Statins and Heart Disease – Do Women Differ From Men?

Recent studies have shown that the symptoms of heart disease may differ between men and women. For example, women are less likely than men to have chest pain while suffering an acute heart attack (acute myocardial infarction). This may delay diagnosis and may partly explain why women seem to fare worse than men under these circumstances. Furthermore, the role of risk factors for heart disease may be different between the two genders.

Statins and Heart Disease - Do Women Differ From Men?

It has also been suggested that treatment with cholesterol lowering drugs, so-called statins may be less effective for women than men, in particular in primary prevention (individuals without known cardiovascular disease).

We had the pleasure to address these important issues recently in my hometown Reykjavik, Iceland, when visited by Barbara H. Roberts MD who is a prominent expert in this field. Dr. Roberts is director of the Women’s Cardiac Center at the Miriam Hospital in Providence, R.I. and associate clinical professor of medicine at the Alpert Medical School of Brown University. She has written two hugely interesting books,  How to Keep From Breaking Your Heart: What Every Woman Needs to Know About Cardiovascular Disease and The Truth About Statins: Risks and Alternatives to Cholesterol-Lowering Drugs.

I ran across Dr. Roberts recent book on statins while visiting New York last December for a cardiovascular meeting. I became very fond of it because it is extremely well written and can easily be read both by laymen and professionals. Her discussion is objective, evidence based, and she does not jump to any conclusions. Although Dr. Roberts has a point to make, her writing is careful and unbiased. Of course, the book has a strong message which I know many of my cardiologist colleagues will not agree with.

The internet may affect our lives more than we sometimes realize. A few days after I finished reading Dr. Roberts book I mentioned it in one of my blog posts because I felt it had an important message to everyone interested in cardiovascular disease and modern-day health care. Statins are used by millions of people worldwide. Whether we like it or not, we have an obligation to look at both the positive and negative effects of this therapy.

By coincidence, Dr Roberts read my article and we became acquainted. Six months later she arrived in Reykjavik to give two talks, a public lecture on how women may reduce their risk of heart disease, and another lecture at aimed at professionals at our University Hospital on statin therapy.

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How to Keep From Breaking Your Heart: What Every Woman Needs to Know About Cardiovascular Disease 

Dr. Roberts gave her first talk on the evening June 18th 2013. It was attended by more than 300 people, mostly women.  I was really proud by the huge interest. Thank you, Icelandic women for showing so much interest in how to improve your health and reduce the risk of heart disease. Dr. Roberts gave a fascinating overview of cardiovascular disease, risk factors, lifestyle and prevention. It was a memorable evening.

She started by addressing the anatomy of the normal heart, the coronary vessels and the blood circulation.  She then discussed important symptoms and disease concepts such as angina pectoris, myocardial infarction or heart attack, congestive heart failure, and palpitations.  She touched on the underlying pathology of cardiovascular disease and introduced important disease mechanisms like atherosclerosis, plaque rupture and clot formation.

Barbara H Roberts
Barbara H Roberts MD is director of the Women’s Cardiac Center at the Miriam Hospital in Providence, R.I. and Associate Clinical Professor of Medicine at the Alpert Medical School of Brown University

Dr. Roberts then went on to describe how the symptoms of an acute heart attack may differ between men and women. Men are more likely to experience chest pain than women. Women are more likely to have nausea, back, shoulder, abdominal or neck pain than men. Women are also more likely to have no chest pain, and just shortness of breath or sometimes fatigue.

Dr. Roberts went through most of the known modifiable risk factors for heart disease like smoking, high LDL cholesterol, low HDL cholesterol, high blood pressure, diabetes, obesity, sedentary lifestyle, the metabolic syndrome and inflammation.

Dr. Roberts dedicated a part of her talk to treatment with statin drugs. Statins are frequently used to lower cholesterol and to reduce the risk of heart disease. It is her opinion that the benefits of statins have been greatly exaggerated and that their dangers have been greatly downplayed. She mentioned the most common side effects of statin therapy like muscle pain, rhabdomyolysis, cognitive dysfunction, tendon and nerve damage, diabetes, liver and kidney damage, fatigue, cataracts and congenital defects in babies exposed before birth. She summarized the results from clinical trials addressing the effects of statins in women. She underlined that no study has ever shown that treating women who do not have established vascular disease or diabetes with a cholesterol lowering medicine lowers the risk of cardiac death or cardiac events.

Dr. Roberts concluded that high levels of LDL cholesterol appear less predictive of cardiovascular risk in women than in men. In women, HDL cholesterol appears more predictive of risk than any other lipid level. She emphasized that abnormal blood cholesterol is but one of many risk factors for cardiovascular disease and that it´s not all about the LDL-cholesterol.

After covering the health risks of diabetes, inflammation, obesity and the metabolic syndrome Dr. Roberts went on to talk about the influence of diets. She mentioned a few dietary fictions like “Eating foods high in cholesterol raises your cholesterol” and “Low fat diets are good for your heart“. She also mentioned a few dietary facts like “Low fat diets lower HDL cholesterol so they are NOT heart healthy. You need to eat heart healthy fats” and “You can eat your way through any cholesterol lowering medicine“. Finally she underlined the strong scientific evidence indicating that a Mediterranean type diet reduces cardiovascular risk.

Dr Roberts concluded her lecture with this message:

Prevention of Heart Disease Made Easy:

  • If you smoke, STOP
  • If your cholesterol is high, get it down
  • If your blood pressure is high, get it down
  • If your blood sugar is high, get it down
  • If your weight is high, get it down
  • Do moderate exercise 30 minutes/day
  • Eat a heart healthy diet
  • Pick your parents wisely
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The Truth About Statins: Risks and Alternatives to Cholesterol-Lowering Drugs

Dr. Barbara Roberts gave her second lecture in Reykjavik on June 19th at Landspitali University Hospital. Again she did a wonderful job with a highly informative and provocative talk. Unfortunately, only about 40 people attended, among them only a handful of cardiologists. I know doctors are busy people, but I have to admit that I would have loved to see more colleagues. Statins are the most frequently prescribed drugs by cardiologists all over the world. Many of us believe they are our most important weapon when it comes to pharmacological treatment of cardiovascular disease. So, I can understand that it may be unpleasant to hear about their presumed bluntness.

m_51ftcwyw3yl._bo2-204-203-200_pisitb-sticker-arrow-click-topright-35-76_aa278_pikin4-bottomright-67-22_aa300_sh20_ou01_Dr. Roberts started by going through many of the advantages and disadvantages of statin therapy.  She quoted Doctor Rita Redberg: “There are millions of women on a drug with no known benefit and risks that are detrimental to their lifestyle — and no one is talking about it”. She also quoted Dr. Sidney Blumenthal: “The totality of the available biologic, observational and clinical-trial evidence strongly supports the selective use of statin therapy in adults demonstrated to be at high risk for heart disease”. So, “are statins angels or devils” she asked?

Next Dr. Roberts took us through the history of the lipid hypothesis, from the work of the German pathologist, Rudolph Virchow on atherosclerosis in 1856, to the modern day clinical trials. She underscored the difference between absolute and relative risk reduction. She summarized data from clinical trials on the use of statins in secondary prevention. The result was that statins significantly reduce the number of cardiac events among individuals with cardiovascular disease, although the effect appears less pronounced among women than men. Again, she underscored the fact that clinical trials have not shown that treating women who do not have established vascular disease or diabetes with a cholesterol-lowering medicine lowers the risk of cardiac death or cardiac events.

Dr. Roberts then went through all the most common side effects of statin therapy. Unfortunately, this list appears to be growing, not unsurprisingly though, considering the huge number of people taking these drugs. Recently the increased risk of diabetes and cognitive dysfunction associated with statin therapy has been highlighted. Finally, she talked about possible alternatives to statin therapy. Again she underscored the positive effects of the Mediterranean diet.
Dr. Roberts final conclusions were:

  • Statins confer a small reduction in the risk of heart attacks and in some studies of dying of heart disease in those with established disease. The benefit is less in women than men.
  • They confer much less benefit in men without disease and none at all in healthy women.
  • The Mediterranean Diet is more effective than statins in lowering risk, WITHOUT ANY SIDE EFFECTS.

The Bottom Line

We, cardiologists tend to focus on the positive effects of statins. This is completely reasonable because clinical trials have shown that these drugs are very effective under certain conditions, and they improve the prognosis of patients with cardiovascular disease. Statins may also be effective among individuals at high risk for developing cardiovascular disease, such as those with diabetes. Nobody doubts the important role of statins in patients with familial hypercholesterolemia (FH).

Sometimes it is much easier for doctors to prescribe a drug than not to do it. Furthermore, the positive effects of statins are highly emphasized by the medical community, and these drugs are generally considered well tolerated. I am much more likely to be criticized by my colleagues if I don´t put a patient on statin therapy who might benefit, than if I put someone on such therapy who will probably not benefit from it. Sometimes we forget the words of our ancestors: Primum non nocere; first do no harm.

Sooner or later we will have to face the fact that many people have side effects from statin therapy. Often, these effects are not obvious. As doctors, we have to be alert and monitor patients for such side effects.

It has been pointed out by some of my colleagues that highlighting the negative effects of statins may encourage some patients to stop taking their drugs. Obviously, if these are individuals who are benefitting from their therapy, this may cause harm. On the other hand, providing truthful unbiased information to our patients can never be ethically wrong. Indeed, such information is necessary for shared decision making. Otherwise, our patients will not be able to make a truly informed decision on whether they want a certain treatment or not.

Finally, I would like to sincerely thank Dr. Barbara Roberts for visiting Iceland and sharing her knowledge and experience. Again, I recommend everyone interested in cardiovascular disease and modern-day health care to read her book on statin drugs. It is a strong reminder of our limited knowledge of the long-term effects of drugs that are being prescribed to millions of people worldwide.

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Mie
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Mie

Dr Roberts’ comments and views are problematic in many ways. 1) Mediterranean diet (from now on: Med) more effective than statins? Err nope, don’t think so. Where’s the evidence? The best piece of evidence to support this comes from the Lyon Diet Heart study, the excellent results of which haven’t been replicated since. However, the bigger problem is that at least I’m not aware of any interventional studies comparing Med with statin therapy (with a separate control group). And you certainly cannot compare & contrast between different studies! Not to mention the issues of adherence and compliance. Several long &… Read more »

Axel F Sigurdsson
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Axel F Sigurdsson

Mie. Thanks for your comments which are thorough and valid as always. You mentioned the Cochrane analaysis when discussion the benefits of statins in women in primary prevention: https://onlinelibrary.wiley.com/doi/10.1002/14651858.CD004816.pub5/full I didn´t find any distinction between men and women in this particular analysis. The authors on the other hand make another interesting point in their discussion: “All but one of the trials had some form of pharmaceutical industry sponsorship. It is now established that published pharmaceutical industry-sponsored trials are more likely than non-industry-sponsored trials to report results and conclusions that favour drug over placebo due to biased reporting and/or interpretation of… Read more »

Mie
Guest
Mie

Axel, I understood that the review refers to CTT 2012. In addition, this isn’t the only recent meta-analysis stating that women benefit from statins. See Kostis et al, “Meta-Analysis of Statin Effects in Women Versus Men”, 2012. The benefits in terms of primary CV endpoints were there for BOTH sexes in both primary and secondary prevention – and the results were statistically significant. Thus Roberts’ claim that healthy women (meaning women without existing CVD) don’t benefit from statins is clearly not valid. I agree with you on that people at low risk of CVD (such as women whose total risk… Read more »

bhrdoc
Guest

Axel thank you for this comprehensive and accurate summary of my remarks. I realize they will spark a lot of argument and controversy. That is not a bad thing especially if it makes us question the preconceptions we all harbor about what is best for our patients.

Doc´s Opinion
Guest

There is an interesting analysis of the risk of diabetes in the statins trials published in a recent issue of Diabetes Care. The risk of new onset diabetes on statin therapy appears higher among women than men.
https://care.diabetesjournals.org/content/36/7/e100.full.pdf+html?sid=b0d9a20c-86c1-470c-afc8-5c9579deea50
The authors point out that among women at low risk for cardiovascular disease who are prescribed statins, the risk of incident diabetes may outweigh the cardiovascular benefit.

Doc's Opinion
Guest

The question whether women benefit from statins in primary prevention depends on how the clinical trials and meta-analyzes are interpreted. In her lecture, as well as in her book Dr Barbara Roberts has criticized the use of the term “need for revascularization” as an end point. She points out that if this end-point is omitted from the major trials on statins in primary prevention which have included women, and only hard end points used, there is no significant effect of statins compared with placebo among women. In their meta-analysis published in JACC (Journal of The American College of Cardiology) 2012,… Read more »

Mie
Guest
Mie

“Secondly, the authors did not have enough data to critically evaluate adverse side effects.” Notice that the Cochrane review addressed this issue, too. Of course, you can always refer to the fact that the number of RCT’s in primary prevention is much smaller than in secondary prevention. However, we’ve got to operate on what we knowledge & data we have. “Thirdly,concerns have been raised about the long term safety of statins for primary prevention, both in men and women, due to a potential increased risk of incident diabetes.” Indeed. However, in high risk patients (seemingly regardless of sex), the benefits… Read more »

Low-fat Richard
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Low-fat Richard

Doc, next time have Bill Roberts speaking at your event instead (American Journal of Cardiology, editor in chief). Bill is a real expert and is not BS:ing his audience into believing there are some other options besides statins or pure (or quasi-pure) vegetarianism. Evaluating lipid-lowering trials in the twenty-first century. “…Only pure vegetarians for practical purposes do not need statins, most of the rest of us do” https://www.ncbi.nlm.nih.gov/pubmed/19406281 There’s only proven approach to diet that is compatible with LDL receptor hypothesis as elucidated by Brown & Goldstein (1984) and that is the Ornish/Esselstyn/McDougall approach. This is a principle as strong… Read more »

Axel F Sigurdsson
Admin
Axel F Sigurdsson

Richard. I don’t disagree with you that a very low fat diet may reduce the risk for developing atherosclerosis. However, there is still a lot of residual risk among those with low LDL cholesterol. Look at the results from the TNT-trial for example (and other statin trials for that matter): https://www.ncbi.nlm.nih.gov/pubmed/15755765. These were patients with stable corornary heart disease. Mean LDL cholesterol was 77 mg/dl (2.0 mmol/l) with 80 mg atorvastatin, vs. 101 mg/dl (2.6 mmol/l) with 10 mg atorvastatin. After a median follow-up of 4.9 years, the primary end-point occurred in 10.9% of the 10 mg atorvastatin group, and 8.7% of the 80 mg atorvastatin group… Read more »

Mie
Guest
Mie

Axel, bear in mind the difference that Richard is talking aboutf life-long risk accumulation in people with no CVD and you’re talking about people with established CVD. You can’t really expect the latter to have zero risk whatsoever. However, I too would like to point out that Richard’s idea of risk modification ever accounting for only LDL in real life setting is … well, daydreaming. People get treated on the basis of clinical evidence from studies, not extrapolations of what we could achieve if things were different. I suspect we’re NEVER going to see LDL levels like that (1,5 mmol/L)… Read more »

Low-fat Richard
Guest
Low-fat Richard

Yes, exactly. Thanks Mi(k)e for saving my time. The mean age at the randomization in typical statin trial is 63. There’s the residual risk. However, I’d like to point out that there will be no talk about residual risk once the PCSKY-9 inhibitors enter the market. This agents allow LDL reduction down to 20’s and 30s (mg/dl). People with existing disease need to treated more aggressively.

Axel F Sigurdsson
Admin
Axel F Sigurdsson

The efficacy of PCSK-9 inhibitors is currently being tested in large scale clinical trials. Until we have the results, it´s an untested hypothesis that further lowering of LDL cholesterol will improve prognosis of individuals with cardiovascular disease. Let´s hope you are right Richard that residual risk will be history when we have the trial results. Remember though that additional lowering of LDL-C by by adding ezetimibe to statins has not been proven to be beneficial in clinical terms. Actually I am principal investigator at one of the FOURIER – trial sites. FOURIER is a huge clinical trial testing the efficacy… Read more »

Richard
Guest
Richard

Sounds awesome, Doc.

The people at UT Southwestern medical center (Brown & Goldstein, etc) seem to be very confident with the approach of further lowering LDL.

“If we get LDL low enough, you cannot develop atherosclerosis, no matter how much diabetes, hypertension or smoking you do” (15min.20sec).

–Darren McGuire
https://www.youtube.com/watch?v=DFMtoafT70c

BTW, Doc! Have you met some of these big names in atherosclerosis research such as Brown & Goldstein, Evan Stein, Steinberg, etc.

Best,
R

Mie
Guest
Mie

“Mie, the idea that Ornish would in par with med diet is ridiculous.” And yet, you yourself state evidence against the feasibility of Ornish: “In Gardner et al, people assigned to read the Ornish book, ate 30% of their calories from fat and had very little resemblance to Ornish diet.” And this happened in a trial where compliance rates & results in dietary intervention are BETTER than in real life. In addition, it’s pretty much a no-brainer that a diet that produces results X in clinical setting with compliance rates of Y isn’t as recommendable as a diet that produces… Read more »

Low-fat Richard
Guest
Low-fat Richard

What Garner et al showed was how obese people respond after reading a popular diet book. I am about being a force of change. There’s not a single people eating according to Ornish approach if they do not know what to expect. I want to change the meat-dairy laden culture to starch/plant-based culture. I am about educating people. This is the whole purpose of public measure’s for health, education, that is. What would have been the outcome if the saturated fat laden diets of the developed world of the 1960s would have continued? Luckily health educators did not just wait,… Read more »

Mie
Guest
Mie

“What Garner et al showed was how obese people respond after reading a popular diet book.”

And these people benefitted most from reading Atkins’ book. 🙂

And if you want results showing something different, check out e.g. Dansinger et al (2005), “Comparison of the Atkins, Ornish, Weight Watchers, and Zone diets for weight loss and heart disease risk reduction: a randomized trial”, where Ornish produced the greatest weight loss but in terms of CVD risk factors there were virtually no differences after 12 months of intervention.

So there.

Low-fat Richard
Guest
Low-fat Richard

Mie, to recommend med- or any other type of diet over the Ornish would be an act of charlatanism. It would be as if the doctor prescribed fibrates alone for his/her FH-patients. To not to encourage patients to adopt low-fat, whole-food plant-based diet (the only diet congruent with the LDL receptor theory), would not be in the best interest of the patient. As Esseltyn commented for New York Times, what PREDIMED actually proved was that the Mediterranean diet promoted heart disease in people that did not have it at the baseline. You cannot recommend a high-fat diet with a proven… Read more »

Mie
Guest
Mie

Richard, once again, your resort to talking BS. 1) There’s no comparative study suggesting that Ornish (or low fat vegan diet by any other name) is superior. There’s evidence showing the benefits of Med, more so than with any other diet (see Mente et al 2009), but all in all, the idea of one single dietary approach being superior isn’t founded in scientific evidence. However, there are a few key issues (plenty of vegetables/legumes/nuts, quality fat in moderation, avoid excess meat & especially processed meat etc. etc.) which are in common to many successful approaches – e.g. Med and Portfolio.… Read more »

Low-fat Richard
Guest
Low-fat Richard

Mie, I have problems with your stance. To my knowledge there’s no other diet than that of the Ornish approach that would be in congruent with LDL receptor hypothesis. Med diet cannot provide physiologic cholesterol levels for most adult humans, it’s too high in fat. And yes, I know olive lowers cholesterol next to butter or beef, but if I was to increase my consumption of oils, my cholesterol levels would go up, since I have low cholesterol already (olive oil is 14% SFA).The studies you cited come within obese, high-risk population, the usual end-point being weight-loss. We need to… Read more »

Mie
Guest
Mie

“I have problems with your stance. To my knowledge there’s no other diet than that of the Ornish approach that would be in congruent with LDL receptor hypothesis. Med diet cannot provide physiologic cholesterol levels for most adult humans, it’s too high in fat.” Err, you do realize that unsaturated fat ENCHANCES LDL receptor activity? This explains why unsaturated fat has been consistently shown to REDUCE LDL levels in human. “And yes, I know olive lowers cholesterol next to butter or beef, but if I was to increase my consumption of oils, my cholesterol levels would go up, since I… Read more »

Low-fat Richard
Guest
Low-fat Richard

Mie, I don’t fail. For the first, the Ornish trial exists already, but even if didn’t, we don’t need trials for everything. It’s good to have them but we can use our logic and fill the missing holes even without them. There’s not a single trial that has established the benefits of smoking cessation (all three trials that tested it failed), lack of exposure to asbestos, seat belts, etc. Trials belong to pharmacology, excessive obsession about them is a thingy of the low-carb/Taubes crew, people who do not believe in the darwinian legacy. The diet story is here, by Brown… Read more »

Low-fat Richard
Guest
Low-fat Richard

Doctors such as Barbara Roberts pushing nonsense about dietary cholesterol not elevating blood cholesterol are the best kept secrets of the statin industry. They provide market for these drugs long into the future. Sure, let’s all pretend the Hegstedt never conducted extremely controlled feeding experiments on dietary cholesterol, let’s all forget Hopkins meta-analysis on dietary cholesterol (1992) and the fact the dietary cholesterol downregulates LDL receptors. Let’s forget that Sacks found that adding 1 egg per day to the usual diet of 17 lactovegetarians whose habitual cholesterol intake was very low (97 mg/d) significantly increased LDL cholesterol level by 12%.… Read more »

Axel F Sigurdsson
Admin
Axel F Sigurdsson

Richard
The main conclusion of a recent meta-analysis published last year in the British Medical Journal was, quote:
“Higher consumption of eggs (up to one egg per day) is not associated with increased risk of coronary heart disease or stroke.”
https://www.bmj.com/content/346/bmj.e8539

Mie
Guest
Mie

Axel, you do realize that Richard’s just going to have a sissy fit and spam that same ol’ BS about “darwinian foundation” and animal studies, instead of looking & criticizing the meta-analysis (since he simply can’t read research literature)? Even though it directly contradicts his absurdities such as these “Instead, lets pretend that Egg center’s gimmicks, feeding egg yolks to overweight diabetic people who are not sensitive to extra dietary cholesterol, that is, is the last word on dietary cholesterol” (Richard, the meta-analysis showed that increased egg consumption INCREASES the risk of CHD in diabetic patients …) So yes, moderate… Read more »

Low-fat Richard
Guest
Low-fat Richard

Axel, highly problematic meta-analysis. For several reasons. Ancel Keys showed already in the 1960s that if the within-person variation is larger than the between-person variation, which is common in homogenous populations where everyone consumes a similar diet, then this will especially bias the findings towards a null association. For example, in a homogenous population with a between-person variation of between 2 to 6 eggs per week on average, the variation of intake of an individual consuming on average 4 eggs per week maybe between 1 to 7 eggs per week. If this person’s diet is measured at a high or… Read more »

Mie
Guest
Mie

And yet another systematic review on eggs:

https://ajcn.nutrition.org/content/early/2013/05/15/ajcn.112.051318.abstract

“This meta-analysis suggests that egg consumption is not associated with the risk of CVD and cardiac mortality in the general population. However, egg consumption may be associated with an increased incidence of type 2 diabetes among the general population and CVD comorbidity among diabetic patients.”

Mie
Guest
Mie

Heck, I’ll give this a brief look since I’ve got the time. 1) The first point (the issue of intra/interindividual variation): irrelevant. This issue is well-known but doesn’t render the findings of ANY given meta-analysis obsolete. Or if they do, then … Well, the logical result is that epidemiological evidence per se is obsolete. Is that really the argument here? If it is, perhaps you should stop referencing epidemiological evidence when it suits your needs. Or even better: perhaps you should go read a book on epidemiology. 2) The second point (reverse causation): cherry-picking. Yes, of course people will adjust… Read more »

Health Longevity
Guest

Mie, 1) If the degree of measurement error in a study is so great that the expected result of an association would be near zero even if the hypothesis is correct, this would mean that null findings would do very little to negate a hypothesis as such results were expected. Nevertheless if a positive association is found it could be hypothesized that this finding would have potentially been attenuated due to measurement error and can still provide support for a particular hypothesis. Epidemiological evidence is especially useful when there is limited evidence from higher quality forms of evidence and should… Read more »

Mie
Guest
Mie

1) Your comment changes nothing. Of course there are differences in study design etc. etc. but that really wasn’t the case here. Unless you can, of course, elaborate why this problem w/ epidemiological evidence seems to concern ONLY this issue? Or are you arguing that e.g. current recommendations for whole-grain which are – to a large extent – based on observational data are misguided? 🙂 2) Problems with compliance are well-known problems in any study involving diet & free-living subjects (of course elsewhere too, but let’s focus on this one). Unless you have plenty of evidence pointing out that one… Read more »

Healthy Longevity
Guest

1) One of the problems with testing the diet heart hypothesis as opposed to testing the health benefits of whole grain with within-population cross-sectional and cohort studies is due to the diet-hearts hypothesis reliance on the intermediate variable of serum cholesterol (which is greatly effected by interindividual variability). Studies looking at the health benefits of whole grains may not suffer as greatly if the beneficial effects are largely independent of blood lipid concentrations. I refer you to Jacobs et al. classical paper from 1979 to explain the reasoning for this as you do not appear to be familiar with these… Read more »

Low-fat Richard
Guest
Low-fat Richard

^A problematic meta-analysis for several reasons. Firstly, the association between egg intake and the risk of cardiovascular disease is meaningless without considering suitable substitutes for eggs. As a lower intake of eggs implies a higher intake of other foods in order to maintain caloric balance, the effect that egg intake has on coronary heart disease depends on which foods eggs are substituted for. For example, data from the Nurses’ Health Study, one of the largest studies included in these meta-analyses suggested that replacing one serving of nuts, but not red meat and dairy with one serving of eggs per day… Read more »

Mie
Guest
Mie

Richard, if you’re not citing the source for the abovementioned, you’re plagiarizing. The text is copy/pasted in pieces from here

https://healthylongevity.blogspot.fi/2013/04/cracking-down-on-eggs-and-cholesterol.html

Unless, of course, you’re the blogger Healthy Longevity, in which case nevermind.

I’ll address the points mentioned once you either ask Axel to remove the plagiarized part or confirm that you are the author.

And of course: Axel, I recommend that you address the issue, too. Of course we can quote other people, but credit where credit is due.

Axel F Sigurdsson
Admin
Axel F Sigurdsson

Thanks Mie. Point taken. For those of you who are copy/pasting or quoting in general, please cite the source.

Mie
Guest
Mie

And why not comment on this one, too? Just got back from a 10-km-long jog & feeling nice and energetic, so … 🙂 “1) Firstly, the association between egg intake and the risk of cardiovascular disease is meaningless without considering suitable substitutes for eggs.” Err, the point of the individual studies included in the meta-analysis was NOT to look at the “best possible option” but to see whether egg intake was associated with increased risk in comparison with a given diet. Complaining about a different focus doesn’t mean the meta-analysis is problematic. “The findings from this meta-analysis should therefore be… Read more »

Healthy Longevity
Guest

It is not merely how researchers of a particular field interpret the conclusions of a study, but perhaps even more importantly how the general population will. This is one of the main reasons why Katan at al. criticized the Siri-Tarino et al. meta-analysis. If a meta-analysis/systematic review concludes that food x is not associated with an increased risk of heart disease people may think it is safe to increase consumption of this food instead of focusing on healthier choices. For example, if a systematic review concludes that refined grains are not associated with an increased risk of heart disease because… Read more »

Mie
Guest
Mie

“It is not merely how researchers of a particular field interpret the conclusions of a study, but perhaps even more importantly how the general population will. This is one of the main reasons why Katan at al. criticized the Siri-Tarino et al. meta-analysis. If a meta-analysis/systematic review concludes that food x is not associated with an increased risk of heart disease people may think it is safe to increase consumption of this food instead of focusing on healthier choices.” I find this VERY problematic. Virtually ALL meta-analyses clearly mention the limitations. You cannot expect different meta-analyses be stopped/go without publishing… Read more »

Healthy Longevity
Guest

It is obvious that I am not suggesting censorship, but a call for more informative conclusions. The researchers should make it clear that the analysis suggests that increasing food or macronutrient x is unlikely to confer any benefit compared to other foods typically not considered health. It is especially problematic when the conclusions appear to be written in a way that is purposely intended to mislead the public. As Hu FB and Sun Q, two authors of the Siri-Tarino et al. meta-analysis pointed out in a different paper they co-authored, “in this meta-analysis saturated fat was compared with other calorie… Read more »

Mie
Guest
Mie

“As Hu FB and Sun Q, two authors of the Siri-Tarino et al. meta-analysis pointed out in a different paper they co-authored, “in this meta-analysis saturated fat was compared with other calorie sources, primarily refined carbohydrates, and high intake of refined carbohydrates has been associated with a high risk of CHD.“ Not only was this not made clear in the conclusions of the original meta-analysis paper, this limitation was not made clear in the paper at all.” Now, it’s kinda hard to assess the claims unless you provide a REFERENCE. I suggest you do so first, then we may continue… Read more »

Healthy Longevity
Guest

In regards to the statement from the paper co-authored by Hu FB and Sun Q here is the link to the paper below: https://circ.ahajournals.org/content/122/9/876.full You did not seem to have any difficulties searching for where Richard copied some of his previous quotes from so obviously you should have been able to find this paper. There is also the other meta-analysis eggs and cardiovascular disease that Richard cited that found that eggs were associated with an increased risk of cardiovascular disease even when they did not restrict the analysis to diabetics. Although I agree more with the conclusions of this meta-analysis… Read more »

Mie
Guest
Mie

Richard, I’ll continue here to avoid the messages becoming too narrow to read properly (damn you, WordPress!) “I don’t fail. For the first, the Ornish trial exists already, but even if didn’t, we don’t need trials for everything. It’s good to have them but we can use our logic and fill the missing holes even without them. There’s not a single trial that has established the benefits of smoking cessation (all three trials that tested it failed), lack of exposure to asbestos, seat belts, etc. Trials belong to pharmacology, excessive obsession about them is a thingy of the low-carb/Taubes crew,… Read more »

Mie
Guest
Mie

Richard,

“And, yes, I know oils have isolated components that lower cholesterol, it’s just that food is package deal. Ornish has written well about oils; 2-piece writing:
The Great Olive Oil Misconception — Dr. Ornish Responds
https://www.rd.com/health/the-great-olive-oil-misconception-dr-ornish-responds/

1) You do realize that Ornish isn’t arguing that oils are unhealthy? Hell, do you even READ what you post?

2) Ornish’s post is creating a false dilemma. Just because cold-pressed canola oil may be healthier, doesn’t mean that olive oil is unhealthy. This isn’t the case of either/or, but BOTH/AND. There’s room for all these oils (canola, olive, fish, flaxseed) in a healthy diet.

Richard
Guest
Richard

Mie & Doc, I should have provided a link. HealthyL is a very good friend who has given me permission to utilize and use his texts how I wish. This was the first time ever I did not cite him properly nor provided the link, I did this because I utilized mostly my own material in Axel’s blog, and used HealthyL’s egg post only for time saving purposes. However, at the risk of me having misunderstood his intentions, I forward this conversation to his email, and if he feels I did wrong, he can let you know, Doc. Right now,… Read more »

Mie
Guest
Mie

“Mie, I do not argue smoking is healthy or harmless, but as HealthlyL elaborated in DietDoc’s blog, there are actually 3 such trials that tested the hypothesis that smoking cessation would lower the risk of lung cancer mortality.” Even though this is completely off-topic, I’ll address this briefly. 1) MRFIT was a multi-factorial trial which wasn’t powered to detect such individual benefits in individual risk factors. Follow-ups have shown that the primary finding was – indeed – the difficulty of smoking cessation: relapse after relapse leads to the fact that people receiving special guidance fared no better than people receiving… Read more »

Healthy Longevity
Guest

The main point I was trying to make when I mentioned the smoking cessation trials was that a few trials that fail to produce statistically significant findings does not necessarily negate a particular hypothesis in the presence of certain limitations, and that a number of problems that plagued the smoking cessation trials also plagued the trials that tested diet-heart hypothesis. The lack of statistically significant decreased risk of lung cancer in the smoking cessation trials is probably due to several limitations and does necessarily negate nor overrule all other forms of evidence that support this hypothesis. All forms of evidence… Read more »

Healthy Longevity
Guest

Please ignore that first comment, I will reword it. I was confused by the e-mail that Richard sent to me which had me assuming that the Doc was the one who left the comment, not somebody else. The main point I was trying to make when I mentioned the smoking cessation trials was that a few trials that fail to produce statistically significant findings does not necessarily negate a particular hypothesis in the presence of certain limitations, and that a number of problems that plagued the smoking cessation trials also plagued the trials that tested diet-heart hypothesis. The lack of… Read more »

Low-fat Richard
Guest
Low-fat Richard

Mie, my blogger friend addressed the findings from tobacco trials as a response to diet-heart denialism and obsession with RCT -trials in the context of lifestyle issues. As I concluded, all 3 trials that have tested whether smoking cessation works have failed. You try to confuse the point being made as you often do. When things don’t go in your way, you resort to creating confusion, bad manners and outward nastiness. I did not not tout these findings as a strong piece of evidence. Shall we go into the details of your favorite Atkins paid RCT’s? I have my favorite… Read more »

Mie
Guest
Mie

“my blogger friend addressed the findings from tobacco trials as a response to diet-heart denialism and obsession with RCT -trials in the context of lifestyle issues. As I concluded, all 3 trials that have tested whether smoking cessation works have failed. You try to confuse the point being made as you often do. When things don’t go in your way, you resort to creating confusion, bad manners and outward nastiness. I did not not tout these findings as a strong piece of evidence.” Err Richard: you do realize that I a) stated it was off-topic but decided to dissect the… Read more »

Low-fat Richard
Guest
Low-fat Richard

Mike, I don’t need to understand much about the Darwinian foundation. I just need to remind you about it. I think it’s enough, I understand the main principles as addressed by Stamler (2010): dietary cholesterol promotes atherosclerosis on numerous different omnivorous species, the most relevant being non-human primates. Dietary cholesterol has unfavorable effects on serum lipids and induces atherosclerotic lesions. Furthermore, there was no evidence of a threshold for dietary cholesterol with respect to an adverse effect on arteries. Long-term feeding of cholesterol in relatively small amounts has actually been shown to induce atherosclerosis in rabbits, chickens, pigeons and monkeys… Read more »

Mie
Guest
Mie

Richard, you can ask him about the cig trials if you wish, but I’m not going to address the issue again in this thread. It’s off-topic, just like I stated, and has gone on long enough. If you can’t be bothered to check the studies yourself, that’s fine by me. If your blogger friend suffers a blow to his ego as a consequence, that’s fine by me, too. 🙂

Low-fat Richard
Guest
Low-fat Richard

Axel, I apologize if this somewhat off-the-main-topic but topics may sometimes receive another tinge or an angle. I feel I still need to address this issue. Mie, I think your arguments about cigerette smoking trials and healthy diet are somewhat flawed. The failure of smoking cessation trials is a fact that ought give us some perspective. Trials are not the last word when it comes to lifestyle. Katan elucidated this very well: “In addition, evidence from epidemiologic, metabolic, and laboratory studies confirms that high intakes of saturated fat do cause heart disease. Ignoring this evidence leads to absurd consequences. For… Read more »

Axel F Sigurdsson
Admin
Axel F Sigurdsson

Apology accepted. I guess nobody’s going to read these lengthy off-topic discussions anyway.

Low-fat Richard
Guest
Low-fat Richard

Healthy Longevity,

excellent remarks. Thanks for your contribution. Doc, what do you think about SFA and dietary cholesterol these days? Have you reconsidered your position? After all, not a single public health authority took the S-T meta-analysis seriously. And now, the results from the recent reanalysis of MRFIT has been brought to your attention. Moreover, I’d like to add that the RRs for SFA and fatal heart event that Stamler reported was 1.32 which is on line or even bigger than that of the RRs between passive smoking and lung cancer.

Axel F Sigurdsson
Admin
Axel F Sigurdsson

Richard. I´m considering my position all the time. I try to keep an open mind. In terms of saturated fats and cholesterol there´s really nothing to reconsider. I have never doubted that avoiding saturated fats will lower blood cholesterol. We totally agree on that. I also believe that plant based diets are very useful when it comes to preventing heart disease. That´s another thing we agree on. I wish more people could stick to such lifestyle. I do recommend it to my patients and have done so for many years. However, there are other issues than blood cholesterol that we… Read more »

Low-fat Richard
Guest
Low-fat Richard

Doc, here’s an MD colleague for you who is also interested in preventative medicine. In the course of three months his cholesterol plummeted from 240 to 150 together with other benefits. An inspiring story for you! Forks Over Knives Changed My Health and How I Treat My Patients “As the director of prevention and wellness at St. Luke’s Hospital in St. Louis, I had always considered myself knowledgeable about the importance of diet and exercise, tried to eat “healthy,” tried to stay active, and counseled my patients to do the same. My “healthy” diet centered on eating plenty of fruits… Read more »

Mie
Guest
Mie

1) Nicely copy/pasted advertisement. Lucky for you that Axel allows this kind of spamming. 2) Concerning the point you made to Axel about MRFIT post-trial: if you (or your blogger pal w/ a bruised ego) knew anything whatsoever about conducting an RCT or statistical analysis, you’d understand that a post-hoc analysis of a MULTIFACTORIAL NON-BLINDED trial is not without problems. Check out this article concerning the problems related to post-hoc analysis: https://www.medscape.com/viewarticle/409693 What a post-hoc analysis of MRFIT tells us is another indication that life-style interventions are worth conducting when treating CVD patients and/or people belonging to risk groups. However,… Read more »

Low-fat Richard
Guest
Low-fat Richard

Mie, what was your point? The tobacco trials were a success, and relying solely on evidence from RCT’s goes without problems in the context of life-style? The point that I and HealthyL tried to convey is that it is important to consider all lines of evidence in regards to the link between diet and chronic disease. You seem to have a problem with this? You don’t have to consider anything else beyond RCT evidence if one is to address the effect of a drug, obviously. Now, in regards to findings from MRFIT (including the ad hoc analysis) do you think… Read more »

Mie
Guest
Mie

“Now, in regards to findings from MRFIT (including the ad hoc analysis) do you think the advice to reduce dietary cholesterol is not based on good science? What was the problem? I apologize if I get it wrong, but it appears to me that you are the one with difficulties in the ego section (see Katan’s reply to someone with an obvious problem, whatever that problem is).” Err, what on earth are you talking about? You do realize that I commented on post-hoc analysis being problematic, not on dietary recommendations concerning dietary cholesterol? And Katan, by the way, is commenting… Read more »

Low-fat Richard
Guest
Low-fat Richard

Mie, Doc wrote a blog post about fats which was somewhat problematic according to me and HealthyL. https://www.docsopinion.com/2013/02/17/fat-and-heart-disease-exploring-the-villain/ He stated that the participants in MRFIT were told to reduce their intake of cholesterol with no results. HealthyL pointed out that INTERESTINGLY a more recent reanalysis of MRFIT which demonstrated a significant decreased risk of CHD and CVD events during the trial and that the non-fatal events during the trial were strongly associated with CVD mortality during the 20 years after the trial ended which demonstrated that the trial was too short to show a significant benefit for the degree of… Read more »

Mie
Guest
Mie

Once again, I can read – apparently better than you. Nothing you wrote changes the fact that post-hoc analyses cannot be used convincingly to argue that a negative trial – hallelujah! – indeed produced the results YOU personally like. At best, it contributes to what you know already of the primary topic (lifestyle interventions in CHD prevention) and also adds to another matter, too (trials need to be designed carefully). Had you read the link I posted, you’d have realized why the authors are correct in pointing that post-hocs should be treated with caution. And what’s even worse, NONE of… Read more »

Low-fat Richard
Guest
Low-fat Richard

Mie, I referred to a wrong link. Doc wrote about the MRFIT here: https://www.docsopinion.com/2012/06/19/should-i-take-cholesterol-lowering-drug-2/ HealthyLongevity quoted Doc directly in his response and thus this should not have been a problem. Not sure, how well good you read after all. I was very busy and screwed it up with the links. What’s your excuse? We, obviously, disagree strongly, but I think it’s a idea to leave it at that. To bring this back to the issue, I think B Roberts ignores the evidence on dietary cholesterol which a) elevates cholesterol and b) is associated with CHD in several prospective cohorts under… Read more »

Mie
Guest
Mie

“I was very busy and screwed it up with the links. What’s your excuse?”

Trusting that you could provide a correct link.

Dietary cholesterol has less influence on plasma cholesterol than e.g. SAFA when we’re talking about people eating a mixed diet. See this

https://www.ncbi.nlm.nih.gov/pubmed/1534437

and figure 2.

It has also been well established that some people react much more severely to dietary chol. than others and thus should watch out for it. For others, this isn’t as important as e.g. quality of fat, intake of fibre etc. etc. issues that influence plasma cholesterol levels.

Low-fat Richard
Guest
Low-fat Richard

I regards to my previous post I just made, I feel slightly bad for being too rough on B Roberts. Apologies! Mie, great to debate with you. Axel, thanks for the patience and tolerance for differing views. Summer calling and I need to leave the scene.

Best,
R

Low-fat Richard
Guest
Low-fat Richard

Mie, I misread your arguments somewhat. Yes, we agree that it’s worth treating risk patients and those with diagnosed CHD. These people benefit from the treatment in terms of substituting SFA and dietary cholesterol with better alternatives. I am confident everyone else will benefit from replacing SFA and cholesterol with minimally refined plant foods even though we do not have any trials directly verifying this. HealthyL’s argument for the diet-heart is not limited to MRFIT alone, he just wanted to address that the diet-heart has a solid foundation. No bruised ego’s. His arguments are in line with those of NHS:… Read more »

Allie Dillard
Guest

If you have established vascular disease — and I analyzed five of the biggest secondary prevention trials, and I looked at the outcomes in men and women. And if you look at these five trials, which included over 33,000 men, the event rate dropped from 25.5 percent in men on placebo to 19.5 percent in men on statins. So there’s a 6 percent absolute risk reduction. But when you read these trials and you read the headlines, they never give the absolute risk reduction.

Mie
Guest
Mie

HL, I’ll continue down here due to WordPress’ tendency to shrink Reply-boxes: “1) One of the problems with testing the diet heart hypothesis …” Not convincing. The direct benefits of whole-grain products are based – in my opinion quite extensively – on blood lipids, too (soluble fibre lowers LDL). And the fact that there are more than just this factor in the picture doesn’t really differentiate them from fats which too have effects on CVD beyond their effect on LDL receptor activity. “2) To suggest that what I said is based on mere speculation and that it maybe almost as… Read more »

Healthy Longevity
Guest

1) As the observed benefit of soluble fiber seen in prospective cohorts is much greater than the predicted effect it has on serum lipids, and as benefit has also been observed for insoluble fiber which his little effect on serum lipids, this suggests that the benefits of fiber (or perhaps foods rich in fiber which fiber intake may merely be a marker of) are largely independent of serum lipids. https://archinte.jamanetwork.com/article.aspx?articleid=216689 I agree that dietary fats probably influence CVD via mechanisms that are also independent of serum lipids, but cohort studies may have limited ability to test the additive effects of… Read more »

Low-fat Richard
Guest
Low-fat Richard

Mie, the points you’ve made, inter alia, are the following: a) Dietary cholesterol is not a top priority for people on mixed diets. b) Trials which have tested the effect of smoking cessation have been successful. c) The magnitude of reverse causation (sick quitter effect) has gone unnoticed in prospective cohorts All of the arguments are flawed. In fact, you act like low-carb apostles with a messianic belief in your own faulty reasoning. So far, you’ve provided very little beyond rudeness, confusion and outward lies. Dietary cholesterol downregulates LDL receptors. If dietary cholesterol is an issue for vegetarians and people… Read more »

Low-fat Richard
Guest
Low-fat Richard

Moreover, as one of the co-authors of the Pedersen et al editorial (Uusitupa & Schwabb 2011) pointed out in a separate publication, the meta-analysis of prospective cohorts do not gauge the structural changes in the diet that already occurred in all developing nations earlier (before the survey): the intake of SFA plummeted. This is a separate issue from the observation that people change their diet DURING the survey as a response to unfavorable blood lipids (sick-quitter effect). Between 1970 and 1995 annual consumption decreased from 310 to 235 eggs per person in US, a one important component of the improved… Read more »

Mie
Guest
Mie

“Did the authors of these new egg reviews discussed these structural changes in the diet that occurred earlier? If they didn’t, I wonder why?”

Oh jeez. Answer: a meta-analysis/review of prospective cohorts need not discuss epidemiological correlations.

This thread of discussion is indeed SO over. Even though it’s been kinda amusing watching both you and HL struggle in a sea of strawmen, off-topic and red herrings, it’s also fundamentally a waste of time.

Mie
Guest
Mie

Richard, it seems that – once again – we’re done. You’re exhibiting the “usual” signs of an Internet crank: “a) Dietary cholesterol is not a top priority for people on mixed diets.” Refusal to study the evidence. I pointed out Hopkins (1997), a meta-analysis of metabolic ward studies, which clearly shows that the effect of dietary cholesterol is negligible compared to e.g. the effects of dietary fat modification – which, in turn is, is again minor compared to a more thorough dietary change. In addition, by replacing the sources of saturated fat in one’s diet with fat sources richer in… Read more »

Healthy Longevity
Guest

“Hopkins (1997)”? Are you confusing Hopkins 1992 and the Clarke et al. meta-analyses of metabolic ward studies? I cannot find such a paper published by Hopkins PN from 1997. The Hopkins 1992 meta-analysis suggests that for a person consuming a near cholesterol free diets, adding cholesterol from a couple large eggs per day would increase serum cholesterol by about 0.5 mmol/l (Fig. 2). This is actually quite considerable and is about the same as change in serum cholesterol that Clarke et al. 1997 found for replacing 10% of calories complex carbohydrates with saturated fat. Even if dietary cholesterol is to… Read more »

Mie
Guest
Mie

“Hopkins (1997)”? Are you confusing Hopkins 1992 and the Clarke et al. meta-analyses of metabolic ward studies?” Indeed, I mentioned the wrong year. Apologies. “The Hopkins 1992 meta-analysis suggests that for a person consuming a near cholesterol free diets, adding cholesterol from a couple large eggs per day would increase serum cholesterol by about 0.5 mmol/l (Fig. 2). This is actually quite considerable and is about the same as change in serum cholesterol that Clarke et al. 1997 found for replacing 10% of calories complex carbohydrates with saturated fat.” Notice that this applies only to people consuming very little dietary… Read more »

Mie
Guest
Mie

Clarification to my messages above, this part:

“Thus when people with higher LDL/TC complied, they lowered the intake of unsaturated fats as …”

What I meant that this presumed compliance to dietary advice may not have changed the dietary fat relations (SAFA/PUFA/MUFA) in connection with TC/LDL that much, if at all, and thus it would bias the results in a way, too.

Not to mention that there is no quantified data on the size and scope of this effect. Therefore, pointing out reverse causation nonetheless remains observative speculation.

Healthy Longevity
Guest

As I provided references to 2 papers in which 3 out of the 4 authors of the S-T co-authored emphasized the issue of saturated fat in the S-T meta-analysis as likely being compared primarily to unhealthy sources of calories, this cannot be simply be passed off as being cherry picked. This is an obvious issue (as well as many others) that merited a greater emphasis in the original meta-analysis (and by others those who cite it). https://ajcn.nutrition.org/content/93/4/684.full#xref-fn-1-1 https://www.ajcn.org/content/93/4/684.full#xref-fn-1-1 In regards to reverse causation and fat between the 1950s and 1980s, for example in the US intake of saturated fat and… Read more »

Mie
Guest
Mie

“You did not seem to have any difficulties searching for where Richard copied some of his previous quotes from so obviously you should have been able to find this paper.” Ahem, whose job is it to provide references to his own claims? As for the point in the paper mentioning S-T et al (2010): yes, the authors were pointing out the correct context for S-T. But as for S-T not mentioning the refined carb -thing: try reading the paper a bit more carefully the next time. Here’s a quote from “Discussion” in S-T: “With respect to dietary carbohydrate, the type… Read more »

Healthy Longevity
Guest

The S-T could not have carried out a full examination into the effect of replacing saturated fat with other macronutrients with the data they used. However, the fact that the greatest source of calories in the studied population was derived from foods rich in carbohydrates and many of the larger studies adjusted for either unsaturated fats, dietary fiber and fruits and vegetables (leaving almost all but refined carbohydrates) strongly suggests that this is what saturated fat was “primarily compared” with. As was my point, it should have been made very clear that saturated fat was likely compared with other sources… Read more »

Doc's Opinion
Guest

There’s been a lengthy discussion here on saturated fats and low fat diets. However, nobody’s mentioned the recent Cochrane meta-anlysis here, or maybe I just missed it.

https://onlinelibrary.wiley.com/doi/10.1002/14651858.CD002137.pub3/abstract

It showed that reducing the total amount of fat in our diet, by replacing them with starchy foods does not reduce the risk of cardiovascular disease. However, modifying the fat we eat, by replacing saturated fat with mono- and polyunsaturated alternitives may provide som protection.

Healthy Longevity
Guest

The reduction in LDL and total cholesterol in these reduced fat randomized controlled trials included in the Cochrane meta-analysis was very minimal. As it has been demonstrated in dozens of rigorously controlled metabolic ward trials that replacing saturated fat with carbohydrates significantly lowers total and LDL cholesterol, the lack of decrease of LDL and total cholesterol likely reflects lack of appropriate dietary changes required to test the diet-heart hypothesis. The RR of 0.96 for cardiovascular mortality in the Cochrane meta-analysis is consistent with the expected results when considering the small decrease in LDL cholesterol. The Womens Health Initiative which was… Read more »

Mie
Guest
Mie

Just like I mentioned, this was quite good stuff. Nice to see you can produce, after all. 🙂 I’d like to add a couple of points: a) Quality of the individual studies (most are quite old, thus problems with methodology) –> the “carbage in, carbage out” is difficult to avoid b) Quality of the fat used in fat modification: many times the amount of PUFA & n-6 increases considerably, which (in the context of otherwise sub-optimal diet, smoking etc. etc.) isn’t prone to improve things However, the lack of statistically significant findings does indeed suggest the need to focus on… Read more »

Mie
Guest
Mie

One correction: the RR for CV mortality was 0.94, not 0.96.

Mie
Guest
Mie

Axel, the discussion has focused on cohort data & eggs. But yes, good point. Let’s see what HL can make out of this.

Mie
Guest
Mie

“As was my point, it should have been made very clear that saturated fat was likely compared with other sources of calories that are not generally considered health.” Made clear despite adequate means to investigate the issue (cherry-picking among studies)? No, most certainly not. It’s clear that you enjoy speculation ONLY when it suits your needs. The rest of us have higher standards. “Furthermore, S-T were only emphasizing the importance of reducing refined carbohydrates instead of both refined carbohydrates and saturated fat. This is one of the many reasons why it was obvious to many prominent researchers that this paper… Read more »

Low-fat Richard
Guest
Low-fat Richard

Axel, the intervention arm in WHI did not increase their consumption of whole-grains, fruits, legumes or vegetables. The intervention group tinkered on fat in the form of choosing animal products lower in fat. The fiber intake was pathetic, 15g/day. This is indeed the “golden standard” of nutrition research as some would say. “Low-fat doesn’t work” is just one one interpretation of the trial, however I think that is a misleading and flawed interpretation. T Colin Campbell pointed out in his book “China Study” that better interpretation of the trial is that diets high in animal products do not work. The… Read more »

Mie
Guest
Mie

Richard, you’re wrong – yet again – in a couple of issues: a) Just because a trial doesn’t produce the results some people wanted doesn’t mean it was badly conducted or “wrong”. WHI showed precisely the same problem as virtually all trials: the difficulties people have in adjusting and modifying their diet & behaviour. There really are no major differences between … well, virtually all known diets. E.g. Ornish and vegetarian diets: adherence and compliance is no better than w/ others. b) This “Darwinian foundation” you speak of is a strawman. Yes, we all have the same origin. But no,… Read more »

Healthy Longevity
Guest

I believe the point Richard is making about the Darwinian foundation of biomedical research is that because it has been demonstrated that elevated serum cholesterol and the feeding of dietary cholesterol and saturated fat accelerates the development of atherosclerosis in virtually all vertebrates (including nonhuman primates) that have been sufficiently challenged (so long as a way is found to raise serum cholesterol high enough for a sufficient period of time), very compelling evidence is required in order to safely say that this does not apply to humans. This is very different than the Taubesians whose claims are based off a… Read more »

Mie
Guest
Mie

“I believe the point Richard is making about the Darwinian foundation of biomedical research is that because it has been demonstrated that elevated serum cholesterol and the feeding of dietary cholesterol … ” … it’s ok for him to refer to animal studies when he sees fit. The ego question again. And false solidarity, in your case. “Furthermore, animal studies have actually been considered when creating guidelines. One example of this is the 1984 NIH consensus …” So nearly 30 years ago animal studies were referenced? Yes, on the issue of experimental pathology/pathophysiology, which is precisely the purpose why animal… Read more »

Healthy Longevity
Guest

When the evidence from animal studies is so compelling it would be preferable to have strong evidence from human studies in order to guarantee the safety of a particular substance. We wouldn’t want those who we care about to consume a substance known to hurt virtually all species of animals without strong evidence demonstrating its safety in humans. Of course, this may not apply to someone like you who appears to prioritize their ego over saving lives.

Doc's Opinion
Guest

Richard.

Back to the Cochrane data I mentioned. This is a meta-analysis, based on a systematic review of randomized intervention trials addressing the issue. This is the clinical data that is available for us to draw our conclusions from. I understand that you hold another opinion, but I don’t believe it is supported by available clinical trial data. Citing epidemiological data won’t change this fact.

Healthy Longevity
Guest

As I pointed out metabolic ward experiments have demonstrated that replacing saturated fat with complex carbohydrates can significantly lower LDL and serum cholesterol. Therefore the fact that the decrease in LDL and serum cholesterol in these trials were very small reflects the lack of appropriate dietary changes required in order to test the diet-heart hypothesis. The Womens Health Initiative which was given the majority of the weight in the Cochrane meta-analysis was not even designed to lower LDL cholesterol, and as a result reductions in saturated fat intake and LDL cholesterol were fairly negligible. The researchers of the WHI pointed… Read more »

Low-fat Richard
Guest
Low-fat Richard

Doc, John McDougall MD certified internist interviewed the chief inspectors of WHI-trial in his radio show. The inspectors believed in moderation. Well, the “low-fat” -group had actually 9% reduction in breast cancer occurrence which was the primary end-point of this failed trial. The whole story can be read here: https://www.drmcdougall.com/res_whi_report.html McDougall came out recently with a new book. The book, Starch solution, was reviewed by the current editor-in-chief of Medcape, the former editor of JAMA, George Lundberg who also sits in at the board of IOM. I recommend McDougall’s new book to everyone interested in preventative med. The diet book… Read more »

Mie
Guest
Mie

Now Richard, this all would mean something if

a) you’d stop the advertising of popular, commercial books

and if

b) McDougall’s diet plan had any scientific evidence to back up his claims

Mie
Guest
Mie

“As I provided references to 2 papers in which 3 out of the 4 authors of the S-T co-authored emphasized the issue of saturated fat in the S-T meta-analysis as likely being compared primarily to unhealthy sources of calories, this cannot be simply be passed off as being cherry picked. This is an obvious issue (as well as many others) that merited a greater emphasis in the original meta-analysis (and by others those who cite it).” And as your “merited a greater …” is still based on … Yes, what (Lack of enough words? Lines?) is it based on? I’ll… Read more »

Healthy Longevity
Guest

You again repeat: “I’ll answer that for you: nonsense & ego.” My point is even that the authors of the S-T meta-analysis pointed out the weakness that saturated fat was likely compared to unhealthy sources of calories and called for more of a focus on studying the effects of replacing foods with other suitable alternatives. These researchers had a good idea of the composition of the diet was of the populations in these studies which is why they are able to make such a statement. It is not very meaningful to compare the worst foods with the worst foods which… Read more »

Mie
Guest
Mie

“It is not very meaningful to compare the worst foods with the worst foods which has been taken advantage of by the food industry and promoters of fad diets in order to promote an unhealthy diet. I strongly agree that food should be compared with other healthy alternatives. This is not nonsense and ego but is about saving lives.” Yes, it is nonsense. You’re essentially claiming that because established methodological solutions can be exploited & twisted by some people, these solutions are to be discarded. That is – simply put – idiotic. An analogous argument would be to stop having… Read more »

Mie
Guest
Mie

It seems that the rest of my reply vanished? I’ll try again from the Howell part:

1) Howell et al 1997 found out that the totality of various lipid changes had an effect of ca. 5% reduction in LDL-C. Yes, 5%!!!

“compliance with current dietary recommendations (30% of energy from fat, < 10% from saturated fat, and w/ HDL, no such thing)

Low-fat Richard
Guest
Low-fat Richard

Mike,

you also dismiss the evidence suggesting that dietary cholesterol influences the risk of CHD independently from serum cholesterol. In other words, dietary cholesterol promotes atherosclerosis under and above its effect on blood cholesterol levels.

Low-fat Richard
Guest
Low-fat Richard

Mie wrote: “Yes, it is nonsense. You’re essentially claiming that because established methodological solutions can be exploited & twisted by some people, these solutions are to be discarded. That is – simply put – idiotic. An analogous argument would be to stop having prospective cohorts because the inherent methodological issues inevitably limit the nature of information we can gain from them.” HL made a valuable point why discussing with you is worthless. You are too opinionated about issues you have no clue. Let go, it’s over. It’s time for you to retire. “For example, it may not be useful, as… Read more »

Healthy Longevity
Guest

You said: “You’re essentially claiming that because established methodological solutions can be exploited & twisted by some people, these solutions are to be discarded.” I am currently debating with a person who refuses to accept this and exploits this data to suggest that diet rich in saturated fat and cholesterol can be healthy. I am not saying that these findings should be discarded but that the findings from these studies should be considered with great caution as the foods/macronutrients at question are most likely being compared to foods that are not likely healthy alternatives. As the researchers of the Astrup… Read more »

Low-fat Richard
Guest
Low-fat Richard

Mie, your ideological belief in the supremacy of the “golden standards of evidence” disappear immediately when HDL-C is being discussed. Where are the trials supporting the HDL-C theory? Your “robust association” disappears immediately when global perspective is taken into consideration. HDL-C levels were once very low in rural China and Okinawa with near-absence of clinical CHD. Moreover, people carrying APo1 Milano mutation in their HDL-C live long with very low rates of heart disease despite having elevated triglycerides and low HDL-C. The best evidence of McDougall approach is that it’s the only dietary paradigm that guarantees biologically normal “physiologic” cholesterol… Read more »

Mie
Guest
Mie

Richard, please stop creating strawmen. I’ve clearly stated that yes, I’m in favour of looking at the evidence as a whole but that I also do regard RCTs (or rather, systematic reviews/meta-analyses of them) as the top of the evidence hierarchy. Which is, BTW, the standard. Now, obviously that doesn’t mean that trial evidence cannot or shouldn’t be scrutinized. If you’d bothered to read (which I’m beginning to doubt) my messages, you’d noticed that I agreed w/ HL’s take on the Hooper et al meta-analysis on fat modification RCTs. Now why would it be any different to take a critical… Read more »

Low-fat Richard
Guest
Low-fat Richard

Doc, what do you think of HDL-C modulation? Have you seen lean & fit people with very low levels of HDL-C? I think there’s only one biomarker in the lipid fraction that is sensitive to diet independent of weight and that is LDL-C. Elevated triglycerides and low HDL-C probably function as a marker of abdominal obesity and HDL-C goes up after weight-loss independent of the mechanism used. In other words, everything goes: amphetamine, chemo therapy, diet; everything that result in weight-loss probably elevates HDL-C on obese people. What do you think, Doc? There are papers that highlight the importance of… Read more »

Axel F Sigurdsson
Admin
Axel F Sigurdsson

At least it appears that HDL-C modulation by drugs hasn´t been successful thus far. HDL-C is a complicated molecule and there are many subtypes which may play a slightly different role. I agree that weight loss usually helps in elevating HDL-C, at least for those who are overweight and/or obese.

Mie
Guest
Mie

Now Richard, have a look at the ESC guidelines for the management of dyslipidemia https://www.escardio.org/guidelines-surveys/esc-guidelines/GuidelinesDocuments/guidelines-dyslipidemias-FT.pdf and notice (p. 1786) that weight loss doesn’t have the same magnitude of effect on HDL-levels as reducing transfat and exercise: If you lose 10 kg of body weight, your HDL can go up ca. 0,1 mmol/L whereas exercising worth 1500-2200 kcal creates the SAME or even LARGER increase.Of course, these need not be mutually exclusive options, not by any means. However, this does put that “amphetamine and chemo” nonsense of yours into context. It would be analogous – and equally stupid – to claim… Read more »

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