Saturated Fat advice from AHA is still 20 years behind science

The new American Heart Association (AHA) position statement on saturated fat and cardiovascular disease is slightly lesswrong and misleading as previous statements they made. [1]

AHA Presidential

First, we do find some common ground

  1. It seems reasonable to us that specific saturated fats, most notably palmitic acid, can have adverse cardiometabolic effects when combined with refined carbohydrates and eaten by people with an excessive postprandial insulin response.
  2. It also seems reasonable that the effects can be quite different outside of this context, and in fact the AHA has cited evidence that shows this, which we will get to later.

We’re not poo-pooing the whole idea or the body of evidence on display here, just pointing out that the AHA’s single-minded obsession with the 10-15% of saturated fat in the average diet has completely blinded them to the effect of the 50-60% of mostly refined carbohydrate, and the value of replacing that with almost anything. We think that in this case the naturally occurring saturated fat in the diet will be harmless and quite possibly somewhat beneficial at a population level.

So how do you wade through and make any sense of the research evidence the AHA has presented? Here’s our attempt.

Meta-analysis of RCTs (we like)

We can start with the new meta-analysis of saturated fat substitution RCTs that the AHA team has done. We’ve never seen a meta-analysis like this. There seems to be no prearranged protocol. What we get instead is the four most favourable studies of PUFA replacing saturated fat, now designated “core studies” and analysed separately from all the RCTs that failed to confirm the hypothesis, using the fixed-effects model. The unfavourable RCTs are dismissed because of confounders that favoured the control diets. However, confounders that favoured the interventions go unmentioned. Controls in the Sydney Diet Heart study may in fact have consumed more trans fats [TFA] than the intervention group for example, which is consistent with the intervention lowering LDL cholesterol; the AHA hypothesis is that lowering LDL cholesterol reduces heart attacks and heart attack deaths, but this is the opposite of what happened in Sydney.[2]

The AHA has rehabilitated the Finnish Mental Hospital Study and included it as a “core study”, and this tells you a lot about their attitude to the scientific method, which Gary Taubes demolishes here. In the FMHS the populations in two hospitals were allocated to different diets, and the patients who ate a high intake of PUFA (from rapeseed oil) replacing SFA saw fewer heart attacks and cardiovascular deaths. This is the SFA-replacement study with the largest reduction in CHD and CVD mortality in the intervention arm (0.59), which may be why the AHA choose to revive it. However, non-CVD deaths rose and the all-cause mortality rate didn’t go down (1.01).
In any case, it’s our view that this study has  important confounders that the AHA hasn’t mentioned. For example, the patients were treated with a cardiotoxic medicine, thioridazine, with overall greater use in the control diet groups (0.63 vs. 0.97 standard doses/day).[2] Thioridazine is an antipsychotic  drug that causes heart attacks as a side effect, which is why it was withdrawn worldwide in 2005. The control diet groups were also fed more trans fats than the intervention groups (2%E vs 0%E in hospital K, 0.6%E vs 0.2%E in hospital N).[2] So the people eating more PUFA may have had fewer heart attacks because of the PUFA, which is plausible because this diet supplied plenty of omega 3 to a population possibly lacking in it, but for all we know it could have been due to the fact that they were being poisoned less often. Or, of course, just due to chance, because this study wasn’t fully randomised a a patient level. Patients were allocated diets on admission to hospital and there were only two hospitals; this is called a cluster trial and it takes more clusters than were in FMHS to equate to a randomised trial.

Now, either the AHA knows about the confounding, and they should, it’s been mentioned in discussions of this trial for years (including their ref. 35) and Steven Hamley covers it in his own recent meta-analysis – the one that tried hardest to account for confounders, and they’ve chosen not to mention it. The alternative is that they don’t know, and are sleepwalking through the science with blinkers on. In general – and probably in toto – the AHA meta-analysis covers only half the evidence on confounders, the half that suits the AHA position, as Gary Taubes found when he analysed the Oslo study. We ask how this gets past independent peer-review?

Fat intolerance and its causes

We don’t have time to check every reference, but as usual we checked the ones that claimed to prove something of interest to us. One of these is the primate studies in which saturated (and monounsaturated) fat is more atherogenic than PUFA (studies in mice and rabbits don’t show this consistently enough to validate the hypothesis). The AHA states:

“To induce hypercholesterolemia and atherosclerotic lesion formation, one group of monkeys typically was fed lard or palm oil at 35% of their daily energy intake and dietary cholesterol to raise serum cholesterol levels into the 300- to 400-mg/dL range to model hypercholesterolemia in human beings at high risk for CHD. A second group of monkeys was fed a monounsaturated fat, high-oleic safflower oil, and a third group was fed a polyunsaturated fat linoleic acid–rich diet using safflower oil. Saturated fatty acids promoted higher LDL cholesterol concentrations and more coronary artery atherosclerosis. Linoleic acid lowered LDL cholesterol concentrations and decreased the amount of coronary artery atherosclerosis.”

How much cholesterol do you need to feed to monkeys to make them intolerant of saturated (and monounsaturated) fat? 0.8mg/Kcal; the equivalent of 1,600mg for a human eating 2,000kcal/day.[3] This is more cholesterol than you should make in an average day, so the monkey cannot downregulate cholesterol synthesis enough to compensate. Humans, with natural diets higher in cholesterol, can usually decrease absorption of cholesterol and increase excretion enough to tolerate such amounts. Indeed in some cases much larger amounts –  but these monkeys can’t.[4] However, the test monkeys were chosen for their response to saturated fat and cholesterol in the first place, they weren’t chosen at random from the monkey population. Monkeys that didn’t respond as desired were excluded from the study.[3] It’s not the saturated fat causing atherosclerosis, or these monkeys would only have needed to be fed saturated fat.

Here’s a question; what factor, if any, could possibly make a human as intolerant of fat as a cholesterol-fed monkey? Surely not fat itself, nor the minor amounts of cholesterol in the average human diet. How about the insulin response to refined carbohydrate? High refined carb diets cause heart disease in monkeys without any need to feed them cholesterol. This is the elephant in the room with the AHA. They do mention that replacing SFA with refined carbs is a bad idea (despite the AHA having recommended this substitution for many decades). You get the impression that they only think it’s bad because it has no effect, not because it’s harmful – more on this later.

Another cause of high cholesterol

In a 1991 cross-over trial, 147 non-obese normotensive subjects (60 females and 87 males) aged 19-78 were placed alternately on high-sodium and low sodium diets. The high sodium diet raised mean arterial blood pressure by a mean of 7.5 mmHg in 17% of the subjects (salt sensitive) – the low sodium diet raised mean arterial blood pressure by a mean of 6 mmHg in 16% (reverse reactors). With dietary salt restriction serum total- and LDL-cholesterol as well as serum insulin and uric acid concentrations increased significantly in all three groups. The largest increases in total (10%) and LDL- (12%) cholesterol occurred in the reverse reactors.[5]

So it would appear that the salt restriction advice the AHA has been giving generally for years, in the face of growing contradictory evidence, can raise cholesterol as much as eating butter can if taken to extremes. Again this is ignored.

Evidence that SFA is safe in low carb diets is cited but concealed

As an example of the AHA”s approach to evidence, consider the reference for this claim.

“Therefore, the effects of replacing carbohydrates with various kinds of fats qualitatively at least may be similar by increasing larger and decreasing smaller LDL sizes. In another study, monounsaturated fat, replacing carbohydrates, reduced medium and small LDL, also shifting the distribution to the larger size.78”

In the context in which it occurs, the statement is far from exciting, but the reference 78 is actually a very valuable experiment and one of the few that answers the question “what is the difference between high saturated fat and low saturated fat in a low carb diet?” This should be something that interests the AHA, but the blinkers mean they can only use this paper to buttress their own position on some minor point while ignoring the main outcomes from this research.

Ref 78 is a Ron Krauss paper in which a low fat diet (54% CHO) is compared with a moderate fat diet (39% CHO) and two low carb (26% CHO) diets, one with 15% SFA, one with 9% SFA. The diets are isocaloric, and the 15% SFA diet is superior to all other diets for four cardiometabolic results. Lower triglycerides, higher HDL, lower total cholesterol/HDL ratio, lower ApoB/ApoA1 ratio, larger LDL particle size.[6,7]

total C HDL

Now, the AHA is quite churlish about particle size. Maybe they’re right, maybe they’re wrong. However, every LDL particle only has one ApoB lipoprotein. The larger the particles, the less ApoB you have at any given LDL concentration. The ApoB/ApoA1 ratio (only slightly) favours the 15% SFA diet. Of course, 26% CHO is a little outside the upper edge of low carb, but this is the best evidence we have to show whether SFA in a low carb diet is a worry or not. The evidence says it’s not. In fact, what this study shows is that carbs are are mechanistic in causing poor lipid profiles as related to cardiometabolic health.

The evidence on carbohydrate

The AHA review also cites observational studies, including the Jakobsen et al and Farvid et al meta-analyses, in which a substitution analysis appears to show that replacing saturated fat with mostly linoleic acid is beneficial. The logic of this is impeccable – “because we can’t find the evidence that we wish existed, that saturated fat is independently associated with heart disease (which would suggest a causal relationship), we are going to compare it with the essential fatty acids, because that makes it look worse”. These studies are out of date because they do not include the two Praagman et al studies from last year, in the larger of which (n=35,597) replacing SFA with PUFA was associated with an increase in ischemic heart disease events.[8]

“Total SFA intake was associated with a lower IHD risk (HR per 5% of energy: 0.83; 95% CI: 0.74, 0.93). Substituting SFAs with animal protein, cis monounsaturated fatty acids, polyunsaturated fatty acids (PUFAs), or carbohydrates was significantly associated with higher IHD risks (HR per 5% of energy: 1.27-1.37).”

In the smaller (n=4,722) study there was no association.[9]

Even so, what do the substitution meta-analyses tell us? That every benefit, if there is a benefit, of replacing SFA with PUFA can also be achieved by replacing carbohydrate with PUFA. By carbohydrate is meant the total carbohydrate from the mixture of refined (flour, sugar) and unrefined (potato, fruit, whole grains, legumes) sources in the usual diet. The AHA fastens on this distinction – not made in the substitution metas – to tell us that replacing 5% of energy from saturated fat with 5% of energy from whole grains will produce some huge associational benefit.

If your diet was about 50% refined carbohydrate, as is normal in Western countries these days, you’d be looking to replace some of that with unrefined carbs, PUFA, MUFA, anything at all, rather than worrying about the 10-15% of saturated fat left in these diets!
Let’s look at this again – you have maybe 50% of energy from junk carbs to replace in the Standard Western Diet. You don’t need any of it – you can replace every last bit of it and only feel better for the effort.

On the other hand you have around 15% of saturated fat at most. Much of this is attached to whole foods – some of it is even in nuts, fish, and vegetable oils!
Priorities, people, priorities.

Even Harvard’s NHS/HPFS study, which has its issues but which the AHA relies on heavily here, predicts that replacing carbs (which includes some unrefined) with fat (which includes some saturated) will be associated with lower mortality, 0.84 (0.81-0.88) and cardiovascular mortality, 0.86 (0.79, 0.93).[10] Similarly, the Malmo Diet and Cancer Study found a significantly lower risk of CVD death (RR 0.65, p=0.028) in men eating the most fat, an average of 47%E.  “No deteriorating effects of high saturated fat intake were observed for either sex for any cause of death”.[11]

But supposing there is a benefit of PUFA? The Farvid meta-analysis predicted that “A 5% of energy increment in LA intake replacing energy from saturated fat intake was associated with a 9% lower risk of CHD events (RR, 0.91; 95% CI, 0.86-0.96) and a 13% lower risk of CHD deaths (RR, 0.87; 95% CI, 0.82-0.94).”[12] One good wholefood source of linoleic acid is nuts. According to a 2016 meta-analysis, just eating 28g of nuts per day was associated with greater decreases in mortality from coronary heart disease, 0.71 (95% CI: 0.63–0.80), cardiovascular disease, 0.79 (95% CI: 0.70–0.88), and all-cause mortality, 0.78 (95% CI: 0.72–0.84) than those predicted by Farvid et al for total PUFA.[13] We have this evidence that PUFA from nuts is beneficial, or at least not harmful. We don’t actually have the same evidence when it comes to PUFA from plant seed oils – no-one has looked at these specifically.

Coconut oil – the rush to judgement

When Ancel Keys chose his 7 countries to study from the 22 or 23 available, he chose Japan as an example of a country with a low fat intake and a low rate of heart disease; but he could have chosen Ceylon, very close to it on the graph, with a similar low rate of heart disease but 4x as much saturated fat as Japan, because the Ceylonese cooked with coconut oil.

As an aside, a recent cohort of 58,472 Japanese followed up 19 years with 11,656 deaths showed that Japanese women with the highest saturated fat intake, and higher total fat intake had lower mortality rates. So, for what is worth, there is some associational evidence that more fat could be protective in the Japanese population.[14]

We don’t know a lot more about coconut oil today than we did in Ancel Key’s day, but the AHA thinks that its effect on serum lipids warrants avoiding it. That makes sense in a country where having higher cholesterol increases the risk of being prescribed unnecessary drugs or having your insurance premiums raised. Viewed in that context, coconut oil could be truly hazardous to your health.

Most of the health claims made for coconut oil can’t be substantiated, because the research hasn’t been done. An exception is this recent paper, which shows that a meal high in coconut oil had a more favourable effect on postprandial lipids than either palm oil or rice bran oil.[15] It’s also interesting because it shows that higher insulin and a higher fasting TG/HDL ratio (1.8 vs 1.1) is associated with an adverse response to palm oil. We’d interpret this as meaning that carbohydrate intolerance (the meal supplied an OGTT dose of refined carbs) drives fat intolerance, as we would expect from the interaction between carbohydrate, insulin, and palmitic acid discussed here.
Another benefit of using coconut oil for meals such as stir fries is that it is much less likely than plant seed oils to produce carcinogenic fumes. Lung cancer risk is greatly increased in non-smokers exposed to heated seed oils in poorly ventilated kitchens, as we discussed here.

The Dog in the Manger

One of the defects of the modern “Presidential” personality type, as we mentioned in the introduction, is that every innocuous question is treated with a partisan bias. Nowhere is this more evident than in the handling of trans fats.

Industrial trans fats probably increase heart disease risk, more by their effect on the metabolism of omega-3 and -6 fatty acids and how this affects blood clotting and inflammation than by any effect on lipids or basic metabolism.

Fact – people were only exposed to industrial trans fats because animal fats were replaced with vegetable fats.

There are also trans fats in dairy – ruminant trans fats. These, as far as we can tell, are associated with better health not worse

The AHA really wants (you) to believe that the effects of ruminant trans fats are similar to those of industrial trans fats.

“Although most human trials were conducted with partially hydrogenated vegetable oil, emerging evidence suggest the ruminant trans fatty acids have similar adverse effects on blood lipids…Although industrial trans fatty acids were consistently associated with total CHD and CHD death in observational studies, ruminant trans fatty acids were generally not. The exact reason for these discrepant relationships remains unknown but may relate to the very low levels of ruminant trans fatty acids in these studied populations (mean intake, ≈0.7% of total energy),112 differences in trans fatty acid isomers between ruminant and industrial trans fatty acids that have diverse biological effects, or confounding by the high amount of saturated fat in the major source of ruminant trans fatty acids.”

Firstly, ruminant trans fats (present in both dripping and dairy fat at around 3%) are products of the fermentation of plants by bacteria. Does anyone still believe that such fermentation is bad for the heart? The dominant ruminant trans fat, CLA, is a cis-trans fat. The cis bond means that it cannot behave like an industrial trans fat in cell membranes. The metabolism of CLA in vivo involves elongation and further desaturation similar to that seen with long-chain polyunsaturates.

The “emerging evidence” that the AHA alludes to involves feeding doses of ruminant trans fats higher than those sourced from diet in supplement form, without their accompanying fats. This is a critical point; the myristic acid in ruminant fats raises the most beneficial forms of HDL, but the benefit of HDL depends on its functionality. Ruminant trans fats by themselves increase HDL functionality, but not mature HDL.[16] The similar benefit of olive oil and red wine polyphenols may also depend on their inclusion in foods that raise HDL.[17] Whole foods beat supplements and refined foods every time.

Interventions in Children

The AHA review mentions a number of intensive healthy-lifestyle interventions in children that reduced saturated fat, always in the context of many other changes including reduced sugar, and had positive effects on various proxies for heart disease risk. We concur that healthy diet and lifestyle choices can overall reduce heart disease risk. What we don’t know is whether saturated fat intake from good-quality sources needs to be restricted to produce these benefits, and whether greater benefits will not in fact follow from a higher fat, lower refined carbohydrate diet that minimises insulin exposure after meals. The least-confounded RCTs of saturated fat reduction suggest that it contributes little if any benefit in adults, and the evidence that specifically relates to low fat vs whole milk, and to fat content overall in the diet of children (including breast-feeding infants, which eliminates reverse causality), suggests that lower fat foods and diets in the general population are associated with higher childhood BMI and therefore greater future cardiovascular risk.[18-23]

Summing up

The recommendation to eat less than 30% of energy as fat, applied to a population with easy access to refined carbohydrates, as promoted by the AHA (which did promote the use of sugar and flour in place of naturally fatty foods for many years) may have increased fat intolerance in the population, mostly with regard to specific saturated fats, mainly palmitic acid.[24] This intolerance, because it is driven by insulin, seems to go away when carbohydrate is restricted. It may also go away to some extent when genuinely unrefined carbohydrate replaces refined starch and sugar, due to the lower insulin AUC.

It would literally take a PhD thesis to fully dissect the AHA presidential advisory and its errors of interpretation and expressions of bias. We’ve only dipped into the areas we already know about, and found the AHA trying to pull a fast one. Which is not to say that every statement or idea in the document is false, but that half the story is hidden in darkness. The public needs bodies like the AHA to adjudicate fairly, not act like a prosecutor for one cause then a defense attorney for another. The AHA’s diet advice may be taken with a grain of salt by many in the know who can afford to ignore it, but not by those fed in institutions or by government programs, and the AHA’s stated positions also influence drug prescribing. If the AHA can’t balance the evidence wisely, and step well beyond the bias of defending their previous assumptions that a high carb, low fat diet low in saturated fat is best for all, we’re in trouble.



[1] Sacks FM, Lichtenstein AH, Wu JHY et al. Dietary Fats and Cardiovascular Disease: A Presidential Advisory From the American Heart Association. 

[2] 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. Nutrition Journal. 2017; 16:30 DOI: 10.1186/s12937-017-0254-5

[3] Rudel LL, Parks JS, Sawyer JK. Compared with dietary monounsaturated and saturated fat, polyunsaturated fat protects African green monkeys from coronary artery atherosclerosis. Arterioscler Thromb Vasc Biol. 1995;15:2101–2110.

[4] Kern F. Normal Plasma Cholesterol in an 88-Year-Old Man Who Eats 25 Eggs a Day — Mechanisms of Adaptation. N Engl J Med. 1991; 324:896-899. DOI: 10.1056/NEJM199103283241306

[5] Ruppert M, Diehl J, Kolloch R et al. Short-term dietary sodium restriction increases serum lipids and insulin in salt-sensitive and salt-resistant normotensive adults. Klin Wochenschr. 1991;69 Suppl 25:51-7.

[6] Krauss RM, Blanche PJ, Rawlings RS, Fernstrom HS, Williams PT.
Separate effects of reduced carbohydrate intake and weight loss on atherogenic dyslipidemia [published correction appears in Am J Clin Nutr. 2006;84:668]. Am J Clin Nutr. 2006;83:1025–1031; quiz 1205.

[7] Feinman RD, Volek JS. Low carbohydrate diets improve atherogenic dyslipidemia even in the absence of weight loss. Nutrition & Metabolism. 2006; 3:24 DOI: 10.1186/1743-7075-3-24

[8] Praagman J, Beulens JW, Alssema M et al. The association between dietary saturated fatty acids and ischemic heart disease depends on the type and source of fatty acid in the European Prospective Investigation into Cancer and Nutrition-Netherlands cohort.Am J Clin Nutr. 2016; 103(2): 356-365.

[9]Praagman J, de Jonge EAL, Kiefte-de Jong JC et al. Dietary Saturated Fatty Acids and Coronary Heart Disease Risk in a Dutch Middle-Aged and Elderly Population.

[10] Wang DD, Li Y, Chiuve SE, Stampfer MJ, Manson JE, Rimm EB, Willett WC, Hu FB. Association of Specific Dietary Fats With Total and Cause-Specific Mortality. JAMA Intern Med. 2016;176(8):1134-1145. doi:10.1001/jamainternmed.2016.2417.

[11] Leosdottir M, Nilsson PM, Nilsson JA, Månsson H, Berglund G. Dietary fat intake and early mortality patterns–data from The Malmö Diet and Cancer Study. J Intern Med. 2005 Aug;258(2):153-65.

[12 Farvid MS, Ding M, Pan A et al. Dietary Linoleic Acid and Risk of Coronary Heart Disease: A Systematic Review and Meta-Analysis of Prospective Cohort Studies.

[13] Aune D, Keum N, Giovannucci E et al. Nut consumption and risk of cardiovascular disease, total cancer, all-cause and cause-specific mortality: a systematic review and dose-response meta-analysis of prospective studies. BMC Medicine. 2016; 14:207
DOI: 10.1186/s12916-016-0730-3

[14] Wakai K, Naito M, Date C, Iso H, Tamakoshi A. Dietary intakes of fat and total mortality among Japanese populations with a low fat intake: the Japan Collaborative Cohort (JACC) Study. Nutrition & Metabolism. 2014;11:12. doi:10.1186/1743-7075-11-12.

[15] Irawati D, Mamo JCL, Slivkoff-Clark KM et al. Dietary fat and physiological determinants of plasma chylomicron remnant homoeostasis in normolipidaemic subjects: insight into atherogenic risk. British Journal of Nutrition (2017), 117, 403–412. doi:10.1017/S0007114517000150

[16] Nicod N, Parker RS, Giordano E et al. Isomer-specific effects of conjugated linoleic acid on HDL functionality associated with reverse cholesterol transport. J Nutr Biochem. 2015 Feb;26(2):165-72. doi: 10.1016/j.jnutbio.2014.10.002. Epub 2014 Nov 12.

[17] Nicod N et al. Green tea, cocoa, and red wine polyphenols moderately modulate intestinal inflammation and do not increase high-density lipoprotein (HDL) production. J Agric Food Chem. 2014; 62(10):2228-32. doi: 10.1021/jf500348u. Epub 2014 Mar 4.

[18] Prentice P, Ong KK, Schoemaker MH, et al. Breast milk nutrient content and infancy growth. Acta Paediatrica (Oslo, Norway : 1992). 2016;105(6):641-647. doi:10.1111/apa.13362.

[19] Vanderhout SM, Birken CS, Parkin PC, Lebovic G, Chen Y, O’Connor DL, Maguire JL; TARGet Kids! Collaboration. Relation between milkfat percentage, vitamin D, and BMI z score in early childhood. Am J Clin Nutr 2016;104:1657–64.

[20] Rolland-Cachera MF, Maillot M, Deheeger M, Souberbielle JC, Peneau S, Hercberg S. Association of nutrition in early life with body fat and serum leptin at adult age. Int J Obes (Lond) 2013;37:1116–22.

[21] Alexy U, Sichert-Hellert W, Kersting M, Schultze-Pawlitschko V. Pattern of long-term fat intake and BMI during childhood and adolescence—results of the DONALD study. Int J Obesity Relat Metab Dis. 2004;28: 1203–9.

[22] Gunnell DJ, Frankel SJ, Nanchahal K, et al. 1998. Childhood obesity and adult cardiovascular mortality: a 57-year follow-up study based on the Boyd Orr cohort. American Journal of Clinical Nutrition 67: 1111–18.

[23] Ness AR, Maynard M, Frankel S, et al. Diet in childhood and adult cardiovascular and all cause mortality: the Boyd Orr cohort. Heart. 2005;91(7):894-898. doi:10.1136/hrt.2004.043489.

[24] Kuipers RS, de Graaf DJ, Luxwolda MF et al. Saturated fat, carbohydrates and cardiovascular disease. Neth J Med. 2011 Sep;69(9):372-8.

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