There may be no country in the world in which a suggested limit on saturated fat has not been followed by a relatively rapid increase in the incidence of diabetes and obesity.
Of course this is a matter of observation not experiment, but so is most of the evidence that various dietary guidelines organizations have relied on over the years.
A particularly egregious case seems to have occurred in Mauritius, after the Mauritian Government changed the fat content of ration oil, a cheap cooking oil used by most of the population, by decree. In 1987 it had been 75-100% (median 87.5%) palm oil, with (by then) some soybean oil – overnight this was changed to 100% soybean oil. This change was based on predictions from the research of Ancel Keys into heart disease, in particular the 7 Countries study and the intervention in East Finland.
This took PUFA intakes (almost all linoleic acid) to 8.6%E for men and 8.8%E for women, and lowered SFA intakes to 7%E and 7.5%E respectively. These were, as reported, not high fat diets, and it may be relevant that Mauritius is a sugar-producing nation.[1,2]
"In the 5-year survey of lipids and other biomarkers, mean population serum total cholesterol concentration fell appreciably from 5.55 mmol/l to 4.7 mmol/l (P<0.001). The prevalence of overweight or obesity increased, and the rates of glucose intolerance changed little."
However, in a letter to the BMJ, N Chandrasekharan, a consultant chemical pathologist and Kalyana Sundram, senior research officer of the Palm Oil Research Institute of Malaysia disputed these findings -
The data for 1992 on the per caput fat intake of 56.2 g per day based on a 24 hour dietary recall is a far cry from the 73.7 g reported by the Food and Agriculture Organisation. The figures for edible oil intake seem erroneous. In 1987 palm oil accounted for only 27.5% of the edible oils consumed and its saturated fatty acids contributed 1.89% of the total energy intake and this fell to 0.33% in 1992."
However, we have previously found FAO fat consumption estimates to be unreliable, overestimating NZ butter consumption in recent years by a factor of 4. And Chandrasekharan and Sundram’s letter contains this statement:
In other words, whatever the effect on fat intakes or cholesterol, the change was a radical one. It put more linoleic acid into the Mauritian food supply, and as in other places, the change in mandated fats would have been accompanied by voluntary changes along the same lines. We may doubt whether cholesterol levels changed, but not that people began to consume more soybean oil.
So what happened? The 1987 intervention included several good ideas – exercise more, smoke less, drink less – as well as less certain ones – eat less salt, eat less saturated fat and more soybean oil.
Mauritius is now #2 in the world for diabetes mortality. However, a coding change in 2004 meant that much of what had been recorded as circulatory disease mortality was shifted to diabetes mortality. What we do know is that diabetes prevalence increased, as has incidence of pre-diabetes.
Note that this contradicts the 1992 claim – by some of the same authors – that “the rates of glucose intolerance changed little” between 1987 and 1992, a discordance not mentioned in the 2002 paper.
The Mauritius fat change paper has been cited just 17
times in 25 years, and not one of the citing papers includes any follow up on the
consequences of the change there. For example, an AHA paper mentions the
Mauritius change in glowing terms without following up whether benefit or harm
ensued, beyond the claimed 5-year drop in cholesterol. Palm oil reduction
was modelled for India in 2013, and a doubled palm oil tax has been implemented
in Fiji since, all in papers citing the 1987-1992 Mauritius cholesterol
But none follows that citation up with any hard outcomes.
It appears now that both saturated fat in the diet, and a low intake of omega 6 linoleic acid, are beneficial in terms of the incorporation of the omega 3 fatty acids EPA and DHA into circulating lipids and cells.[10, 11, 12, 13] EPA in particular is anti-inflammatory, and is an approved drug for the prevention of CVD.
The conversion of linoleic acid to arachidonic acid, and the peroxidation of arachidonic acid to aldehydes which interfere with insulin signaling, as well as its conversion to cannabinoids which increase adipocyte growth, in a context of decreased omega 3 availability from high LA and low SFA diet, are pathways that may explain the eventual adverse outcomes in Mauritius, especially in a population with high sugar availability.[15,16]
It seems that, in the matter of diet, public health experts cannot be relied on to investigate the possibility that they have made a mistake. They control the narrative so that a (questionable) historical change in cholesterol within a 5-year period is considered evidence that a lifetime intervention is valuable, yet a nation-wide worsening of hard endpoints after that intervention can be ignored. Certainly the diabetes disaster in Mauritius can have had many causes, but the possibility that the soya bean oil intervention was one of them has not even registered in the medical literature over a 30 year period, let alone been tested.
H/T Louise Stephen @LouiseStephen9 author of
Postscript: it will be obvious to students of evidence-based medicine that the quality of evidence used to create this argument has left much to be desired. With the exception of the date and intent of the intervention and the diabetes incidence data, nothing here tells us quite what we want to know. For example, circulatory disease as a percentage of mortality is a suggestive but imperfect measure, even before the coding change. So there will be those who read this article and feel justified in dismissing the need for it.
But I ask them to look at things another way - the data in this page is, to the best of my knowledge, the sum total of the published, peer-reviewed evidence on the subject. The Mauritius intervention - a legal disruption of the saturated fat supply to replace it with unsaturated fat within an entire community, in a way designed to target its most vulnerable members - has been the masturbation fantasy of a certain type of public health epidemiologist for as long as I can remember. There is a constant supply of peer-reviewed publications modelling the long-term effect of such an intervention on the putatively preventable causes of mortality, and there have been none directly investigating the impact on those causes in this case - where the long-planned intervention actually happened.
The reasons for this neglect are a matter for conjecture; we may hear future tales of suppressed data and publication bias as we did with the Sydney Heart Study and Minnesota Coronary Experiment studies (both of which also involved changes of fat products given to a population, rather than the less certain changes of mere advice given in most other diet-heart studies) but the conclusion ought surely to be that the modelling should stop until the facts have been checked.
H/T Louise Stephen @LouiseStephen9 author of'Eating Ourselves Sick' for bringing this intervention to my attention.
 Dowse GK, Gareebo H, Alberti KGMM, Zimmet P, Tuomilehto J, Purran A, et al. Changes in population cholesterol concentrations and other cardiovascular risk factor levels after five years of the noncommunicable disease intervention programme in Mauritius. BMJ 1995;311:12259.
 Uusitalo U, Feskens EJM, Tuomilehto J, Dowse G, Haw U, Fareed D, et al. Fall in total cholesterol concentration over five years in association with changes in fatty acid composition of cooking oil in Mauritius: cross sectional survey. BMJ 1996;313:10446.
 Chandrasekharan N, Sundram K. Fall in cholesterol after changes in composition of cooking oil in Mauritius. BMJ. 1997;314(7079):516. doi:10.1136/bmj.314.7079.516
 Morrell, S., Taylor, R., Nand, D. et al. Changes in proportional mortality from diabetes and circulatory disease in Mauritius and Fiji: possible effects of coding and certification. BMC Public Health 19, 481 (2019) doi:10.1186/s12889-019-6748-7
 Söderberg S, Zimmet P, Tuomilehto J, de Courten M, Dowse GK, Chitson P, Gareeboo H, Alberti KG, Shaw JE. Increasing prevalence of Type 2 diabetes mellitus in all ethnic groups in Mauritius. Diabet Med. 2005 Jan;22(1):61-8.
 Magliano DJ, Söderberg S, Zimmet PZ, et al. Explaining the increase of diabetes prevalence and plasma glucose in Mauritius. Diabetes Care. 2012;35(1):87–91. doi:10.2337/dc11-0886
 Mozaffarian D, Afshin A, Benowitz NL, et al. Population approaches to improve diet, physical activity, and smoking habits: a scientific statement from the American Heart Association. Circulation. 2012;126(12):1514–1563. doi:10.1161/CIR.0b013e318260a20b
 Basu S, Babiarz KS, Ebrahim S, Vellakkal S, Stuckler D, Goldhaber-Fiebert JD. Palm oil taxes and cardiovascular disease mortality in India: economic-epidemiologic model. BMJ. 2013;347:f6048. Published 2013 Oct 22. doi:10.1136/bmj.f6048
 Coriakula J, Moodie M, Waqa G, Latu C, Snowdon W, Bell C. The development and implementation of a new import duty on palm oil to reduce non-communicable disease in Fiji. Global Health. 2018;14(1):91. Published 2018 Aug 29. doi:10.1186/s12992-018-0407-0
 Gibson, Robert A. Musings about the role dietary fats after 40 years of fatty acid research. Prostaglandins, Leukotrienes and Essential Fatty Acids, Volume 131, 1 – 5
 Garg ML, Thomson ABR, and Clandinin M T. Interactions of saturated, n-6 and n-3 polyunsaturated fatty acids to modulate arachidonic acid metabolism.
The Journal of Lipid Research, February 1990 , 31, 271-277.
 Dabadie H, Motta C, Peuchant E, LeRuyet P, Mendy F. Variations in daily intakes of myristic and alpha-linolenic acids in sn-2 position modify lipid profile and red blood cell membrane fluidity. Br J Nutr. 2006 Aug;96(2):283-9.
 Dias Cintia B, Wood LG, and Garg Manohar L. Effects of dietary saturated and n-6 polyunsaturated fatty acids on the incorporation of long-chain n-3 polyunsaturated fatty acids into blood lipids. European Journal of Clinical Nutrition. 2016; 70: 812-818
 Budoff M, Brent Muhlestein J, Le VT, May HT, Roy S, Nelson JR. Effect of Vascepa (icosapent ethyl) on progression of coronary atherosclerosis in patients with elevated triglycerides (200-499 mg/dL) on statin therapy: Rationale and design of the EVAPORATE study. Clin Cardiol. 2018;41(1):13–19. doi:10.1002/clc.22856
 Madsen L, Kristiansen K. Of mice and men: Factors abrogating the antiobesity effect of omega-3 fatty acids. Adipocyte. 2012;1(3):173–176. doi:10.4161/adip.20689
 Clark TM, Jones JM, Hall AG, Tabner SA, Kmiec RL.
Theoretical Explanation for Reduced Body Mass Index and Obesity Rates in
Cannabis Users. Cannabis Cannabinoid Res. 2018;3(1):259-271. Published 2018 Dec
 Ramsden Christopher E, Zamora Daisy, Majchrzak-Hong Sharon, Faurot Keturah R, Broste Steven K, Frantz Robert P et al. Re-evaluation of the traditional diet-heart hypothesis: analysis of recovered data from Minnesota Coronary Experiment (1968-73) BMJ 2016; 353 :i1246