The Empire Strikes Back – American Heart Association gets Presidential on Saturated Fats.

These days most people associate the word “Presidential” with a lot of bluster that tends to disguise real problems and do more harm than good, as well as a partisan approach to any question. In the US at least, being “presidential” means a pathological inability to admit error, and a cavalier approach to the evidence and the scientific method.

The question is whether this trait is moving elsewhere?  We’d say that these vices are on full display in the new American Heart Association (AHA) position statement on saturated fat and cardiovascular disease.[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 deaths. This is the only SFA-replacement study with a significant reduction in all-cause mortality in the intervention arm, which may be why the AHA choose to revive it. But any two hospital populations can experience different death rates regardless of diet. 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.


  1. So much work to dissect a document that should never have been published in the first place. Hat tip to you sir!

  2. Dr Chris Leathart · · Reply

    Thank you for your excellent dissection of the latest “presidential” advice from the AHA.
    I have had a look at the article “Dietary Fats and Cardiovascular Disease: A Presidential Advisory From the American Heart Association” that you refer to. It makes your head spin! Thats’s because it IS so full of spin.
    This is just the latest learned looking article attempting to prop up the Diet Heart Hypothesis. The fact that it is from the AHA and the lead author is Frank Sacks MD, Professor of Cardiovascular Disease Prevention at the Harvard School of Public Health make it appear to be authoritative. But is actually a blatant example of pseudoscience. It is dogma and because it is from such a prestigious source it seems unassailable.
    Pseudoscience has many definitions, but essentially it starts with a hypothesis that seems credible and is emotionally appealing. Then you only look for evidence that supports it and ignore evidence that refutes it. The supporters of the Diet Heart Hypothesis do just that. This puts them in the same league as climate deniers, intelligent design creationists, astrologers, UFOlogists, parapsychologists and practitioners of alternative medicine. Like most promulgators of pseudoscience they are too invested in their views to ever admit they may be wrong. We will have to wait for the current generation of Diet Heart Hypothesis supporters to retire and die off before we will ever see more a scientific and evidence based approach to dietary advice coming from institutions such as the AHA.

    I am a GP and at the coal face of practicing medicine. Over the years I have become very skeptical of dogma. So I have spent a lot of time reading up about nutrition and it relationship to health.
    I have come to the conclusion that spending so much time and effort identifying those with high cholesterol and giving them advice on a “healthy” low fat diet is mostly a waste of time with comes with a huge opportunity cost.
    What we should be doing is making efforts to identify those who fit the criteria for metabolic syndrome. Metabolic syndrome is strongly linked to an increased risk of cardiovascular disease and type 2 diabetes.
    Total cholesterol and LDL levels do not feature in the criteria for diagnosing metabolic syndrome. Instead high triglycerides and low HDL are the markers along with obesity, hypertension and elevated blood glucose. The cause of metabolic syndrome is not yet proven but the work of Dr Robert Lustig is, I believe, pointing us in the right direction. He has done work which shows that excess fructose ( a 50% component of table sugar/sucrose) in the diet leads to high triglycerides. Triglycerides and HDL have an inverse relationship so when triglycerides are high, the HDL is usually low. The glucose that comes with the fructose causes high insulin levels which in turn leads to storage of calories as fat leading to obesity, and elevates blood pressure. High triglycerides have been shown to interfere with insulin signalling and contribute to insulin resistance, with consequent elevation of blood glucose and then type 2 diabetes. Fructose is a metabolic poison but a very slow acting one.
    Excessive alcohol is also a cause of high triglycerides but in my practice I have found that patients with high triglycerides rarely have excessive alcohol intake, but readily admit to high sugar intake.
    So my advice to my patients with metabolic syndrome is to drastically cut down on sugar consumption. Increasing exercise is also helpful as it increases muscle mass and therefore increases the number of mitochondria to help burn off the excess glucose.
    There are many diets to choose from, but the diets associated with lower risk of CVD all share the feature that they are low sugar diets.

    Sugar is the new cholesterol and needs the spotlight of good science shining on it.

    1. It’s a curious thing Chris, but people with high cholesterol who go on the LCHF diet often tell us their LDL has gone down, even though they are likely to be eating more saturated fat. This is not universal, but it seems to apply more to those people who are overweight or have other risk factors for CVD, whereas lean, healthy, low risk individuals might see it go up.
      This is just an impression, mind you, not a statistical survey, but I think it can be explained – in someone with hyperinsulinaemia LDL can be high because insulin drives cholesterol synthesis and cholesterol in the liver downregulates LDL receptors. So the inhibition of cholesterol synthesis by statins upregulates LDL receptors and lowers serum LDL, and lowering insulin has the same effect in these cases. Something like that anyway – so the story is more complex than the AHA thinks; in Framingham, cholesterol didn’t correlate with saturated fat.
      The story of the monkeys shows that free access to sugar can cause heart disease, whereas it takes unnatural levels of dietary cholesterol to make fat atherogenic in animals.

      1. chris c · ·

        Anecdotally, but N=thousands, HDL generally increases often spectacularly on LCHF and trigs generally plunge equally spectacularly. When this fails to happen in trials IMNSHO it’s an indicator that the trials have not been done properly.

        LDL may increase, decrease, or stay the same. Mine initially increased, then went back down by exactly the same amount that HDL increased, with the addition of more saturated fat. Pretty sure I’ve seen evidence of this in GENUINE low carb diets. However another explanation, for which I’ve also seen evidence, is that LDL increases during active weight loss, and decreases again when weight restabilises, when the fat is body stores rather than dietary in origin.

        There’s a funky paper by Krauss that shows different pathways, AFAICR controlled by different genes, are responsible for generating the different sized LDL particles. This made me ponder why we would have a number of different pathways to much the same outcome. My thought was that it was to enable the pathways to be run in parallel when large quantities of LDL were required, probably for nutrient transport, either dietary or body fat, and from an evolutionary point of view it wouldn’t matter much if some of the LDLs were a bit wonky since they wouldn’t stay in the bloodstream long enough to do any harm – UNLESS you were eating a high carb diet and getting most of your energy from glucose, and whacking up your insulin levels to where fat metabolism is impeded.

        Until the ongoing work by Dave Keto

        I had no idea (and I suspect nor did many other people) just how much and how quickly LDL responded to dietary changes.

        There seems to be a pattern emerging here, no?

      2. Here’s a classic paper which thoroughly debunks both the coconut oil and the monkey lines of thought in the AHA paper

        Relative Failure of Saturated Fat in the Diet to Produce Atherosclerosis in the Rabbit
        By William E. Connor, M.D., Jay J. Rohwedder, M.D.,and Mark L. Armstrong, M.D.

        Three “saturated” fats of vegetable origin were fed to different groups of
        rabbits for periods up to 1 year. Cocoa butter and a hydrogenated vegetable
        oil shortening produced no hypercholesterolemia. Coconut oil feeding increased
        the serum cholesterol concentrations for 4 months, but a decline to baseline
        values occurred after 6 months. No gross atherosclerosis occurred in any animal
        fed coconut oil or the hydrogenated vegetable oil shortening. Slight atherosclerotic
        lesions were found in 50% of the rabbits fed cocoa butter. Aortic
        cholesterol content was slightly increased in animals fed coconut oil and
        cocoa butter. Dietary fats, even when highly saturated, had only a minimal
        capacity to produce atherosclerosis in the rabbit, a species usually highly
        susceptible to the induction of atherosclerosis. When a moderate amount of
        cholesterol was added to the diet, the serum cholesterol levels increased greatly
        and considerable atherosclerosis resulted.

        So the cocoa butter, which produced some lesions in 50% of animals, is the fat that’s high in palmitic and stearic acid, as well as oleic acid, and all of these are products of carbohydrate metabolism. The (partially) hydrogenated vegetable oil wasn’t atherogenic – this stuff isn’t toxic because it raises cholesterol but because it interferes with blood clotting, inflammatory catabasis, and so on. It causes heart attacks but may not be a driver of atherosclerosis per se (similarly omega-3 fats do the opposite).
        And the coconut oil raises cholesterol, in the very sensitive rabbit model, for no longer than 6 months before it returns to normal. The AHA coconut oil warning is based on very short term feeding studies.

        Coconut oil does induce hypercholesterolemia in
        man (16). The periods of feeding have usually
        been 60 days or less, so that there is the
        possibility that even man might eventually
        adapt to coconut oil feeding

        As with Rudel’s monkeys, fats only became atherogenic in the presence of added cholesterol – something which mimics an effect of hyperinsulinaemia in humans (consistent with stearate and palmitate combos being most atherogenic here). And the corn oil plus cholesterol combo greatly elevated cholesterol in the liver – as we would expect given that 12.5% of the carbon from linoleic acid, but none from SFAs, is converted to sterols in the liver.

        Fat wasn’t fattening, either;

        Animals fed these different saturated-fat
        diets were healthy and active for the duration
        of the experiment. Their fur remained in
        good condition. Weight gain occurred steadily
        in all animals; adiposity was’ found at
        autopsy. For example, animals fed cocoa butter
        gained a mean weight of 1,017 g over the
        12-month period of feeding. The control rabbits
        fed only chow without added fat had a
        similar mean weight gain of 997 g.

        There’s a recent paper on SGLT2 inhibitors, which are ketogenic, reduce CVD deaths (mostly heart failure) but increase LDL levels, which says that this increase in LDL is a sign of a shift to higher fat oxidation. Similarly with HDL, I suppose if you’re burning fat in place of glucose you need more of the fat support crew in the blood stream, and you’ll need reverse cholesterol transport increased with less glucose/insulin, which for some reason signals an increase in whole-body cholesterol (never mind the serum levels, also consider the cellular and hepatic content).

  3. chris c · · Reply

    Look, it’s obvious! Low fat diets based on “vegetable” oils reduce CVD. This is a Known Fact and must never again be questioned. The proof is that CVD has gone down while everyone eats low fat. We must stop diets based on science and other fads.

    So how has obesity, diabetes etc. increased so dramatically?

    Look, it’s obvious! No-one is actually eating low fat diets.

    oh . . . wait . . . (fx. sound of brain imploding)

  4. Steve Hamley, who is an expert on meta-analysis of diet heart RCTs, has made the following point about the “core studies” in his review of the AHA paper

    While the high PUFA group in LAVAT and FMHS had a lower risk of CHD and CVD mortality (RR = 0.80 and 0.59), they had a near identical risk of total mortality (RR = 0.98 and 1.01), because non-CHD/CVD mortality was higher [8] [26]. As those trials were both many times larger than ODHS and MRCT, and therefore have a much larger weighting, the pooled RR of the AHA’s core trials for total mortality is 0.98 (CI = 0.90-1.07, P = 0.65).

    So will replacing SFA with PUFA reduce your risk of dying? Even with the AHA’s selection of trials and even while ignoring the major issues in LAVAT, ODHS and FMHS, the answer is still no.

  5. chris c · · Reply

    Like statins, it may marginally change what you die from, but not when.

    I just LOVE these old studies you and others are digging out. So much information which was once known and then ignored – and is now being rediscovered by even more modern researchers.

    I typoed unformation just then, on reflection I think it should become a valid word.

  6. Warrick · · Reply

    Picking up your reference 5 (salt reduction) – I noted “These results do not support a general recommendation to reduce sodium intake.” 1998 review. And even the 2017 Cochrane review suggests very limited blood pressure effect but a significant increase in cholesterol and triglycerides.
    I noted with interest that sodium restriction increased uric acid (ref 5 above). Gout is reasonably commonly associated with diabetes – yet US dietary guidelines recommend sodium restriction for diabetics. provides an interesting hypothesis on the uric acid/sodium link with hypertension.

    1. Thanks for those references Warwick. Sodium restriction seems to be most strongly associated with CVD in type 2 diabetes, and those mechanisms help explain why.
      Sodium restriction raises LDL, yet the AHA recommends it. Carbohydrate restriction tends to lower LDL in the obese and diabetic – that is, in those individuals at highest risk of heart attacks – but can elevate it in healthy lean people. The AHA does not recommend it. Long-term fasting lowers LDL in obese and diabetics but strongly elevates it in healthy lean individuals. Anorexia is associated with very high LDL cholesterol.
      A question – has anyone ever suggested that atherosclerosis is caused by under-eating?
      I thought not.

      1. chris c · ·

        Likewise has anyone suggested hyperthyroid as a valid LDL-lowering intervention? I thought not either, though IME it works as well as a statin – yet “strangely” when my thyroid is most overractive and my LDL at its lowest is when my leg arteries become blocked up.

        I can recall a now long-retired doctor saying that whenever he saw high “cholesterol” he suspected hypothyroid and ordered a TSH, but then this stopped being related – obviously when metabolic syndrome/IR became so common.

        Increasingly I’m seeing “lipid panels” as indicators of other processes at work, and for personal/familial reasons I look at insulin levels and IR.

        It’s like the computer in my car which shows me fuel consumption in the moment, and a rolling average. My previous car (Renault) was most economical between 1500 – 2500 rpm. This one (Nissan with essentially the same Renault engine, only tuned differently) is most economical between 1200 – 2000 rpm. It will pull like a train from 1000 rpm and spin away to 2500 but at both ends the fuel usage ticks up sharply. Hey look, a metabolic advantage – a VW I had briefly was hard pressed to make 50 mpg, the Renault did over 60, the Nissan is bigger and heavier with much more performance but still averages over 56. The computer only feeds me information though, I use the information to choose what revs and in which gear.

        Likewise I see the lipids as providing information – high trigs = excess carbs, especially fructose, high HDL = suitable fat consumption in the excess of the carbs, LDL = not really an indicator of anything much of interest *for me* though it might be if I was APO E3 or 4.

        The whole field makes me think of a crime movie where the FBI have “cholesterol” under 24 hour surveillance while insulin and its gang are going round completely unobserved creating mayhem.

      2. That last bit made me laugh!
        Dr Bernstein recommends using thyroxine supplementation to correct high LDL, which might make sense in type 1 where other mechanisms are not available, but in terms of low carbers in general T3 will be decreased and some replaced with rT3 in some – because T3 just isn’t needed as much with lower carb intakes. In fact Kopp has a hypothesis about this –

        “An increased iodine requirement as a result of significant changes in human nutrition rather than a decreased environmental iodine supply is suggested to represent the main cause of the iodine deficiency disorders (IDD). The pathomechanism proposed is based on the fact that serum concentrations of thyroid hormones, especially of trijodothyronine (T3), are dependent on the amount of dietary carbohydrate. High-carbohydrate diets are associated with significantly higher serum T3 concentrations, compared with very low-carbohydrate diets. While our Paleolithic ancestors subsisted on a very low carbohydrate/high protein diet, the agricultural revolution about 10,000 years ago brought about a significant increase in dietary carbohydrate. These nutritional changes have increased T3 levels significantly. Higher T3 levels are associated with an enhanced T3 production and an increased iodine requirement. The higher iodine requirement exceeds the availability of iodine from environmental sources in many regions of the world, resulting in the development of IDD.”

        Things get even more interesting when we see that IGF-1 lowers LDL in hypothyroidism

        Of course lower exposure to IGF-1 is one of those things that is supposed to be beneficial for longevity…

  7. chris c · · Reply

    Ooh! Fascinating how it all ties in together. I thought the iodine, and selenium, were related to the T3/T4 conversion which seems to be broken in many hypothyroids.

    My T3 and T4 (I managed to get both tested, not always available) seem to track the inverse of TSH closely, so more tests I no longer bother with. Allegedly my hyperthyroid is Graves – autoimmune and unrelated to diet, same as what happened to my father, but hypothyroid is the one that has really taken off on the same timescale as HCLF. Yet again insulin is there behind the curtain.

    I would be VERY careful manipulating thyroid out of range, neither end is pleasant. AFAICR I started with TSH of 0.001something (whenever tested in the past it was always around 1) with T4 over 40 and T3 over 14: then every so often the thyroid spikes and I have to increase the carbimazole, after which it often suddenly rebounds low – TSH shot up to 44, then it returns to normal on my usual dose. All started after about ten years of LCHF and presumed low IR and normalised insulin – which I seriously wish I could get tested. I suspect a pocket insulin meter would be a very useful gadget in so many diseases, probably why it hasn’t been invented yet.

    ps/ I suspect coconut oil is one of the culprits in blocking my kitchen sink drain – at room temperature, if your arteries are at room temperature you have bigger problems than “cholesterol”. On the other hand do not even TRY to find out what happens when you put “Heart-Healthy” oatmeal down the drain . . .

    . . . now to dig out the drain rods, then go for a walk now my thyroid is relatively normal again, followed by liver and bacon with mushrooms and runner beans with EVOO and butter. Probably the only “meal” I’ll have all day, apart from a small breakfast and maybe a late snack I spend most of my time running on stored energy/ketones/fat. Those AHA guys would have a heart attack if they knew. So would their sponsors.

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Richard David Feinman

Richard Feinman, the Other

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