbohydrate diets.”

    Willet, W. ,”Reduced Carbohydrate Diets: No roll in weight management?”, Ann Intern Med. 18 May 2004;140(10):836-837
    http://annals.org/article.aspx?volume=140&page=836

  49. Patohaz says:

    I see a lot has happened. Unfortunately I have no time to read through posts in the past two days.

    However, I have some comments on Dr. Hall’s post and to Alia from before Saturday morning. I am probably breaking blogging protocol, but the consensus committee invited agreed.

    @Alia
    Glad it works. You have very impressive self-discipline. Keep doing what you are doing [my advice is no way intended to take the place of professional medical advice. Consult a physician prior to making any changes in diet].

    @Dr. Hall
    Taubes points out clearly in his book that the USDA dietary guidelines were also adopted before being tested, and there was no consensus at the time. You seem to have no problem with this.

    In your post you state:

    “He [Taubes] says that [restricting carbohydrates]…leads to weight loss and particularly fat loss, independent of the calories we consume from dietary fat and protein. We know that the laws of physics have nothing to do with it.

    This is simply not true. The laws of physics are unavoidable. His demonization of the calories-in/calories-out principle strikes me as a bit of a straw man argument. He says exercising and reducing total calorie intake don’t work; moreover, he says they can’t work. Most of us would argue that they can and do; the problem is not with the principle, but with its implementation. Simple physics requires that to lose weight, we must burn more calories than we ingest: that is indisputable. The devil is in the details. It takes a lot of exercise to burn off a few calories, so exercise is not a practical solution; and it has proved very difficult in practice to get people to reduce their calorie intake significantly over long periods of time. Weight loss is simple, but it is not easy; and those of us who rely on the calories- in/calories-out principle have never suggested that it was. We don’t just berate obese people for lack of will power. We try to understand why most people find it so difficult to lose weight. Perhaps the more intriguing question is why some people maintain a low weight throughout a long lifetime of varying food intake, including people who eat a lot of carbohydrates.”

    The laws of physics are unavoidable, but you leave out all of the details. Thermodynamics is far more complicated and not limited to the first law. A review of why the type of fuel is important is found here:
    Feinman R and Fine E. “A calorie is a calorie” violates the second law of thermodynamics, Nutrition Journal 2004, 3:9 http://www.nutritionj.com/content/3/1/9

    If provoked I will provide more on this point.

    You go on to state that “There are social and cultural influences and practical considerations; but the basic problem is that because of their genetic makeup, some people’s bodies are more efficient at storing calories.”

    Does this not violate calories in/out? Actually it doesn’t, if you accept the second law – that various inefficiencies in chemical loops, or cycles will vary for individuals, but you clearly state a calorie is a calorie. Which is it?

    If you need a more concrete example of calories not balancing in the expected way, refer to the WHI initiative I cited earlier, and that was included as the largest study in the meta-analysis that Dr. Novella cited. You can also look at this study, which maintained a calorific deficit constant, but showed significantly more weight loss for low carbohydrate diets. There are more studies, too.

    JS Volek*, MJ Sharman, AL Gómez, DA Judelson, MR Rubin, G Watson, B Sokmen, R Silvestre, DN French and WJ Kraemer, Comparison of energy-restricted very low-carbohydrate and low-fat diets on weight loss and body composition in overweight men and women, Nutrition & Metabolism 2004, 1:13 http://www.nutritionandmetabolism.com/content/1/1/13

    You cite the following: JAMA. 2003 Apr 9;289(14):1837-50.
    Efficacy and safety of low-carbohydrate diets: a systematic review.
    Bravata DM, Sanders L, Huang J, Krumholz HM, Olkin I, Gardner CD, Bravata DM.

    From the article body (not the abstract!):
    “Of the 34 [references] 21 ,26 ,39 ,42 – 43 ,53 ,67 ,75 – 76 ,78 – 80 ,82 ,84 ,88 – 89 ,95 – 98 ,102 ,106 ,109 ,111 – 112 ,116 – 118 ,121 of 38 lower-carbohydrate diets for which weight change after diet was calculated, these lower-carbohydrate diets were found to produce greater weight loss than higher-carbohydrate diets (absolute summary mean [SD] change, 16.9 [0.2] kg; 95% CI, 16.6-17.3 kg vs 1.9 [0.2] kg; 95% CI, 1.6-2.2 kg) (Table 5). Because the 95% CIs for the lower- and higher-carbohydrate diets do not overlap, it suggests that a difference may exist in weight change between the 2 types of diets. However, the highly heterogeneous nature of the 34 diets is reflected in the significant Q statistic associated with the summary mean changes in weight calculated when all studies were included in the analysis. Given this heterogeneity, little can be concluded about the summary mean change in weight loss when all studies are combined. When only the randomized controlled trials and the randomized crossover trials in the analysis are included, the result of the Q statistic suggests that the studies are homogeneous. From this selected group of relatively similar randomized studies of 7 lower-carbohydrate diets [references 21 ,26 ,39 ,42 - 43 ,53 and 75] higher-carbohydrate diets we found that the absolute summary mean [SD] change decrease in weight for lower-carbohydrate diets was 3.6 (1.2) kg (95% CI, 1.2-6.0 kg) and for higher-carbohydrate diets was 2.1 (0.3) kg (95% CI, 1.6-2.7 kg). This overlap in 95% CIs suggests no difference in weight loss between the lower- and higher-carbohydrate diets.”

    I am not an expert in statistics, however something looks like it needs a bit more explaining. 16.9 kg vs 1.9 kg is a rather big difference favoring low carb diets. And it is fascinating to see the writing style. “Because the 95% confidence intervals do not overlap, it suggests that a difference may exist…”, a basic lesson in stats 101 for dummies followed by discussion of Q statistic without stating it? I am (genuinely!) interested if the Q statistic could completely eliminate the relevance of this difference, and why was it not stated. Or if it would be more appropriate to stated in the article that although there was statistically more weight loss on carbohydrate restricted diets the highly heterogeneous nature of the diets resulted in a high Q statistic suggesting that the result may not be valid”

    You then make a very odd statement:

    “He admits that it is a real challenge to overcome carbohydrate cravings, which amount to an addiction. He admits that high protein diets can be toxic. He also admits that people who restrict carbohydrates tend to eat less, and he says their energy expenditure increases. Wait! This sounds like support for very calories-in/out principle that he rejects.

    That fact that he admits that overcoming carb cravings is difficult – this is why it is hard to lose weight while eating a diet containing significant amounts of carbs, and is part of his argument for eating low carb foods. Protein he already dealt with, based on, if I recall, problems experienced by the Inuit when deprived of enough fat. “He also admits” – you mean he states that people eat less and have more energy on low carb diets. Yes, but you are in the paradigm of the first law and reject the second. Consider that if you are in ketosis, you have ready access to an order of magnitude more stored energy than if you rely on glucose/glycogen and that one is not fighting cyclical crashes in blood sugar. There is more going on that the first law which says nothing about kinetics.

    The 2001 Cochrane review and selective quoting – you mean he actually read the article not just the abstract? How dare he! You go on to selectively quote the abstract. [For those confused, read Dr. Hall’s post and the article.]

    Your 2010 article regarding Swedish men is observational only as is your next citation Nurses’ Health Study and Health Professionals’ Follow-up Study, and the China Study. Why not WHI, a RCT and a big one at that?

    You then cite an article by Sacks et al. which was completely irrelevant. From the article:

    “The nutrient goals for the four diet groups were: 20% fat, 15% protein, and 65% carbohydrates (low-fat, average-protein); 20% fat, 25% protein, and 55% carbohydrates (low-fat, high-protein); 40% fat, 15% protein, and 45% carbohydrates (high-fat, average-protein); and 40% fat, 25% protein, and 35% carbohydrates (high-fat, high-protein).”

    No low carb group in the study at all, and pretty sad results all around. And then you go to cite the editorial on the article. Well, how about this one, [@WLU and SH: note the author, if appeals to authority are your thing]. I am jetlagged and will be leaving you alone for now and end with Uncle Walt:

    “For decades, nutritionists and dietitians have disparaged the very-low-carbohydrate Atkins diet because it is high in saturated fat and because its purported benefits had not been tested in formal studies. According to the conventional wisdom, a diet low in fat and high in starch reduces the risks for heart disease and cancer and promotes weight loss. However, these claims do not have solid evidence to support them.”

    “The primary remaining justification for high-starch diets diets has been weight control, but even this rationale is on shaky ground.”

    “We can no longer dismiss very-low-carbohydrate diets.”

    Willet, W. ,”Reduced Carbohydrate Diets: No roll in weight management?”, Ann Intern Med. 18 May 2004;140(10):836-837
    http://annals.org/article.aspx?volume=140&page=836

  50. estockly says:

    Oops, I was looking at the right blog post, but the wrong study. So I thought he was misinterpreting an HDL study. My mistake. Turns out he was misinterpreting an article referencing an LDL study. My bad.

    Also just a comment on the quality of your links. Generally they are bloggers who are linking to articles written about studies.

    So, by the time you write about the issue you’re four or five steps from the original source.

    When I linked to diet doctor, he provided a brief quote from the study and a link to the full text of the study in a few cases. In other cases just the link to the study itself.

    Much simpler.

    ES

  51. willywisp says:

    @estockly

    The debate is becoming long-winded enough that I’m losing the desire to continue responding. Especially since I haven’t encountered any new information in your responses yet (except for the bit about atherosclerosis reversal). I’ll try to be as terse as possible.

    > The brain regulates appetite, but even that is somewhat in response to hormones.

    This is more accurate wording, but it doesn’t change the fact that appetite regulation is a major factor in body fat regulation. When I see the term “regulate,” I think homeostasis. In this sense, insulin itself does not “regulate” fat storage, it promotes it. If anything, you should be arguing that the pancreas regulates fat storage by choosing when to secrete insulin.

    > Fat is stored rather quickly, breakdown of TG is a slower process, particularly when metabolic requirements have dropped. (overnight).

    If you replace carbohydrate with dietary fat, where do you think that energy is stored? As more body fat. To my knowledge, TG breakdown speed is independent of dietary calorie source. This is consistent with the observation that energy expenditure is equivalent at isocaloric intakes of varying carb:fat ratios.

    By the way, ASP accelerates fat storage _without_ a carbohydrate-like insulin response. ASP production is stimulated by chylomicrons, which come from fat in the diet. If you think insulin is a problem, you should also be looking at ASP.

    > Many overweight and obese have high fasting insulin levels.

    And they release as much or more free fatty acids from adipose tissue as lean people with baseline insulin. So you cannot argue that their higher fasting insulin is preventing them from mobilizing their fat stores.

    The problem is that just because fat is in circulation does not necessarily mean it’s getting burned for energy. If you are weight-stable, the net flux in/out of the fat cells remains zero. This is another reason why the focus on insulin misses the bigger picture.

    > Insulin does not drop between meals and overnight for everyone.

    Again, any time insulin is active, energy expenditure does not decrease. If someone is “covering” the day with HCLF snacks, there isn’t as much dietary fat to store in the first place, so it makes sense for insulin to help burn the available carbohydrate instead.

    > If that puts you at a deficit your brain will seek more food. Your metabolism will slow to conserve energy.

    But when is insulin high? When glucose is plentiful. Under normal circumstances, insulin is triggered exactly when you don’t aren’t in a deficit.

    > Compared to high protein diets, people on low carb diets burn more fat and preserve or build more lean tissue.

    Preservation of lean body mass is thought to be due to dietary protein, not carbohydrate or fat.

    > The II does not account for insulin spikes, but total insulin produced.

    Fat oxidation is not an on/off switch. As insulin rises, fat oxidation decreases as a proportion of total calories burned. This is why total insulin production counts.

    > Those two foods are simple carbs which which cause the fastest and highest blood sugar/insulin spikes.

    You seem to think refined carbohydrates are simple carbs. Not so. Wheat (and all starches, refiend or not) are complex carbohydrates. They often cause greater insulin responses than pure table sugar, because fructose does not illicit an insulin response.

    > But, to say that Carbs as a food group don’t stimulate appetite because corn and beans and rice don’t is equally inaccurate.

    No, it’s accurate. I bet you’d agree that saturated fat doesn’t stimulate appetite because coconut and raw cacao and lard don’t. Carbohydrates containing gluteomorphine are the exception, rather than the rule.

    Fructose is indeed more general. But Robert Lustig is rightly singling out fructose for this effect, rather than calling all carbohydrates addictive.

    > Does that mean you disagree with the study findings that LCHF diets lead to improved risk factors for CVD and other chronic diseases and result in burning more fat while preserving lean tissue?

    I admit that I don’t have interest or time to go through the studies you linked. Here is what I would look for in them. If you’re really interested in the truth, you will consider these questions with an open mind:

    - Can increased protein intake account for the preservation of lean tissue?
    - Can differences in weight loss account for any of the resulting changes in risk factors? How many of the studies reported better LDL on low-carb?
    - Was the LC diet a high protein diet? You recommend a HF diet, but how many of these RCTs actually study the absolute levels of fat intake you think are healthy?
    - How much fiber was in the HC diet? A low-fiber intake suggests “junk food” carbohydrates, which nobody is defending.

    > So if carbs are high (more then 50% of cal) or moderate (more than 30% of cal) the studies don’t apply to LCHF.

    The point I’m making is that you can reduce small-dense LDL even while increasing carb intake. Eating LC is not the only way to reduce small-dense LDL.

    > Are you saying that post wasn’t about what he talked about in his lead and the headline?

    I still think we’re talking about different links :) The one I’m referring to was titled “Another devastating blow to the cholesterol deniers”, and it only talks about LDL, not HDL:

    http://www.plantpositive.com/blog/2012/4/11/another-devastating-blow-to-the-cholesterol-deniers.html

    Since you seem to be allergic to Plant Positive, I’ll link you directly to the resource:

    http://www.healio.com/endocrinology/cardiometabolic-disorders/news/online/%7BF2F80A78-E72C-40AD-BF3B-19907E4EA7F7%7D/Lifelong-reductions-in-LDL-linked-to-consistent-reduction-in-CHD-risk

    > What I’ve said repeatedly is LDL is not a risk factor and may be protective.

    Let me clarify. For a given LDL-C level, I don’t think the large pattern will make it worse.

    However, high LDL-C is atherogenic regardless of particle size, because it usually indicates elevated LDL-P. The genetic evidence lends support to the lipid hypothesis throughout the entire spectrum of LDL-C ranges.

    > High HDL (not induced by drugs) and low TG do lead to halting and reversing atherosclerosis.

    This is a claim I’d be interested in learning more about. Can you point me to a reference?

  52. estockly says:

    >>> The brain regulates appetite, but even that is somewhat in response to hormones.
    This is more accurate wording, but it doesn’t change the fact that appetite regulation is a major factor in body fat regulation.

    It is a secondary factor. Maybe the most important, but insulin regulates fat storage on a cellular level. If you keep protein moderate and eat very little carbs there will be very little fat storage and stored fat will be metabolized and the brain has nothing to say about it no matter how much is has you eat or exercise.

    The brain can influence the availability of fat and glucose, but does not regulate cellular storage of fat. That is insulin.

    >>In this sense, insulin itself does not “regulate” fat storage, it promotes it.

    It does three things, promotes uptake of fatty acids into adipose tissue; promotes formation of TG; inhibits breakdown of TG. That is regulation of fat storage. If FFA and glycerol don’t go into adipose tissue, there is no fat to store; if TG are not formed inside cells, the FFA will circulate out and there is no fat to store; if TG breakdown is not inhibited TG will breakdown and stored fat will be released.

    I think the precise and accurate term is regulate. The difference is insulin initiates fat storage and allows for release of stored fat. Nothing else has such a strong regulatory on those two aspects of fat storage than insulin

    Other hormones and factors can influence somewhat how much of that happens, but insulin is in the drivers seat, the rest are back seat drivers.

    >>If anything, you should be arguing that the pancreas regulates fat storage by choosing when to secrete insulin.

    The reason we don’t say that is because the pancreas doesn’t choose when to secrete insulin. When blood sugar is high, insulin gets secreted. (Also when certain hormones like cortisol are present, but that’s not that common or significant in healthy people).

    >>>If you replace carbohydrate with dietary fat, where do you think that energy is stored? As more body fat.

    Nope. Body fat is only stored when insulin is high. If insulin is not high then that energy is not stored.

    >>To my knowledge, TG breakdown speed is independent of dietary calorie source.

    That is true. So when you replace carbs with fat and insulin stays low, circulating TG breakdown and circulate as FFA; TG in adipose tissue breakdown and circulate as FFA; and dietary fat circulates as FFA. Very little is stored.

    As the body needs energy there’s plenty available in circulation. The brain doesn’t get the hunger signals it usually gets when blood sugar drops, because blood sugar stays at a stable and fairly low level.

    >>If you think insulin is a problem, you should also be looking at ASP.

    I don’t think insulin is a problem. It’s a good hormone and part of the many things it does is regulate fat storage. Carbs are the problem.

    ASP does have influence, but insulin is what regulates fat storage. ASP influences, insulin regulates.

    > Many overweight and obese have high fasting insulin levels.
    And they release as much or more free fatty acids from adipose tissue as lean people with baseline insulin. So you cannot argue that their higher fasting insulin is preventing them from mobilizing their fat stores.

    Sure you can. You see, they have lots of fat stores. You see they are obese and that’s what that means. A single molecule of insulin does not shut down all TG breakdown. It is proportional to how much fat there is. (Although a little insulin goes a long way).

    >>The problem is that just because fat is in circulation does not necessarily mean it’s getting burned for energy.

    That means it’s available for metabolism (if it’s circulating as FFA.)

    >>If you are weight-stable, the net flux in/out of the fat cells remains zero.

    You can’t assume that. You could be building muscle while burning fat or metabolizing lean tissue while storing fat.

    >>This is another reason why the focus on insulin misses the bigger picture.

    Insulin is the big picture.

    >>Again, any time insulin is active, energy expenditure does not decrease.

    No one is saying it does…

    >>If someone is “covering” the day with HCLF snacks, there isn’t as much dietary fat to store in the first place, so it makes sense for insulin to help burn the available carbohydrate instead.

    If someone is eating a HC diet, the body is not in fat burning mode and it makes sense for insulin to encourage the body to get rid of the glucose through metabolism. Storing fat helps.

    >>>But when is insulin high? When glucose is plentiful.

    And people tell me I over simplify!

    Insulin rises when blood glucose is high and stays elevated even after glucose levels drop. That’s why people experience low blood sugar spells and become lethargic and crave snacks. If you’re insulin resistant, insulin gets higher than needed for the level of glucose and then drives glucose lower than normal.

    >> Preservation of lean body mass is thought to be due to dietary protein, not carbohydrate or fat.

    Who thinks that? Preservation of lean body mass results when the body has sufficient energy in circulation that it doesn’t have to metabolize lean mass. That energy can be FFA or glucose.

    >> The II does not account for insulin spikes, but total insulin produced.
    Fat oxidation is not an on/off switch. As insulin rises, fat oxidation decreases as a proportion of total calories burned. This is why total insulin production counts.

    Sure it counts, but insulin spikes account. Gram for gram a simple carb will produce as much glucose and insulin as a complex carb. The difference is that all the simple carb hits the blood stream immediately spiking glucose, spiking insulin and stressing the liver and pancreas. A complex carb takes longer to bread down so glucose never gets as high and insulin never gets as high and the liver and pancreas don’t have to work so hard.

    >>You seem to think refined carbohydrates are simple carbs. Not so.

    It is so. They are almost synomomys.

    >>Wheat (and all starches, refiend or not) are complex carbohydrates.

    No. Not the case at all. In fact many of the products sold as “whole wheat” are also simple carbs that have been remixed with fiber, etc.

    >>They often cause greater insulin responses than pure table sugar, because fructose does not illicit an insulin response.

    Right, so gram for gram only half of sucrose becomes blood sugar, but for refined wheat flour, more like 70% becomes blood sugar.

    >> But, to say that Carbs as a food group don’t stimulate appetite because corn and beans and rice don’t is equally inaccurate.

    >>But Robert Lustig is rightly singling out fructose for this effect, rather than calling all carbohydrates addictive.

    Nobody is calling all carbohydrates addictive. I mentioned sugar and wheat.

    >>I admit that I don’t have interest or time to go through the studies you linked. Here is what I would look for in them.

    So you won’t read actual studies published in peer reviewed journals, but instead rely on opinionated bloggers! And criticize me for not reading your bloggers’ diatribes.

    >>If you’re really interested in the truth,

    If you are you’d read the studies.

    - Can increased protein intake account for the preservation of lean tissue?

    It can help. Generally protein is not metabolized for energy, but can be through gluconeogenesis. When the body metabolizes lean tissue it’s doing the same thing, creating glucose from protein, only the protein is coming from muscle or organs or even the brain.

    The studies that you won’t read make it clear that on a low-carb high-fat moderate protein diet, the body metabolizes more fat and preservers or builds more lean tissue than on other diets.

    - Can differences in weight loss account for any of the resulting changes in risk factors? How many of the studies reported better LDL on low-carb?

    Yes, and the second is not an easy question. I’d have to go back and look it up, which I won’t do for this discussion. But I can say that in general LCHF diets had minimal impact on LDL-C and a significant favorable impact on LDL-p

    - Was the LC diet a high protein diet? You recommend a HF diet, but how many of these RCTs actually study the absolute levels of fat intake you think are healthy?

    Some diets were LCHP. Atkins never was. At least read the abstracts, that would answer those questions. A minority of them were isocaloric with the other diets in the trial. The rest were fat ad lib. I don’t think there is a standard healthy level of fat intake. You should eat fat ad lib, that will be higher some days than others, way low at times, but if you listen to your body and avoid carbs your hunger and satiety system will keep you healthy.

    >>- How much fiber was in the HC diet? A low-fiber intake suggests “junk food” carbohydrates, which nobody is defending.

    Which HC diet? What are you referring to?

    >>The point I’m making is that you can reduce small-dense LDL even while increasing carb intake. Eating LC is not the only way to reduce small-dense LDL.

    Fine. I don’t think I ever said it was the only way to do that. Just the only way to improve HDL; TG; LDL p; blood pressure; body fat percentage.

    >>I still think we’re talking about different links

    Whatever, if you can’t be bothered to look at studies in peer reviewed journals I’m not going to read an anonymous blogger with an axe to grind.

    The one I’m referring to was titled “Another devastating blow to the cholesterol deniers”, and it only talks about LDL, not HDL:

    > High HDL (not induced by drugs) and low TG do lead to halting and reversing atherosclerosis.
    >>This is a claim I’d be interested in learning more about. Can you point me to a reference?

    It’s in some of those studies. You’ll have to read them all to find it.

    >>The debate is becoming long-winded enough that I’m losing the desire to continue responding.

    Got it.

  53. weing says:

    “So when you replace carbs with fat and insulin stays low, circulating TG breakdown and circulate as FFA; TG in adipose tissue breakdown and circulate as FFA; and dietary fat circulates as FFA. Very little is stored.”
    Huh? What are you talking about? Circulating FFAs cause insulin resistance and increase insulin levels.
    http://www.ncbi.nlm.nih.gov/pubmed/15929861

  54. weing says:

    @estockly,

    Oh. I see your are one of those who think size matters. I’m more of a numbers guy. You are correct that elevated HDL and low TGs are correlated with less CHD. But I don’t know of any studies showing that raising HDL or lowering TGs is cardioprotective. Actually the studies have shown the opposite. If someone has low HDL, your best approach is to lower the LDL. That does work. TGs over 500 may cause pancreatitis. That is the reason to treat them.

  55. weing says:

    @Patohaz,

    I attended a talk by Dr. Willett last year at a lipid conference. His conclusions regarding the saturated fat vs carbs issue were that it depends on the type of carbohydrate, adiposity/insulin resistance, maybe on the type of saturated fat, maybe on the food sourse of the saturated fat, but nothing clear there. And replacing saturated fat with carbohydrate will have minimal effect on CHD risk.

  56. estockly says:

    >>Huh? What are you talking about? Circulating FFAs cause insulin resistance and increase insulin levels.

    The impact of FFA’s on insulin resistance and increasing insulin levels is not as strong when carbohydrates are reduced. When blood sugar is high, circulating FFA amplify the insulin response and interfere with insulin’s ability to lower blood sugar.

    ES

  57. weing says:

    “The impact of FFA’s on insulin resistance and increasing insulin levels is not as strong when carbohydrates are reduced. When blood sugar is high, circulating FFA amplify the insulin response and interfere with insulin’s ability to lower blood sugar.”
    News to me. That’s not how I learned it. Do you have any studies backing this up? Are you sure you don’t have it bass-ackwards?

    http://www.jci.org/articles/view/118742

    http://ajpendo.physiology.org/content/295/1/E38.full

    http://www.jbc.org/content/275/40/30749.full?ijkey=3a42b0b1399059d3cc869c1133a47ed9988287d9&keytype2=tf_ipsecsha

    http://jn.nutrition.org/content/134/9/2444S.full

  58. Patohaz says:

    @weing

    Thanks. I have no argument with the statement of Dr. Willett that you relay. I also agree with Dr. Hall that long-term studies are needed regarding low carbohydrate diets and await the results.

  59. estockly says:

    This answers some questions that were raised earlier. I will go back and look for the FFA info. What I recall is that on LCHF diets when insulin is stays low and stable, while FFAs circulate.

    Thanks for the links!

    ES

    “Meta-analysis carried out on data obtained in 1,141 obese patients, showed the LCD to be associated with significant decreases in body weight (−7.04 kg [95% CI −7.20/−6.88]), body mass index (−2.09 kg m−2[95% CI −2.15/−2.04]), abdominal circumference (−5.74 cm [95% CI −6.07/−5.41]), systolic blood pressure (−4.81 mm Hg [95% CI −5.33/−4.29]), diastolic blood pressure (−3.10 mm Hg [95% CI −3.45/−2.74]), plasma triglycerides (−29.71 mg dL−1[95% CI −31.99/−27.44]), fasting plasma glucose (−1.05 mg dL−1[95% CI −1.67/−0.44]), glycated haemoglobin (−0.21% [95% CI −0.24/−0.18]), plasma insulin (−2.24 micro IU mL−1[95% CI −2.65/−1.82]) and plasma C-reactive protein, as well as an increase in high-density lipoprotein cholesterol (1.73 mg dL−1[95%CI 1.44/2.01]). Low-density lipoprotein cholesterol and creatinine did not change significantly, whereas limited data exist concerning plasma uric acid.”

    http://onlinelibrary.wiley.com/doi/10.1111/j.1467-789X.2012.01021.x/abstract;jsessionid=7396D07C42DB2B84642D35158B132AF9.d04t04

  60. estockly says:

    >>I also agree with Dr. Hall that long-term studies are needed regarding low carbohydrate diets and await the results.

    That raises a few questions.

    What do you mean “long-term studies”? How long is long-term?

    According the criteria on the National Weight control registry that RD pointed to, long term is one year. (I don’t consider that long term.)
    http://www.nwcr.ws/

    SkepticHealth says it’s better to recommend a low-fat diet than a low-carb diet. Where are the long-term studies that show the benefit of low-fat diet?

    Why wait longer for long term results for Low Carb than low fat, when it’s clear that in the short term Low Carb is significantly better?

    ES

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