WHO draft guidelines on dietary saturated and trans fatty acids: time for a new approach?BMJ 2019; 366 doi: https://doi.org/10.1136/bmj.l4137 (Published 03 July 2019) Cite this as: BMJ 2019;366:l4137
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SATURATED FATTY ACIDS (SFAs) SHOULD NOT BE DOWN-PLAYED Re: WHO draft guidelines on dietary saturated and trans fatty acids: time for a new approach?
Astrup and 18 co-authors [half of them consultants to the dairy industry] in their article “WHO draft guidelines on saturated and trans fatty acids: time for a new approach” 1 are largely repeating the 2011 Astrup et al article 2 against general advice to reduce saturated fatty acids [SFAs] to limit coronary heart disease [CHD]. The response to the 2019 paper stands the same as the critiques in 2010-2011 by experts in the field, Stamler 3, Kromhout et al 4 and Pedersen et al 5 on the importance of reducing SFAs.
Astrup’s team place too much trust in meta-analysis of prospective studies, that have not found SFAs associated with CHD. In these prospective studies, exemplified by Siri-Tarino et al 6, 93 % of the 208,823 subjects reporting CHD had their food intake estimated only ONCE by a Food Frequency
Questionnaire [ these had 30 to 276 food items] and follow up was for 6 to 23 years! Reliability here is very much less than in the classic studies, randomized controlled trials 7, 8, the Seven Country Study and metabolic ward studies 9.
Questioning the value of reducing SFAs has the potential to weaken the public health strategies that have been so effective in the USA, western Europe and Australasia. In contrast to the inconclusive prospective studies, CHD mortality [age standardized in men] from the peaks in 1967-8 to 1994 (the start of general use of statins), fell from 640 to 200 ( per 100,000) in the USA, from 690 to 300 in Finland and from 600 to 180 in Australia 10. During this period butter and red meat consumption went down in the USA 11, with SFAs from 18 -20% energy to 12-13 % 12. In Finland SFA consumption went from 18% to 13 % energy 13. In Australia the government’s advice was “Eat a diet low in fat and, in particular low in saturated fat” 14.
Fatty acid patterns of serum lipids—phospholipids or triglycerides nearer the CHD event should be a more reliable indicator of what fatty acids people have than FFQs many years in the past. They have shown association of SFAs with CHD 15-17.
The term “Saturated fat[s]” is by now well established among people working with foods and diets and food labelling. It has an official dietary reference value in the UK and is used by the European Food Safety Authority [ who recommend  “lower the better”]. But 12:0, 14:0 and 16:0 belong within the realms of biochemists and food analysts. We have known since 1956 & 7 that butter, red meat and coconut oil raise plasma [LDL]cholesterol 18, 19. The fat in beef is not only stearic acid;
most of consists of SFAs that raise the cholesterol level 20.
A. Stewart Truswell, is an Emeritus Professor of Human Nutrition, Human Nutrition Unit, University of Sydney. He published 19 articles ABC of Nutrition in 1985 in BMJ, later published in book form for 4 editions to 2003, and some editorials in BMJ.
1. Astrup A, Bertram HC, Bonjour JP, et al. WHO draft guidelines on dietary saturated and trans fatty acids: time for a new approach? BMJ 2019;366:l4137. doi: 10.1136/bmj.l4137
2. Astrup A, Dyerberg J, Elwood P, et al. The role of reducing intakes of saturated fat in the prevention of cardiovascular disease: where does the evidence stand in 2010? American Journal of Clinical Nutrition 2011;93:684-8. doi: 10.3945/ajcn.110.004622
3. Stamler J. Diet-heart: a problematic revisit. American Journal of Clinical Nutrition 2010;91:497-9. doi: 10.3945/ajcn.2010.29216
4. Kromhout D, Geleijnse JM, Menotti A, et al. The confusion about dietary fatty acids recommendations for CHD prevention. British Journal of Nutrition 2011;106:627-32. doi: 10.1017/s0007114511002236
5. Pedersen JI, James PT, Brouwer IA, et al. The importance of reducing SFA to limit CHD. British Journal of Nutrition 2011;106:961-3. doi: 10.1017/s000711451100506x
6. Siri-Tarino PW, Sun Q, Hu FB, et al. Meta-analysis of prospective cohort studies evaluating the association of saturated fat with cardiovascular disease. American Journal of Clinical Nutrition 2010;91:535-46. doi: 10.3945/ajcn.2009.27725
7. Truswell AS. Review of dietary intervention studies: effect on coronary events and on total mortality. Australian and New Zealand Journal of Medicine 1994;24:98-106.
8. Mozaffarian D, Micha R, Wallace S. Effects on coronary heart disease of increasing polyunsaturated fat in place of saturated fat: a systematic review and meta-analysis of randomized controlled trials. PLoS Medicine 2010;7:e1000252. doi: 10.1371/journal.pmed.1000252
9. Clarke R, Frost C, Collins R, et al. Dietary lipids and blood cholesterol: quantitative meta-analysis of metabolic ward studies. BMJ 1997;314:112-7. doi: 10.1136/bmj.314.7074.112
10. Truswell AS. Cholesterol and Beyond: The Research on Diet and Coronary Heart Disease 1900–2000: New York: Springer 2010:162-166.
11. Higgins M, Thom T. Trends in CHD in the United States. International Journal of Epidemiology 1989;18(3 Suppl 1):S58-66.
12. Stephen AM, Wald NJ. Trends in individual consumption of dietary fat in the United States, 1920-1984. American Journal of Clinical Nutrition 1990;52:457-69. doi: 10.1093/ajcn/52.3.457
13. Valsta LM, Tapanainen H, Sundvall J, et al. Explaining the 25-year decline of serum cholesterol by dietary changes and use of lipid-lowering medication in Finland. Public Health Nutrition 2010;13(6a):932-8. doi: 10.1017/s1368980010001126
14. National Health and Medical Research Council. Dietary Guidelines for Australians. Canberra: Australian Government Publishing Service 1991.
15. Miettinen TA, Naukkarinen V, Huttunen JK, et al. Fatty-acid composition of serum lipids predicts myocardial infarction. BMJ 1982;285:993-6. doi: 10.1136/bmj.285.6347.993
16. Simon JA, Hodgkins ML, Browner WS, et al. Serum fatty acids and the risk of coronary heart disease. American Journal of Epidemiology 1995;142:469-76. doi: 10.1093/oxfordjournals.aje.a117662
17. Clarke R, Shipley M, Armitage J, et al. Plasma phospholipid fatty acids and CHD in older men: Whitehall study of London civil servants. British Journal of Nutrition 2009;102:279-84. doi: 10.1017/s0007114508143562
18. Ahrens EH, Jr., Insull W, Jr., Blomstrand R, et al. The influence of dietary fats on serum-lipid levels in man. Lancet 1957;272:943-53. doi: 10.1016/s0140-6736(57)91280-1
19. Bronte-Stewart B, Antonis A, Eales L, et al. Effects of feeding different fats on serum-cholesterol level. Lancet 1956;270:521-6. doi: 10.1016/s0140-6736(56)90592-x
20. Keys. A, Blackburn. H. Effect of dietary stearic acid on plasma cholesterol level. New England Journal of Medicine 1988;319(16):1089-90. doi: 10.1056/nejm198810203191611
Competing interests: No competing interests
There are many ways that I could rebut the authors' statements in this opinion piece that suggests that advice to reduce saturated fat might lead people to exclude foods that are rich in nutrients.
I will first point out the obvious, that there are a plethora of nutrient rich foods that do not contain saturated fats.
It should be concerning that the authors have voluminous competing interests particularly from the dairy industry.
It should be concerning that the authors do not cite the many consensus statements from large reputable organizations, and seem to have disregarded rigorous science and massive data.
For example, the American Heart Association recently issued a Presidential Advisory that reviewed the scientific evidence (including recent studies) on the effects of dietary saturated fat intake – and its replacement by other types of fats, as well as carbohydrate intake – on cardiovascular disease. They looked at randomized controlled trials that lowered the intake of dietary saturated fat and replaced it with polyunsaturated fats, and they found that replacing the saturated fat with polyunsaturated fat reduced CVD by around 30%. They state: "Replacement of saturated with unsaturated fats lowers low-density lipoprotein cholesterol, a cause of atherosclerosis, linking biological evidence with incidence of CVD in populations and in clinical trials."
See: Dietary Fats and Cardiovascular Disease: A Presidential Advisory From the American Heart Association http://circ.ahajournals.org/content/early/2017/06/15/CIR.0000000000000510
The European Atherosclerosis Society Consensus Panel recently issued a consensus statement as well. After a very comprehensive review of the evidence that LDL cholesterol causes heart disease, namely:
-Several large meta-analyses of prospective observational epidemiologic studies with data from 1,194,767 participants in the studies.
- Evidence from Mendelian randomization studies involving more than 300,00 participants.
- Compelling evidence from randomized clinical controlled trials including almost 170,000 individuals
"Considered together, the strong and consistent evidence from the genetic studies, prospective epidemiologic cohort studies, Mendelian randomization studies, and randomized intervention trials discussed here, supported by mechanistic evidence to be presented in the second Consensus Statement on LDL causality, establishes that LDL is not merely a biomarker of increased risk but a causal factor in the pathophysiology of ASCVD.
- Cumulative LDL arterial burden is a central determinant for the initiation and progression of atherosclerotic cardiovascular disease.
- The lower the LDL cholesterol (LDL-C) level attained by agents that primarily target LDL receptors, the greater the clinical benefit accrued.
- Both proportional (relative) risk reduction and absolute risk reduction relate to the magnitude of LDL-C reduction.
- Lowering LDL-C in individuals at high cardiovascular risk earlier rather than later appears advisable, especially in those with familial hypercholesterolaemia."
For additional expert opinions on this opinion piece, please see: https://www.sciencemediacentre.org/expert-reaction-to-opinion-piece-ques...
Competing interests: No competing interests
We welcome Astrup at el conclusions that the WHO should reconsider their recommendations on the reduction in total saturated fatty acids and introduce a food based approach in their future guidelines.
The recommendation of the reduction of saturated fats and replacing them with vegetable oils was first introduced in the US dietary guidelines in 1977.1 Since then we have seen the worldwide obesity epidemic. Vegetable oils have been promoted as healthier alternatives to saturated fats, as they can reduce cholesterol levels, and consequently their consumption has dramatically increased.2 However, vegetable oils are high in omega-6 PUFAs, and the intake of these fatty acids was historically low in the human diet.3 Experimental work shows that linoleic acid is toxic to beneficial bacteria in the gut,4 which may explain why the increased ratio of omega-6 to omega-3 has been linked with inflammation, obesity and metabolic disorders.5 6
Furthermore, the reduced saturated fat content in foods has also resulted in a steady increase in food additives.7 Emulsifiers and enzymes such as transglutaminase are added to increase shelf life or improve consistency, texture and palatability of foods in a range of products, such as low fat dairy, reconstituted meat, cereals, etc.8 9 Animal experiments have shown that emulsifiers damage the mucus structure that protect the intestinal wall and trigger inflammation and metabolic syndrome and obesity through changing the microbiota.10-12 Currently, there are 1400 molecules are approved as food additives by the EU https://www.food.gov.uk/business-guidance/eu-approved-additives-and-e-nu.... The metabolic consequences of these additives are poorly understood.
The NOVA classification system has recently been introduced as a framework for categorising the degree of industrial food processing.13 In general, ultra-processed foods are high in sugars and fats and low in natural protein.7 14 Studies based on NOVA found exponential growth in consumption of ultra-processed products and show that they have gradually been displacing unprocessed or minimally processed foods and freshly prepared meals. Moreover, ecological and epidemiological studies have shown a link with increased rates of obesity and metabolic disorders. Research suggests that in high income countries, more than half of the foods consumed are ultra-processed for most age groups, including children.15 16 This may even be an underestimate, as 75% of supermarket foods include added sugars, which is a marker of ultra-processed foods.17 These shifts in the food environment have resulted in dramatic increases of obesity and related chronic noncommunicable diseases, most notably diabetes and metabolic syndrome, at first in high- and middle-income countries, and now also in lower-income ones.18 19 Ultraprocessed food consumption is higher in lower socioeconomic groups,16 20, resulting in reduced dietary protein density and increased sugar intake,21 22 which in turn is linked with higher rates of obesity, metabolic disorders. The WHO should focus on reversing this trend as part of the work of the UN Sustainable Development Goals and its Decade of Nutrition.7
1. USDA. Dietary Guidelines Advisory Committee Report. Appendix 5: History of the Dietary Guidelines for Americans
2. Naughton SS, Mathai ML, Hryciw DH, et al. Australia's nutrition transition 1961-2009: a focus on fats. Br J Nutr 2015;114(3):337-46. doi: 10.1017/S0007114515001907
3. Saini RK, Keum YS. Omega-3 and omega-6 polyunsaturated fatty acids: Dietary sources, metabolism, and significance - A review. Life Sci 2018;203:255-67. doi: 10.1016/j.lfs.2018.04.049
4. Di Rienzi SC, Jacobson J, Kennedy EA, et al. Resilience of small intestinal beneficial bacteria to the toxicity of soybean oil fatty acids. Elife 2018;7 doi: 10.7554/eLife.32581
5. DiNicolantonio JJ, O'Keefe JH. Good Fats versus Bad Fats: A Comparison of Fatty Acids in the Promotion of Insulin Resistance, Inflammation, and Obesity. Mo Med 2017;114(4):303-07.
6. Naughton SS, Mathai ML, Hryciw DH, et al. Linoleic acid and the pathogenesis of obesity. Prostaglandins Other Lipid Mediat 2016;125:90-9. doi: 10.1016/j.prostaglandins.2016.06.003
7. Monteiro CA, Cannon G, Moubarac JC, et al. The UN Decade of Nutrition, the NOVA food classification and the trouble with ultra-processing. Public Health Nutr 2018;21(1):5-17. doi: 10.1017/S1368980017000234
8. Chassaing B, Koren O, Goodrich JK, et al. Dietary emulsifiers impact the mouse gut microbiota promoting colitis and metabolic syndrome. Nature 2015;519(7541):92-6. doi: 10.1038/nature14232
9. Cani PD. Metabolism: Dietary emulsifiers--sweepers of the gut lining? Nat Rev Endocrinol 2015;11(6):319-20. doi: 10.1038/nrendo.2015.59
10. Viennois E, Chassaing B. First victim, later aggressor: How the intestinal microbiota drives the pro-inflammatory effects of dietary emulsifiers? Gut Microbes 2018:1-4. doi: 10.1080/19490976.2017.1421885
11. Chassaing B, Van de Wiele T, De Bodt J, et al. Dietary emulsifiers directly alter human microbiota composition and gene expression ex vivo potentiating intestinal inflammation. Gut 2017;66(8):1414-27. doi: 10.1136/gutjnl-2016-313099
12. Halmos EP, Mack A, Gibson PR. Review article: emulsifiers in the food supply and implications for gastrointestinal disease. Aliment Pharmacol Ther 2019;49(1):41-50. doi: 10.1111/apt.15045
13. Monteiro CA, Cannon G, Levy RB, et al. Ultra-processed foods: what they are and how to identify them. Public Health Nutr 2019:1-6. doi: 10.1017/S1368980018003762
14. Martinez Steele E, Popkin BM, Swinburn B, et al. The share of ultra-processed foods and the overall nutritional quality of diets in the US: evidence from a nationally representative cross-sectional study. Popul Health Metr 2017;15(1):6. doi: 10.1186/s12963-017-0119-3
15. Bielemann RM, Santos LP, Costa CDS, et al. Early feeding practices and consumption of ultraprocessed foods at 6 y of age: Findings from the 2004 Pelotas (Brazil) Birth Cohort Study. Nutrition 2018;47:27-32. doi: 10.1016/j.nut.2017.09.012
16. Rauber F, da Costa Louzada ML, Steele EM, et al. Ultra-Processed Food Consumption and Chronic Non-Communicable Diseases-Related Dietary Nutrient Profile in the UK (2008(-)2014). Nutrients 2018;10(5) doi: 10.3390/nu10050587
17. Lustig RH. Processed Food-An Experiment That Failed. JAMA Pediatr 2017;171(3):212-14. doi: 10.1001/jamapediatrics.2016.4136
18. Monteiro CA, Moubarac JC, Cannon G, et al. Ultra-processed products are becoming dominant in the global food system. Obes Rev 2013;14 Suppl 2:21-8. doi: 10.1111/obr.12107
19. Rodgers A, Woodward A, Swinburn B, et al. Prevalence trends tell us what did not precipitate the US obesity epidemic. Lancet Public Health 2018;3(4):e162-e63. doi: 10.1016/S2468-2667(18)30021-5
20. Baraldi LG, Martinez Steele E, Canella DS, et al. Consumption of ultra-processed foods and associated sociodemographic factors in the USA between 2007 and 2012: evidence from a nationally representative cross-sectional study. BMJ Open 2018;8(3):e020574. doi: 10.1136/bmjopen-2017-020574
21. Martinez Steele E, Raubenheimer D, Simpson SJ, et al. Ultra-processed foods, protein leverage and energy intake in the USA. Public Health Nutr 2018;21(1):114-24. doi: 10.1017/S1368980017001574
22. Martinez Steele E, Baraldi LG, Louzada ML, et al. Ultra-processed foods and added sugars in the US diet: evidence from a nationally representative cross-sectional study. BMJ Open 2016;6(3):e009892. doi: 10.1136/bmjopen-2015-009892
Competing interests: No competing interests
I applaud the authors for highlighting the limitations of the WHO guidelines on saturated fat. The recommendations for adults are based on only two studies: a Cochrane review by Hooper  that included 15 RCTs assessing the impact of replacing SFAs with CHOs, PUFAs, MUFAs, and/or protein on mortality and cardiovascular morbidity; and a systematic review by Mensink  that included 84 RCTs assessing the effects of specific fats on blood lipids.
This review included studies with substantial differences in treatments/diets between control and intervention groups, preventing clear conclusions about the impact of saturated fat intake on CVD. For example, they included the 1966 Oslo Diet-Heart study, in which the treatment group, in addition to replacing saturated fat with soybean oil, received a large dose (~5 g/day) of EPA/DHS from sardines canned in cod liver oil and was advised to restrict sugar and refined carbohydrates. They also included the 2006 Women’s Health Initiative, in which the treatment group, in addition to lowering total and saturated fat, increased intake of fruits/vegetables. These are just two examples of included studies that did not isolate the effect of saturated fat on CVD and mortality. Nevertheless, while the review found a modest reduction in risk for the treatment versus control groups on combined cardiovascular events (RR 0.83 [0.72, 0.96]), it found no difference on cardiovascular mortality (0.95 [0.80, 1.12]) or all-cause mortality (RR 0.97 [0.90, 1.05]).
This review provides evidence that replacing SFAs with PUFAs or MUFAs can improve blood lipid markers, but it’s unclear whether this lowers cardiovascular morbidity or mortality. Increased intake of stearic acid had no effect on blood lipids, and increased intake of lauric acid lowered the total to HDL cholesterol and LDL to HDL cholesterol ratios compared with a mixture of carbohydrates.
The WHO guidelines also cite a meta-analysis of RCTs by Mozaffarian  which found replacing SFAs with PUFAs resulted in reduced CVD events (RR 0.81 [0.70, 0.05]). However, this study included trials with substantial differences in diets between treatment and control groups––the 1996 Oslo Diet-Heart study described above and other problematic studies. For example, the Finnish Mental Hospital study was not a RCT––all participants from one hospital were assigned to treatment, all from a second hospital to control. Additionally, participants in the control group were disproportionally exposed to a cardiotoxic drug thioridazine.
There are important systematic reviews and meta-analyses of RCTs and observational studies that conflict with WHO guidelines. Conclusions differ substantially depending on included/excluded studies. The two studies included for adults in the WHO guidelines have weaknesses and are not representative of the totality of evidence, which may lead to misguidance. Additional important studies highlighted below.
Authors analyzed unpublished data from the Minnesota Coronary Experiment, which replaced SFAs with LAs in the treatment group and conducted a meta-analysis of RCTs. The analysis of the Minnesota Coronary Experiment data showed that while the treatment group had substantially lower serum cholesterol, there was no mortality benefit in the intervention group and that there was a 22% higher risk of death for each 30 mg/dL reduction in serum cholesterol (HR 1.22 [1.14, 1.32]). The meta-analysis showed no benefit of cholesterol-lowering interventions on mortality from CVDs (HR 1.13 [0.83, 1.54]) or all causes (HR 1.07 [0.90, 1.27]). Authors included different studies in the meta-analysis than Mozaffarian  or Hooper .
This analysis critically reviewed the inclusion/exclusion of controversial studies and conducted a meta-analysis of adequately controlled RCTs that replaced SFAs with omega-6 PUFAs. It found no differences between treatment and control groups for total CVD events (RR 1.02 [0.84, 1.23]), CVD mortality (RR 1.13 [0.91, 1.40]), or total mortality (RR 1.07 [0.90, 1.26]).
This systematic review and meta-analysis included prospective observational studies and RCTs of the impact of different fats. In observational studies there was no increased risk in coronary disease from higher saturated fat intakes (RR 1.03 [0.98, 1.07]) or other fats, between the top and bottom thirds of baseline intake. Long-chain omega-3 fats showed a benefit in reduced coronary disease (RR 0.87 [0.78, 0.97]). There were no significant results for RCTs or overall.
De Souza 
This systematic review and meta-analysis included observational studies that reported associations between saturated fat and all-cause mortality, CHD/CVD mortality, total CHD, ischemic stroke, or type 2 diabetes. Saturated fats were not associated with all-cause mortality, CVD, CHD, stroke, or type 2 diabetes.
This meta-analysis included prospective observational studies analyzing the association between saturated fat intake with CHD/CVD or stroke. Intake of saturated fat was not associated with an increased risk of CHD, stroke, or CVD.
There are also important findings from the 18-country observational PURE study. Dehghan : Total and specific fats were not associated with CVD, myocardial infarction, or CVD mortality, whereas saturated fat had an inverse association with stroke. Mente : Reducing saturated fat intake and replacing it with carbohydrate had an adverse effect on blood lipids. Substituting saturated with unsaturated fats might improve some risk markers but worsen others. Simulations suggest the ApoB-to-ApoA1 ratio provides a good indication of the effect of saturated fats on CVD risk. Focusing on a single lipid marker such as LDL cholesterol does not capture the net clinical effects of nutrients on cardiovascular risk.
Individual dietary components are not eaten separately, they are bundled together as diets. The impact of any one nutrient, such as saturated fat, varies depending on the food matrix and total diet. For example, a RCT by Shih  found that in the context of a weight-loss diet, people on a high-quality low-fat diet developed increased risk of CVD, compared to those on a high-quality low-carbohydrate diet higher in saturated fat. Refined carbohydrates were an important risk factor for CVD, not the proportion of total or saturated fat. Overall diet quality influences the impact of saturated fat on CVD risk––consuming > 10% of energy from saturated fat may be healthy if the diet is energy-balanced, composed of high-quality whole foods, and low in refined carbohydrates.
1 Astrup A, Bertram HC, Bonjour J-P, et al. WHO draft guidelines on dietary saturated and trans fatty acids: time for a new approach? BMJ 2019;366:l4137. doi:10.1136/bmj.l4137
2 Hooper L, Martin N, Abdelhamid A, et al. Reduction in saturated fat intake for cardiovascular disease. Cochrane Database of Systematic Reviews Published Online First: 10 June 2015. doi:10.1002/14651858.CD011737
3 Mensink RP. Effects of saturated fatty acids on serum lipids and lipoproteins: a systematic review and regression analysis. 2016.
4 Mozaffarian D, Micha R, Wallace S. Effects on Coronary Heart Disease of Increasing Polyunsaturated Fat in Place of Saturated Fat: A Systematic Review and Meta-Analysis of Randomized Controlled Trials. PLoS Med 2010;7:e1000252. doi:10.1371/journal.pmed.1000252
5 Ramsden CE, Zamora D, Majchrzak-Hong S, et al. Re-evaluation of the traditional diet-heart hypothesis: analysis of recovered data from Minnesota Coronary Experiment (1968-73). BMJ 2016;:i1246. doi:10.1136/bmj.i1246
6 Hamley S. The effect of replacing saturated fat with mostly n-6 polyunsaturated fat on coronary heart disease: a meta-analysis of randomised controlled trials. Nutr J 2017;16:30. doi:10.1186/s12937-017-0254-5
7 Chowdhury R, Warnakula S, Kunutsor S, et al. Association of Dietary, Circulating, and Supplement Fatty Acids With Coronary Risk: A Systematic Review and Meta-analysis. Ann Intern Med 2014;160:398. doi:10.7326/M13-1788
8 de Souza RJ, Mente A, Maroleanu A, et al. Intake of saturated and trans unsaturated fatty acids and risk of all cause mortality, cardiovascular disease, and type 2 diabetes: systematic review and meta-analysis of observational studies. BMJ 2015;:h3978. doi:10.1136/bmj.h3978
9 Siri-Tarino PW, Sun Q, Hu FB, et al. Meta-analysis of prospective cohort studies evaluating the association of saturated fat with cardiovascular disease. The American Journal of Clinical Nutrition 2010;91:535–46. doi:10.3945/ajcn.2009.27725
10 Dehghan M, Mente A, Zhang X, et al. Associations of fats and carbohydrate intake with cardiovascular disease and mortality in 18 countries from five continents (PURE): a prospective cohort study. The Lancet 2017;390:2050–62. doi:10.1016/S0140-6736(17)32252-3
11 Mente A, Dehghan M, Rangarajan S, et al. Association of dietary nutrients with blood lipids and blood pressure in 18 countries: a cross-sectional analysis from the PURE study. The Lancet Diabetes & Endocrinology 2017;5:774–87. doi:10.1016/S2213-8587(17)30283-8
12 Shih CW, Hauser ME, Aronica L, et al. Changes in blood lipid concentrations associated with changes in intake of dietary saturated fat in the context of a healthy low-carbohydrate weight-loss diet: a secondary analysis of the Diet Intervention Examining The Factors Interacting with Treatment Success (DIETFITS) trial. Am J Clin Nutr 2019;109:433–41. doi:10.1093/ajcn/nqy305
Competing interests: No competing interests
This article contradicts many of the most established and agreed tenets regarding association with saturated fat , LDL and cardiovascular and overall mortality, as per response above. Anyone reading this article MUST be aware that the authors are heavily remunerated by or funded by some of the wealthiest dairy and agriculture organisations in the world, which is a massive conflict of interest and raised huge questions over the validity of their conclusions and motives behind this work. That the list of conflicting interests is perhaps one of the longest on record is does not completely invalidate the paper of course, but the information already provided in the response regarding flaws in the conclusions is a fairer reflection of where we are with the evidence.
Competing interests: Founding member of the non profit health through nutrition supporting organisation Evidence Based Eating New Zealand EBE.nz.
The links between saturated fats and chronic diseases are very clear.
Through a reduction in smoking and saturated fat intake, the North Karelia Project achieved an 80% reduction in male heart disease (our number one killer) for the 35-64 yr olds and a 96% reduction in the 35-44 yr olds.
At the same time a 37% reduction in animal fat combined with an 80% increase in female smoking resulted in a 27% cancer mortality reduction in North Karelia (and 29% reduction over the whole of Finland combined with a 15% increase in smoking).
Hence both our number one and number two killers are linked to the consumption of animal fat. Considering the Finish Female experience, the influence of animal fat on cancer rates would appear to be significantly bigger than that of smoking.
This can be explained through the saturated fats containing fat soluble estrogens which have been labelled by the World Health Organization as a class one (i.e. definite) human carcinogen.
The likely pathway of estrogens causing cancer is not through DNA damage but through undermining the human cancer immunological responses through interfering and hindering apoptosis.
Ref.: Grott M et al. Progesterone and estrogen prevent cisplatin-induced apoptosis of lung cancer cells. PubMed. [Online] 2013. https://www.ncbi.nlm.nih.gov/pubmed/23482746
The latest developments in cancer research and treatment utilizes different forms immunotherapies. Hence we have arrived at the point where on one hand we are stimulating our immune system to fight cancer while at the same time we are continuing animal food consumption leading to Acquired Cancer Immunodeficiency Disorder.
Ref.: The North Karelia Project - Pekka Puska
The only diet that has ever demonstrated reversibility of heart disease and its risk factors including diabetes type 2 is a low fat whole plant based diet.
Ref.: Dr Esselstyn’s article about reversal of coronary artery disease demonstrates this in figure 2: http://dresselstyn.com/JFP_06307_Article1.pdf
This is further supported by a RCT by Dr Dean Ornish et al: “Intensive Lifestyle Changes for Reversal of Coronary Heart Disease” - https://www.ornish.com/wp-content/uploads/Intensive-lifestyle-changes-fo...
According to epidemiologist Sir Bradford Hill, reversal is strong evidence of causality.
Competing interests: No competing interests
This paper makes some good points about understanding the need to consider the food matrix before rating a food as more or less desirable for frequent consumption. However, it's a good idea to read the list that shows the potential conflicts of interest for many of the authors of this paper.
Let's also remember that foods do not contain a single fatty acid. Chocolate for example is listed as a source of stearic acid - which may not raise serum cholesterol, but chocolate is also a rich source of palmitic acid.
Competing interests: No competing interests
I am not a a medical professional however having read this article what struck me is it appears bias.
It does not seem to take into consideration people live well on low saturated fat Whole Plant Based diets. Using language like “may” or “could” in relation to nutrient deficiencies feels alarmist. See extract below:
“A recommendation to reduce intake of total saturated fat without considering specific fatty acids and food sources is not evidence based; will distract from other more effective food based recommendations; and might cause a reduction in the intake of nutrient dense foods that decrease the risk of cardiovascular disease, type 2 diabetes, other serious non-communicable diseases, malnutrition, and deficiency diseases and could further increase vulnerability to nutrient deficiencies in groups already at risk”
It does not seem to take account of the considerable evidence that exists which demonstrates the benefits of low saturated fat Whole Plant Based Diet esp. reduction in obesity.
Lastly, the article does not take “Ecosystem” or “Health Service” sustainability into consideration which are equally important to survival of the population.
Andrew Reid BSc MBCS CIPT
Competing interests: No competing interests
I fully agree with the authors that the focus of nutrition guidelines should be food-based not nutrient-based. However, it is inaccurate and potentially dangerous to state that saturated fat consumption is not a concern on a population level.
Most national and international health organisations, including the WHO, agree that the healthiest diet/food pattern is one centred around minimally processed fruits, vegetables, whole grains, legumes, nuts and seeds, whilst minimising meat and full fat dairy. Such a diet is naturally low in saturated fat, which is predominately derived from animal foods. This type of diet pattern has been associated with the lowest incidence of chronic disease, specifically cardiovascular disease, diabetes, cancer, dementia and obesity and can also reverse already established disease. In fact, diet patterns used in clinical practice, such as the DASH (dietary approaches to stop hypertension) diet, are based on the vegetarian diet pattern and emphasis whole plant foods, whilst minimising meat and dairy, and therefore are low in saturated fat. They have been shown to be very effective at reducing hypertension, biomarkers of cardiovascular disease and diabetes.
A diet emphasising whole plant foods and de-emphasising meat and dairy is established as healthy and nutritionally complete by most dietetic organisations, without concerns about nutrient deficiencies if planned with care, as all diets should be. In fact diets that emphasise meat, eggs and dairy, as recommended by the authors, are often low in fibre, potassium, folate and, magnesium to name a few nutrients. There are no long-lived, healthy populations that consume diets high in saturated fat.
The meta-analyses on saturated fat consumption and health outcomes cited by the authors do not tell the full story. The analyses didn't take into account what was being substituted for saturated fat in the diet of participants. When saturated fat is replaced by refined carbohydrates and free sugars, health outcomes are equally bad. However, when you avoid/minimise both saturated fat and refined carbohydrates, as is the case in a healthy vegetarian diet, the risk of heart disease is reduced in the order of 30%.
The PURE study has been heavily criticised previously and does not exonerate saturated fat, but again tells us that replacing saturated fat with refined carbohydrates can be worse for health. What the PURE study actually told us was that consumption of saturated fat is associated with higher education and socioeconomic status and thus better access to healthcare, which all contribute to improved health outcomes.
As a global population we need to move towards eating a predominately plant-based diet, not only for human health but for the health of our planet. We need to move away from our reliance and want of meat, eggs and dairy as this is no longer sustainable.
Reference. Food in the Anthropocene: the EAT–Lancet Commission on healthy diets from sustainable food systems
Prof Walter Willett, MD Prof Johan Rockström, PhD, Brent Loken, PhD , Marco Springmann, PhD, Prof Tim Lang, PhD
Sonja Vermeulen, PhD et al. The Lancet Published:January 16, 2019.
Competing interests: I also work for the University of Winchester.