A new review on dietary fats: Putting its findings in context

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Lisa Te Morenga, Jim Mann, Murray Skeaff, Rod Jackson, Tony Blakely, Nick Wilson, Rachael McLean

Bowl of almondsThis blog considers a newly published review on the evidence around dietary fat intakes and coronary heart disease. We have concerns about some aspects of this review, in particular the lack of context around the totality of the evidence. Hence we suggest that the best evidence for national guidelines is still that which encourages the replacement of saturated fats with polyunsaturated fats – with the latter ideally being long-chain omega-3 fatty acids (as found in fish, flax seed and nuts).

The issue of whether the current evidence base is sufficient to advise populations to reduce saturated fat intakes is one that remains controversial. A just published systematic review and meta-analysis examining the association between dietary fatty acids and coronary heart disease (CHD) by Rajiv Chowdhury and colleagues has appeared in the journal “Annals of Internal Medicine”. The authors, conclude that “current evidence does not clearly support cardiovascular guidelines that encourage high consumption of polyunsaturated fatty acids and low consumption of total saturated fats”, and that such guidelines may need reappraisal to reflect the current evidence. They found no significant association between CHD outcomes and intakes of saturated fat, monounsaturated fat, and both omega-3 and omega-6 polyunsaturated fats.

At first glance you might think then that this review offers substantially new insights into the effects of dietary fats on CHD. However this is not the case. This new review essentially repeats the findings of earlier reviews (i.e., by Skeaff and Miller in 2009 and by Siri-Tarino and colleagues in 2010). Each of these reviews acknowledges the limitations inherent to dietary assessment methods which make accurate measurement of the exposure variable difficult. These include reporting biases, particularly those in response to snack foods which can contain high amounts of fats. Chowdhury & colleagues try to account for these limitations by including prospective cohort studies which have examined associations between CHD and fatty acid intake biomarkers – a theoretically more objective measure of intake. Previous reviews have already suggested a protective effect of omega-3 long-chain polyunsaturated fatty acids (measured as intake biomarkers) on CHD outcomes and this new review confirms these earlier findings (statistically significant results for 4 different such fatty acids circulating in the blood). However it also examines associations with saturated and monounsaturated fatty acid blood biomarkers, as well as omega-6 polyunsaturated fatty acids. In accordance with their findings based on dietary intake reports they show no association between saturated or monounsaturated fatty acids with the exception of a protective effect from C17:0 margaric acid (consistent with some other evidence around its presence in dairy fat intake). However the even-chain saturated fatty acid biomarkers reflect both saturated fat intakes and endogenous synthesis from carbohydrates and alcohol so are not ideal intake biomarkers. Thus the lack of association could be confounded by other nutrient intakes, particularly carbohydrate, which have not been adjusted for.

Possibly the best of recent systematic reviews examining this fat/disease issue is one by Jakobsen et al in 2009. This review reported a pooled analysis of individual level data from 11 prospective cohort studies examining associations between energy intake from monounsaturated fatty acids, polyunsaturated fatty acids and carbohydrates, and risk of CHD. Only studies where dietary intake was measured using validated questionnaires, which examined replacement of macronutrients, and which reported similar endpoints were reported. Jakobsen et al found that substitution of 5% of energy from saturated fat with 5% of energy from polyunsaturated fat was associated with a significant reduction in CHD events and CHD deaths whereas substitution with monounsaturated fat was associated with a borderline increased risk in CHD events. Substitution with carbohydrate on the other hand, was associated with significant increase in risk of CHD events in women.

The above review was followed by another key one by Mozaffarian et al 2010 which was a meta-analysis of eight randomised controlled trials. It provided further evidence that replacing saturated fat with polyunsaturated fat reduced CHD events. The new review by Chowdhury & colleagues does not address the question of what nutrients replace saturated fat (and they fail to mention the previous review findings by Jakobsen et al and Mozaffarian et al). If saturated fat is replaced with refined carbohydrate then we would not expect to see a reduction in CHD event risk. Even the use of dietary biomarkers in this new study does not answer this important question of substitution.

Despite the mixed body of evidence from dietary studies described above, advice to reduce saturated fat intakes over the past several decades has been accompanied by substantial reductions in mortality from CHD which have occurred in parallel with reductions in saturated fat intake and serum cholesterol concentrations in much of the Western world. These ecological observations are also supported by findings of cohort studies and clinical trials examining the association between raised blood cholesterol levels and CHD. A meta-analysis of prospective cohort studies involving over 900,000 adults shows a linear association between blood cholesterol concentrations and CHD mortality. Numerous high quality experimental trials have provide unequivocal evidence that dietary saturated fat raises serum cholesterol concentrations in comparison to poly and monounsaturated fat, although not in comparison with refined carbohydrate, and clinical trials show that cholesterol lowering with drugs reduces CHD risk.

We agree that more high quality research is needed to properly understand the role of dietary fats in CHD (and stroke). Such research also needs to clarify if foods high in particular fatty acids also have other beneficial or problematic aspects (e.g., the problem of mercury accumulation in some fish species and also the sustainability of modern fisheries).

But given the overall evidence at the present time, we still think the best advice in national guidelines is to reduce the intake of saturated fats and to replace this with healthier fats, ideally with more omega-3 polyunsaturated fats (e.g., from fish, flax seed and nuts etc). Governments should also state more clearly that replacing saturated fat with refined carbohydrates is very likely to be hazardous to health.

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18 thoughts on “A new review on dietary fats: Putting its findings in context

  1. Essential fatty acids are essential. Perhaps the reduction in SFA was not required for the effect of increased PUFA. On the face of this evidence it would seem wiser to replace carbohydrates with PUFAs.
    Haven’t smoking rates been decreasing, and isn’t this one of the alternative explanations for a drop in CHD?

    • Hi George,
      Our reading of the evidence is that reducing SFA (saturated fatty acids) if replaced with PUFAs (Poly unsaturated fatty acids) is beneficial for CVD health, but perhaps not is SFAs are replaced with carbohydrates. Which is pretty close to your take on it.
      The fall in smoking rates, improved treatments, etc, and reduction in SFAs have all made important contributions to falls in CVD incidence and death rates – in our view.
      Best, Tony

      • Thanks Tony.
        I guess the case is that optimising PUFA without reducing SFA is not something that has been tested. The research has until now been predicated on the theory that SFA was bad and needed replacing, so always involves SFA substitutions, which may turn out to be red herrings.
        The parsimonious explanation may be, that PUFAs include essential fatty acids, and that some people in any population with low PUFA intakes are deficient in one or both of these at any time. PUFAs also have anticoagulant effects. There may be no reason why dietary SFA or MUFA would inhibit these effects.

        My concern is that targeting SFA in this way reduces the consumption of whole foods. People become afraid to eat, or feel guilty about eating, whole milk, cheese, whole meats, and are more likely to eat low-fat processed meats, or sweetened low-fat yoghurt, or processed foods promising less fat, less cholesterol and so on.
        In my opinion a 13% reduction in the incidence of one disease (not all-cause mortality or the various other types of morbidity in our population) is not enough to justify guidelines that are open to abuse or ripe for misunderstanding. The 2.7 OR between high sugar consumption and CHD recently reported, if it can be confirmed, may well be of a sufficient order of magnitude.
        I appreciate the comments in the post about dairy fat and food sources of omega-3 fatty acids, because the effect of particular foods and types of foods is often lost in discussion of macronutrients.
        Almonds and non-dairy spreads are both sources of linoleic acid, but I know which I would rather feed to my children.

  2. It should be obvious by now that findings based on dietary intake reports and Random Clinical Trials are not sufficient to resolve the saturated fat controversy. But perhaps biochemistry is. The biochemistry of inflammation clearly indicates that excessive insulin levels and high omega-6 intake promote inflammation. Excerpt from Page 191 of “The Modern Nutritional Diseases: and How to Prevent Them” by Fred and Alice Ottoboni:

    “BIOCHEMICAL LESSON: The significant point is that good health depends on regulating the D5D enzyme. High insulin levels due to dietary sugar and starch and high dietary omega-6 to omega-3 ratios, stimulate the D5D enzyme, and move the biochemical set point from normal toward inflammation. On the other hand, control of dietary sugar and starch, reduction of LA [linoleic acid, an omega 6 FA that is common in US diet in oils such as safflower, grapeseed, soybean, etc, and putatively ‘bad’ – PHE ed] in the diet, and a daily supplement of fish oil to provide EPA will inhibit the D5D enzyme so that the appropriate amounts of both proinflammatory and anti-inflammatory eicosanoids are produced. Keep in mind that all of the eicosanoids, both the so-called good and bad, are important. The body is designed to use eicosanoids with opposing effects to control vital functions. In a state of optimum health, the good and the bad eicosanoids balance one another.”

    Scientists are beginning to pay attention to what biochemists like Fred Kummerow have been saying for decades. Excerpt from a recent New York Times article:

    In the past two years, he (Kummerow) has published four papers in peer-reviewed scientific journals, two of them devoted to another major culprit he has singled out as responsible for atherosclerosis, or the hardening of the arteries: an excess of polyunsaturated vegetable oils like soybean, corn and sunflower — exactly the types of fats Americans have been urged to consume for the past several decades. http://www.nytimes.com/2013/12/17/health/a-lifelong-fight-against-trans-fat.html?_r=0

    Back in 2010 Lipid experts from different countries gathered in Munich, Germany to discuss governments’ recommendations to replace saturated fats with polyunsaturated seed oils. From Abstract and concluding remarks:
    “Background/Aims: The importance of reducing saturated fatty acid intake to prevent cardiovascular disease and rec- ommended intakes for omega-6 polyunsaturated fatty acids (PUFAs) are controversial. Therefore, experts debated these topics at the biennial meeting of the International Society for the Study of Fatty Acids and Lipids (ISSFAL), in May 2010…The debate concluded with agreement by all that we need a randomized controlled trial to compare the effect of low and high intakes of LA. The trial should have typical US intakes of omega-3 PUFAs, with 7.5% energy from LA (the current US intake) in one group and 2.0% LA (historical intake) in the other. It would study cardiac endpoints and continue for about 5 years.” ISSFAlL 2010 Dinner Debate, http://www.karger.com/Article/Pdf/324749.

    Hopefully, such a trial is underway. Meanwhile there’s this:

    “Traditional Mediterranean, rural Japanese, and other populations with very low CHD risk have uniformly low LA intakes. Two US prospective cohort studies have reported inverse associations between LA intake and CHD risk. However, because LA intake was uniformly high, severalfold higher than evolutionary intakes and those of modern groups with very low CHD rates, these studies provide little insight into optimal LA intakes. Moreover, both studies relied on food frequency questionnaires, which have well-known limitations and may not be able to disentangle the effects of LA and n-3 ALA [alpha linoleic acid, an omega 3 FA commonly found in seeds, nuts, and many common vegetable oils, and putatively ‘good’ – PHE ed]. Controlled trials in which high-LA oils replaced TFA- and SFA-rich fats have shown conflicting results, despite the fact that LA was accompanied by large amounts of medium- and long-chain n-3 PUFAs. A single small trial testing the specific effects of LA without n-3 PUFAs found increased CHD risk. The only long-term trial that reduced n-6 LA intake to resemble a traditional Mediterranean diet (but still higher than preindustrial LA intake) reduced CHD events and mortality by 70%. Although this does not prove that LA intake has adverse consequences, it clearly indicates that high LA intake is not necessary for profound CHD risk reduction.” http://www.ncbi.nlm.nih.gov/pubmed/19627662

    Note, the reduction in n-6 intake in the Lyon Trial referred to here was inadvertent but the results were dramatic. https://circ.ahajournals.org/content/103/13/1823.full

  3. With regards to biological hypotheses, the strongest evidence is that serum total cholesterol concentration, a causal risk factor for CHD, is lowered when n-6 PUFA or MUFA replace dietary saturated fat. The inflammatory hypothesis has supportive mechanistic evidence, but gaps remain, particularly in the identification of a causal risk factor.

    Dispassionately examined, it is difficult to ignore the large and consistent body of evidence from RCTs that dietary fat affects serum cholesterol and serum cholesterol affects CHD risk. This evidence underpins most dietary guidelines about saturated, monounsaturated and n-6 polyunsaturated fat, but critics, justifiably ask, where is the evidence of a direct link of fat intake with CHD outcomes? Herein lies the uncertainty and confusion. A number of researchers have independently undertaken to review the epidemiological evidence, but rather than finding clarity, divergent results and interpretations have emerged, from largely the same set of studies. In our opinion the highest quality review of the observational evidence is by Jakobsen et al. In an individual participant data meta-analysis, which overcomes many of the limitations of meta-analyses of aggregated results, they found that a 5% lower energy intake from SFA combined with a higher intake of polyunsaturated fat was associated with a 26% reduction coronary death based on 2155 deaths amongst 344,696 person followed-up for 4-10 years.

    The randomised controlled trials examining reduced saturated fat intake were, with a couple of exceptions, conducted 30-50 years ago, and a few of them involved multiple interventions, and had variable degrees of compliance.

    The Lyon Diet and Heart Study also involved a change in dietary pattern, so the dramatic effects on CHD can not be attributed solely to dietary fat.

    • But. Murray, “a 5% lower energy intake from SFA combined with a higher intake of polyunsaturated fat” is a multiple intervention.
      There are two things going on.
      Of course some people need more PUFA – there are always people deficient in any given nutrient in any population.
      And if the diet is high in refined starch (as in MOH guidelines to “fill up on bread rice and pasta”), and/or sugar, which elevate LDL cholesterol, this may increase the dose of PUFA needed to normalise cholesterol.
      None of which proves that lowering SFA was necessary or desirable. Lowering carbohydrate looks better.
      Choosing Jakobsen et al. over RCTs and other meta-analyses does look a bit like cherry-picking the study that best suits the existing position, rather than taking the trouble to see if it can be improved on.

    • “With regards to biological hypotheses, the strongest evidence is that serum total cholesterol concentration, a causal risk factor for CHD, is lowered when n-6 PUFA or MUFA replace dietary saturated fat.”
      Except that Jakobsen says that MUFA in place of SFA increases CHD risk.
      So you’re only left with two planks of the classic lipid hypothesis – trans fats raise LDL and CHD risk, and so does sugar. Nothing much else does (although refined starches haven’t really been investigated properly, and I’m sure there are also a few toxins that will also raise LDL and CHD risk).

  4. “With regards to biological hypotheses, the strongest evidence is that serum total cholesterol concentration, a causal risk factor for CHD, is lowered when n-6 PUFA or MUFA replace dietary saturated fat.”

    The original cholesterol hypothesis was based on the assumption that a fatty acid that lowers total cholesterol is good and a fatty acid that raises total cholesterol is bad. Only three chain lengths of saturated fatty acid raise total cholesterol to varying degrees – lauric, myristic, and palmitic. http://ajcn.nutrition.org/content/80/3/550.long

    Interestingly, omega-3 fatty acids also raise LDL cholesterol but are considered good because they lower triglycerides. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2683599/?tool=pmcentrez http://ajcn.nutrition.org/content/79/4/558.full

    Replacing carbohydrate with monounsaturated and or saturated fats lowers triglycerides also. Excerpt:

    “Evaluation of the overall health effects of saturated fat requires consideration of markers in addition to LDL-cholesterol. Isocaloric replacement of carbohydrate with any type of fat results in decreased triglycerides and increased HDL-cholesterol, the effect on HDL-cholesterol being greater for saturated fat compared to unsaturated fat. Reductions in saturated fat also adversely affect HDL subpopulations by decreasing larger HDL2-cholesterol concentrations, whereas increases in saturated fat increase this antiatherogenic fraction. Furthermore, very low-carbohydrate diets rich in saturated fat increase LDL size and conversion from a high-risk pattern B to a lower risk pattern A phenotype. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1208952/

    Finally, when total cholesterol is plotted against all cause mortality we see a j-shaped curve with the lowest death rate in the 200 to 240 mg/dL range. http://www.tvandijk.nl/wp-content/uploads/2012/10/cholesterol-mortality-chart.pdf

    • Hi David,

      A note of caution on HDL. An important and massive analysis of many studies published in the Lancet in 2012 found no association of HDL with myocardial infarction (or heart attacks). This study used a genetic technique call Mendelian Randomisation, which strips away (in theory, and I believe in practice in this paper) all the confounding that plagues observational studies. Thus, it appears that it is LDL – not HDL – that has a causal association with coronary heart disease.
      Reference: Voight BF, Peloso GM, Orho-Melander M, et al. Plasma HDL cholesterol and risk of myocardial infarction: a mendelian randomisation study. The Lancet 2012;380(9841):572-80 doi: 10.1016/s0140-6736(12)60312-2[published Online First: Epub Date]|.

      Best, Tony

  5. “The inflammatory hypothesis has supportive mechanistic evidence, but gaps remain, particularly in the identification of a causal risk factor.”

    I’m wondering. What is the nature of these gaps? As noted in my original post, the inflammatory hypothesis has been elucidated by biochemists. Excerpt from page 190 of “The Modern Nutritional Diseases”:

    The position of the D5D enzyme in the flow of the omega-6 cascade is of vital importance because it acts as a valve that directs DGLA either toward anti-inflammatory eicosanoids or proinflammatory eicosanoids. When this valve is open (the enzyme is stimulated), DGLA is transformed to AA, the precursor of a large number of proinflammatory eicosanoids. At the same time, DGLA is diverted away from the production of anti-inflammatory eicosanoids PGE-1 and HETrE. When the valve is closed very little DGLA is converted to proinflammatory AA but rather is directed toward the production of the good anti-inflammatory eicosanoids, PGE-1 and HETrE.

    The D5D enzyme is opened (stimulated) by two dietary factors. One stimulating factor is high blood insulin levels caused by dietary sugar and starch (high glycemic carbohydrates). The other stimulating factor is high omega-6 to omega-3 ratios in the circulating blood, also caused by diet. Such stimulation of D5D over a period of years by sugar, starch, and/or high omega-6 to omega-3 ratios is a major underlying cause of chronic inflammation and the diseases discussed in this book. The D5D enzyme is closed (inhibited) by a healthful diet, namely one low in high glycemic carbohydrates, low in LA, and adequate in EPA.”

    For what it’s worth, my own experience with excessive omega-6 intake is in agreement with the above explanation. I used to eat a peanut butter sandwich for lunch almost daily during the work week. When National Institutes of Health scientist Bill Lands mentioned that there are 4,000 milligrams of omega-6 in each 28 gram, one ounce serving of peanuts, I realized my mistake and stopped eating peanut butter. Within two months my leg pains subsided. A year or so later I noticed that my gingivitis had cleared up. And now, 4 years later, my blood pressure is normal (113/58) and my total cholesterol has dropped from 256 to 221mg/dL. Best of all, I have regained much of the strength and stamina I lost as I approached retirement age. https://www.youtube.com/watch?v=ZJ9i-9JcTF4

    Regarding my gingivitis, in a recent article entitled “New Wrinkles in the Dietary Fat Story” Bryant Stamford wrote, “Since inflammation is bad news, what kinds of things favor and promote inflammation? In past columns I pointed a finger at gingivitis, a low-grade gum infection common in the U.S. that provides a launching pad for inflammation throughout the body. Thus, a strong argument can be made for flossing and good dental hygiene as important for overall health. Dietary factors have now pushed their way into the inflammation spotlight, and spearheading the move is dietary fat. However, the dietary fat in the inflammation spotlight is not saturated fat or trans fat. There’s another bad guy involved, in other words. Now, here’s where it gets really interesting. Unsaturated fat, the kind we have been promoting for decades as a healthy alternative to saturated fat, appears to be feeding inflammation. Oops!” http://www.courier-journal.com/article/20140306/FEATURES03/303060083/Body-shop-New-wrinkles-dietary-fat-story

  6. Apparently the smaller, more artery-clogging particles are increased not by saturated fat, but by sugary foods and an excess of carbohydrates, Dr. Chowdhury said. “It’s the high carbohydrate or sugary diet that should be the focus of dietary guidelines,” he said. “If anything is driving your low-density lipoproteins in a more adverse way, it’s carbohydrates.”

  7. Biochemical chemical research provides insights into how specific metabolic pathways work and generates new hypotheses on the relationship between food and health which can then be explored further in animal and human studies. However since humans, behaviour and their diets are so variable, such hypotheses are difficult to prove in real life settings.

    A recent dietary intervention study in obese adults comparing diets high in n-6 PUFA (planto oils) or saturated fat (butter) found that high n−6 PUFA intake did not cause any signs of inflammation or oxidative stress http://ajcn.nutrition.org/content/95/5/1003.short

    As for personal experiences with food/health relationships, although very important and meaningful to an individual, do not generate the evidence required to justify changes to public health recommendations. I am reminded of a young nutrition student who claimed that she had gained 40kg in 2 years while carefully eating a diet consisting mainly of steamed vegies and lean meat. After giving this up she went back to a less healthy diet involving regular fast food meals and beer and claimed she had started to lose weight. Despite her apparent success I would certainly not advocate this diet!

  8. I have read estimates that high blood pressure and diabetes are much larger risk factors for CVD than are the various lipid markers.
    These are things that can be influenced by diet, more clearly than the “lipid hypothesis” mechanisms. Furthermore, they are more susceptible to a “common sense” nutrition approach of wholesomely prepared, unrefined, minimally processed animal and vegetable foods, without as much need to calculate and restrict the macronutrients in these foods.
    The benefits of fresh vegetables and fruits cannot easily be explained in terms of macronutrient analysis. The complex interplay between the effects of fibre, micronutrients, electrolytes, polyphenols, and other phytochemicals makes any scientific analysis of “5+ a day” a baffling proposition.
    Similarly, it is hard to evaluate any intervention that increases PUFA without knowing what foods are supplying the PUFA, and what the breakdown of subtypes is.
    The same with knowing what foods are restricted when SFA is restricted. It may be a good thing overall to replace vegetable shortening with say sunflower seed oil, but a bad thing to replace butter with margarine (whatever that is), simply because the less processed foods in that example are the better sources of vitamins and antioxidants.

  9. Last month my doctor wanted to conduct a lipid panel test on me and when I suggested to him that his standard HDL/LDL/Trig tests don’t prove anything in isolation and that it is more appropriate to look at particle size and concentration if we want to investigate possible risk factors, he sheepishly asked me if I knew something about the apolipoproteins. When I replied in the affirmative, he tore up the instructions for the test he was going to have me take and wrote a new one to test for apolipoprotein. When I got to the lab the person taking my blood had never heard of the test and had to look it up. This was all good to me since I had been under the impression we didn’t do this sort of test in NZ.

    My question is about the elephant in the room. People here seem to be talking about the elevations in blood pressure and serum cholesterol as if those are the cause of ill health. Why don’t we consider these as the symptoms of ill health and recognise them as the body’s mechanism to heal itself? Rather than try to reduce these by such ill-founded dietary interventions as reducing SFAs and increasing CHO, wouldn’t we be better served by investigating what is causing the symptoms and treating that instead?

    Case in point: My brother-in-law had a severe CVD event (ambulance was called and he was found near to death) a couple of years ago which required him to have stents put in. He was sent home with a fear of saturated fats and a prescription for statins. He has always had a “high cholesterol” profile in spite of being a much more outdoorsy person than I. (I’m now sixty and a year or two older than him). He has always made an effort to limit animal fats in his diet – as opposed to me always making a pig of myself with red meat and fat.

    The point of difference between us is in how we handle stress. He has always complained about the stresses in his jobs, with back-biting co-workers and unappreciative employers making unrealistic demands. His life has been one long worry about his employment. I, on the other hand, have been choosing occupations which I enjoy and discarding them when I no longer do so.

    While we may rightly attribute obesity, diabetes, dementia and other adverse health trends to a rise in refined CHO and a decrease in protective SFA in our diets over the last 200 (and more markedly), 40 years, we should be looking at going back to a diet that has helped us evolve to where we are now and then looking at the role stress plays in our life and how we can change that. Government and ‘expert’ intervention in our diet has only worsened the situation.

    • Hi Gregg. Lots of interesting comments. Just a couple of replies from me.
      1. One of the most succesful treatments ever put into practice in medicine is lipid lowering drugs. Thus, if only for this reason blood test of cholesterol (LDL and HDL) seem warranted.
      2. To be clear, our assessment of the saturated fat evidence here at Public Health Expert is that reducing saturated fat is beneficial for heart disease prevention – SO LONG as the saturated fat is replaced with polyunsaturated (‘good’) fats not carbohydrate.
      3. Modern diets are not perfect – far from it (witness the obesity epidemic). But the reduction in aturated fat since the 1960s has alomost certainly contriubted to falls in heart disease and stroke rates.
      3. Heart disease, and many other disease, are largely a lottery. We can change the odds of you winning the lottery by chagning risk factors – but there is still a large element of chance (and genetics), which probably explains the difference between you and your brother.

      Best, Tony

      • Thanks for the reply Tony. There is clearly some disagreement in the ranks of scientists over some of these matters.
        1. Doctor Malcolm Kendrick writes convincingly about the role of lipid lowering drugs and would maintain the the “success” you allude to has mainly been to the benefit of the bank accounts of the drug companies. Would we similarly treat infection by finding drugs to limit the body’s ability to create white blood cells.
        2. I haven’t seen evidence of ANY benefit from reducing saturated fat in the diet. In fact, from the research I’ve done, it would seem the opposite is true. We have reduced saturated fat in the diet at a population level yet our key health indicators are all adverse. Is this one correlation that might be causation? What if dietary saturated fat is in fact protective against things like lung cancer, dementia, diabetes? Haven’t we then been going down the wrong track in experimenting with population level dietary advice?
        3. I would take the opposite view and suggest that the reduction in saturated fat has contributed to the increase in all cause mortality, particularly when you factor in the negative health associated with inflammation attributable to imbalances in omega 6 and omega 3 as well as the oxidation in the grain oils we’ve replaced SFAs, not to mention the effect of increased sugar consumption (because taking SFA away makes food taste awful).
        4. It was my brother-in-law I referenced – no genetic relation. Are you suggesting that mental stress is not a great factor in CVD? My reading would be that most doctors regard it as perhaps the main contributor.

      • With your first point, do you refer to statins? Because they have antiinflammatory effects. The benefit of the drug might very well be due to the antiinflammatory effect and not the lipoprotein lowering effect.

  10. I have a question about the Jakobsen meta-analysis; it states, in you words,
    “Jakobsen et al found that substitution of 5% of energy from saturated fat with 5% of energy from polyunsaturated fat was associated with a significant reduction in CHD events and CHD deaths ”
    My question: what was the range of PUFA intake to which the reported reduction in CHD events and deaths relates?
    This is not obvious from the paper and no commentary has mentioned it.
    Is it, for example, the difference between 1%E PUFA and 6%E? Or between 6%E and 11%E?
    These cannot (surely) have the same value.

    In this matter it is relevant to consider what Ancel Keys and his co-workers wrote in the Seven Countries analysis:
    ‘The coronary incidence rate of the cohorts was not significantly correlated with the percentage of calories in the diet provided by proteins or by polyunsaturated fatty acids. In regard to the latter, the averages for the cohorts ranged from 3 percent to seven percent of calories from linoleic acid, with only trivial contributions from other polyenes. These findings conform to the general picture that in no natural diet of man so far studied do polyunsaturated fatty acids contribute more than a very small fraction of the total calories. Accordingly, it must be expected that in such natural diets variations in the amount of polyunsaturated fatty acids will have at most only a trivial effect on the concentration of cholesterol in the blood serum or risk associated with it.’
    from page 253 of Chapter 14 of Keys, A., Aravanis, C., Blackburn, H., et al. 1980. Seven Countries A Multivariate Analysis of Death and Coronary Heart Disease. Harvard University Press, Cambridge, Massachusetts.

    If we factor in those other polyenes, the range of PUFA seen in “natural” diets in the Mediterranean might have reached 5%E, but the effect on serum cholesterol of these amounts was “trivial”.

    Any discussion of Jakobsen et al. has to be informed by the similar 2014 analysis by Farvid et al. in which PUFA (linoleic acid) has the same correlations whether it replaces SFA or carbohydrate. Thus the association between PUFA and CHD is shown to be independent of SFA (or equally dependent on any other calorie source except protein, which has not yet been compared).
    A finding which can be confirmed by a thoughtful reading of Jakobsen et al.

    Dietary Linoleic Acid and Risk of Coronary Heart Disease: A Systematic Review and Meta-Analysis of Prospective Cohort Studies
    Farvid MS, PhD; Ding M, MS; Pan A et al. DOI: 10.1161/CIRCULATIONAHA.114.010236

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