This is a good little watch. Last month I sat down with Todd Scott CEO of the National Business Review, and Chris Keall also at NBR. Chris had let his weight get away on him and needed to front up to this. Todd was in pretty good shape, but is always aiming to be a high performer. He was looking at a reset to be in his best possible shape.
So they took on a fasting challenge following our “super fasting” protocol in What the Fast?
Here’s the full article and video here, it’s a great little video of the outcomes 4 weeks later …some great men’s weight loss results for both Todd and Chris, as well as some interesting mental health (including medication reduction) outcomes for Todd.
Cardiovascular Disease Risk Assessment and Management for Primary Care.
Its the same stuff – saturated fat is bad for you. Avoid it, and replace it with polyunsaturated and monounsaturated fats
But hang on minute, is this still the best advice you have? And will it really prevent people getting cardiovascular disease?
The advice to limit saturated fat misses more important effects?
We think there are a few holes in the argument. Or at least we aren’t getting the full story.
“Substituting dietary saturated fat with mono and polyunsaturated fats is the most effective dietary approach to reducing low-density lipoprotein cholesterol (LDL-C) while maintaining or increasing high-density lipoprotein cholesterol (HDL-C).”
But we think this misses the mark – polyunsaturated and mono-unsaturated fats lower LDL because of their effect on the LDL-receptor and on ApoB catabolism. But they only raise HDL when substituted for carbohydrate, because they are fats, and fats in general stimulate the release of ApoA1, the seed of HDL, from gut and liver cells.
A high intake of linoleic acid lowered LDL and raised HDL when it was added to the baseline fat intake (e.g. replaced carbohydrate in the diet), but lowered both LDL and HDL when it replaced saturated fat.
This might seem to be picking on the details, but we think it is important. As it stands above replacing saturated fats isn’t the most effective way of changing the fats in your diet to improve your chances of avoiding clogged arteries.
We think better advice might to be to replace the carbs your eat with fats from minimally processed foods.
The classic feeding study meta-analysis of Mensink et al. makes clear the benefits of replacing carbohydrate with various fats. This is worth quoting at length.
The cis MUFAs had a modest but significant LDL cholesterol–lowering effect relative to carbohydrates. All 3 classes of fatty acids increased HDL cholesterol relative to carbohydrates. Unsaturated fatty acids increased HDL cholesterol less than did SFAs. As a result, the replacement of 1% of energy in the form of SFAs with an equal percentage in the form of cis MUFAs is predicted to lower HDL-cholesterol concentrations by 0.002 mmol/L. A similar decrease is expected when 1% of energy in the form of MUFAs is replaced with an equal percentage in the form of PUFAs. These effects, however, are small compared with those of replacement of carbohydrates with any of the 3 classes of fatty acids. Replacement of carbohydrates with any class of fatty acids decreased fasting serum TG concentrations (Table 1). The effect was slightly but not significantly larger for PUFAs than for other fatty acids. This contrasts with the powerful TG-lowering effect of n−3 PUFAs from fish, which is evidently not shared by linoleic acid, the major n−6 PUFA. Replacement of carbohydrates with SFAs did not change apo B concentrations. The cis unsaturated fatty acids, however, decreased apo B, and this effect was slightly stronger for PUFAs. SFAs and MUFAs increased apo A-I concentrations relative to carbohydrates. PUFAs did not significantly change apo A-I concentrations.
In other words, all benefits expected in terms of increasing unsaturated fats are seen when fat replaces carbohydrate, and this has the additional benefit of decreasing triglycerides – it’s better for the TG/HDL ratio. We explained how this effect plays out in terms of ApoB and ApoA1, even if saturated fat increases, in an earlier blog.
The substitution meta-analysis of Farvid et al makes it clear that a similar effect – an association with risk here, not just risk markers – is even seen in prospective cohort studies, confounded though those are.
“9 cohort studies evaluated substitution of LA for carbohydrate showed that substituting 5% energy intake from LA for carbohydrates lowered risk with about 10%. A slightly lower risk benefit was seen for substitution of LA for SFA.”
So if it’s better, or at least not worse, to replace carbs with unsaturated fats and leave saturated fats as they were, why isn’t this offered as advice?
The most at risk benefit the least from current advice
The problem with the existing advice is is, that even the expected effects of replacing SFA with unsaturated fats are unlikely to be seen if you are overweight or insulin resistant. The studies being relied on for guidelines are based, overall, on healthy volunteers – unfortunately for people depending on these results, insulin sensitive people are at very low risk of CVD, and LDL has little correlation with their risk, but the opposite is true for the insulin-resistant.
Design: A randomized, double-blind, 3-period crossover controlled feeding design was used to examine the effects on plasma lipids of 3 diets that differed in total fat: the AAD [designed to contain 38% fat and 14% saturated fatty acids (SFAs)], the Step I diet (30% fat with 9% SFAs), and the Step II diet (25% fat with 6% SFAs). The diets were fed for 6 wk each to 86 free-living, healthy men aged 22–64 y at levels designed to maintain weight.
Results: Compared with the AAD, the Step I and Step II diets lowered LDL cholesterol by 6.8% and 11.7%, lowered HDL cholesterol by 7.5% and 11.2%, and raised triacylglycerols by 14.3% and 16.2%, respectively. The Step II diet response showed significant positive correlations between changes in both LDL cholesterol and the ratio of total to HDL cholesterol and baseline percentage body fat, body mass index, and insulin. These associations were largely due to smaller reductions in LDL cholesterol with increasing percentage body fat, body mass index, or insulin concentrations. Subdivision of the study population showed that the participants in the upper one-half of fasting insulin concentrations averaged only 57% of the reduction in LDL cholesterol with the Step II diet of the participants in the lower half.
Whereas the drops in HDL and rise in TG (from the stepwise reductions in fat and replacement with carbs) probably cancelled out any benefit from lower LDL in responders here, the most IR subjects weren’t even getting the benefit of lower LDL! That’s where a low carb approach to lipid management would have come in handy – if insulin and body fat % became lower, these subjects would experience a greater response to any PUFAs and MUFAs in their diet.
What is LDL anyway?
The LDL-cholesterol (LDL-C) in a standard lipid panel is just a calculated proxy for ApoB. On a low carb diet, with low TGs, you’ll start to get discordance between LDL-C and ApoB. That is, sometimes the LDL-C count can go up even when there’s a reduction in ApoB; this is because the ApoB particles become larger and less atherogenic. We see this in the Virta Health type 2 diabetes study – there’s a 9% rise in LDL cholesterol but ApoB has decreased non-significantly, LDL-P (the actual number of LDL particles) has decreased, small LDL-P (the actual number of the most atherogenic type of LDL particle) has decreased massively, and of course everything else has improved.
Curiously, triglycerides are only mentioned in the new guidelines as a risk factor for pancreatitis, which is one pathway to diabetes, and not as a CVD risk factor (and the cut off here is 11 mmol/L. Wow). We’re not sure why this is. Has the new shift to non-fasting tests made it impossible to use the old risk calculations, which clearly defined risk in terms of LDL, TG, and HDL? Is there an assumption that because everyone in NZ should be eating a high carb diet, there is no point giving advice to lower TGs? It’s a mystery. TGs (with more reasonable cut-offs) are still a risk factor for people with LDL controlled by statins.
Triglycerides are important
Here’s a rare, good quality study (n= 3590) from the Framingham Offspring Cohort that actually looked at risk based on all 3 lipid measures, in a population not taking any lipid-lowering drugs. The high/low cut of for HDL was 40 mg/dL for men and 50 mg/dL for women, which some labs will tell you is still too low (we can do better !). The lowest TG cut-off of 100 mg/dL is also a bit high (again, we can do better !) – the 2 cut-offs combined give a TG/HDL ratio of 2.5 for men and 2 for women, whereas the insulin-sensitive groupings in other studies tend to have a mean TG/HDL ratio of ~1.1 (consistent with LDL particle size in people with type 2 diabetes improving below a TG/HDL ratio of 1.5).
Even so, you can see that if HDL is high and TG low, risk is low, and any difference in the LDL level has little effect. Note that this population wasn’t screened for familial hypercholesterolaemia genes, which would have impacted risk across all higher LDL categories.
Statins – good for some?
When statins (okay we will wade into this just a little) are prescribed in secondary prevention (i.e. after a heart attack), they are very effective in preventing a second event in the most insulin-resistant people, calculated by the TG/HDL ratio. The NNT (number needed to treat) over 6 years in the IR group in the 4S study was 6, which is amazingly good – but statins didn’t really make much difference to the most insulin-sensitive, who are at an almost equally low risk if taking a placebo – their NNT in 4S was 36.
Remember, these insulin sensitive cases, who don’t seem to benefit much from LDL lowering, are also the ones likely to see the biggest LDL drop if they replace saturated fats with unsaturated fats (it’s the opposite with statins, so the insulin-sensitive people below were actually on a higher statin dose to get the same LDL reduction – so much for extrapolating between diet and drug effects).
Age increases risk?
It’s also worth questioning the use of age as a continuous variable in risk calculations. Of course your risk of dying from any disease goes up as you age, but trials of statins in elderly populations for primary prevention are few, and include 1) the ALLHAT open-label trial where statin use was not beneficial in a post-hoc analysis of the elderly patients (n=2867): this was a rare trial not funded by industry and came closest to a real-world model of prescribing.
The hazard ratios for all-cause mortality in the pravastatin group vs the UC group were 1.18 (95% CI, 0.97-1.42; P = .09) for all adults 65 years and older, 1.08 (95% CI, 0.85-1.37; P = .55) for adults aged 65 to 74 years, and 1.34 (95% CI, 0.98-1.84; P = .07) for adults 75 years and older. Coronary heart disease event rates were not significantly different among the groups.
2) The PROSPER RCT (n=5804) in which CHD was reduced, but all-cause mortality was not affected (0·97 (0·83–1·14)) due to increases in other causes of death.
3) The JUPITER and HOPE3 trials, in which a recent post-hoc sub-group meta-analysis has revealed benefit for the elderly patients. (JUPITER was a statin trial targeted at patients with low LDL but high CRP, i.e. inflammation, and had most clear evidence of benefit in cases with low HDL at baseline, which again is evidence of statins being far more effective in the insulin-resistant). The older people were, the more likely they were to stop taking statins, but we can’t say how much of this is due to increasing side effects with age, because side effects were poorly recorded in these early statin trials.
Risk management in the elderly may also be complicated by the fact that total cholesterol and LDL are often protective risk markers in older populations. For example, in the Danish registry of people without pre-existing heart disease or diabetes higher LDL is associated with lower mortality, compared with LDL under 2.5 mmol/L, in those over 50. That this included those with very high LDL – above 4 mmol/L – rules out reverse causality. Though statin use (by about 1 person in 4) was also associated with lower mortality in this population, there was no interaction between statin and cholesterol (i.e. statins didn’t explain the LDL difference either way). HDL between 1-2 mmol/L was protective compared with HDL <1 mmol/L (39 mg/dL); HDL ≥ 2 mmol/L was protective in women but not men (very high HDL levels can reflect heavy drinking), and higher TG was associated with increased mortality. In other words, the TG/HDL ratio – which correlates with fasting insulin, the 2-hour insulin response to glucose, and measures of insulin resistance – still predicted the risk of dying even in a population where LDL was pointing the other way.
Better diet prescription?
If we’re going to prevent diabetes and cardiovascular disease, it’s obvious we need to identify insulin resistance and prescribe diets accordingly. Prescribing diets that seem to lower LDL based on studies in healthy, insulin-sensitive people isn’t going to achieve much for the insulin-resistant who are most at risk, especially if these are still high carb, fat-phobic diets. At the very least, people at risk should be told to cut out sugar and refined starches, the products driving their insulin and triglycerides.
Whichever way you look at it – whether you think low carb is best, or you just favour a real food or Mediterranean diet with less sugar and processed food – the diet advice given in these guidelines, and supposed to be passed on by every GP in the country, represents a wasted opportunity.
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, , , , Primary Prevention With Statin Therapy in the Elderly: New Meta-Analyses From the Contemporary JUPITER and HOPE-3 Randomized Trials.
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Our health system is awesome at fixing up sickness, if I have an accident or get an infectious disease, get ear ache or a sore tooth, then it’s good to know that we have world class medical professionals and a system to deal with all of that.
But, let’s face it, our health system is not so awesome at preventing us getting sick, and providing us with the tools to have a great life where we are the best we can be.
Let’s face it, we spend billions on sickness and very little on health.
Let’s face it, we need to change medicine.
I’m a big fan of what has been achieved in medicine. We stand on the shoulders of giants in so many ways – Louis Pasteur, Florence Nightingale, Marie Curie, Joseph Lister, Otto Warburg, Watson and Cricks….
We’ve come so far, but each change has been painful and slow.
It took more than 50 years to move on the evidence that smoking kills to doing something about it. It took about the same time for the evidence that asbestos caused lung cancer to doing something about it. Also, in 1846, Hungarian doctor Ignaz Semmelweis found that hand washing after autopsy of dead mothers reduced neonatal death from sepsis 9-fold. He never got to see his breakthrough as he was ostracised, institutionalised, and in a twist of fate died himself of sepsis.
The time has come for change. Nutrition as medicine is a no brainer. The evidence is already there.
What’s different this time is that we have the crowd. Just like the consumer is demanding a change in regard to single-use plastic bags so to is the consumer now beginning to ask for change in the medical arena. We expect our doctors to understand nutrition and lifestyle medicine. So #letschangemedicine. We don’t have to wait for another 50 years.
Here’s what to do:
Step 1: Watch this TedX talk on the video below – just out by NZ researcher Julia Rucklidge on nutrition and mental health. It’s a game changer.
Step 2: Start making a noise yourself. People want to listen, they will follow!
Step 3: Stand by, we’ve got some bigger announcements coming in the next couple of weeks about how we are going to contribute to #letschangemedicine
It’s out! I’m honoured to be part of an authorship team with Prof Robert Lustig and Cardiologist Dr Aseem Malhotra, two rock stars of nutritional science and public health. These two guys are driving change and challenging dogma.
The paper, just published here in the Journal of Insulin Resistance, is an up to date report on the science of sugar, and offers an eight-point plan to reverse the diabetes epidemic within three years.
From the press release….
“Three international obesity experts, NHS Consultant Cardiologist Dr Aseem Malhotra, Professor Robert Lustig of the University of California San Francisco and Professor Grant Schofield, Auckland University of Technology have authored the most comprehensive up to date report on the science of sugar with an eight-point plan that if implemented will result in a reversal in the epidemic of type 2 diabetes within 3 years.
We have particularly focused on the tactics of the food industry, acting in the same way as Big Tobacco does. We are calling out The US Academy of Nutrition and Dietetics, British Dietetic Association (BDA), and the Dietitians’ Association of Australia who all receive annual contributions from the food industry.
Here’s our eight-point plan, all of which are evidence based to reduce population sugar consumption, and all of which were successful in curbing tobacco use.
- Education for the public should emphasise that there is no biological need or nutritional value of added sugar. Industry should be forced to label added and free sugars on food products in teaspoons rather than grams, which will make it easier to understand. GS comment: We need a better food labelling system and all free sugars should be included in this. It should be obvious to the consumer how much sugar there is in products.
- There should be a complete ban of companies associated with sugary products from sponsoring sporting events. We encourage celebrities in the entertainment industry and sporting role models (as Indian cricketer Virat Kohli and American basketballer Stephan Curry have already done) to publicly dissociate themselves from sugary product endorsement. GS comment: Like alcohol and tobacco in sport, the tide has turned and the untrue associations between sporting success and sugar are no longer tolerable to society. The gig’s up Big Sugar!
- We call for a ban on loss leading in supermarkets, and running end-of-aisle loss leading on sugary and junk foods and drinks. GS comment: Supermarkets in New Zealand can’t loss lead on tobacco and alcohol, just add sugary drinks and junk food as well.
- Sugary drinks taxes should extend to sugary foods as well. GS comment: NZ needs to join the club on sugary drink taxes, but if we want to change the three As (affordability, accessibility, and accessibility) then this tax must also extend to other junk foods. We could use the money for public health. Of our billions spent on health, the fact is most of it goes on sickness.
- We call for a complete ban of all sugary drink advertising (including fruit juice) on TV and internet demand services. GS comment: As above, like tobacco and alcohol the tide has turned. Big sugar should be on notice.
- We recommend the discontinuing all governmental food subsidies, especially commodity crops such as sugar, which contribute to health detriments. These subsidies distort the market, and increase the costs of non-subsidised crops, making them unaffordable for many. No industry should be provided a subsidy for hurting people. GS comment: Why do some counties make sugar cheaper yet healthy real food is costly. Sugar=wrong thing to subsidise.
- Policy should prevent all dietetic organisations from accepting money or endorsing companies that market processed foods. If they do, they cannot be allowed to claim their dietary advice is independent. GS comment: Let’s save these guys because they clearly can’t identify that taking food industry money is a serious conflict of interest and undermines their credibility.
- We recommend splitting healthy eating and physical activity as separate and independent public health goals. We strongly recommend avoiding sedentary lifestyles through promotion of physical activity to prevent chronic disease for all ages and sizes, because “you can’t outrun a bad diet”. However, physical (in)activity is often conflated as an alternative solution to obesity on a simple energy in and out equation. The evidence for this approach is weak. This approach necessarily ignores the metabolic complexity and unnecessarily pitches two independently healthy behaviours against each other on just one poor health outcome (obesity). The issue of relieving the burden of nutrition-related disease needs to improve diet, not physical activity. GS comment: Being fit is really good for you, but unfortunately big food is using it to confuse us about the solution to nutritional-related disease. Let’s treat these two things as important and separate, not run them against one another.
The retrospective econometric analysis and prospective Markov modelling both predict that the prevalence of type 2 diabetes will start to reduce three years after implementing these measures. This calamity has been 40 years in the making — three years is not too long to wait!
Here’s some great expert reaction so far….
“The science against sugar, alone, is insufficient in tackling the obesity and type 2 diabetes crises — we must also overcome opposition from vested interests”
Martin McKee, Professor of European Public Health London School of Hygiene and Tropical Medicine said, “We now know how Big Tobacco works, pushing products that kill millions. This paper makes a compelling case that Big Food is doing the same. Maybe these corporations don’t care how they are seen. But if they do care about their reputation, then this paper shows that they have a lot to do to clean up their act.”
Tim Lang, Professor of Food Policy, City University of London, Centre of Food Policy said, “This is an important paper with fair but firm recommendations. Slowly but surely, evidence and awareness are growing that a fundamental change is needed to national and international food policies. Food manufacturing has sweetened diets unnecessarily. Influence is bought by funding arms-length organisations who take the money and cloak themselves in spurious arguments on consumer freedom. Actually, the public worldwide is conned. The impression is given that a tweak here or there will sort out obesity and the runaway non-communicable disease toll. Media ought to realise they give airtime and space to what are effectively anti public health fronts. Declaration of funding should be made before airtime is given.”
Simon Capewell, Professor of Clinical Epidemiology
Department of Public Health and Policy, University of Liverpool said, “BigSugar, Big Tobacco and Big Food all use the same HARMS tactics to deny culpability: H Heaps money for politicians, journalists & scientists
- H Heaps money for politicians, journalists & scientists
- A Attack PH opponents & groups
- R Recruit cronies
- M Misinformation
- S Substitute ineffective interventions.
Simon Chapman, Emeritus Professor, Sydney School of Public Health University of Sydney, AUSTRALIA said, “The 2005 satirical movie Thank you for smoking featured a triumvirate of tobacco, alcohol and firearms lobbyists, sharing their strategies at weekly meetings they call The MOD Squad (Merchants of Death). If the movie was remade today, a fourth member from Big Sugar would be mandatory.
These modern chronic disease vectors all use the same playbook. If you want to control malaria, it’s essential you control mosquitos. If you want to control obesity, diabetes and cardiovascular disease, you must control the mosquito’s equivalent – the food industry”
Patti Rundall OBE, Policy Director of Baby Milk Action said, “A key tactic used by the food industry and all industries whose harmful practices should be regulated, is to create ‘front groups’ that represent their interest while sponsoring individuals in positions of influence – especially health professionals or anyone holding a position of trust. This allows them to secretly hijack the political and legislative process; manipulate public opinion and appear respectable. Since 1996, eight world Health Assembly Resolutions have called for conflict of Interest safeguards for those working in infant and young child feeding. These safeguards need to be implemented and extended to all those providing nutrition advice – transparency is an essential first step.”
After a big year of research, writing, and testing of our low-carb fasting method – “Super fasting” we are finally good to go.
We are super excited about What the Fast!, and how it continues the challenge on conventional nutritional-science wisdom. We’ve wrapped up the latest science, practice and yum recipes to provide you with a brilliant structure to mange your eating week (the sub-title is “How Monday and Tuesday will change your life”).
I really want to take the opportunity to thank the team, especially my co-authors Dr Caryn Zinn (aka the Whole Food Dietitian) and Craig Rodger (aka The Michelin-trained Chef), as well as Blackwell and Ruth our publishing partners.
I really hope you like it.
The book is available for pre-order now at whatthefatbook.com
There is a limited initial print run available and we expect this will sell out.
Thanks again everyone for all your support, its been quite a journey over the last few years.
Professor of Public Health
Director Human Potential Centre
If you have a spare 30 mins, then you might want to go to 1.03 on the fitter podcast. An interview closing sport performance, low carb, and fasting – especially concentrating on our soon to be released book “What the Fast”
You might have noticed claims in the media in the last few days that
New research conducted by Deloitte Access Economics and Nutrition Research Australia shows that if every New Zealand adult adds three serves of high fibre grain food to their daily diet, it could save the economy an estimated $607 million a year in reduced healthcare costs and lost productivity, and potentially avert 34,000 new cases of cardiovascular disease and 68,000 new cases of type 2 diabetes.
This is from a report (dae-nz-fibre-economics) that Deloitte produced for Kellogg’s. Industry funding was a conflict of interest properly reported by media. We have a rough rule of thumb around this – when industry funds basic research in labs – experiments – that’s not necessarily a bad thing, because science always needs funding, and we want answers to questions. When industry funds reviews and modelling, these are more likely to be subject to cherry-picking to favour the sponsor – they are questions of interpretation, so the risk of bias is higher.
The causes of disease and mortality that grain fibre is supposed to be able to prevent are cardiovascular disease and type 2 diabetes.
Based on data from published meta-analyses, the number of cases averted was estimated by assuming that a one-gram increase in grain fibre reduces the risk of CVD by 1.1% and T2D by 2.5% (Threapleton, 2013; InterAct Consortium, 2015).
We took a closer look at the evidence used to calculate the larger of the two benefits, that for type 2 diabetes. This was the EPIC-InterAct study and meta-analysis; the EPIC-InterAct study was a multicentre European observational study that didn’t find a protective association for grain fibre once adjusted for BMI (but there are some interesting details we’ll discuss later), so the authors added a meta-analysis (a statistical method that pools all available studies world-wide) that did find a protective association with grain fibre.
“However, the findings from our updated meta-analysis of prospective studies do support an inverse association between total fibre and cereal fibre intake and risk of type 2 diabetes, with a 9% and 25% lower RR per 10 g/day, respectively, independent of BMI.”
So an extra 10g of grain fibre reduces your risk of type 2 diabetes by 25%. Or does it? Actually, it depends on where you live.
There are many countries in EPIC-Interact without a protective association between grain fibre and type 2 diabetes, including France with a non-significant HR of 1.72 (that’s 72% worse). Another exception is the UK with a non-significant HR of 0.74 (26% better).
What are the differences in these populations? The French cohorts, for some reason, are all 100% female, which isn’t the case for any other country. And the largest of the two UK cohorts is EPIC-Oxford. “The majority of participants recruited by the EPIC Oxford (UK) centre consisted of vegetarian and “health conscious” volunteers from England, Wales, Scotland, and Northern Ireland”. So these health conscious volunteers are probably being compared with people with lower fibre intakes in the less health-conscious UK cohort.
Sweden always interests us because one of their two cohorts is the Malmö Diet and Cancer Study, which unlike the usual observational diet studies in this, or any other meta-analysis, uses the more accurate 7-day food diary for all subjects, and in Sweden the HR is a more reasonable 0.96. So less confounding by conscientiousness and more accurate diet recall tends to minimize the cereal fibre and type 2 diabetes association. If cereal fibre prevented type 2 diabetes in any important or unique way, it should probably show up in most of these populations, not just a few.
What about the other countries in the meta-analysis? Most of the weighty studies in favour of fibre for type 2 diabetes prevention in the EPIC-Interact meta-analysis come from the USA. There are two important facts about the USA – low fibre intakes are lower than they are anywhere else (so basically a high intake of deep fried food, white breads, and sweetened soda in these low-fibre groups), and conscientiousness is an identifiable confounding factor in many populations. For example, the Nurses’ Health Study and Health Professionals’ Follow-up Study; here we have the populations not only given the most advice about fibre being healthy, but also given the job of passing it on to the other US populations. In other words, grain fibre – like red meat – is one of the signifiers separating conscientious Americans from other Americans (it’s harder to eat fruit and vegetables without their fibre, and vegetables in the US includes fried potatoes). It’s almost a class distinction.
Closer to home, there are 3 Australian studies, two small ones with protective associations between grain fibre and type 2 diabetes (smaller studies have less weight in a meta-analysis) and a large one, Hodge 2004, with none. However Hodge 2004 finds that white bread is associated with type 2 diabetes, and that lower GI carbs, including sugar, aren’t.
White bread in Australia is so bad that even sugar looks good by comparison.
Does it follow that putting a few grams of bran in white bread will make it safe, or even good for you? Why not just say “avoid white bread”? This would definitely be our advice! Anyway, if fibre isn’t associated with type 2 diabetes in a fairly large sample of Australians, who tend to have fairly high fibre intakes anyway (by OECD standards), do Kiwis still need to take their lead from the USA?
“The mean±SD fibre intake in the [European] subcohort was 22.9± 6.2 g/day (ranging from 19.9 g/day in Sweden to 25.2 g/day in Denmark; data not shown).”
These figures for European countries are very similar to the averages for New Zealand – 22.8 g/day for men and 17.9 g/day for women.
Germany (7.40%) and Denmark (7.20%) have higher diabetes prevalence rates than Sweden (4.70%). USA’s mean total fibre intake is 16.1 g/day and diabetes prevalence is 10.80%. This would suggest that there is a suboptimal fibre intake, or perhaps just a protective effect of the real food, higher fat diets eaten in a place like Sweden, where (in Malmö) dairy fat has a protective association with type 2 diabetes, total fat has a protective association with CVD mortality in men, and fibre is protective against heart attacks only in combination with saturated fat (most of this is grain fibre in Malmö, probably from rye bread).[4,5] Sucrose – sugar – is the only nutrient/food/ingredient significantly associated with increased heart disease risk in Malmö. Its effect on the lipid profile is to increase triglycerides.
Participants who consumed >15 % of their energy intake (E%) from sucrose showed a 37 (95 % CI 13, 66) % increased risk of a coronary event compared with the lowest sucrose consumers (<5 E%) after adjusting for potential confounders. The association was not modified by the selected lifestyle factors.
There are no nutrients unique to grains. But some grain fibres, especially oat bran, are a very good source of silicon, a mineral which might be more important for cardiovascular health than is currently recognised. Other good sources of silicon are mineral water (the higher the total dissolved solids, the higher the silicon content is likely to be), green beans (especially) and other crunchy fibrous vegetables, bone broth, red wine and beer, and some herb teas, especially horsetail, oatstraw, and nettle. Oat bran is low in digestible carbohydrate and could definitely be included in the LCHF diet if anyone thought this necessary (it makes a great binder for mince patties).
The push from Kelloggs is to increase fibre by eating more grains and cereals – this is conflating any benefit of fibre with the effect of starch (and sugar if we’re talking breakfast cereals). Indeed fibre might be healthful but if you get it by adding extra bread and breakfast cereal what does that mean? for example, from EPIC-Netherlands:
Dietary GL was associated with an increased diabetes risk after adjustment for age, sex, established diabetes risk factors, and dietary factors [hazard ratio (HR) per SD increase: 1.27; 95% CI: 1.11, 1.44; P < 0.001] [corrected]. GI tended to increase diabetes risk (HR: 1.08; 95% CI: 1.00, 1.17; P = 0.05). Dietary fiber was inversely associated with diabetes risk (HR: 0.92; 95% CI: 0.85, 0.99; P < 0.05), whereas carbohydrate intake was associated with increased diabetes risk (HR: 1.15; 95% CI: 1.01, 1.32; P < 0.05). Of the carbohydrate subtypes, only starch was related to increased diabetes risk [HR: 1.25 (1.07, 1.46), P < 0.05]. All associations became slightly stronger after exclusion of energy misreporters.
And don’t forget the PURE study, as well as the Czech ecological analyses (below) – there are protective effects from moderate amounts of high fibre foods, but replacing fat with lots of carbohydrate is overall associated with a worsened metabolic profile and higher mortality.[10, 11]
The aim of this study was a large-scale ecological analysis of nutritional and other environmental factors potentially associated with the incidence of cardiovascular diseases (CVDs) in the global context. Indicators of CVDs from 158 countries were compared with the statistics of mean intake (supply) of 60 food items between 1993 and 2011, obesity rates, health expenditure and life expectancy. This comparison shows that the relationship between CVD indicators (raised blood pressure, CVD mortality, raised blood glucose) and independent variables in the global context is influenced by various factors such as short life expectancy, religiously conditioned dietary customs, the imprecision of some statistics and undernutrition. However, regardless of the statistical method used, the results always show very similar trends and identify high carbohydrate consumption (mainly in the form of cereals and wheat in particular) as a dietary factor most consistently associated with the risk of CVDs. These findings are in line with the changing view of the causes of CVDs.
From this evidence, it might be better to get the fibre from the low-starch foods; but if you do eat grains (not everyone is or needs to be low-carb), eating only whole grains, i.e. grains that you can see are whole or minimally broken, in relatively small amounts, and avoiding refined grains as far as possible is the pattern associated with most benefit.
The Bottom line: there are almost certainly people at higher risk of type 2 diabetes and cardiovascular disease because their diets are too dependent on refined and processed carbohydrate foods, especially sugars and grains. Their risk would indeed be lower if they replaced these with whole grains – brown rice, barley, oats and so on. This may be due in part to the fibre content, but it may also be due to the slower release of glucose and thus healthier insulin response to a grain when it hasn’t been powdered; fibre in a powdered grain doesn’t do much to reduce its impact. Yer dreamin if you think that just adding bran to processed carbs – which is what Kellogg’s products do – is going to make an impact on disease rates. Eating whole foods instead of food products might give us a chance.
For people with carbohydrate intolerance, grains are too carbohydrate-dense a food to consume in any quantity, but other fibre-rich foods are available to substitute.
However, to say that high-fibre diets are better is a generalisation – the benefits of fibre require the cooperation of gut bacteria and the gut, and quite a few people who look to diet to improve their health find that lower-fibre diets such as FODMAP exclusion diets and occasionally even zero-carb carnivore diets give significant improvement where high-fibre diets fail.
The What The Fat? diet is high-fibre because fibre increases satiety and there is some evidence for other health benefits, but fibre isn’t necessarily something there should be a bulk ruling about.
P.S. Ironically, when the Herald ran a news story on the Deloitte/Kellogg’s report, the high fibre success story they spoke to was a low(er) carber! There are only a couple of slices of brown bread in this story.
 The InterAct Consortium. Dietary fibre and incidence of type 2 diabetes in eight European countries: the EPIC-InterAct Study and a meta-analysis of prospective studies. Diabetologia. 2015;58(7):1394-1408. doi:10.1007/s00125-015-3585-9.ghb
 The InterAct Consortium, Langenberg C, Sharp S, et al. The InterAct Project: An Examination of the Interaction of Genetic and Lifestyle Factors on the Incidence of Type 2 Diabetes in the EPIC Study. Diabetologia. 2011;54(9):2272-2282. doi:10.1007/s00125-011-2182-9.
 Hodge AM, English DR, O’Dea K, Giles GG. Glycemic index and dietary fiber and the risk of type 2 diabetes. Diabetes Care. 2004;27:2701–2706. doi: 10.2337/diacare.27.11.2701
 Wallström P, Sonestedt E, Hlebowicz J, et al. Dietary Fiber and Saturated Fat Intake Associations with Cardiovascular Disease Differ by Sex in the Malmö Diet and Cancer Cohort: A Prospective Study. Obukhov AG, ed. PLoS ONE. 2012;7(2):e31637.
 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. link
 Warfa K, Drake I, Wallström P, Engström G, Sonestedt E. Association between sucrose intake and acute coronary event risk and effect modification by lifestyle factors: Malmö Diet and Cancer Cohort Study. Br J Nutr. 2016 Nov;116(9):1611-1620. Epub 2016 Oct 24.
 Sonestedt E, Hellstrand S, Schulz C-A, et al. The Association between Carbohydrate-Rich Foods and Risk of Cardiovascular Disease Is Not Modified by Genetic Susceptibility to Dyslipidemia as Determined by 80 Validated Variants. Müller M, ed. PLoS ONE. 2015;10(4):e0126104. doi:10.1371/journal.pone.0126104.
 Loeper J, et al. Study of fatty acids in atheroma induced in rabbits by an atherogenic diet with or without silicon IV treatment . Life Sciences 1988, 42:2105-2112.
 Sluijs I, van der Schouw YT, van der A DL, Spijkerman AM, Hu FB, Grobbee DE, Beulens JW. Carbohydrate quantity and quality and risk of type 2 diabetes in the European Prospective Investigation into Cancer and Nutrition-Netherlands (EPIC-NL) study. Am J Clin Nutr. 2010 Oct;92(4):905-11. doi: 10.3945/ajcn.2010.29620. Epub 2010 Aug 4.
 Dehghan M, Mente A2, Zhang X, et al. Prospective Urban Rural Epidemiology (PURE) study investigators. Associations of fats and carbohydrate intake with cardiovascular disease and mortality in 18 countries from five continents (PURE): a prospective cohort study. Lancet. 2017 Nov 4;390(10107):2050-2062. doi: 10.1016/S0140-6736(17)32252-3. Epub 2017 Aug 29.
 Grasgruber P, Cacek J, Hrazdíra E, Hřebíčková S, Sebera M. Global Correlates of Cardiovascular Risk: A Comparison of 158 Countries. Preprints 2018, 2018020066 (doi: 10.20944/preprints201802.0066.v1).
Cholesterol is a molecule required by every cell of the body in fairly large amounts. It can be easily synthesised by these cells, or taken up by them from LDL and other ApoB lipoproteins, but cannot be broken down. Cholesterol is not soluble in water, and thus must be carried through the blood on lipoprotein particles. When the cholesterol produced or taken up by the cells of the body becomes surplus to requirements it is extracted by HDL (ApoA1 lipoproteins) and carried back to the liver for disposal as bile salts and acids (most of this cholesterol is reabsorbed and recycled, but there is also a variable amount lost in faeces). Reverse cholesterol transport (RCT) is the term used for this extraction of unneeded cholesterol. Here we describe a simplified version of reverse cholesterol transport, how this has been modified by new research into HDL, and we explain the effect of raising or lowering insulin and insulin sensitivity on RCT.
This video gives a good overview of the systems we’ll be describing. (The brain has its own, largely separate cholesterol system which we’ll ignore for now).
Cholesterol and insulin
We have about 30g of cholesterol in our bodies, and synthesise well over a gram a day. Only 10% of this is synthesised in the liver, and even less if we eat cholesterol or have a reduced requirement. Our requirement goes up when we are growing (cells are expanding and new cells being made) and down when we are fasting or losing weight (when fat cells and glycogen cells are shrinking, and autophagic processes are clearing unwanted cells). Thus it makes sense, and helps to keep cholesterol in balance with requirements, that cholesterol synthesis is stimulated by insulin (the fed state hormone) and inhibited by glucagon (the fasting state hormone). An additional check on cholesterol synthesis in the fasting state is the activation of AMPK by the ketone body B-hydroxybutyrate. No surprises then that cholesterol synthesis is found to be increased in type 2 diabetes.
If scientists want to create the early signs of heart disease in animals, they need to feed them doses of cholesterol much larger than the total capacity of the body to make cholesterol. However, Jerry Stamler, one of the founding fathers of the diet heart hypothesis, found in the early 1960’s that animals treated in this way got better when the cholesterol feeding stopped – unless they were given extra insulin. This vital clue was missed in the later rush to change our diets – Jerry Stamler advised the population to avoid egg yolk and replace fat with refined carbs, yet human diets never supplied the amount of cholesterol he fed his animals – unfortunately, the new, modified human diet would start to increase insulin to the high levels seen in those chickens once the diabesity epidemic got underway.
Reverse Cholesterol Transport
Fortunately our gut and liver cells make a protein called ApoA1, which the liver turns into something called a nascent HDL particle. Unlike VLDL and the other ApoB particles, which are released from the liver as large, fat and cholesterol laden spheres, HDL is produced in an embryonic state, just a few proteins with little if anything in the way of lipids (lipid-poor ApoA1), and only becomes what we call HDL by performing its cholesterol-gathering role out in the body.
If we focus on the cells believed to play the major role in atherosclerosis, macrophages (large immune cells) which can turn into foam cells if they become overloaded with cholesterol, we can see HDL at work. Macrophages clear the blood of infectious agents and damaged particles, and have a particular affinity for oxidised LDL particles (oxLDL). LDL becomes oxidised if it stays in the blood too long (more likely with higher levels or small, dense particles) and is exposed to excessive glucose and fructose levels after meals, or to smoking and other oxidative stressors.[7,8,9] Brown and Goldstein, who won the Nobel Prize for discovering the LDL receptor, estimated that 30-60% of LDL is cleared from circulation by macrophages. (Macrophages exposed to excess insulin increase their uptake of oxLDL by 80%). The oxLDL is then broken down and the cholesterol stored – remember it can’t be broken down. As in other cells, any excess is sent to the surface of the cell, to transporters and other structures that make it available for HDL to pick up, as free cholesterol (cholesterol efflux). If this doesn’t happen for some reason, over a long period, there’s a risk of foam cell formation and atherosclerosis. (Macrophages exposed to excess insulin decrease their efflux of cholesterol to HDL by 25%).
LCAT and esterification
After HDL picks up free cholesterol, this is esterified by an enzyme called lecithin cholesterol acyltransferase (LCAT), making the HDL particle larger. Cholesteryl ester (CE) is cholesterol joined to a fatty acid, usually an unsaturated fatty acid, which is supplied from the phospholipids also picked up from cells by HDL. The more effectively HDL can esterify cholesterol, the sooner it can return to pick up more from the macrophage (or other cell) – this is called HDL efflux capacity – and the phospholipids found in egg yolk have been shown to increase HDL efflux capacity. Phospholipids, found in all whole foods, especially fatty ones like eggs, nuts, seeds, liver, shellfish, and soya beans, are good things to have in your diet; you won’t get them from eating flour, sugar, and oil.
CETP – swapping cholesteryl esters for triglycerides
HDL renews itself in the bloodstream by moving cholesteryl esters onto VLDL and other ApoB particles, in more-or-less equal exchange for triglycerides (TGs), through a banana-shaped protein tunnel called Cholesteryl Ester Transport Protein (CETP) which docks between ApoA1 and ApoB particles. HDL can then shed the TGs picked up to help feed cells along its path (as ApoB particles also do), turning them into free fatty acids and glycerol by the action of lipase enzymes. However, the CETP exchange is another place where things can go wrong. If there are too many TGs on VLDL, and too many TG-rich VLDL particles, and fats are not being burned by the body (yes, we’re talking about insulin resistance again), then the piling of TGs onto HDL via CETP will result in its recall to the liver after limited efflux. Carrying lots of TGs back to the liver that made them is not a good use of HDL’s time. And the cholesterol esters being transferred to former TG-rich VLDL is what makes the “Pattern B” lipoproteins, small dense LDL, which are more likely to oxidise and more easily taken up by macrophages. LDL really, once it’s done its job of delivering fat, cholesterol, antioxidants and proteins to cells that need them, ought to be helping in reverse cholesterol transport by ferrying the extra cholesterol esters it received from HDL back to the liver. Large, cholesterol-dense LDL particles – “Pattern A” – are better at this. Small, dense LDL particles aren’t taken up as avidly by the liver, so tend to stay in circulation and oxidize. Hence the TG/HDL ratio is a critical predictor of cardiovascular risk, whether or not we factor in LDL.
The exchange via CETP action is thought responsible for the inverse relationship between levels of TG and HDL-C. Specifically, the larger the VLDL pool (higher TG level), the greater the CETP-mediated transfer of CE from HDL to VLDL in exchange for TG, resulting in TG-rich small, dense HDL which are catabolized more rapidly, leading to low levels of HDL-C. These small, dense HDL also have reduced antioxidant and anti-inflammatory properties. Thus, the greater the increase in hepatic VLDL-TG synthesis and secretion that characterizes insulin-resistant/hyperinsulinemic individuals, the lower will be the HDL-C concentration.
Fasting, weight loss, and LDL
People who are naturally lean and active and have good insulin sensitivity are at very low risk of cardiovascular disease; they tend to burn fat and have low TG/HDL ratios on any diet. Paradoxically, LDL rises sharply when such people fast for long periods. Despite this, no-one as far as we know has ever suggested that not eating enough causes atherosclerosis. Of course TGs and insulin also fall, while HDL stays the same. But strangely, this rise in LDL does not happen in obese people or people with atherosclerosis.
Phinney and colleagues found that LDL first fell, then rose significantly, during major weight loss. They calculated that this was due to the delayed removal of around 100g extra cholesterol from the adipose of obese people. LDL became normal when a weight maintenance diet replaced the (low fat, reduced calorie) weight loss diet.
Think about this – all of this extra 100g of cholesterol, 3x the usual whole body content, was eventually removed by reverse cholesterol transport. Some of it ended up on LDL, increasing the LDL count to the level where statins would be indicated according to guidelines. This did not prevent its removal. There is no “LDL gradient” that forces cholesterol back into the body. The LDL level doesn’t tell you whether cholesterol is coming or going – the TG/HDL ratio is the best guide to that.
Hepatic lipase – burning fat.
ApoA1 and HDL production increases the release of hepatic lipase, so in a sense ApoA1 is a fat-burning protein, which helps to explain why eating fat increases ApoA1 output.[18, 19] More lipase means lower TGs all round. So, making more HDL can lower TGs, just as making too many TGs can lower HDL – but only the latter is likely to be harmful.
Of course, a low fat, high carbohydrate diet decreases ApoA1, but this doesn’t mean it’s bad if you’re insulin sensitive and have low TGs (and low LDL) eating such a diet, as many people do; the lower lipid circulation all round probably just means that less ApoA1 will be required for equilibrium. However, the old assumption that the lower fat higher carb diet is the “Prudent” diet hasn’t aged well.
We have previously reported that apoA-I and HDL directly affect HL-mediated triacylglycerol hydrolysis, and showed that the rate of triacylglycerol hydrolysis is regulated by the amount of HDL in plasma.
The antioxidant and antiinflammatory benefits of HDL.
Reverse cholesterol transport is the core business of HDL, but it isn’t the only business; HDL is like a busy doctor with a useful bag of healing tricks trundling up and down your bloodstream. For example, HDL carries an antioxidant protein, PON1. When a fatty hamburger meal rich in lipid peroxides was fed to 71 subjects, those with higher HDL experienced a much smaller rise in oxLDL.
The pre-meal HDL level was associated with the extent of the postprandial rise in oxidized LDL lipids. From baseline to 6 h after the meal, the concentration of ox-LDL increased by 48, 31, 24, and 16 % in the HDL subgroup 1, 2, 3, and 4, respectively, and the increase was higher in subgroup 1 compared to subgroup 3 (p = 0.028) and subgroup 4 (p = 0.0081), respectively. The pre-meal HDL correlated with both the amount and the rate of increase of oxidized LDL lipids. Results of the present study show that HDL is associated with the postprandial appearance of lipid peroxides in LDL. It is therefore likely that the sequestration and transport of atherogenic lipid peroxides is another significant mechanism contributing to cardioprotection by HDL.
Tregs or T regulatory cells are a type of immune cell that switches off inflammatory responses. They are also a type of cell that takes up HDL, and HDL selectively promotes their survival. This is a good thing.
Can LDL help in reverse cholesterol transport?
The answer is yes – if it’s large LDL particles (Pattern A), not so much small dense ones. Triglycerides and VLDL, on the other hand, are no help at all.
There are two pathways by which RCT can occur. In the first, the scavenger receptor class B type 1 (SRB-1) mediates hepatic uptake of CE from HDL particles without uptake of apoA-I or the whole HDL particle . In the second pathway, cholesteryl ester transfer protein (CETP) catalyzes the transfer of CE from HDL to apoB-containing lipoproteins (VLDL and LDL) in exchange for TG from the apoB-containing lipoproteins (Fig. 1) [21, 75]. This exchange results in apoB-containing lipoproteins which are enriched with CEs and depleted of TGs, and HDL particles which are depleted of CEs and enriched with TGs. The TG-rich and CE-poor HDL particles are catabolized faster than large, CE-rich HDL (apoA-I FCR is increased as noted in Fig. 1), a finding resulting in lower levels of HDL-C in the setting of high TG levels . The apoB-containing lipoproteins, now enriched in CE, can also be taken up by the liver receptors as previously described . When TG levels are high, the apoB particles are TG-enriched and hepatic lipase then hydrolyzes the TGs within the TG-rich LDL to release FFAs, a process which remodels the LDL particles into smaller and denser LDL particles which can enter the arterial intima more easily than larger LDL particles, thus making them more atherogenic (Fig. 1). Small, dense LDL particles also bind less avidly to the LDL receptor, thus prolonging their half-life in the circulation and making these particles more susceptible to oxidative modification and to subsequent uptake by the macrophage scavenger receptors .
An unusual experiment (using a radioactive nanoemulsion mimetic of LDL) showed that LDL cholesterol is removed from circulation more rapidly in resistance-trained healthy men than in sedentary healthy men. oxLDL was 50% lower in the resistance-trained men – but total LDL levels were the same, probably as a result of increased beta-oxidation (fat burning).
Why are doctors being confused about HDL and reverse cholesterol transport?
There’s a trend in mainstream medicine to be dismissive of HDL and treat reverse cholesterol transport as unimportant; LDL lowering is the thing. New evidence from genetics, epidemiology, and drug trials is increasingly misinterpreted in this way – probably because drugs that increase HDL have, with some exceptions, been failures. However, drugs that raise HDL, and lower LDL, by inhibiting CETP are not helping either particle do its job; so far, they have neither decreased nor increased the rate of heart attacks in people taking them. Drugs that raise HDL by increasing ApoA1 and nascent HDL output, like the fibrates (e.g. gemfibrozil), do decrease CHD – but only in people with lower HDL and higher TGs! Moderate alcohol use, which also increases ApoA1 output, seems to have a similar effect, though the first randomised controlled trial of this observational hypothesis is only beginning.[23, 24] Even statins help with RCT by decreasing the synthesis of cholesterol in peripheral tissues, thus leaving more room on HDL for efflux cholesterol – again, statins only seem to reduce CHD in the subgroup of people with lower HDL. Clearly reverse cholesterol transport is very important, and efficient reverse cholesterol transport can best explain why so many people with high LDL and high cholesterol do enjoy long lives free from cardiovascular disease. Some ApoA1 genes that especially promote RCT are associated with reduced CVD risk, notably ApoA1 milano – which is actually associated with low HDL, because HDL clearance is so rapid – a paradox which highlights the trickiness of measuring a dynamic process across all tissues only by what appears in the blood. Efficient RCT is associated with lean genes, but it’s largely something you have to work for – eating right, exercising, and looking after yourself in various ways – including giving up smoking, or not starting – which may be why the drug industry has largely given up on it.
We observed that normolipidemic smokers present higher total plasma and HDL phospholipids (PL) (P < .05), 30% lower postheparin hepatic lipase (HL) activity (P < .01), and 40% lower phospholipid transfer protein (PLTP) activity (P < .01), as compared with nonsmokers. The plasma cholesteryl ester transfer protein (CETP) mass was 17% higher in smokers as compared with controls (P < .05), but the endogenous CETP activity corrected for plasma triglycerides (TG) was in fact 57% lower in smokers than in controls (P < .01). Lipid transfer inhibitor protein activity was also similar in both groups. In conclusion, the habit of smoking induces a severe impairment of many steps of the RCT system even in the absence of overt dyslipidemia.
The latest study on very, very high HDL – why isn’t it good?
Last year we wrote about the CANHEART study, which seemed to show adverse health effects of higher HDL. We wrote then that this was probably showing an effect of alcoholism, hereditary CETP defects, and other factors, and not an increase in heart disease. A new study allows us to look at this problem in more detail.
When compared with the groups with the lowest risk, the multifactorially adjusted hazard ratios for all-cause mortality were 1.36 (95% CI: 1.09–1.70) for men with HDL cholesterol of 2.5–2.99 mmol/L (97–115 mg/dL) and 2.06 (1.44–2.95) for men with HDL cholesterol ≥3.0 mmol/L (116 mg/dL). For women, corresponding hazard ratios were 1.10 (0.83–1.46) for HDL cholesterol of 3.0–3.49 mmol/L (116–134 mg/dL) and 1.68 (1.09–2.58) for HDL cholesterol ≥3.5 mmol/L (135 mg/dL).
Those are some very high HDL levels, and not surprisingly fewer than 4% of men and even fewer women had HDL levels so high that they were associated with any extra risk.
Compare that with 40% of both men and women having low HDL levels that were associated with an equally elevated risk!
Further, the risk associated with very high HDL, though it does include cardiovascular deaths, doesn’t seem to include much increased risk of heart attacks and strokes.
This is consistent with alcoholism (a confounder not measurable with accuracy, as we described in the CANHEART analysis) increasing deaths from heart failure, cancer, and other causes, and with no further benefit (but maybe not much harm overall) from CETP variants elevating HDL. Furthermore, interactions between heavy alcohol consumption and genes associated with higher HDL have been noted in some populations.
Note that the HDL level associated with lowest heart disease and stroke incidence in this study is well to the right of the bell curve of population HDL distribution. Most of these people could have done with more HDL.
Madsen et al discuss their results soberly; although they fail to discuss the potential role of alcohol, which would explain the exact pattern of increased mortality seen well, and don’t highlight the 10-fold larger impact associated with low HDL in their study, there is nothing biased about their analysis. The European Heart Journal’s editorial was also worth reading.
However, as reported in medical media, the message changed a bit.
“It appears that we need to remove the focus from HDL as an important health indicator in research, at hospitals and at the general practitioner. These are the smallest lipoproteins in the blood, and perhaps we ought to examine some of the larger ones instead. For example, looking at blood levels of triglyceride and LDL, the ‘bad’ cholesterol, are probably better health indicators,” he notes.
Well yes, looking at everything is good, and TGs and the TG/HDL ratio as well as LDL will give you extra information about the likely reasons for low HDL and whether you need to worry about it. However, Denmark, where the extremely high HDL study was done, is a place where high LDL (the ‘bad’ cholesterol, remember) is associated with lower all-cause mortality in those over 50 free from diabetes or CVD at the start of the study. Over 50 is when most CVD and type 2 diabetes is diagnosed, so LDL might not be all that informative unless you can look at the subclasses of oxLDL, sdLDL, particle number, and so on (of course part of the effect of LDL in Denmark will be due to that country’s higher dairy fat intake, which will also raise HDL and LDL particle size, maybe helping to explain why the association is so favourable in that population).
If we look at the PURE study, higher fat consumption is associated with both higher LDL and higher ApoA1 and HDL, with saturated fat (like all fat types) tending to improve the ApoB/ApoA1 ratio. This is consistent with many other lines of evidence.
Intake of total fat and each type of fat was associated with higher concentrations of total cholesterol and LDL cholesterol, but also with higher HDL cholesterol and apolipoprotein A1 (ApoA1), and lower triglycerides, ratio of total cholesterol to HDL cholesterol, ratio of triglycerides to HDL cholesterol, and ratio of apolipoprotein B (ApoB) to ApoA1 (all ptrend<0·0001).
This is just what fat-burning does, and there’s maybe not a lot of reason to think it’s good or bad per se. What is good about it is, that fat burning lowers insulin. Insulin is what makes your cells hoard cholesterol, and it’s also one of the things that can mess with reverse cholesterol transport. If you’re making or using excess insulin, the switch to a fat burning metabolism allows the insulin to normalise and causes your cells, including the macrophages, to let go of cholesterol – and when they do, the lipoproteins are there ready to carry it away.
Reverse cholesterol transport manages cholesterol flux through all cells and helps us reach a healthy old age.
LDL cholesterol is not a reliable guide to the state of cholesterol flux unless TG/HDL (and HbA1c) are factored in as well. LDL may increase when cholesterol is being removed or in states where it is not being taken up by cells.
Reverse cholesterol transport can remove prodigious amounts of cholesterol from the body during weight loss.
Excessive triglycerides due to insulin resistance can impair reverse cholesterol transport, as can smoking.
Various nutritional factors found in whole food diets have been found to assist in reverse cholesterol transport (including phospholipids, CLA, and polyphenols).
HDL in the high (if not the “extremely high”) range usually correlates with efficient reverse cholesterol transport and has benefits for cardiovascular health, inflammation, antioxidant status etc, but people with HDL outside (higher or lower than) the ideal range can be equally healthy if their overall metabolic health (insulin sensitivity) is good.
The TG/HDL ratio is a good measure of insulin sensitivity, and if excessive can be improved by lowering excessive insulin levels. A low carb diet, intermittent fasting, exercise, or weight loss are all effective ways to correct the TG/HDL ratio.
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 Phinney SD, Tang AB, Waggoner CR, Tezanos-Pinto RG, Davis PA. The transient hypercholesterolemia of major weight loss. Am J Clin Nutr. 1991 Jun;53(6):1404-10.
 da Luz PL, Favarato D, Faria-Neto JR Jr, Lemos P, Chagas ACP. High ratio of triglycerides to HDL-cholesterol predicts extensive coronary disease. Clinics. 2008; 64:427-32
 Ramsamy TA, Boucher J, Brown RJ et al. HDL regulates the displacement of hepatic lipase from cell surface proteoglycans and the hydrolysis of VLDL triacylglycerol. The Journal of Lipid Research. 2003; 44: 733-741.
 Chatterjee C, Sparks DL. Hepatic Lipase, High Density Lipoproteins, and Hypertriglyceridemia. The American Journal of Pathology. 2011;178(4):1429-1433. doi:10.1016/j.ajpath.2010.12.050.
 Tiainen S, Ahotupa M, Ylinen P, Vasankari T. High density lipoprotein level is negatively associated with the increase of oxidized low density lipoprotein lipids after a fatty meal. Lipids. 2014; 49(12): 1225-32. doi: 10.1007/s11745-014-3963-y. Epub 2014 Oct 31.
 Rueda CM, Rodríguez-Perea AL, Moreno-Fernandez M et al. High density lipoproteins selectively promote the survival of human regulatory T cells. J Lipid Res. 2017 Aug;58(8):1514-1523. doi: 10.1194/jlr.M072835. Epub 2017 Apr 4.
 da Silvaa JL, Vinagrea CGCM, Morikawa AT et al. Resistance training changes LDL metabolism in normolipidemic subjects: A study with a nanoemulsion mimetic of LDL.
Atherosclerosis. 2011; 219(2): 532-537.
 Mukamal KJ, Clowry CM, Murray MM, et al. Moderate Alcohol Consumption and Chronic Disease: The Case for a Long-Term Trial. Alcohol Clin Exp Res. 2016 Nov;40(11):2283-2291. doi: 10.1111/acer.13231. Epub 2016 Sep 30. Review.
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 Madsen CM, Varbo A, Nordestgaard BG. Extreme high high-density lipoprotein cholesterol is paradoxically associated with high mortality in men and women: two prospective cohort studies. European Heart Journal,. 2017; 38(32): 2478–2486, https://doi.org/10.1093/eurheartj/ehx163
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 Volcik K, Ballantyne CM, Pownall HJ, Sharrett AR, Eric Boerwinkle E. Interaction Effects of High-Density Lipoprotein Metabolism Gene Variation and Alcohol Consumption on Coronary Heart Disease Risk: The Atherosclerosis Risk in Communities Study. Journal of Studies on Alcohol and Drugs, 68(4), 485–492 (2007).
 Barter PJ, Rye K-A. HDL cholesterol concentration or HDL function: which matters? European Heart Journal. 2017; 0: 1–3
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Lancet Diabetes Endocrinol 2017 Published Online August 29, 2017 http://dx.doi.org/10.1016/S2213-8587(17)30283-8
PURE lipids and BP
We’re recruiting participants for a research study about low carbohydrate diets.
The study “How low do you need to go? Comparing symptoms of diet induction and mood with outcomes from diets containing differing levels of carbohydrate restriction” seeks to help us understand the effects of differing types of low-carb diets on symptoms of carbohydrate withdrawal (known as ‘Keto-Flu’) and on outcomes from dietary intervention.
We are seeking healthy, non-diabetic people aged between 24 and 49 who are currently seeking weight loss. Please be aware that due to the nature of this study those who are currently, or have previously followed a ketogenic diet may be ineligible and people who are current or former clients of mine or my Secondary Supervisor Caryn Zinn Dietitian are ineligible to participate.
Find out more and register your interest here: http://www.carbappropriate.study/
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.
First, we do find some common ground
- 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.
- 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.
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). 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). 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. 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. 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. 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.
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]
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.
“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.
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). 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”.
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).” 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. 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.
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. 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. The similar benefit of olive oil and red wine polyphenols may also depend on their inclusion in foods that raise HDL.
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]
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. 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.
 Sacks FM, Lichtenstein AH, Wu JHY et al. Dietary Fats and Cardiovascular Disease: A Presidential Advisory From the American Heart Association.
 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
 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.
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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.
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[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.
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