Yet another major review finds no reason at all to limit saturated fat in the diet

Conventional nutritional advice varies a bit depending on who you ask, but there are a few constants. One is the importance of limiting saturated fat in favour of polyunsaturated fat. Most Governments, doctors and dieticians would therefore have us eschew foods such as red meat, dairy products and butter in favour of vegetable oils, oily fish and margarine.

This week saw the publication of the largest and most comprehensive review to assess the relationship between specific dietary fats and heart health, as well as the evidence for the supposed benefits of supplementing the diet with polyunsaturated fats [1]. The study was carried out by researchers from the University of Cambridge and MedicalResearchCouncil,University of Oxford, Imperial College London, University of Bristol, Erasmus University Medical Centre and Harvard School of Public Health, and was partly funded by the British Heart Foundation.

The study brought together two types of evidence:

1.    Epidemiological evidence

Evidence where associations between different fats in the diet and risk of heart disease were assessed.

This sort of evidence itself came in two types:

a.    studies where associations between dietary intake of specific fats and heart disease were assessed

b.    studies where associations between body levels of specific fats (e.g. as measured in the blood) and heart disease were assessed

2.    Randomised controlled trials

Where individuals were treated with specific dietary fats to see what effect this had on heart disease risk over time.

45 epidemiological and 27 randomised controlled trials were pooled in this review. The total number of subjects involved in these studies was more than 650,000.

Here’s a summary of the results:

Epidemiological studies of dietary fat and heart disease risk:

Saturated fats – No association

Monounsaturated fats – No association

Omega-3 fats – No association

Omega-6 fats – No association

Trans fatty acids  – Increased risk

Epidemiological studies of body levels of specific fats and heart disease risk:

Saturated fat – No association other than one specific type of saturated fat (margaric acid) that was associated with reduced risk

Monounsaturated fat – No association

Omega-3 fats – Reduced risk

Omega-6 fats – No association other than arachidonic acid (found in meat, eggs and dairy products) which was associated with reduced risk

Trans fatty acids  – No association

Randomised controlled trials of supplementation with:

Alpha-linolenic acid (a type of omega-3 fat found in plants including flaxseed/linseed) – No reduction in risk

Omgea-3 fats such as those found in oily fish – No reduction in risk

Omega-6 fats such as those found in vegetable oils – No reduction in risk

The authors of the review conclude:

…the pattern of findings from this analysis did not yield clearly supportive evidence for current cardiovascular guidelines that encourage high consumption of polyunsaturated fatty acids and low consumption of saturated fats. Nutritional guidelines on fatty acids and cardiovascular guidelines may require reappraisal to reflect the current evidence.

Should we be surprised?

Last year, a review published in the British Medical Journal pooled together studies in which saturated fat in the diet was replaced with polyunsaturated fats [2]. Overall, the review found no evidence of benefits when saturated fat was replaced with omega-6 fats. However, there was evidence of benefit when saturated fat was replaced with a mix of omega-6 and omega-3 fats, suggesting that omega-3 fat may be beneficial (but not omega-6).

Another major review, however, have found no good evidence that omega-3 supplementation reduced the risk of heart disease [3]. Yet another recent review found no reduced risk of heart attack when saturated fat was replaced with supposedly healthier fats in the diet [4].

Also, previously, overall the epidemiological evidence has failed to support the idea that saturated fat is linked with heart disease [5,6].

There is some variation in what the scientific literature appears to show in terms of the impact different dietary fats have on heart health. However, if I were to summarise what the evidence points to as a whole, I would say:

1.  There appears to be no good evidence to fear fats found naturally in the food supply (including saturated fat)

2.  Processed fats (e.g. industrially produced trans fats) should be avoided.

In other words, eat real, unprocessed food, and perhaps forget about the amount and types of fat in that food.


1.    Chowdhury R, et al. Association of Dietary, Circulating, and Supplement Fatty Acids
With Coronary Risk: A Systematic Review and Meta-analysis Ann Intern Med. 2014;160(6):398-406-406. doi:10.7326/M13-1788

2.    Ramsden CE, et al. Use of dietary linoleic acid for secondary prevention of coronary heart disease and death: evaluation of recovered data from the Sydney Diet Heart Study and updated meta-analysis BMJ 2013;346:e8707

3.    Skeaff CM, et al. Dietary fat and coronary heart disease: summary of evidence from prospective and randomised controlled trials. Annals of Nutrition and Metabolism 2009;55:173-201

4.    Hooper L, et al. (2012). Reduced or modified dietary fat for preventing cardiovascular disease. The Cochrane Library. Published online 16 May 2012 DOI: 10.1002/14651858.CD002137.pub3

5.    Mente A, et al. A Systematic Review of the Evidence Supporting a Causal Link Between Dietary Factors and Coronary Heart Disease. Arch Intern Med. 2009;169(7):659-669

6.    Siri-Tarino PW, et al. Meta-analysis of prospective cohort studies evaluating the association of saturated fat with cardiovascular disease Am J Clin Nutr 2010;91(3):535-46

36 Responses to Yet another major review finds no reason at all to limit saturated fat in the diet

  1. Chris 21 March 2014 at 10:02 am #

    The theoretical link between saturated fat and cholesterol levels in the blood was pure supposition on the part of Dr Ancel Keys, and the supposed epidemiological evidence he then supplied to back up his theory represented by his six countries was revealed as a misuse of data (cherry-picking six data points from a possible 22) was exposed by Yerushalmy and Hilleboe in 1957.
    Keys interpreted the write-up of the work of Anitschkov and Chalatov (1913) to reliably infer that cholesterol was an atherogen that resulted cholesterol-fed rabbits developing atheromas (the beginnings of cardiovascular disease).
    Seifter studied cholesterol, dyslipidemia, and atherogenicity in rabbits using both dietary methods and endocrinological manipulation. His work threw up anomalies that cast a question over the ‘raised cholesterol causes cardiovascular disease theory’. Seifter hosted an open workshop discussion in 1956 and additional parties took up with interest. Two delegates, Feiser and Schwenk raised the matter of the ease with which distilled cholesterol can spontaneously form oxidised sterols when handled, presumably via exposure to air. So they cast a question over the matter of confounding errors in all previous work. Oxidised sterols might account for the findings of Anitschkov and Chalatov, and might also account for Seifters anomaly, if the cholesterol they used in dieatry inteventions on rabbits and chickens was contaminated by oxidised sterols, and not the cholesterol itself.
    Eventually Hideshige imai et al clarified the matter in 1976. Oxidised cholesterol, not pure cholesterol accounted for the atherogenicity apparent in all experiments involving animals. When viewed from that perspective all trials have been consistent.
    If epidemiological ‘evidence’ ever supported a link with a lame-duck hypothesis established upon a confounding error, pure invention and outright fruad then one should suppose it could only be down to chance, bias, an agenda to deceive, or another confounding error.

  2. LeonRover 21 March 2014 at 11:22 am #

    Ever since the work on trans- vs cis- hydrogenation,I have been expecting such a report.

    I note the irony of naming:

    margaric acid occurs in goats’ milk while margarine is composed of cell wall threatening trans-fats.


  3. stan 21 March 2014 at 11:59 am #

    Well done, John, nice to have your conclusion that puts my mind at rest. It did seem a bit ‘wishy-washy’ on the TV extracts.

  4. Sean Raymond 21 March 2014 at 1:12 pm #

    Thankyou Dr Briffa for bringing this to my attention – I have no idea how I missed this?

    As a recently qualified Dietitian I am worried about what these findings suggest for my training was un-equivocally geared towards the sat fat-heart hypothesis. It is clear now that the link between saturated fat and heart disease has not been conclusively shown – I have no idea how to reconcile this fact with the health messages, I am almost strait jacketed into giving by the guidelines I must adhere too, which say sat fat will cause a coronary event. I am to give a diet-heart presentation to cardiac patients soon and my confidence in my material is being shot to bits by what I am starting to read. At UNI I had no time to question anything (although this is apparently the best time to do so) – I was focussed on learning and that was it. Now what if much of that learning is wrong?

    I believe the evidence for saturated fat raising cholesterol is pretty tight – this has been shown by metabolic studies which have shown at least a transient raising of LDL from saturated fat (transient due to the fact these experiments cannot be carried out for a long time). However these studies cannot be conducted for long enough to examine the long term impact this would have on health and so we cannot use such studies to show elevated cholesterol increases CVD risk. The studies we can use produces data that is very limited and open to many confounding variables to show saturated fat and or cholesterol will raise the risk of cardiovascular disease. HOWEVER I believe the same is true to prove the theory that cholesterol DOESN’T cause heart disease also – so either way it is clear greater reserach is needed to prove if raised cholesterol is harmful or not.

    I think one of the best pieces of literature I have read regarding a link between sat fat and CVD was actually a rebuttal of a meta analysis published in the American Journal of Clinical Nutrition by Siri Tarino et al which suggested saturated fat was not associated with CVD. This rebuttal, by Jeremiah Stamler called ‘Diet-Heart: a problematic revist’ actually did seem to find a strong relationship between saturated fat and CVD (if I remember correctly). However, when I look at my university work on this area to furtehr support it – the best evidence I have comes from the ‘7 countries study’ by Ancel Keys, Smith et al 1972, Kris-Etherton et al, 1999. Hopper et al 2001, and MRFITS (which showed cholesterol to be a biomarker for CVD).However, these really do not show cause at all but more an association and so I am astonished that us Health Profesionals are being taught something that actually has not been conclusively proved. The idea is simple – saturated fat appears to raise cholesterol and cholesterol is what blocks arteries – bingo! My oh my.

    My assumption is that there is a link between cholesterol and heart disease but maybe it is not in the way we think – cholesterol has a crucial role in furring up arteries but is it the amount of cholesterol in the blood that is important? Or is it more about the particle size of the LDL ? Or is it more about the number of LDL particles in the blood rather than the amount of cholesterol that is being carried? Or both? Then we must ask what is causing the cholesterol to get into the intima of the artery in the first place…..

    Anyway – I am incoherently rambling with no purpose – I suppose I just need to express my shock at these findings and hope this starts a real mainstream debate which will, if anything, allow me to be able to advise that saturated fat may has not been shown to cause heart disease to patients and not worry about getting sacked (that is hypothetical as I am actually looking to start my career in Dietetics but thus far haven’t).

    Erm – Cheers Dr Briffa once again!

    • Snazgul 21 March 2014 at 4:02 pm #

      Fascinating to read the dieticians dilemma. As a GP I have had the same problem though am far less straight-jacketed in what I can say. I do confess to patients that I am a ‘heretic’ and disbelieve the official line. Actually then are far more often receptive and understanding than not, especially when I tell them what my diet actually is i.e. what I do believe in.

      One grouse, a big and regular one…. how come research that is in major part indirectly funded by the public through taxes and charitable giving is published behind a pay-wall that I cannot penetrate? Dr B’s analysis sounds spot on but I have no access to the original paper to check it. Big -Food, Big-Pharma… Big-Medicine too!

      • Jonathan Bagley 21 March 2014 at 5:54 pm #

        It is regrettable that you, as a GP, have no access to this journal. I am surprised the BMA does not subscribe to journals on behalf of its members. I think that Manchester University, where I studied and work, grants library membership to former students, although I dimly recall this doesn’t include access to online journals. Have you tried contacting the medical school at which you studied? They might do you a favour, or at least come to some financial arrangement. It does seem odd that I, a mathematician, with no medical knowledge, can read this paper, whereas you, a doctor who might benefit, cannot.

    • Chris 21 March 2014 at 4:21 pm #

      “Then we must ask what is causing the cholesterol to get into the intima of the artery in the first place…..”

      I’m not convinced cholesterol is being pressed into the intima of the artery. Save for neurons most cells can synthesise cholesterol, so the cholesterol that is found in an atheroma may not have to be the result of transportation. Plus, analysis of the gunk that is found in atheromas reveals other constituents in addition to cholesterol.

      What is happening, I think, is that certain cells present in the endothelial layer of the arterial wall cease to behave in precisely the way nature intended while under the influence of ‘something’. That ‘something’ is an atherogen for it induces the beginings of atherogenesis and leads to the formation of atheromatous plaques – those fatty streaks. Cholesterol cannot be an atherogen – it occupies to prestigious and important a place in biology and human physiology.

      Oxidised cholesterols and homocysteine have been reliably identified as atherogens, while the history of cholesterol science indicates that cholesterol was held accountable for effects induced by oxidised cholesterol [See my comment at the top of the thread]. There are three possible forms of oxidised cholesterol cholesterol and one has three atoms of oxygen added. They call this cholestane triol, and cholestane triol seems to be the most potent atherogen presently known to man.

      That cholestane triol induces accompanies cholesterol on its travels is an increased prospect if high levels of oxidative stress are a feature of a persons physiology, and potential oxidation of molecules of cholesterol in LDL or other lipoproteins seems an increased prospect is there are plenty of reactive oxygen species about and few antioxidants available to ‘zap’ them. Homocysteine looks to be the more potent oxidisin gagent capapble of commuting oxidative stress to cholesterol.

      I guess in some ways cholestane triol mimics the properties of cholesterol sufficiently well to access the same places cholesterol can, but once their it confounds some aspect of the cells metabolism, perhaps it ‘meets’ an enzyme that mistakes it for cholesterol itself and then confounds it. Howsoever, the presence of homocyteine or oxycholesterol (cholestane triol) reliably predicts atherogenesis. Smooth muscle cells suffer degeneration of necrosis in their presence, and that I think is the axial nature of atherogenecity from which atheromas develop.

      You might find, Sean, that the later works written about homocysteine, say in the last 15 years, have trended to perceive homocysteine as a conveyor of oxidative stress that bears upon cholesterol to result in some molecules being converted to cholestane triol, and cholestane triol is toxic or injuries to several cell types and in several potential locations. The later work which Kilmer McCully has written or edited may aid your search for the truth. Killan Robinson is another name to seek out.

      I hope that helps, and FYI, that’s where I’m headed next.

    • Simona 21 March 2014 at 4:42 pm #


      It might help if you look at Chris Masterjohn’s articles on cholesterol on his two blogs.

    • Gabriella in Santa Barbara, CA 21 March 2014 at 6:20 pm #

      Hello’, Sean Raymond –
      There is an organization here in the US that has debunked all of that nonsense about saturated fats and has actually showed that, especially in older individuals, cholesterol is actually your friend not your enemy. I am talking about the Weston A Price Foundation. Their web site is full of incredible information but I will give you just a link to the cholesterol article that you should read about cholesterol:

      I am an Italian-American and grew up in Tuscany, Italy. I have stuck throughout my life to the ways we eat there, that is plenty of saturated fats and olive oil plus all the other good stuff Tuscany is famous for. I avoid like the pest sugar, polyunsaturated “vegetable” oils (Industrial oils), most grains and processed foods. I am 77 years old and in fine shape. I am not overweight or diabetic. I keep my cholesterol in spite of doctor’s advice to take statins because I believe that cholestorol is good for you. It is a substance essential to life and keeps one’s brain sharp and muscles in good shape.

      I hope you will educate yourself and give your patients GOOD, SOLID advice. DO NOT blindly recite mainstream crap. Do your research! I am glad you also read Dr. Briffa’s blog. His advise is solid. Thank you, Dr. Briffa!

      Good luck to you, Sean, and best wishes, Gabriella

    • Robert Park 21 March 2014 at 8:04 pm #

      While in harness I was required to lecture to college recruits on a an aspect of the company in which I was national manger and of which I had an intimate knowledge. To my amazement, on assuming this role, I discovered that the company’s manual had described the system wrongly but on drawing this to the attention of the college principal it was dismissed as if it was myself who was mistaken. The result was that I was obliged to teach the recruits what was in the manual rather than what occurred in the field. This, of course, was necessary to enable the recruits to pass their examination but which would confuse and confound them on taking their places in the field which sounds similar to your experience Sean. Your problem is not unique and is a feature of all organisations which raises the question, ‘should I be a fool among others or should I be a fool alone,’ remembering, that ‘baby, it’s cold outside’!

      Later, when in-charge of an operational branch, a common complaint of staff was the lack of personnel who passed the promotion examination. On examining this feature with the local training officer he assured me that he taught what was provided by the college. On reading through the literature it was frequently punctuated by errors showing that whoever provided the information knew little of the organisation’s structure or its legislature. On enquiry of who was the author of the information the TO nearly fell off his chair and said in exclamation, it comes from the staff college, as if somehow that made it right and unquestionable.

      You may subsequently learn that the downside of all teaching and training is the mass of misinformation that is provided suggesting that colleges also teach ignorance. Now you know in advance of having to learn the hard way!

      It might be best to speak in two tongues and maintain your own counsel. Remember, he who wields the sword never wears the crown.

    • George Henderson 21 March 2014 at 8:11 pm #

      Consider that sugar and refined starch do reliably elevate LDL and TGs.
      There’s your “bad cholesterol”.
      Also consider that some of the people eating least PUFA will be deficient in EFAs. This might explain difference better than SFA being bad for us.

      • Auggiedoggy 22 May 2014 at 5:05 pm #

        Personally, I’m more concerned with SFA intake. I achieved my highest cholesterol levels ever while on a LCHF diet back in 2007. My father, back in the early 70’s was told in drink full fat milk for his stomach ulcer. That was the advice back then. He ended up gaining weight and probably set him up nicely for that double-bypass surgery he had at age 60. Fortunately for me I got off that LCHF diet and adopted a plant-based diet. I included lean meats and fish later. I would never try LCHF again.

    • Frances Kelly 21 March 2014 at 9:02 pm #

      Hello Sean,

      with regard to your comment about “cholesterol furring up arteries”, may I guide you towards a brilliant resource on Cholesterol. Chris Masterjohn has a blog entitled The Daily Lipid & he is the go-to guy on all things Cholesterol. It’s fairly in-depth but I’m sure you’ll have no problem with it.

      The concept of cholesterol furring up arteries just as cooking fat blocks drains is deeply flawed and this blog will show you how. Cholesterol may be found in arterial plaques but it is probably there in a restorative capacity. A bit like finding ambulances at a road accident & blaming them for causing it.

      Atheroma develop behind the lining of the arteries. I believe current thinking is pointing towards oxidised LDL, not cholesterol. Apologies to John & his fine work but you can also look at Dr Malcolm Kendrick’s website for information on Cholesterol. Hope that helps,

      • Chris 22 March 2014 at 10:15 am #

        “I believe current thinking is pointing towards oxidised LDL”

        To clarify the point it is impossible for a a particle of low-density lipoprotein to become oxidised. However it is entirely plausible that any lipoproteins could become contaminated by fat soluble reactive oxygen species.

        When cholesterol becomes subject to oxidative stress it can form new oxy-sterols that are identical to cholestrol save for the addition of oxygen atoms. As a term ‘oxycholesterol’ means much the same thing, There are three possible oxycholesterols. One of them has three atoms of added oxygen to a parent molecule of cholesterol. They call this particular oxycholesterol ‘cholestane triol’. Cholesteane triol is an identified atherogen. It is entirely plausible that under certain conditions cholestane triol may be found in lipoproteins, and LDL may the particular faction that conveys cholestane triol to the scene of the crime.

        It has been proven that cholesterol itself is not at all atherogenic, and sound reason says LDL can only be atherogenic if an atherogen is present within.

        • Frances Kelly 22 March 2014 at 3:58 pm #

          Hi Chris,

          I’m interested in your clarification…..

          can you explain how LDL cannot become oxidised? I’m currently reading Denise Minger’s book “Death By Food Pyramid” & she asserts that LDL-c leaves the liver with a supply of antioxidants. For whatever reason, when these antioxidants become depleted, the LDL reacts with unstable molecules, becoming oxidised. She also states that once this occurs, the LDL is seen by the body as a foreign invader, resulting in an auto-immune cascade. She was actually referring to Familial Hypercholesterolaemia which causes the LDL to remain in the bloodstream rather than link up to LDL receptors. This book was written last year, so are there any recent research findings that contradict her information?

    • M. Penney 28 March 2014 at 8:30 pm #

      major study into the saturated fat = heart disease question has been running for more than 50 years in Frammingham, USA, and has found no link at all. Rabbits are vegetarian, so not a good subject for cholesterol resrch

  5. John Walker 21 March 2014 at 3:43 pm #

    These findings need to be brought to the attention of the public, in the same way that the makers of ‘pro-active’ drinks pimp up their products. Repeated advertising, over and over, until general awareness is realised. Until this is done things won’t change much, and Celebrity chefs, like James Martin, and the Hairy Bikers (Random selection) will continue to talk about saturated fats being bad, and a guilty pleasure. A couple of nights ago, we had one spokesman for a two minute slot, in which he summarised the studies, and said, ‘It appears the advice to avoid saturated fat was wrong.’ Since then I have heard nothing more about it, until this mention by Dr. John. Sadly I don’t think things will change. The belief in fat is bad dogma has been pounded home for too long. It’s almost a religion, and committed followers will never change, no matter what is explained to them. Maybe if food manufacturers, advertising the ‘benefits’ of their low-fat spreads or dishes, were prosecuted under the Advertising Standards legislation, we might get somewhere.

    • Cindy C 21 March 2014 at 10:50 pm #

      I just put into a yahoo search Dr Chowndhury saturated fats. A hundred or more news reports did a story on the study, Some from many other countries. Each reporter did a different take on it, many quoting ” experts” who disagreed. Some had very sensational titles(read me!!).The press release is easy to find on line, but wonder where those reporters got the auxiliary info/other experts. I actually read the study myself, and realize some publications have bias against meat and fat.

    • Gregory Barton 23 March 2014 at 2:14 am #

      “Maybe if food manufacturers, advertising the ‘benefits’ of their low-fat spreads or dishes, were prosecuted under the Advertising Standards legislation, we might get somewhere.”

      That needs to happen.

  6. Liz Smith 21 March 2014 at 4:20 pm #

    At college in mid 90’s we did in our Aromatherapy/reflexology course a month of nutrition. I am told that Doctors spend less than a day in their study on nutrition? It was explained to us that saturated fats were ok, but that vegetable oils (other than Olive, Avocado,coconut) would go toxic when heated up. From then we stopped buying the so called healthy fats and went back to full fat milk, Danish butter and cream, and ate the fat off meat and enjoyed the flavour.

    When people asked what we ate I said ‘all the good things but ‘as I was not a doctor” they usually ignored me. It takes a bit of time for change to register, and now I’m constantly being asked if I take my Vit D3 or what oils I use. Seems the latest oil for all to be told to use is Canola, which if it tastes as foul as the rape seed honey, the mind boggles how it improves the cooking.

  7. Robert Park 21 March 2014 at 5:11 pm #

    What is actually being admitted is that the scientific establishment is halfway to confessing (which it obviously won’t do) that it was mistaken! Allow me to add some anecdotal information. For 17 years I was a vegetarian yet had to have an emergency quadruple by-pass. Interestingly my diet then consisted principally of both mono and poly unsaturated fats. Afterwards I abandoned vegetarianism and returned to a standard diet. I then noticed that I suffered from severe bouts of angina and observed a connection to that of polyunsaturated fat in my diet. On ramping-down down my intake of PUFAs the severity and incidence of angina almost but not quite dispersed. Further observation brought to attention that MUFAs (olive oil) also caused angina but not to the same frequency nor severity but then MUFAs were low in my diet. On reducing this too I no longer suffered from angina (hope you are listening Doc)! It seems best to ignore the science and learn from observation and experience; it almost guarantees better health and longevity.

    • Jonathan Bagley 21 March 2014 at 6:01 pm #

      Yes, it is halfway to confessing and the U turn will be in very small stages to avoid loss of face. The concession that sugar causes obesity will slowly change to include other carbohydrates – they will pick on white flour first and leave porridge till last, or the advice will be to eat more nuts, without without explicitly stating they are high in protein and fat, which will replace carbohydrate in the diet.

      • Robert Park 21 March 2014 at 8:50 pm #

        I am reminded of a study done on plaque from cadavers which appears to have disappeared into the annals of the archives. What was discovered was that a massive 70% of plague arose from PUFAs, 23% from saturated fats, and 7% from other sources. It is said that saturated fat also contains in its structure both poly and mono unsaturated fats from which it can be reasonably deduced that saturation per se is not problematic.

        It is also understood that the traditional Inuits ate a diet consisting principally of marine life and containing a high element of polyunsaturated fat (no vegetable or fruit) and they were relatively free of cardiac problems yet looked older than their Western counterparts and did not survive longer. What appears to have caused their demise was either bleeding to death through injury or aneurysms owing to their blood being very thin which seems to have adversely affected the artery linings. Only when the Inuit’s diet became Westernised with the introduction of carbohydrates did the incidence of ill-health increase and match that of the West.

        Two separate studies with a common theme suggesting that fat alone is not problematic and becomes so only in the presence of carbohydrates in the diet. It sounds as if their may be a connection here to glycation.

  8. Fiona 21 March 2014 at 5:36 pm #

    For further reading, Dr Malcolm Kendrick (author of ‘The Great Cholesterol Con’) also put out a blog on 19.3.14, ‘Althogh now dead, the Cholesterosaurus will march on’.

  9. Dina Junkermann 21 March 2014 at 7:13 pm #

    Interesting discussion. What I am finding fascinating is how the British Heart Foundation, having part-funded the study, can not now bring itself to embrace the findings, falling back on the old ‘more research is needed’ and continuing to push the ‘eatwell’ (hah!) plate for healthy eating. You get the impression they would far rather not mention the study at all, but that’s not really an option for them once it’s been outed in the press!

  10. Susan Fairbairn (nee Kirk) 21 March 2014 at 8:54 pm #

    Did the study take into account the participants with hypertension? Isn’t that a risk factor for heart disease? What about the cholesterol levels of the different groups? I take a personal and professional interest in the cholesterol myth. My levels were 13 at one stage. I got the usual advice and script for statins. I did my own research didn’t like what I read but found it hard to discredit our much esteemed medical establishment and came off the statins and went pescatarian, but still consumed saturated fats, cheese, milk, butter etc. My cholesterol is now 5.4. My doctor still finds this alarming (the 5.4 reading) but no longer tries to convince me to take my statins. So Doc, if you’re talking about oxidative damage, then it still would be wise wouldn’t it to have a low level of blood cholesterol? Or ramp up the ROS somehow?

  11. daz 21 March 2014 at 9:55 pm #

    Hi Dr Briffa,

    Do you (or any of your readers) have access to this study published last month,
    i would loved to hear your comments.

    Their conclusion is “…overeating SFA promotes hepatic and visceral fat storage whereas excess energy from PUFA may instead promote lean tissue in healthy humans.”

    But i’m sure (hope?) there is something hidden in the detail that may be confounding this conclusion.

    Here’s the press release link,
    & heading & first para,

    “Abdominal fat accumulation prevented by unsaturated fat”

    “New research from Uppsala University shows that saturated fat builds more fat and less muscle than polyunsaturated fat. This is the first study on humans to show that the fat composition of food not only influences cholesterol levels in the blood and the risk of cardiovascular disease but also determines where the fat will be stored in the body. The findings have recently been published in the American journal Diabetes.”

    • George Henderson 22 March 2014 at 12:12 am #

      This is consistent with evidence that PUFA promotes fat-burning when a) refined carbs are restricted and b) protein intake is high.
      On the other hand, high sugar or high-GI starch, high linoletate, low protein is a recipe for diabetes.
      Even omega 3 becomes obesigenic in a high-sugar, low-protein diet.

      Paleolithic diets seem to have supplied about 1/3 fat as PUFA, in a high-protein, low-carb milieu. The PUFA was relatively low in linoleate, but higher in longer-chain fats such as EPA, DHA, DPA and AA. And these are the fats that are most associated with benefits.

  12. Vince 21 March 2014 at 11:23 pm #

    Hi Sean,
    I hope you will be able to research the concept of ” cognitive dissonance “. I first experienced it in my youth via the Origin of Species. I guess like a lot of folks out there. My second exposure was when I discovered, many years ago now that my fixation on cholesterol and the diet heart hypothesis was smoke and mirrors. And although I had two degrees in Medicine from Scotland I had had very little nutritional teaching ( or fell asleep in the lectures as ” you are never going to get a question in nutrition anyway, so forget it ” ). Then 15 years ago my T2DM arrived via my genes and inspite of a life of athleticism. That really started my nutritional study and conversion to a low carb life. I am still a busy Dr. and have no more cognitive dissonance regarding things like low carb and cholesterol / diet heart theory and sat fat will kill and butter and eggs are bad and other such silliness.
    Sorry mate, but I never send my patients to Dieticians for diabetic advice. Lovely folks all, but stuck in time with paradigm paralysis. Don’t come to my part of Australia and try to work with me or you will go broke. But stick to the lots of other places in ( lovely ) Oz where what you have been taught is still the standard mantra.
    And as a final little anecdote, I have a daughter who like all my children is a low carb convert and who has belatedly been studying Medicine at one of our prestigious universities. She has had to sit through ” the worse lecture so far, Dad ” on nutrition by a Dietician . Yes, you guessed it. And at the end of the lecture the students who were all “‘getting it” were rewarded with a chocolate…
    Sometimes I despair, but like Dr John here, I keep on and think I see the circle turning. Sadly, like molasses uphill.

  13. George Henderson 22 March 2014 at 12:16 am #

    Here’s a good article defending the “saturated fat bad, PUFA good” position. I mean, if you are going to defend that position, this is how it should be done; with the selective presentation of good science.

    Does not convince me that it is necessary to restrict SFA in order to get what benefits there may be from PUFA. It would be more logical to restrict carbohydrate.

  14. Lobstergirl 23 March 2014 at 8:28 pm #

    I just came across this article by Dr Mcdougall

    Any comments?

  15. Jennie McGinlay 24 March 2014 at 6:34 pm #

    The study was reported on Radio 4 of course, and a representative from the British Heart Foundation was interviewed. He was asked “Does this mean we can all go back to eating butter then?” He replied “Oh no, you mustn’t eat too much of ANY fat, because it will lead to obesity” (not his exact words, but along those lines).
    How is it that I, having merely read a few books (John Briffa, Gary Taubes, Robert Lustig etc) have grasped the principles of healthy eating and what makes people fat, and someone from the BHF doesn’t get it?!

    • Cindy C 25 March 2014 at 2:03 am #

      I read the actual study, and in it, Dr Chowndhury mentions about carbohydrates ( de novo synthesis) references study numbers 33, 34, 36, 37. (Volk, Phinney and others). That representative does not keep up with current science, and did not read all the references. A quote from the study

      We saw heterogeneity of effect across circulating
      composition of specific saturated fatty acids. This could, at
      least in part, reflect biology because circulating saturated
      fatty acid fractions reflect both consumption and endogenous
      metabolism and synthesis (33). For example, the influence
      of metabolism seems particularly relevant for the
      de novo synthesis of even-numbered saturated fatty acids
      in the body, compositions of which are largely determined
      by dietary factors, including carbohydrate and alcohol consumption
      (33–35), and other metabolic pathways (36, 37)
      rather than direct dietary intake.

  16. LJ 28 March 2014 at 3:38 pm #

    Fats, functions & malfunctions

    ‘Saturated fatty acids terminate the stress reactions, polyunsaturated fatty acids amplify them.

    The most highly unsaturated fats, including DHA, accumulate with aging, and their toxic fragments are increased in Alzheimer’s disease.

    The most highly unsaturated fats found in fish oil break down into chemicals that block the use of glucose and oxygen.

    The ratio of saturated fatty acids to polyunsaturated fatty acids is decreased in cancer. Omega-3 fats promote metastasis.’

  17. John Walker 16 May 2014 at 5:38 am #

    Saw a TV programme last night ‘The Food Inspectors’. They were discussing the perils or otherwise of ice cream. I was horrified to see one presenter literally ‘brainwashing’ schoolchildren into being disgusted by the sight of lard; representing the fat that is in true ice-cream, made with double cream. All because they still cling to this belief that fat is the villain. When will the BBC either learn the truth, or admit to the evidence they must know is there. Or is this yet another attempt by the grain and sugar industries to fight back against the recent attacks on their products? The message was being pushed so aggressively, that I was infuriated, and I had to stop watching.


  1. Yet another major review finds no reason at all to limit saturated fat in the diet « wchildblog - 27 March 2014

    […] By Dr John Briffa on 21 March 2014 […]

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