Fat and Heart Disease – The Changing Landscape

Fat and Heart Disease - The Changing LandscapeMost of us know that the risk of heart disease can be modified by lifestyle. For more than fifty years, that’s what we’ve been taught by the people we trust, scientists, medical professionals and public health officials.

But the doubters have always been out there, and they ask questions. How do these people know what’s good and bad for us? Well, of course we’re aware that their evidence is based on scientific data. But, is the data reliable and has it been interpreted correctly?

For decades we’ve been told that saturated fat, the type found in meat, butter and cheese, raises the risk of heart disease. Health officials have urged the public to avoid saturated fat as much as possible, saying it should be replaced with unsaturated fats like that found in nuts, fish, seeds and vegetable oils. In fact, many consider this to be conventional wisdom, which basically mean that it’s undebatable. However, recent research has challenged this view, and the debate on the risk associated with consuming saturated fat has grown louder by the years.

One of the main reason saturated fat has historically had a bad reputation is that it increases LDL-cholesterol, the type of cholesterol that is supposed to raise the risk for heart attacks. But the effects of saturated fat on blood cholesterol are probably more complex than that. For example saturated fat also increases HDL-cholesterol, the so-called good cholesterol. However, the effect of polyunsaturated fat (PUFA) on blood cholesterol and traditional lipid profile is generally considered more favorable than the effect of saturated fat.

A few days ago, a scientific study published in the Annals of Internal Medicine caught the headlines of news media around the world. The main reason for the attention is the fact that the study did not find that people who ate more saturated fat had more heart disease than those who ate less. Furthermore, the study did not find less heart disease in those eating higher amounts of omega-6 PUFA or those eating more monounsaturated fat.

The study deserves our attention, not only because it challenges current wisdom and modern dietary guidelines, but because it summarizes a very large amount of data from three different types of studies. However, because it’s not an open access paper, and because it’s a landmark study, I thought it would be proper to summarize the main findings as I see them.

The Study Design

The study was performed by researchers from the UK, USA and the Netherlands and was led by a team at the University of Cambridge in the UK. It was a systematic a review and meta-analysis of available scientific data addressing the association between dietary fatty acid intake, fatty acid biomarkers (measured in blood or adipose tissue), or fatty acid supplementation and the risk of coronary heart disease (CHD).

The investigators performed a systematic review of the scientific literature in order to find studies that fitted for their meta-analysis. The studies selected were both observational studies as well as randomized controlled clinical trials. To be eligible, the studies had to fulfill certain criteria. For example, observational studies were eligible if they were prospective in design with at least one year follow-up and involved participants from a general population (not people with known heart disease). Intervention studies were eligible if they were randomized and recorded CHD outcomes. A total 72 studies of more than 600 thousand individuals were selected for the final meta-analysis.

In order to grasp the results of the paper, it is important to understand that the meta-analysis consisted of three parts. Firstly, the association between the intake of different dietary fats with CHD was studied. Secondly, the association of measurements of fatty acid biomarkers with CHD was addressed. Thirdly the association between fatty acid supplements and CHD was studied.

Saturated fat, Omega-6 and Monounsaturated Fat Don’t Affect Risk

There was no statistically significant association between dietary saturated fatty acid intake and the risk of CHD. Furthermore, intake of omega-6 PUFA was not associated with the risk of CHD. The authors of the paper therefore conclude: “Our findings do not clearly support cardiovascular guidelines that promote high consumption of omega-6 polyunsaturated fatty acids and suggest reduced consumption of total saturated fatty acids”.

When studying measurements of biomarkers, it is important to keep in mind that there are many types of saturated fatty acids and many types of PUFA’s. Palmitic and stearic acids are saturated fats that were not significantly associated with the risk of CHD. However, margaric acid was significantly associated with lower risk of CHD. Margaric acid is an odd-chain saturated fatty acid. It’s levels are moderately correlated with milk and dairy consumption. The findings support the possibility that odd-chain saturated fats reflecting milk and dairy consumption, may be less harmful in terms of risk for CHD. Arachidonic acid was the only omega-6 fatty acid that correlated with lower risk of CHD.

Studies of dietary intake and biomarker studies did not find any significant association between monounsaturated fat and the risk of CHD.

Dietary Long Chain Omega-3 PUFA’s Are Protective

Dietary long-chain omega-3 PUFA was associated with lower risk of CHD. These findings were supported by the blood biomarker studies which showed some evidence that circulating levels of eicosapentaenoic acid (EPA) and docosahexaenoic acid  (DHA) (the two main types of omega-3 PUFA) are associated with lower risk of CHD. Alfa-linolenic acid was neutral in terms of risk.

On the other hand, meta-analysis of omega-3 and omega-6 PUFA supplements suggests that supplementation with these nutrients does not significantly affect the risk of CHD. However, the authors point out that more data is needed because the available data is limited. There is a large ongoing trial on the effects of omega-3 PUFA in primary prevention (VITAL). This study will also address the efficacy of vitamin D.

Trans-Fats Increase the Risk of Heart Disease

Not surprisingly, dietary trans-fats were associated with increased risk of heart disease. However, only five published prospective cohort studies contributed to this analysis.

The Changing Landscape

For the last five years, a number of reports (12345) have concluded that there is a weak association between the consumption of saturated fat or major foods that contain saturated fatty acids (meat and milk) and the risk of CHD. The above study certainly adds strength to these conclusions. It appears that the advice to encourage high consumption of polyunsaturated fatty acids and low consumption of saturated fats is not based on solid scientific evidence, and needs to be reconsidered. In fact, the study suggests that dietary fat composition me play a much smaller role for cardiovascular risk than previously thought.

Finally, a few questions need to be asked. Firstly, is this the final verdict? Well, I guess not. But certainly these new results have to be taken seriously. Secondly, how did public health authorities manage to get it wrong for fifty years? Was it because the available scientific data was unreliable, or was it because the data was wrongly interpreted? Was it because the pieces of the puzzle had to fit into a preconceived notion? And thirdly, how will we get it right? How will the new landscape on dietary fats and heart disease be introduced to the public, and how will this landscape affect the food industry?

I know for sure that many experts will cover their ass by suggesting that the macro-nutrient approach is outdated, and they’re probably right. Dietary recommendations focusing on how much to eat of different types of fats and how much of our daily energy intake should be carbohydrates, protein or fat, are both misleading and impractical. So maybe we will soon see a paradigm shift in the way medical professionals and public health officials educate people about the effect of diet and nutrition on health and disease.

Comments

  1. says

    I agree with you Axel. I find this meta-analysis compelling. Let’s hope that professional medical organizations like the AHA and its corollaries abroad admit that they’ve been giving dubious advice about diet for decades.

  2. RichardOrnishForLife says

    Dr. Chowdhury has admitted to a half dozen errors in his paper that he says do not affect his conclusions. This was partly in response to the comments of Walter Willett, Frank Sacks, and Meir Stampfer, who called his conclusions about MUFAs and PUFAs “seriously misleading.”

    • FrankG says

      Good ol’ dependable R O F L.. straight in there with an appeal to the authority of the establishment.. while simultaneously seeking to discredit the study’s authors :-P

      Speaks volumes about how weak your own position must be.

      Where is your source for the “half a dozen errors”..?

      In the Medscape article, I see…

      Regarding assertions of errors in the report, Di Angelantonio [senior author Dr Emanuele Di Angelantonio (University of Cambridge)] said, “We recently spotted some minor mistakes in some of the data that will not in any way affect the main results of the study.” He confirmed that another group contacted him and his coauthors about “some other minor mistake,” adding, “We are making an erratum that will be sent to [Annals of Internal Medicine] in the next 24 hours, so there will be an updated version. But it’s unlikely that the main conclusions will change.”

      Maybe that “other group” should perform their own meta-analysis and elevate the discussion to one of scientific method and review, rather than unsubstantiated opinion?

      Is this yet another example of your reading comprehension issue perhaps?

      Nullius addictus iurare in verba magistri, — quo me cumque rapit tempestas, deferor hospes

  3. Mie says

    I brought up a couple of problems with this meta-analysis in the previous discussion (the low carb thread). Should I copy/paste them here, or could you answer the questions I raised, Axel? I would deem it more fruitful to discuss to quality and nature of the meta-analysis critically than merely repeat the findings as such. Perhaps others are willing to contribute, too.

    BTW, the meta-analysis found that n-3 fatty acids had NO statistically significant effect on coronary effects, not in cohort studies nor in trials. Therefore to state that “omega 3 is protective” is somewhat misleading. In addition, serum TFA had NO statistically significant effect on coronary events (based on cohort studies), either – and at least I would consider serum TFA to be more accurate estimate of the actual intake than estimates of dietary intake, as the human body doesn’t produce TFA.

    • Axel F Sigurdsson says

      Yes Mie. Why don’t you copy your comments here as well.

      For coronary outcomes in the prospective studies of dietary fatty acid intake, the RR was 0.87 (CI, 0.78-0.97) for total long chain omega-3 PUFA’s which is statistically significant. RR was 1.16 (CI, 01.06-1.27) for trans-fats which is also statistically significant. This is very clearly illustrated in figure one of the paper.

      The authors conclude that “dietary long-chain omega-3 polyunsaturated fatty acids was associated with lower risk of coronary disease“. They also conclude that “total dietary trans fatty acid intake was positively associated with coronary disease risk in our meta-analysis

      • Mie says

        Hmm? According to the table on Medscape

        http://www.medscape.com/viewarticle/822092

        the results for n-3 fatty acids were as I mentioned. Mistake on Medscape.

        With TFA: notice that I mentioned circulating TFA. The results didn’t reach statistical significance there.

        And here’s the copypaste:

        “The authors chose not to consider fat modification/exchange properly and also decided to analyze n-3 and n-6 fatty acid intake separately. If you’ve read the full text, could you explain the rationale behind this? E.g. Ramsden et al 2010 showed that mixed n-3 and n-6 diets had beneficial effects on CHD end points.”

      • Axel F Sigurdsson says

        Mie.
        You’re right. To me it looks like there is an error in the table published on Medscape. The numbers are different than those published in figure 1 in the original paper. As I said the RR for Total long chain omega 3 PUFA´s is 0.87 (0.78-0.97), thus statistically significant.

      • Mie says

        Ok.

        Now, have you read the whole paper? If so, could you comment on the two issues I brought up above? And any ideas about the lack of statistical significance in the case of circulating TFA & CVD?

  4. RichieProOrnish says

    Harvard School of Public Health has weighted in:

    “Dr. Willett emphasized that because this meta-analysis contains multiple serious errors and omissions, the study conclusions are misleading and should be disregarded”
    http://www.hsph.harvard.edu/nutritionsource/2014/03/19/dietary-fat-and-heart-disease-study-is-seriously-misleading/

    Jeremiah made an astute observation (2010) the strenght of the association between SFA and CHD becomes stronger in studies utilizing superior methodology, again many people seem to think that every study bears an equal value.

    Good points Mie, well done. At this point, Doc, I tried to warn you not making too much out of this meta-analysis in order to protect your audience from unnecessary confusion, but of course, you wouldn’t listen. That’s a pitty.

    • FrankG says

      Well there you have it! If a prestigious edifice like the Harvard School of Public Health has “weighted” (sic) in with an opinion, who are we to try and discuss the science? Heck when a prestigious edifice like the Harvard School of Public Health proclaims an opinion, we should all just shut up and listen! Who even needs the scientific method when we have a prestigious edifice like the Harvard School of Public Health to tell us what to think?

      Walter Willett’s, ( with co-signers Frank Sacks’ and Meir Stampfer’s) OPINION that this meta-analysis is “misleading and should be disregarded” is just that… an OPINION.

      If a prestigious edifice like the Harvard School of Public Health truly does speak with a single voice that, in and of itself, would be a cause of great concern to me, because unbiased science is not based on a consensus. It beggars the question, who is funding the Harvard School of Public Health?

      Obviously not all studies are of equal quality, methodology etc… but that is not to say an higher quality necessarily means the authors are correct in their conclusions. Or that a “weighty” body of evidence cannot be overturned by a single study — a “black swan”

      And the funniest thing is that Dickie-Poo is so cocky about his (repeated and obvious) appeal to authority that he now feels an “I told you so” is in order! R O F L ;-P

      • Mie says

        Frank,

        would you like to comment on the two things I mentioned above: the issue of fat modification/exchange missing and the decision to treat n-3 & n-6 fatty acids separately? “Richard” is obviously not going to provide a critical look into the matter, so it’s up to rest of us.

      • FrankG says

        Just to add that my understanding of n-3 and n-6 is that: rather than focusing on absolute amounts of each (within reason), health is a matter of balancing the ratio of the two and that the modern industrial diet tends to lead to an imbalance (in favour of higher n-6). Grass-fed and finished beef (as one example) apparently provides an healthier balance of the two as compared to beef finished in a CAFO. I know some will supplement with fish oils (for example) to redress this balance but my preference is to use real whole food over supplements.

        e.g. http://www.ncbi.nlm.nih.gov/pubmed/15189133

        That said I am puzzled as to why this analysis would treat them separately… without access to the full paper, I’d also be keen to hear what Dr Sigurdsson has to say in this regard.

      • Axel F Sigurdsson says

        Frank.

        I don’t think it’s wrong to treat n-3 and n-6 PUFA’s separately. The dietary sources of these two types of fats are very different. The study didn’t find a significant association between dietary n-3 consumption and CHD, while dietary long-cahin n-3 (EPA and DHA) was associated with lower risk of CHD.

        In fact this does not contradict the results of the meta-analysis by Ramsden and coworkers who concluded that trials that substituted n-6 PUFA for saturated fat, without simultaneously increasing n-3 PUFA produced an increase in risk of death that approached statistical significance.

        So, I guess replacing SFA with n-6 PUFA’s won´t reduce risk unless you at the same time increase n-3 PUFA’s.

      • Mie says

        Thanks Frank and Axel. Yes, I agree that we do indeed need both, just like Ramsden’s paper suggests.

        Axel, you stated:

        “The dietary sources of these two types of fats are very different.”

        To some extent, yes. But then again, foods such as nuts and seeds and olive oil which are more n-6 heavy are quite solidly connected to better CVD health, just like foods like salmon and other types of fatty fish which have a smaller n-3/n-6 ratio. To me, this hints that n-6 problems originate from elsewhere, e.g. industrial & refined foods.

      • Axel F Sigurdsson says

        Your right of course Mie. We need both n-6 and n-3. More importantly, we have to look at the food in itself, not only the fat composition. Maybe fat composition plays a much smaller role for cardiovascular risk than we’ve believed so far. The “issue” with industrial and refined foods has to do with many other factors than n-6.

      • Mie says

        It’s kinda hard to make exact comments when the expressions you used are anything but quantatitive. But then again, it IS difficult to quantify the effects exactly in these matters, so I cannot blame you. At least not much. :-)

        Yes, compared to entire diets, the role of fats in CVD is bound to be minor. But since they are one key factor in e.g. the Mediterranean diet, you really cannot say that the type of fat doesn’t matter, period. That’s a blanket statement, and they’re BS, virtually without exceptions (due to the fact that they ignore the different conditions, contexts and uses for different diets). In addition, that’s inverse reductionism, isn’t it? Plus bear in mind that virtually ALL good options (Med.diet, paleo, certain forms of low carb etc. etc.) do have something in common in the fat department …

        And of course the problem with industrial and refined foods has to do with many other factors besides n-6. But in observational studies you really CAN’T control the role of the sources of a given nutrient that carefully. BTW, here’s Willett et al’s take on the new paper

        http://www.hsph.harvard.edu/nutritionsource/2014/03/19/dietary-fat-and-heart-disease-study-is-seriously-misleading/

        and they point out this same thing (the source of n-6 fatty acids).

        Of course, this works in both ways: the good qualities of e.g. olive oil cannot be reduced to just mufa – what about e.g. polyphenols?

        Where does that leave us?

        Entire diets. Just like you stated:

        “I know for sure that many experts will cover their ass by suggesting that the macro-nutrient approach is outdated, and they’re probably right.”

        Scratch the silly remark about covering one’s ass and the word “probable”, and you’re right on the money.

      • Someone says

        Really nice to notice that there is actually really good discussion going on here :). In my opinion it’s been far too long about “satured/unsatured” battle.

        I believe that quality matters. It matters in case of animal fats(crass fed etc.) as well as it matters for vegetable fats (extra virgin olive oil etc.). One reason for contradictory research results is probably that we have over simplified the matter to satured/unsatured battle, now it’s time go forward.

  5. says

    The meta-analysis by Ramsden and coworkers is often cited to support that replacing saturated with PUFA’s is beneficial. However it is important to keep in mind that the same meta-analysis showed that trials that substituted n-6 PUFA for saturated fat, without simultaneously increasing n-3 PUFA produced an increase in risk of death that approached statistical significance. Ramsden concluded that the advice to specifically increase n-6 PUFA intake, based on mixed n-3/n-6 RCT data, is unlikely to provide the intended benefits, and may actually increase the risks of CHD and death.

    http://journals.cambridge.org/action/displayAbstract?fromPage=online&aid=7930322

    • Mie says

      As far as I know, no one’s recommending an increase in n-6 fatty acids in particular, at least not up to the region of 12-15% of total E (which was the case in the studies Ramsden et al reviewed).

  6. charles grashow says

    http://ht.ly/uXmB1
    Scientists Fix Errors in Controversial Paper About Saturated Fats

    Chowdhury says the paper’s conclusions are valid, however, even after the corrections. Randomized clinical trials are the “hardest” kind of evidence, he says, and they don’t show a significant effect of saturated or unsaturated fats. But even one of the paper’s authors, Dariush Mozaffarian, of the Harvard School of Public Health, admits that he is not happy with the key conclusion that the evidence does not support a benefit from polyunsaturated fats. “Personally, I think the results suggest that fish and vegetable oils should be encouraged,” he says. But the paper was written by a group of authors, he points out. “And science isn’t a dictatorship.”

    Another study author, Emanuele Di Angelantonio of the University of Cambridge, says the main problem is that the paper was “wrongly interpreted by the media.” “We are not saying the guidelines are wrong and people can eat as much saturated fat as they want. We are saying that there is no strong support for the guidelines and we need more good trials.”

  7. says

    Axel and Mie, your dispute on the outcomes regarding omega-3 fatty acids seem to be due to an error in the first release of the original paper. The error was corrected a couple of days later into the original paper, but Medscape published their text before the correction took place (and never revisited their story?).

    I think it boils down to what are the sources of saturated fats in western diets. Dairy foods do not seem to increase the risk of CHD in meta-analyses but processed meat does. Processed meat also increases CVD mortality in meta-analyses but dairy does not. Dairy is neutral and biggest contributor to total sat fat. Butter usually constitutes only some 20% of total sat fat intake in western populations.

    I have not seen a meta-analysis on the effect of sheer butter on CHD incidence (neither on margarine). There is one on CVD mortality (O’Sullivan et al. 2013).

  8. charles grashow says

    http://wholehealthsource.blogspot.com/2014/03/corrections-to-new-review-paper-on.html

    “In my view, the most important question is “what foods should I eat”? The answer depends on the individual, but here are my general opinions. Eating synthetic trans fat is probably a bad idea, and it’s generally found in low-quality processed food anyway. Refined seed oils like corn and soybean oil are the nutritional equivalent of white sugar, oxidize during high-heat cooking, and also tend to be found in low-quality processed food, making them a poor choice. I haven’t seen much evidence that makes me concerned about eating the fat naturally contained in meat and dairy, so I view those as acceptable, in moderation. Nuts and wild seafoods seem to be healthy, whether or not that relates to their fatty acid profile, so it makes sense to eat them regularly. Extra-virgin olive oil appears to be one of the healthiest fats, so it’s logical to gravitate toward it as the default added fat.”

    “The primary critiques were 1) that the data were over-adjusted because some of the data had been pre-adjusted for circulating cholesterol levels, and 2) Dr. Ronald Krauss has received funding from the dairy industry. Further analysis by Dr. Krauss’s team confirmed that the result was the same whether one considered studies that had been adjusted for cholesterol, or those that had not. Dr. Krauss was actually not receiving funding from the dairy industry at the time he wrote and published the paper, but in any case this argument is weak unless specific instances of bias can be identified in the paper. “

  9. Mie says

    Thanks Reijo, it seems you’re correct.

    Guyenet’s post (thank you Charles for linking it) brings out many good points. In particular, I would point out that the Hooper et al. which he’s referring to is precisely the case of “devil being in details”. Since it seems that in many RCT’s people simply cannot reach the treatment targets, the results are less than impressive (three little letters: WHI). Now, this doesn’t necessarily mean that the goals itself aren’t worth reaching for. Heck, if that were the case, then lifestyle interventions would be useless – see e.g.

    http://www.ncbi.nlm.nih.gov/pubmed/15824290

    and we’d all be better off on statins. And yet, as trials like Lyon Diet Heart – or to lesser extent, PREDIMED – have shown, the benefits can very, VERY substantial – and not just in the case of CVD. And, of course, medication itself isn’t the “one size fits all” solution: people with a low risk are unlikely to get that much benefit and can be harmed instead.

    I personally take this to mean that more effort is needed and that interventions in fighting CVD need that “extra kick” in addition to what health professionals can provide, for instance, support from the government in the form of legislation and taxation.

    (That was me being optimist. Ask me another day and I might wallow in self-pity. :-) )

  10. Someone says

    I agree with Reijo’s points. If anything I think we should give some slack for dairy products. I also think that it’s fair question to ask that is it the satured fat at the end that is the responsible of the negative results for processed read meat. It could be high sodium content, higher heme iron etc. Or maybe all of them together…

  11. RichardOrnishForLife says

    Guyenets response is a good example why we ought to be cautious with bloggers from the paleo-sphere. Reijo repeated the exact same flawed arguments in Guyenet’s comment section

    “The primary critiques were 1) that the data were over-adjusted because some of the data had been pre-adjusted for circulating cholesterol levels….Further analysis by Dr. Krauss’s team confirmed that the result was the same whether one considered studies that had been adjusted for cholesterol, or those that had not.

    The meta-analysis by S-T contained 2 kind of studies in regards to cholesterol:

    a) Studies that had over-adjusted for serum lipids
    b) Studies that did non include information about the serum lipids

    S-T simply reported seperately the results for the SFA-CHD link in regards to studies, b. They did have any additional information of the vast body of studies that had over-adjusted for lipids. They did not reconsider these studies.

    Adjustements for cholesterol was only one problem with S-T meta-analysis from the countless of others (Stamler 2010). Perhaps the most compelling argument in my view is the fact that, as Stamler pointed out, the stronger and superior the methodology of the study, the stronger the link between SFA-CHD. In meta-analysis the effects of garbage dilutes the pearls, this is a problem when trying to combine studies that are vastly heterogenous in material.

  12. FrankG says

    @ R O F L

    “…the stronger and superior the methodology of the study, the stronger the link between SFA-CHD. In meta-analysis the effects of garbage dilutes the pearls…”

    Which of the studies included in this particular meta-analysis would you (or Stamler) consider to fit in the category of “pearls”… those with a “stronger and superior the methodology”..? Perhaps, instead of trying to discuss innuendos, we should see how well each of these individual studies stands up to scrutiny?

    Meantime I note that you have failed to mention some other potential problems of meta-analyses, that: on occasion, a study — favourable to an agenda — will be re-published multiple times under different titles and altered author lists, or where the findings of a study were not favourable to an agenda, so it is withheld and not published at all… thus “rigging the votes” as it were.

  13. RichardProOrnish says

    ^I have my favorite pearls, sure.

    Referenced as Oxford Vegetarian. Relative risk: 2.77 for dietary SFA (Mann, 1997).

    “A gradient of risk is apparent with increasing intake of total animal fat, saturated fat, and dietary cholesterol as well as some of the major food sources of these nutrients.”

    To be more precise. Scarborough (2010) pointed out that the meta-analysis by S-T included MOSTLY studies that over-adjusted for serum lipids and that did not have any information on serum lipids. S-T & Co simply reported the SFA-CHD link in regards to the studies that did not have any information on circulating blood cholesterol. They did not go back to raw data of the original studies.

  14. FrankG says

    @ R O F L

    Is this the one you mean? I’d prefer to read the source rather than predigested opinion by ideologues like Plant Positive (Pee Pee)…

    http://www.ncbi.nlm.nih.gov/pubmed/10479226

    Was this study included in the meta-analysis we are discussing here? What exactly is your basis for promoting this study as using a “stronger and superior the methodology” than some of the others included… other than its conclusions obviously suiting your own agenda?

    And your “to be precise”…comment… is that an attempt to “move the goalposts” of this discussion..? As there is no clear line of causality between “circulating blood cholesterol” — at least in so far as when you put it so simply — and CHD, then maybe we should stick to studies showing the relationship of SFA to CHD end-points? In other words I’m not prepared to take “circulating blood cholesterol” by itself, as a sign of CHD. There may well be a relationship but it is obviously not as clear cut as you may suit you to suggest

  15. FrankG says

    Thanks Charles..

    Yes I had found that PDF but I’m still not sure this study was included in the meta-analysis we are discussing, or why R O F L thinks it is of an higher standard than others… or even if it is the same study as he (or PP) alluded to.. this is dated 1999 not 1997? At first glance I see questionable elements like: the use of diet questionnaires/records, broad groupings like “meat-eaters” vs “non-meat eaters” (even tho’ some 23% of “non” ate meat on occasion) — what else did they eat?, talk of relative risk (as opposed to absolute)….

    Do you see the “A gradient of risk is apparent…” quotation in the PDF.. I haven’t found it so far.. so what is its source? An opinion by Mann or PP perhaps??

    Again I question this “house of cards approach” where SFA has some effect on “lipids”, “everyone knows” that “lipids” inevitably leads to CHD and that CHD inevtitably leads to early death GASP!!! shock
    horror!!!! Except it ain’t anywhere near that simple, nor straightforward.

    Of course I realise that diet-trials with humans are fraught with challenges but I repeat that: I do not see a, established direct line of causality from dietary SFAs->”circulating blood cholesterol”->CHD.. let alone that you can skip over the middle part and jump straight from SFAs to CHD… or stop part way before CHD has been demonstrated. If you want to show that dietary SFA’s leads inevitably to CHD, then demonstrate that.

  16. FrankG says

    @ R O F L

    …you make a big deal above about researchers not going back to the raw data and also use the word “garbage” in respect to some of the trials included in this meta-analysis… then you offered one which you claim to be of an higher standard…

    This is how they describe the methodology for collecting the plasma lipid data, used in the Oxford Vegetarian Study (above)…

    “Between April 1984 and January 1986, all surviving subjects under age 70 y were sent a kit … We obtained plasma lipid measurements for 3773 subjects, a response rate of <40%. Total cholesterol concentration was measured directly and LDL- and HDL-cholesterol concentrations were calculated by subtraction as described elsewhere (4). Triacylglycerol concentration was not measured because, for practical reasons, it was not possible to ensure that the blood samples were collected under fasting conditions."

    So less than 40% actually had a (single) blood test, with no concern for fasting or not.

    Sure the researchers then go on to create all kinds of impressive-looking data and statistics from what they have collected but there is another saying related to handling data, “garbage in, garbage out”

  17. Z.M. says

    For the sake of consistency, since Richard is usually concerned about conflicts he could have pointed out that at least two of the Oxford authors are essentially vegetarian activists.

  18. charles grashow says

    @FrankG

    Here’s the paper where the quote came from

    http://heart.bmj.com/content/78/5/450.full
    Dietary determinants of ischaemic heart disease in health conscious individuals

    “The findings support the hypothesis that the nature and quantity of dietary fat and cholesterol are key determinants of IHD mortality.2 3 A gradient of risk is apparent with increasing intake of total animal fat, saturated fat, and dietary cholesterol as well as some of the major food sources of these nutrients. Further indirect support for a key role of dietary saturated fat and cholesterol in promoting IHD comes from the difference in serum cholesterol between vegetarians and meat eaters; we and others have reported differences of between 0.4 and 0.6 mmol/l.18-20Law et al estimated that a 0.6 mmol/l difference in total serum cholesterol would cause a 27% difference in IHD mortality and a 10% difference in all cause mortality,21 predictions that are close to those observed in a meta-analysis including our own and four other studies of vegetarians.12 Serum cholesterol differences of this magnitude would be predicted on the basis of the difference in intake of saturated fat and cholesterol between vegetarians and non-vegetarians.13 22″

  19. FrankG says

    Thanks again Charles… yes I noticed the other paper was also replete with “predictions” about the health outcomes. I’d rather see the conclusions on observed outcomes, than what they “think” might happen.

    Also worth noting that here we have a prime example of multiple papers, with different titles and different publication dates but both are based on the same study. Great way to skew meta-analyses to an agenda…

  20. Mie says

    Am I the only one who finds it … odd that the blogger chooses to a) include studies which – according to e.g.Stamler (who he cites) – were of “low methological quality” and b) studies that didn’t report CHD deaths accurately?

  21. FrankG says

    @ Mie… you mean HealthyLongevity (gotta love these names)..?

    What do you expect… this is just another anonymous veg*n blogger – why do they feel the need to slink around anonymously when they have such conviction about their message… it just makes me think they are not to be trusted –

    As with R O F L, you really can’t expect rational discussion… all bets are off when the only motivation is to reinforce their agenda, by any means

  22. RichardOrnishForLife says

    Am I the only one who finds it … odd that the blogger chooses to a) include studies which – according to e.g.Stamler (who he cites) – were of “low methological quality” and b) studies that didn’t report CHD deaths accurately?

    But these were the exact studies that were used in both S-T meta-analysis and in the new meta-analysis published in the Annals of Internal medicine. HealthyL writes:

    In order to ensure that the methods used for the statistical analysis were consistent with those used by Siri-Tarino and colleagues, I performed the meta-analysis in Review Manager (from The Cochrane Collaboration), and pooled the estimates using the random effects model for both within-study and between-study variation. Similarly, risk ratios and 95% confidence intervals were log transformed to derive the corresponding standard error for beta-coefficients by using Greenland’s formula.23 Otherwise, the exact P-value was used where available to derive the corresponding standard error.

    In a meta-analysis including 14 studies, dietary saturated fat intake was associated with a statistically highly significant 24% increased risk of death from coronary heart disease (Fig. 1). Similarly, for the 11 studies included in the Siri-Tarino meta-analysis, saturated fat was associated with a statistically highly significant 26% increased risk of death from coronary heart disease (RR=1.26 [95% CI, 1.14-1.40]). In order to ensure that the methods used for the statistical analysis were consistent with those used by Siri-Tarino and colleagues, I performed the meta-analysis in Review Manager (from The Cochrane Collaboration), and pooled the estimates using the random effects model for both within-study and between-study variation. Similarly, risk ratios and 95% confidence intervals were log transformed to derive the corresponding standard error for beta-coefficients by using Greenland’s formula.23 Otherwise, the exact P-value was used where available to derive the corresponding standard error.

  23. RichardOrnishForLife says

    Moreover Mie,

    HealthyL performed a separate sub-analysis excluding the 40% of studies that controlled for either serum or LDL cholesterol. SFA was associated with statistically significant 30% increased risk of death from coronary heart disease, consistent with the findings of Stamler (2010).

  24. Mie says

    Frank: that was more of a rhetorical question. I’ve debated with HL here on Axel’s blog before. I know the type: some good points but also suffering from bias.

    As for anonymity, I don’t consider it an issue – though I may be biased for an obvious reason :-). The information value of a statement doesn’t depend on the person uttering it.

  25. Mie says

    Richard:

    “But these were the exact studies that were used in both S-T meta-analysis and in the new meta-analysis published in the Annals of Internal medicine.”

    I know. I merely pointed out that it’s a bit … strange that one should BOTH embrace Stamler’s points AND yet use the same studies. Plus include studies that didn’t have accurate information on CHD deaths. If that isn’t precisely missing “the devil in the details” – on purpose, as it seems – I don’t know what is.

  26. RichardOrnishForLife says

    Mie,

    the problem is not about using poor data per se. The problem was that both S-T and especially Chowdhury made extravagant conclusion and confused the public. These people did not factor the poor methodology of the type of studies they used in their conclusions. And this is a problem, as Willet pointed out. And, S-T did not even look at the link between SFA and CHD mortality in their original paper. HealthyLongevity attempted to clear this confusion. SFA increases the risk of premature death significantly (the strength of this association is most likely diluted due to number of reasons) even when looked at more reductionist, single nutrient fashion.

    David Katz had some excellent remarks of this paper as well; even if this was a sound study (which it wasn’t), it merely illustrated that in the context of Western diet, people eating higher or slightly lower amounts of SFA will have equally much heart disease, roughly speaking; those with SFA intake at the lower end, actually had less CHD (albeit statistically significant finding). However, we just know how to fare much better and butter really does not have a place in these arrangements that fare better (Ornish/McDougall; DASH, Lyon diet, etc).
    http://www.huffingtonpost.com/david-katz-md/bittman-butter_b_5042270.html

Let me know what you think!