Exposing the Cholesterol Con

[Just a quick off-topic aside. Darya Pino at Summer Tomato did a mildly critical but fair & balanced post on paleo dieting. Go take a look and drop a comment about your own experience if it suits you. From my perspective, we out to be able to take fair criticism to refine & strengthen our message.]

This is just a rather quick hit & run with some excerpts and commentary that I wanted to post because it's nice to finally see something in the mainstream news that echos what I and my fellow bloggers have been saying all along, for nearly three years in my case. From MSNBC:

Bad cholesterol: It’s not what you think

Yea, no shit. And it never was. And there was little justification to ever create the "tidy narrative" in the first place.

For decades, a tidy narrative about the relationship between LDL cholesterol and heart disease has affected everything from the food we eat to the drugs we take to the test results we track and the worries we harbor. This oversimplified view of cholesterol — that all LDL is the same and that all LDL is bad — has enabled the adoption of an accompanying oversimplified dietary belief, that all saturated-fat consumption raises your risk of heart disease.

Oversimplified view of cholesterol --> oversimplified view of diet --> complex and dangerous drugs --> obesity --> diabetes --> more complex and dangerous drugs --> lots of drug company profits --> lots of assholes still out needlessly scaring people to death.

The LDL hypothesis has also encouraged many of us to swallow the most-prescribed class of drugs in recent history. Americans spent more than $14 billion on LDL-lowering medications in 2008. Whether that money came out of their own pockets — straight up, or through ever-escalating co-pays — or out of the hemorrhaging U.S. health-insurance system known as Medicare, it's a huge expenditure. Twenty-four million Americans take statins, and the latest health directives suggest that those numbers should be higher. And why stop at grown-ups? Some pediatricians want to start feeding Lipitor (and the like) to kids.

$14 billion for something with tons of side-effects and of dubious, nonexistent value for all but a small subset: men under 65 who've already had a coronary event. Sure, if you've had a heart attack already, go right ahead and "trust your heart to Lipitor."

LDL comes in four basic forms: a big, fluffy form known as large LDL, and three increasingly dense forms known as medium, small, and very small LDL. A diet high in saturated fat mainly boosts the numbers of large-LDL particles, while a low-fat diet high in carbohydrates propagates the smaller forms. The big, fluffy particles are largely benign, while the small, dense versions keep lipid-science researchers awake at night.

But here's the problem: The typical LDL test doesn't distinguish between large and small LDL particles — it can't even spot the difference. And people can have mostly large LDL or mostly small LDL in their overall LDL, depending upon a host of genetic, lifestyle, and environmental factors. Your own personal mix may make all the difference between living to a heart-healthy old age and becoming a Monday-morning casualty at your desk.

Right. And Americans are spending $14 billion per year on statins and it's based on irrational, uncorrelated, unproven associations with a measurement technology that "can't even spot the difference." I'll bet the drug companies are all over getting this new measurement technology into wide usage. Yea, right.

Now, to heap even more outrage on the deal, how long back has it been since it was known that the small-dense sub-particles associated and reasonably predicted heart disease risk? 1976, almost 35 years ago. Dr Krauss recounts:

The heart-disease community was not impressed. "It took me 4 years to publish that paper," he says, recalling his early work on sub-particles in the late 1970s. "That's beginning to tell you some of the obstacles I was going to face."

Big surprise, eh? There's more.

But during experiments, Dr. Krauss discovered that while a diet high in saturated fat from dairy products would indeed make your LDL levels rise, "saturated fat intake results in an increase of larger LDL rather than smaller LDL particles," as he wrote in an American Journal of Clinical Nutrition review he co-authored in 2006. A diet heavy in full-fat cheese and butter — but not overloaded in calories — triggered the relatively harmless health profile described as pattern A. [...]

Not only is dairy fat unlikely to increase heart-disease risk, Dr. Krauss and others have learned, but reducing saturated fat in a way that increases carbohydrates in a diet can shift a person's LDL profile from safe to dangerous. That's pretty much what happens whenever some well-meaning person with "high LDL" starts eating "low-fat" frozen dinners filled out with corn-derived additives, all the while engaging in the customary ravaging of a basket filled with dinner rolls.

Well that should do it. You might want to check out the inane comment from Dean "Chubby Faced Diet" Ornish.

Comments

  1. Carbs = heart disease. I am so tired of arguing this to people. They act like it is a mystery that heart disease is ubiquitous in America while pushing a diet that they know causes it. Ever since the rise of agriculture based societies, we have succumbed to a diet which does not behoove us.

    • If your studies have led you to the conclusion that carbs=heart disease you have not been paying very good attention. Fructose, industrial seed oils and wheat are the main culprits in heart disease as best we can figure from the most current scientific evidence. Using the term “carbs” to describe the problem is not only an oversimplification but a dangerous generalization of the truth.

      Kitavans eat 70% carbs for the entire span of their lives and heart disease is unheard of on Kitava. As long as you eat whole foods as close to their natural state as possible you have a wide range of macro nutrient ratios to choose from and still remain healthy. Yes, some tweaking will be required based on individual body chemistry but the point remains valid nonetheless.

      Personally I do well with a 60/25/15 ratio of fat/protein/carb but I’m still losing weight. Once I get to my ideal weight I doubt that adding significant amounts of starch from whole foods such as yams will affect my health in any negative way.

      In any event, back to my main point…such generalizations do no one any favors, especially those who are new to the paleo/low-carb way of eating and who are still open to persuasion.

  2. The link below is for those who want to take a look at an actual photo of LDL particles, as well as VLDL (LDL’s precursor), HDL, and chylomicrons.

    http://healthcorrelator.blogspot.com/2010/02/large-ldl-and-small-hdl-particles-best.html

  3. I don’t think “carbs = heart disease” is a fair assessment. I got through a couple of pounds of carrots a week, but I don’t eat bread. What do you think of my chances?

    • babblefrog says:

      A kilo of carrots has 100 grams of carbs, of which 30 are fiber. Over the course of a week? You are going to have to try harder :-) Maybe eat several kilos a day?

      • Hehe, I better renew my membership at CostCo then, that’s a lot of carrots! LOL I wonder if my skin would start turning orange at that point…

      • It will, my mother was drinking close to a litter of carrot juice a day, and after about 3 month she started looking much more like an umpa lumpa.


  4. “The typical LDL test doesn’t distinguish between large and small LDL particles – it can’t even spot the difference.”

    Hell, the typical LDL test doesn’t even measure the actual amount of LDL in the blood! It’s calculated with a mathematical formula using the other lipid values. It’s pretty accurate if your triglycerides happen to be between 100 and 400, but if you have low triglycerides, the formula significantly overestimates the amount of LDL.

  5. Richard –

    Just for giggles check out the “Can Fat Produce Sugar” forum over at PaNu.
    djinn won’t need to rant for a week.

  6. Here’s the story arc as I’ve interpreted it. First cholesterol was bad, and no mistake. Second… well, it turns out that there are good and bad cholesterols, HDL being a life-saver and LDL, a stone-cold killer. Now, umm, we seem to have found (while unfairly trying to convict the murderous LDL) that we ought distinguish between “good” bad (large) and “bad” bad (small) LDL particles.

    Next will be good good bad and bad good bad, probably some bad bad bad, with the implication that there exists a form of cholesterol which is, by its mere presence, a causative factor in disease. Let us spend billions of research dollars attempting to find whatever form of LDL particle we are able to prove as disease’s cause.

    Or… could we not avoid such complications by recognizing that cholesterol is a fact of life, ours anyway, and that it is always adaptive, the various types telling us which diseases we are at risk for not because of the presence of the cholesterol itself but the cholesterol’s adaptive purpose as regards its cause, mainly, diet?

    Or are we not ready to complicate what we know to be true, that cholesterol is BAD, and may big pharma save us all?

    • “Next will be good good bad and bad good bad, probably some bad bad bad…”

      LOL

      • Peter actually has blogged on that some time ago – a 4×4 matrix of good/good ,bad/ good, good/bad and bad/bad cholesterol.

        It’s all nonsense really. These are all MARKERS of a diet – which may or may not be healthy.

        You do know the kitavans have BAD levels of GOOD cholesterol, right? they have pretty low HDL because of their carb consumption. Yet they don’t seem to die of heart attacks too much.

        The story is inflammation and repair. I don’t think LDL causes it anymore than HDL cures it, not literally. I am not sure if I buy that sdLDL burrows into your arteries on a ccount of it’s size, or if it just reflects a non-atherogenic and anti-inflammatory diet bereft of oxidized lipids and oxidizing sugars like fructose – I suspect the latter.

      • Yep, I know. The Kitavas have “lousy” lipids. But as Peter says, the bad lipids do no harm because it’s the diet, not the lipids.

        It gets the primary cause wrong. Saying that cholesterol is the _cause of heart disease is like saying the cause of death from a gunshot wound is that you’re not bulletproof.

      • My favorite simple metaphor is police and crime. We note high correlation between police density and crime statistics, so we unburden the municipalities with lots of police of their uniformed officers in order to improve the crime rate, and then are shocked when the crime gets worse.

        This is the kind of thinking that gave us torcetrapid, and has cardiologists still looking for ways to block CETP.

      • Interesting point about their low HDLs. I’ve been reading about paraoxonase of late- it’s an HDL associated enzyme that supposedly takes the oxidized lipids in LDL and gets rid of them, hence removing the inflammatory component. Having a high HDL level could mean higher paraoxonase levels, or maybe it’s the enzyme concentration on the HDL particles that’s important. I remember reading something about the levels of paraoxonase being inducible, so maybe something in the Kitavan diet increases the enzyme without raising HDL.

        Or maybe it’s just better thyroid health from the high iodine…

  7. Davies had a post re saturated fat increasings small LDL particle size in some.
    Not sure if it was the sat fat or the polys:
    http://heartscanblog.blogspot.com/2010/02/genetic-vs-lifestyle-small-ldl.html

    • Please read my and especially Peter’s comments there before you decide to fear saturated fat. I pointedly asked Dr. Davis to confirm (3 times) whether he had actually observed sdLDL increase in response to a known increase in saturated fat. He did not directly answer me directly, so make your own conclusions carefully.

      • Kurt, I’m not convinced its the sat fat. Dr Davis didn’t seem to answer your question. The example of the guy with small ldl that he used and the diet he was on didn’t look high in sat fat but poly fat.

      • I think before we make any conclusions about what Dr. Davis thinks or doesn’t think… I think indeed Davis may not know, or has never in advance set up proper controls for a sdLDL and sat fat increase observation. In the post Sue mentioned, I think he mentioned very clearly that this is a “presumptive designation”, something he needs to reflect on further, something he may not be ready to comment on further.

        Kurt, you’re an expert in radiology. Not that that disqualifies you, but it may make it more difficult to face down the cardiology mafia. Without careful consideration such a definitive statement might ruin Davis’ credibility as our greatest paleo heart expert spokesman and champion, creating either paleo doubters for his practice, or silly CW naysayers mocking Davis if he missteps.

        Quite simply, he may be just working with this hypothesis and doesn’t want to comment further on it. As with your undefined position on milk (meaning, you’re not totally sure), I think Davis’ post here is in the same vein, he’s sharing observations, and not conclusions, and doesn’t imply otherwise. How/when Davis wants to clarify his position is his choice, and yes I agree with your point to not rush to conclusions, I think that rush is coming from others not from him.

      • Let me ask you, do you know if he has directly observed such a change? If he had he could have said so but he did not. The clear impression he gave with the initial post was that there are a subset of us that have a different response to increased sat fat in the diet, and he implied it was therefore DANGEROUS to eat sat fat. I have a right to conclude that he is speculating that there would be such an effect, as he did not respond (even to say I don’t know, as I did with dairy) when I put the question to him three times.

        When you blog you can say whatever you want, but if you don’t choose to elaborate or back up your claims with details folks are allowed to draw their own inferences.

        Being a radiologist makes it very easy to “face down the cardiology mafia”, actually. I don’t get what you mean at all about “definitive statement”. Saying “I am speculating that sat fat addition to the diet can raise sdLDL in someone not on statins, but I have not directly observed this” -how would that upset either sat fat acifionados or other cardiologists?

        And no one is asking him to rush , just to clarify the basis for his initial claim that some of us are in DANGER.

        I do think the idea that Dr. Davis has ever advised someone to increase saturated fat on purpose and then observed the results serially seems doubtful. As recently as 2006, he wrote a book that advocated eating as little sat fat as possible for best health on a plant and nut and oil-based diet. Now he seems to think carbohydrate restriction might be alright.

        As Peter says, maybe some day he will come the rest of the way ’round and see animal fats (heavy in saturated and mono) as the perfect human fuel source.

        Maybe someday I will denounce all dairy, too. But until I do, any time you ask me, I’ll tell you why I think what I do, or what I don’t know if I don’t know it.

      • We may agree to disagree, but I don’t think that he implied there was any danger involved for the subset that he has observed that may have a different uptake to sat fat. I think he was sharing his observations, and reasoning it out loud on his blog.

        I think Davis as a cardiologist may learn a lot from someone like Peter and you, too, and I hope he’s open to it, because with Peter’s research experience and your willingness to look at other fields I think it would be great if Davis benefited from both of these points of view.

        I think in his original publication of “The Paleo Diet” Cordain may be to blame that he let marketers get a bit carried away with Sat Fat catch phrases, and Cordain has backtracked from some of that as he conducted/read more studies and corrected some of his anthropological data on diet, as well. Regarding diet, I think there’s a lot of evidence regarding dairy and autoimmune diseases that Cordain has published among many others you may want to read.

        I think you’re a strong voice in this community, I think as a radiologist/MD you have a unique perspective. But before you make comments like:
        “He is not an MD and I believe his PhD is exercise science. Not that that disqualifies him, but it may make it more difficult to face down the cardiology mafia.”
        “If I have a problem with Cordain’s methodology, it’s that he seems to decide that something should be bad, then marshalls everything he can find to prove it so.”
        -Kurt Harris regarding Cordain’s qualifications

        These comments whether intended or not are rather invalidating. I think you may want to read his published papers and the many references that it includes on dairy especially. Whether it’s a researcher or an MD, when people learn something new and their opinions evolve, their previous held statements and opinions shouldn’t be used to discount everything they say thereafter. I believe that’s the implication (not sure whether it was intended) that you’ve made regarding Cordain, thought it may be good for you to know.

        Again, we may agree to disagree here, just thought you may wanted the feedback as I think your message is worth hearing.

      • You are cherry picking the negative things I have said about Dr. Cordain out of context, a pioneer whom elsewhere on my blog I have praised many times and whom I link to. I stand by those comments (which were in response to queries )and I’m not terribly concerned if you disapprove of them.

        My comment about the cardiology mafia (like I was supposed to know that was some clever quip?) is that Cordain is an not an MD and does research with MD cardiologists on whom he has been somewhat dependent – more dependent than if he were an MD himself. I think it is easier for an MD to criticize the dominant paradigm from within it -and I think both I and Dr. Davis are doing just that. I hope that recontextualizes that comment to your satisfaction, it was meant to be more exculpatory than critical.

        Moving on, Davis’ original post said:

        “If, on the other hand, your small LDL is genetically programmed, then saturated fat will increase small LDL. In other words, saturated fat tends to increase the dominant or genetically-determined form of LDL. If your dominant genetically-determined form is small, then saturated fat increases small LDL particles.

        So to say that saturated fat increases large LDL is an oversimplification, one that can have DIRE CONSEQUENCES in the wrong situation.

        How do you square his assertion of “dire consequences” for those with genetic small sdLDL with your assertion that:

        “I don’t think that he implied there was any danger involved for the subset that he has observed…”

        Yo must think I misread what he wrote. I think dire consequences imply danger, so I don’t think I did.

        So on that we disagree.

      • Oh, and let me add, I strongly object to you saying “Harris on Cordains qualifications”

        The first sentence you quoted says DOES NOT DISQUALIFY HIM

        and the second has zero to do with his qualifications.

        You are sounding like one of those pissed off dairy people.

      • Kurt,
        I was simply giving you feedback that sometimes you make some sweeping statements that indeed perhaps could give people the wrong implication from what you were trying to say. I’m a fan of your work and was giving you feedback on perhaps how to craft your message in a manner that may be better received. You may take what you want from it, I’m neither pissed as a “dairy” person, nor disappointed if you didn’t approve of some of my perspective. I think your prescription regarding Davis investigating Sat Fat further may be worth you taking a look at regarding dairy, that’s my point. I’ll continue to be a supporter of your work, and wish you continued success getting your message (and the paleo community’s message write large) out there to people that truly need it.

      • meant “writ large”, btw

        Oh, and one other thing to imply that you saying,
        “If I have a problem with Cordain’s methodology, it’s that he seems to decide that something should be bad, then marshalls everything he can find to prove it so.”
        isn’t a statement commenting on his qualification is rather interesting. Just saying.

        Enjoyed the exchange. And appreciate you being one of the few folks in this community that will flat out say, “Hey, I’m not sure yet what my opinion on that is on that.” Truly, that’s definitely appreciated and shows your willingness to have an open mind. I agree with you that I hope Davis may further put his observations with further analysis regarding Sat Fat. Best to you.

      • I do have to admit that the “feedback” thing just kind of rubs me the wrong way. If I ever want feedback on anything from my blog, I have plenty of people I can ask, or I could just look at the thousands of blog comments on my blog. Having 4000 comments on my blog, about a quarter of which were written by me, I am sure you could mine it for snippets like the one you found all day long.

        I still can’t for the life of me see what Cordain has to do with what Davis is saying.

        But as I suppose Richard would say, there it is.

        And yes, the thing you quoted, again, has absolutely nothing to do with his qualifications, it is speaking to his apparent biases.

      • Kurt, the thing in common with this Davis issue and Cordain is just the way you go about discussing things with people, that’s all. As a nutrition researcher I think what you said invalidates would invalidate that person’s qualification regarding his methodology. Just saying, it might in turn rub people the wrong way. Yes, there it is. I’m not trying to be personal, just having a conversation.

      • compare how Peter’s comment challenging Davis’ opinion, and yours… which one endears an atmosphere of exchanging ideas with Davis? Granted Davis didn’t answer either of you! so touche to you.

      • Zach, Where did you get the idea that Davis is Paleo? I don’t believe he is. If from my blog you assumed so, then you are wrong.

        Often it is indiscrete dietary carbs that raise sdLDL (NOT saturated fat) — doesn’t take much. Even > 20-40 grams daily depending on how ‘broken’ metabolism, hormones and the liver are…

        Do you think Stan was lying about his carb intake?

        Most patients do… as they also lie about saturated fat too (EXCEPT primal/xfit folks *haa*).

      • Indeed, he is not paleo. I meant to suggest that he is probably the biggest cardiologist voice out there that support a message that paleo adherents may reference and learn from. His Sat Fat observation very well could show that Sat Fat in the presence of PUFAs and/or carbohydrates could lead to dire consequences more so than for others and/or for all of the reasons that Peter suggest. Davis bringing this into the discussion is a positive step forward.

      • Ok, here we go

        “His Sat Fat observation very well could show that Sat Fat in the presence of PUFAs and/or carbohydrates could lead to dire consequences more so than for others and/or for all of the reasons that Peter suggest”

        Peter definitely did not say that and neither did Davis!

        Davis also did not say what his sat fat observation was, exactly. He just asserted it could have dire consequences.

        How is terrifying people about sat fat with no details providing a step forward?

        And what paleo message that we can learn from do you see on Davis’ blog? I am not saying he does not have some good content, but what message that is paleo? Vitamin D and thyroid I’ll grant, if that is what you mean.

      • “His Sat Fat observation very well could show that Sat Fat in the presence of PUFAs and/or carbohydrates could lead to dire consequences more so than for others and/or for all of the reasons that Peter suggest”

        His Sat Fat observation (MEANING DAVIS’ observation from his post) may be that Sat Fat is more harmful in the presence of PUFAs and/or higher level of carbs, that’s me saying that maybe it’s like Feinman says:
        “The deleterious effects of fat have been measured in the presence of high carbohydrate. A high fat diet in the presence of high carbohydrate is different than a high fat diet in the presence of low carbohydrate.”

        OR, Peter’s comments on Davis’ referenced post from the Track Your Plague blog may be absolutely correct, which given how much respect I have for Peter’s writings is most likely the case.

        Not wheat, thyroid advice, no wheat, etc., are one of many things that a paleo adherent can learn.

        Your tone gets the best of you sometimes, you may take this as friendly advice or not, I still think you’re great. You may think I’m an asshole just for trying to tell you have a bit of snot coming out of your nose, that’s fine, I’m actually a good guy and a huge supporter of your site.

        “I pointedly asked Dr. Davis to confirm (3 times) whether he had actually observed sdLDL increase in response to a known increase in saturated fat.”
        (AS IF YOUR QUESTIONING 3 TIMES IS OF SIGNIFICANCE, THE IMPLICATION IS CLEAR)

        Your questions were posed rather harshly to Davis on his post, I can see why though your questions were very spot on and hopefully stimulated thought on Davis’ part, why he didn’t jump to answer you.
        ______
        “Oils = olive oil, flaxseed oil, canola oil (yes, yes, I know), avocado, almond, oils from raw nuts and meats.

        No polyunsaturates here. You’ve got the wrong guy.”

        But Dr. Davis, those all chock full of PUFAs

        (DON’T YOU THINK YOU COULD HAVE SAID THAT A BIT MORE CORDIAL?)
        ________

        Can I assume when you say “seems to be deterioration” and “there is a suggestion that saturated fat increases small LDL” and “saturated fat is the exception” that this is based on the observation of serially increased sdLDL NMR values after increasing only saturated fat intake in these 100 or so patients?

        If this is what you have, serial NMRs that show increased sdLDL with increased saturated fat intake, why not say so explicitly?
        ___________

        I have been very polite in this exchange, and I hope you take my remarks in the respectful tone and intention they were given. Peace to you, and hope to continue dialog here and/or elsewhere on things we agree and/or disagree on. Good to have someone like you on the side of the barricades I reside.

      • Folks, I think this topic has been beat to death: the dispute between Dr. Harris & Dr. Davis in terms of what one said but really meant and wether it was too rude and on and on and on.

        Please let’s move on an discuss the topic of the post if anything.

      • Yep, I agree. I take his lack of response as evidence that he is speculating about the increase due to sat fat and has not directly observed it.

      • Sorry to bring it up again but I don’t think Kurt was rude to Davis at all. Just trying to clarify. Anyway, it would be interesting to observe what would happen to the small LDL with very low carb, increased sat fat and minus the polys.

  8. Oops – I meant Davis.

  9. Can someone explain this to me?

    Okay, there’s LLDL, MLDL, SLDL, and VSLSL. There’s also HDL. The common trait these all share, besides being lipoproteins, is that they’re measured by their density. Now, LLDL (“large low density lipoprotein”) is benign, where are MLDL (“medium…”), SLDL (“small…”), and VSLDL (“very small…”) are bad for you, and each one is worse than the next.

    That makes sense: the denser the lipoprotein, the worse it is. But remember, all of these are “LDLs” (ie: low density). Presumably, that means that while they’re all bad (except for LLDL, which is benign), they’re not as bad as HDL (“high density lipoprotein”). Yet, HDL is what everyone says is the “good cholesterol.” Even the people who think that all types of LDL are bad admit that HDL is good.

    At least using all of this terminology, wouldn’t HDL be the absolute worst type of cholesterol-carrying lipoprotein? After all, it is the densest, isn’t it?

    • Yes, but not nearly as dense as the anti-chloresterol theorizers.

    • Grant said…
      “At least using all of this terminology, wouldn’t HDL be the absolute worst type of cholesterol-carrying lipoprotein? After all, it is the densest, isn’t it?” It’s not just about density. It’s about where the particles go. HDL has apoA in its outer coat which means that it’s taken up by the liver. LDL has ApoB in its outer coat which means that it’s taken up by cells, artery walls etc. Please read Cholesterol And Coronary Heart Disease.

  10. I have to say, that for this to appear on a mainstream site like MSNBC – and for Dr. Ornish’s only comeback to be little more than “oh, yeah? well… that’s not what I said”… I feel like the CW wall just took another huge crack. Pretty soon there will be naught but a little Dutch boy standing there with his finger trying to plug it up.

  11. Thanks for the mention and for inspiring a great conversation today!!

    • Thanks Darya for such a fair critique of Paleo. And nice blog. I’d seen if a few times in the past and glad I was able to find something to comment on and introduce my readers to.

      BTW, since you’re pursuing a PhD in neuroscience if I recall correctly, you might be interested in the blog of Dr. Stephan Guyenet who just recently completed his PhD in neurobiology. One of the best Whole Health Sources on the Internet. He’s more WAPF (Weston A Price Foundation if you don’t know) but also very sympathetic to Paleo and his approach is to evaluate the health science he blogs about through the lens of human evolutionary biology.

      http://wholehealthsource.blogspot.com/

  12. This post reminded me of the T Colin Campbell thing. I went back and re-read his rebuttal and he makes some remarks about aristocracy in the 18th & 19th centuries which reminded me about Jean-Anthelme Brillat-Savarin who wrote about the food habits of the aristocracy at that time. Some very interesting observations are made about the types of foods the overweight people were eating (potatoes & bread) and what the slim people were eating (meat, fat, vegetables), among the wealthy. Very entertaining read, though not rigorously scientific.

  13. I have to thank Lyle for pointing me in the direction of the following study.
    There are some people whose serum cholesterol goes sky-high on a diet with a high percentage of energy from fats. See Some Metabolic Changes Induced by Low Carbohydrate Diets. Subject CF’s total cholesterol goes up to 500mg/dL (12.9mmol/L). What’s the effect of that high a cholesterol level even if LDL particles are large and HDL is high? We just don’t know.

    • Interesting Nigel. We have certainly had a few high-fat guys report this sort of high C experience. I’ll have to keep this study handy.

      • What would be interesting is finding out if people with high serum Cholesterol (with mostly large LDL) have any measurably bad changes in Coronary Artery Calcium, Carotid Intra-Media Thickness, Arterial Stiffness, Flow-Mediated Dilation, non-invasive measurements that are now available.

        I know that Peter of Hyperlipid has a total chol of 8mmol/L (310mg/dL) but has good CAC & AS scores. Low CAC doesn’t guarantee freedom from stenosis, as per Stenosis Can Still Exist in Absence of Coronary Calcium.

    • That was a weird study (1967) what I could make of it.
      The obese subjects were on 70% fat and 30% protein then it changed to 50% fat and 50% protein.
      With 12g carbs daily.

      • RE Fats & Proteins: That’s not correct. Re-read Table 1.

      • The men did all the stages but the women only did 3 stages of the diet. The men were prisoners. The women they mention that they didn’t have much time with (as not prisoners)?

      • It’s irrelevant anyway. I’m only trying to show that we are not all the same. There is no 1 diet that suits absolutely everybody. I am not criticising LCHF diets.

      • The fats were mostly omega-6 PUFA 13-35 grams worth (e.g. 13,000 to 35,000 mg). H*lluva lot of pufas… Ancient hunter-gatherers are predicted to have 5000 mg/d which is where I try to keep mine (nuts, seeds, meat, dairy, etc). See Table 1.

        I take nothing from the study except that omega-6 are VERY BAD — look at the Trigs in that trial despite a very low carb diet 150-200s which indicate inflammation and insulin resistance (and likely leptin resistance as well). The LDL increase is very likely ALL sdLDL if they actually examined more closely.

  14. Once again it is proven, Nigel, we are not all the same… There are still many unknowns out there …

  15. frankifries says:

    Oh man, this is a wonderful mainstream article to slap a few of my indoctrinated FB friends with. I get tired of getting stupid comments–”that pork butt looks like a heart attack” “why are you making so much butter” “you should drink soy milk”–on the pics of my primal foods/meals.
    Thanks for this, cuz I wouldnt have gone searching on msnbc for it!

  16. Slightly off post, but I hope I’m not the only one glad to see the blog back to it’s more colorful language. Ahh….feels like home again.

  17. Working at a cardiovascular agency, the whole cholesterol thing is frustrating. I just took a look at our dietary advice we give heart patients. In my opinion, a low fat Omega 6 disaster. Nonfat milk, vegetable oils, skinless chicken. Keep those statins coming though…

    • I finally found a doctor who agrees with me that the low-fat high-carb diet is nonsense I got so sick of hearing about low-fat this, low-fat that, eat only a card deck-sized portion of meat each day. It’s like being hounded by some strange cult: Just eat the purple wheat and all will be well ……

  18. Brian Seitz says:

    Hi! I’ve been reading awhile and really enjoy the discussions. I am a chiropractor who works in an interdisciplinary medical group. I have slowly been helping them see the light, but then this type of bs gets published (from a lipid update):
    Optimizing Statin Use at the Population Level: What Is the Best Approach?
    In a simulation study, improving patient adherence produced better outcomes than lowering the treatment threshold.

    The benefits of statin therapy in patients at risk for coronary disease is unquestioned. However, many patients who would benefit from statin use are not taking them. Expanding statin use could be achieved in two ways: (1) lowering the treatment threshold, or (2) improving adherence. To compare how implementing these strategies would alter the population-level benefit of statin therapy, Shroufi and Powles used data from the prospective Melbourne Collaborative Cohort Study, involving 41,141 participants, to conduct a simulation study.

    In the U.K., the National Institute for Health and Clinical Excellence (NICE) recommends that adults with a 20% or greater 10-year risk for heart disease should receive statin therapy. For the model based on a lower treatment threshold, the investigators assumed that adults with a 15.5% or greater 10-year risk would be eligible for statin therapy. For the improved-adherence model, the authors assumed an increase in adherence (defined as taking 80% of the prescribed monthly dose) from 50% to 75%.

    The improved-adherence strategy resulted in about twice as large a reduction in cardiovascular deaths as did the lower treatment-threshold strategy. The improved-adherence strategy also showed a modest improvement in averting the onset of cardiovascular disease, compared with the lower treatment-threshold strategy.

    Comment: According to this study, twice as many cardiovascular deaths could be prevented by a 50% improvement in statin adherence under current prescribing guidelines than by lowering the baseline risk threshold. Physicians, families, and pharmacists should increase their efforts to ensure that patients take their prescribed medications.

    — Joel M. Gore, MD

    Published in Journal Watch Cardiology February 17, 2010

  19. Yea, no shit. And it never was. And there was little justification to ever create the “tidy narrative” in the first place.

    It reminds me of the anthropogenic global warming B.S. a lot of people including so-called “scientists” (glorified technicians who couldn’t legitimately think their way out of an English-hedgerow maze) religiously believe in.

    Come to think of it, it reminds me of the religion a lot of people religiously believe in.

  20. Thanks for the post and interesting discussion. Now I am going to pay more attention to cholesterol. My blood lipids results (LDL=271mg/dL) have made me cut down on sturated fat. I don’t know if I should worry or not, but if indeed H-Gs have/had low LDL, I want to go lower as well ASAP, rather than wait for more studies to be published. I reported more details on my blog:
    http://paleoclinic.blogspot.com/2010/02/ldl-cholesterol-goes-sky-high-on-fatty.html

  21. Lyle? Lyle McDonald? Is that where you got that study, Nigel? All it showed was that cholesterol was higher in the two prisoners whose very low carb diet was supplemented with fifty grams of carbohydrate a day. It might be useful in an argument between low and zero carbers. But not very.
    Even in 1967, I think these researchers probably knew very well that those 50 grams of carbohydrate would lower the useless marker of total cholesterol.

    • Yes, Lyle McDonald! He (& I) are only trying to show that we are not all the same. Do you agree with that?

      When I posted that study on Nephropal, people thought that I was attacking LCHF diets due to the summary in that study. I’m not. People are over-analysing things.

  22. “Almost everything is blamed asthe
    cause of obesity except for two of mankind’s
    most common faults-greed and
    laziness. In searching for the easy way to
    weight loss, almost every conceivable diet
    may be attempted from time to time, such
    as the currently popular low-carbohydrate”

    I’m usually a pretty polite guy, Nigel. But based on this quote from the beginning of the study you mentioned, the people who wrote this study were a bunch of f**kwads, and really don’t deserve our attention. It’s a hatchet job.

  23. Maybe I’m beating a dead horse here. But that can be fun sometimes. Dr BG mentioned the high intake of polyunsaturated in this study.

    http://www.ajcn.org/cgi/reprint/20/2/139.pdf

    So the high fat part of the diet was achieved at least in part by adding plant oils. But the dietary cholesterol strongly tracks the fat intake. Higher fat, higher cholesterol. I think the diet was manipulated to ensure that the highest fat intake was paired with the highest cholesterol.

    These guys were looking for high cholesterol at the high fat end of the study, and exploded kidneys at the high protein end.

    • Could you please point out to me where oil is mentioned in the above study as I’m buggered if I can find any mention of it. TIA.

  24. Lyle? Lyle McDonald? Is that where you got that study, Nigel? All it showed was that cholesterol was higher in the two prisoners whose very low carb diet was supplemented with fifty grams of carbohydrate a day. It might be useful in an argument between low and zero carbers. But not very.
    Even in 1967, I think these researchers probably knew very well that those 50 grams of carbohydrate would lower the useless marker of total cholesterol.

    I guess everybody’s probably moved on by now… but I meant to say that the carb-supplemented prisoners had lower total cholesterol, not higher, in the first part.

  25. So, does it not boil down to this: look at the very oldest living heathy people (not the ones who are simply alive because they’re not technically deceased yet). Next, look at how many of them eat meat, and how many are veg. Dollars to donuts none of them are vegitarians. They’re more than likely our great grandmothers and grandfathers who grew up on farms eating pastured meat and eggs and raw milk and getting lots of sunshine and meaningful physical movement.

  26. Thanks for this post! I’ve been primal for the last two years and got my bloodwork done only to find out the LDL was relatively high (166). However, with an HDL of 79 and tri’s at 26, I feel a whole lot better knowing what the numbers really mean. Lucky for me, my doc didn’t even mention statins!

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