How much evidence do you need to make recommendations about what the public should eat?
It depends really.
“On fair evidence we might take action on what appears to be an occupational hazard. For example, we might change from a probably carcinogenic oil to a non-carcinogenic oil in a limited environment and without too much injustice if we are wrong. But we should need very strong evidence before we made people burn a fuel in their homes that they do not like or stop smoking the cigarettes and eating the fats and sugar that they do like.”
This a quote from a great framework used in public health for making such decisions. It was put forward by Austin Bradford Hill in the 1960s, and has become known as the “Bradford Hill criteria“. It’s a set of conditions that should be met, or tests that should be made, before public health people start to make recommendations about what to avoid and what to do instead.
See also, Austin Bradford Hill, “The Environment and Disease: Association or Causation?”
Proceedings of the Royal Society of Medicine, 58 (1965), 295-300.
So what does this have to do with margarine?
In the previous post, we learned that New Zealanders on average consume around 4.9Kg of butter per capita each year, as well as a similar amount of palm oil, around 8.5Kg of canola oil, and around 2.7Kg of soy bean oil (a total of 21Kg of added fat, similar to the totality of 1966 butter intake). Much of the latter three oils goes into non-dairy spreads (along with smaller amounts of other oils such as corn, olive, rice bran, and sunflower, figures for which were not available). So what do we know about these oils and spreads, and their health effects, and should we be telling people to eat them especially over butter?
What are non-dairy spreads?
Butter is butter; its composition will vary slightly depending on what the animal is fed, so that winter silage produces a paler fat, lower in carotenoids, and the feeding of palm kernel expeller produces a fat in which the beneficial trans, cis fat rumenic acid (or CLA) is partly replaced by other trans fats, the importance of which is still uncertain, but these differences are very small compared to the differences that exist within the categories of margarine and non-dairy spreads. Although we’ll use the terms interchangeably here, food labelled “margarine” (a word few food producers seem to use today), as chemist Laurence Eyres reminded us in the Listener, must by law contain at least 80% fat, whereas spreads are usually lower fat. What Eyres doesn’t tell us is that this can be animal fat – there are budget spreads in the supermarket that contain beef fat as an ingredient. Not that there’s anything wrong with that, but obviously the idea that we can “replace animal fat with non-dairy spreads” is a bit misleading.
It’s curious that no-one who supports the substitution of margarine for butter mentions this, and the reason may be that the substitution exists in their heads as a theoretical one – they don’t actually go down to the supermarket and read the labels on the different products that people are buying and eating, or if they do, they only read the saturated fat information on the label.
A lot is made of the use of partially hydrogenated oils (PHO), a source of trans fats, in margarine, and how these are being removed from the food supply by a voluntary arrangement, with labeling still optional. Other countries have made greater efforts to label and remove industrial trans fats than New Zealand, Australia, and the UK. India introduced mandatory labelling and limits on trans fats from PHO within a short period, and the US FDA withdrew the GRAS (generally recognized as safe) classification from PHO, with a complete ban (barring any exemptions being granted) effective later this year. Note that other sources of saturated fats, and of naturally occurring trans fats, are still GRAS and always will be, so that attempts to combine “trans fat and saturated fats” into some common category of “bad fats” have no validity. But why was PHO included in margarine to begin with?
Butter has a spreadable consistency (at least at the right temperature), partly because its saturated fat content ensures that it is not too runny, and partly because the phospholipids and cholesterol it contains allow the fats to form an emulsion with its small amount of water. The trans fats in PHO were straight chains like saturated fats, so had a similar consistency, while appearing as unsaturated fats when tested in the laboratory (they also, unlike saturated fats, interfered with the conversion of polyunsaturated fats into various signaling molecules, which was a bad thing). So they have had to be replaced with more saturated fats, such as beef fat or palm oil. Lighter spreads that don’t contain these fats need to include emulsifiers and stabilizers; this gives them more in common with other highly processed foods, and also means that you’re paying extra for water. The technology of interesterification means that oils can now be made harder by switching fatty acids around on the glycerol backbone of triglycerides, changing their interactions with one another and thus their consistency, but this technology is only used in some of the spreads on the NZ market.
Vegetable spreads – what evidence is there for benefit?
So is there anything (causally) harmful or good about these products? Do they have health benefits? Bearing in mind the Bradford Hill criteria which look at the scientific evidence. The evidence should be tested against these criteria:
- Strength (effect size): A small association does not mean that there is not a causal effect, though the larger the association, the more likely that it is causal.
- Consistency (reproducibility): Consistent findings observed by different persons in different places with different samples strengthens the likelihood of an effect.
- Specificity: Causation is likely if there is a very specific population at a specific site and disease with no other likely explanation. The more specific an association between a factor and an effect is, the bigger the probability of a causal relationship.
- Temporality: The effect has to occur after the cause (and if there is an expected delay between the cause and expected effect, then the effect must occur after that delay).
- Biological gradient: Greater exposure should generally lead to greater incidence of the effect. However, in some cases, the mere presence of the factor can trigger the effect. In other cases, an inverse proportion is observed: greater exposure leads to lower incidence.
- Plausibility: A plausible mechanism between cause and effect is helpful (but Hill noted that knowledge of the mechanism is limited by current knowledge).
- Coherence: Coherence between epidemiological and laboratory findings increases the likelihood of an effect. However, Hill noted that “… lack of such [laboratory] evidence cannot nullify the epidemiological effect on associations”.
- Experiment: “Occasionally it is possible to appeal to experimental evidence”.
- Analogy: The effect of similar factors may be considered.
Criteria 1 and 2: Strength and consistency of epidemiological evidence
There is a body of epidemiological research that claims that replacing saturated fat (or carbohydrate) with polyunsaturated fat reduces cardiovascular risk. Unfortunately, the association isn’t consistent (there are populations where no association, or the opposite association has been seen, at least from theoretically replacing saturated fat with polyunsaturated fat).[1, 2] However, even in the populations where this association has been seen, there’s no clear evidence that margarine, or cooking oil, is the source of it. The problem is that many minimally refined foods are also good sources of polyunsaturated fat, especially chicken and pork, nuts and seeds, olives and avocadoes, but also meat and dairy; all whole foods add more polyunsaturated fat to the diet than sugar and flour do. There don’t seem to have been many attempts to isolate the polyunsaturated fat in oils and spreads and compare it with that in whole foods and animal fats.
There have only been a few epidemiological studies comparing margarine with butter. In Framingham, which was the original large population followed to test the lipid hypothesis (it didn’t work out – there was never any neat linear association between saturated fat in the diet, LDL cholesterol, and heart disease), using margarine instead of butter was associated with no change in heart disease during the first 10 years, then an increase over the 10 years following. This was attributed to trans fats, but that doesn’t explain the different effects over 10 and 20 years.
“Adjusted for age and energy intake, the risk ratio for CHD for each increment of 1 teaspoon per day of margarine was 0.98 [95% confidence interval (CI) = 0.91-1.05] for the first 10 years of follow-up and 1.10 (95% CI = 1.04-1.17) for follow-up years 11-21. Butter intake did not predict CHD incidence.”
Recently, a study was published claiming a theoretical benefit from margarine use instead of butter for heart attack (MI) risk over a 13 year period.
“Substituting butter or stick margarine with tub margarine was associated with lower risk of MI (HRs = 0.95 and 0.91). Subgroup analyses, which evaluated these substitutions among participants with a single source of spreadable fat, showed stronger associations for MI (HRs = 0.92 and 0.87). Outcomes of total CHD, ischemic stroke, and atherosclerosis-related CVD showed wide confidence intervals but the same trends as the MI results.”
Unfortunately, this study is one we don’t have access to, and the methods are not obvious; however, no number of events is given in the abstract, so it is possible that “theoretical” just means calculated risk from serum lipids. Still, it’s noticeable that even in this study, substituting one type of margarine for another was associated with more benefit than replacing butter.
(Given the variety of non-dairy spreads on the market, and the inconsistency of their ingredients, it might be more helpful if the experts fought over what sort of margarine people should use, rather than whether they should use it instead of butter).
There may be other evidence that using margarine, specifically, is associated with beneficial outcomes, but if so we haven’t been able to find it.
Criteria 4 and 6: Temporality and Biological plausibility
What about oils? There’s an interesting paper from the Nurse’s Health Study that looked at two different sources of the omega 3 fat ALA. A higher consumption of ALA from (soy) oil-and-vinegar salad dressing was associated with a lower risk of fatal heart attacks, RR 0.46 (0.27, 0.76), whereas a higher consumption of mayonnaise was not, RR 0.84 (0.50, 1.44). Yet mayonnaise is the richer food and contributed more ALA to diets than oil-and-vinegar salad dressing (16.7% vs 12.2%). This study didn’t look at intake of margarine as a source of ALA (6.8%). A relevant point is that much of this population was probably deficient in omega-3 fats (American’s don’t eat much fish, and median daily energy-adjusted ALA intake ranged from 0.71 g in the lowest quintile to 1.36 g in the highest quintile), so we are probably looking at the effects of correcting a deficiency of an essential nutrient. Of course, if you’re using lots of oil-and-vinegar dressing, or, to a lesser extent, mayonnaise, you’re also eating a very different type of diet from someone who isn’t.
In this case we have a plausible mechanism, and a suggestion of temporality – correcting a historical deficiency of omega-3 fats in a population with very low intake of them would be expected to improve the blood clotting aspect of fatal heart attacks. Other foods could have supplied the ALA, but soy oil happened to be the source available. The association was only significant when the oil was used in salads, and stronger in women taking vitamin E supplements, but in these cases it satisfied the Bradford Hill criteria for strength, and is broadly consistent with the RCT analysis of Ramsden et al.
This example seems to satisfy all Bradford Hill criteria to some extent, if considered as an correction of a deficiency analogous to the correction of a vitamin deficiency, but much less so if considered as the effect of a substitution for saturated fat (especially considering the body of evidence that a substitution for carbohydrate would be at least as beneficial).
On balance we’d say there isn’t a case as far as Bradford-Hill’s criteria are concerned to say anything about spreads and benefit.
Vegetable oils and spreads – some evidence for harm?
So – is there any evidence that non-dairy spreads and cooking oils have harmful effects? You’ll find plenty of mechanistic arguments and non-human experimental evidence that they do in the literature. But remember Bradford Hill’s criteria – an epidemiological association is convincing when it’s attached to mechanisms, but is also strong (RR approaching 2 or greater is best, though 1.5 is usually accepted), consistent (not contradicted by directly comparable studies), and has a dose-response (more seems worse).
Criteria 3, 5, and 7: specificity, biological gradient, and coherence
Age-related macular degeneration is a common cause of visual impairment and blindness in older people.
A case-control study gave the following results.
Higher vegetable fat consumption was associated with an elevated risk for AMD. After adjusting for age, sex, education, cigarette smoking, and other risk factors, the odds ratio (OR) was 2.22 (95% confidence interval [CI], 1.32-3.74) for persons in the highest vs those in the lowest quintiles of intake (P for trend,.007). The risk for AMD was also significantly elevated for the highest vs lowest quintiles of intake of monounsaturated (OR, 1.71) and polyunsaturated (OR, 1.86) fats (Ps for trend,.03 and.03, respectively). Higher consumption of linoleic acid was also associated with a higher risk for AMD (P for trend,.02). Higher intake of omega-3 fatty acids was associated with a lower risk for AMD among individuals consuming diets low in linoleic acid, an omega-6 fatty acid (P for trend,.05; P for continuous variable,.03). Similarly, higher frequency of fish intake tended to reduce risk for AMD when the diet was low in linoleic acid (P for trend,.05). Conversely, neither omega-3 fatty acids nor fish intake were related to risk for AMD among people with high levels of linoleic acid intake.
This was followed by a prospective study by the same authors looking at AMD progression (important because temporality, the presumed cause preceding the effect, which cannot always be shown in case-control studies, is another of the Bradford-Hill criteria), which confirmed the associations above, but also found that nut consumption was protective. This is interesting, because nuts are a good source of linoleic acid, indicating that linoleic acid in whole foods (where some of it is in phospholipid form) may behave differently from linoleic acid in vegetable oils, where the phospholipids have been removed by refining.
The prospective study found that all fats were associated with AMD – however, there was no dose response in the case of saturated fats. Dose response is an important part of the Bradford Hill criteria – if something is truly harmful, more should (usually) do more harm than a little.
One study, NHANES II, did not find a significant correlation between dietary fats and AMD, however this study failed to separate vegetable oils from other sources of fat, and did not provide a sufficiently detailed breakdown of its results.
This is an example that fulfills many of the Bradford Hill criteria. Indeed it already appears in textbooks as an example of the role of peroxidation in oxidative stress diseases. It has specificity because the retina of the eye is exposed to concentrated UV radiation, and plausibility because linoleic acid and ALA are uniquely prone to peroxidation in vivo. It is known not to be the only factor in AMD, yet shows a strong association, increasing our confidence that it is a factor increasing risk.
One of the predicted harms of higher vegetable oil intake is increased cancer risk, due to the peroxidisabilty of polyunsaturated fats, as well as their use by some types of cancer cells. However, this correlation is not usually a strong or consistent one, because exposure to carcinogens and diet both vary by occupation and socioeconomic class, and because cancer, unlike heart disease, subdivides into many discrete diseases, the risk of which is relatively rare. Further, just agreeing to be in a diet study has a significant effect on reducing future cancer risk. However, there are some exceptions.
The use of vegetable oils for high temperature cooking is fairly consistently associated with lung cancer risk in women using them, for example in this case-control study of women in Gansu, China using rapeseed oil (as far as we can tell, this is the name for canola oil in modern China; at any rate, it comes from the same species and is thought to be healthy) for wok cooking.
A useful feature of this study was that rates of two important confounders, deep fryer cooking and smoking, were very low.
The odds ratio (OR) for lung cancer associated with ever-use of rapeseed oil, alone or in combination with linseed oil, was 1.67 (95% CI 1.0-2.5), compared to use of linseed oil alone. ORs for stir-frying with either linseed or rapeseed oil 15-29, 30 and > or =31 times per month were 1.96, 1.73, and 2.24, respectively (trend, P=0.03), relative to a lower frequency of stir-frying. Lung cancer risks also increased with total number of years cooking (trend, P<0.09). Women exposed to cooking fumes from rapeseed oil appeared to be at increased risk of lung cancer, and there was some evidence that fumes from linseed oil may have also contributed to the risk.
In a Hong Kong case-control study in which deep frying was a common style of cooking, the risk was even higher – indeed, similar to that of smoking. Peanut, corn, and canola were the main oils used (there was little difference between them in this study).
The ORs of lung cancer across increasing levels of cooking dish-years were 1, 1.17, 1.92, 2.26, and 6.15. After adjusting for age and other potential confounding factors, the increasing trend of ORs with increasing exposure categories became clearer, being 1, 1.31, 4.12, 4.68, and 34. The OR of lung cancer was highest for deep-frying (2.56 per 10 dish-years) followed by that of frying (1.47), and stir-frying had the lowest OR (1.12) among the three methods.
The first study is curious because linseed oil, an oil very high in ALA, and one which no-one in the West would use for cooking, seemed safer than rapeseed oil. In the recent Harvard study on dietary fat and mortality, based on Nurse’s Health Study data, ALA was associated with cancer mortality (HR 1.12; 95% CI, 1.04, 1.20). There was both a dose-response and a temporal response (the association was only seen with longer exposure). This association is weak, but lung cancer is only one type of cancer, canola oil only one source of ALA, and ALA rich foods can be used in various ways. The Harvard research analyses foods, rather than the ingredients they are made with, so there’s no information on how much canola oil was being used, but in NZ it seems to be the most common cooking oil. However, the idea that cooking oil fumes cause lung cancer seems to be accepted; yet, here in New Zealand, we’re told to use canola oil in place of animal fats or coconut oil (saturated fat wasn’t associated with cancer mortality in the Harvard study).
This is a case that not only fulfills Bradford Hill criteria for causality (the product of heating the ALA in these oils protects lung cancer cells against apoptosis in vitro), but also fulfills his example of a practical intervention. We could look for less probably carcinogenic oils and fats and introduce (or re-introduce) them into the limited environments of kitchens without too much injustice if we are wrong, provided they are no more harmful once eaten.
Since the removal of PHO trans fats from the food supply, the use of palm oil, the vegetable oil highest in the main saturated fats palmitic and stearic acid, has increased in NZ. Palm oil consumption is equal to that of butter, and most of it goes into non-dairy spreads and other processed foods. The “Myth Buster” section of the Listener article we responded to in the last post failed to mention palm oil use in spreads. Palm oil contains a greater amount of the supposedly “bad” saturated fat palmitic acid than butter, thus defeating the point of using margarine. (However, as the amount of palmitic acid in the blood is controlled by the amount of carbohydrate we eat, and we usually eat much more carbohydrate than palmitic acid, it makes more sense to reduce carbohydrate first, and avoid palm oil, before looking at butter. Coconut oil is very low in palmitic acid). Palm oil production has become a far greater environmental disaster internationally than dairying is said by its worst critics to be for New Zealand. To make matters worse, the European Food Safety Agency recently issued a warning that palm oil contains higher levels of the carcinogen glycidyl, caused by refining at temperatures above 200 degrees C, than those found in other processed oils. New Zealand is still awaiting legislation for the mandatory labelling of palm oil, which often appears on food labels as “vegetable oil”. Remember, the New Zealand population has only been exposed to trans fat, palm oil, and interesterified fat products because locally produced animal fats like butter have been supposed, on inadequate evidence, to be harmful, and because a massive international industry exists to profit by supplying us with artificial substitutes.
So there could be a future increased health risk, as well as the ongoing environmental disaster, caused by our rush to consume palm oil, all in the name of avoiding butter and animal fats. However, there’s no epidemiological study looking at the impact of palm oil in Western countries (nor any for interesterified fats). Bradford Hill can’t help us when studies don’t ask the right questions. Most of the studies we’ve looked at weren’t designed to tell us whether getting our polyunsaturated fats from refined oils instead of real foods was a good idea or a bad one, though we can be pretty sure that they’re not as healthful as they were once heated above 200 degrees C, whether in cooking or refining.
We love the way that Bradford Hill’s thinking does more than just help us decide whether to say yes or no to the question of “does X cause (or prevent) Y?”- it can also lead us into a deeper understanding of what the evidence really means.
The case for benefit from PUFA oils and spreads isn’t met, except for the case for correcting a deficiency of LA or ALA – directly analogous to correcting a vitamin deficiency (analogy). Regarded in this way only, the case for benefit should be clear, but can only apply to oils and spreads in cases where oils are the only source of these fats – this doesn’t have to be the case for ALA, and of course it is not the case for LA in normal diets.
Anyone eating a higher fat, real food diet is likely to have an optimal intake of LA and at least a sufficient intake of ALA or other omega-3 fats without relying on these supplementary sources.
A low-butter spread you can make at home.
Supposing you like the taste of butter, want to avoid potentially harmful refined oils, but are also interested in reducing the amount of saturated fat you eat. Or maybe you want to do your bit to reduce the environmental impact of dairy farming. We suggest adapting a recipe for “Sunbutter” from Gayelord Hausers'”Treasury of Secrets” (1963 edition).
Gayelord Hauser was a diet adviser to the stars in the golden age of Hollywood, who advocated (among other things) low carb diets for weight loss, and the use of what later became known as “health food supplements” such as brewer’s yeast, molasses, and wheat germ oil. His books contain a simple recipe for a low-saturated fat spread, using a pound of butter and a cup of sunflower oil. In our new updated version, you’d heat and blend together equal parts butter and extra virgin olive oil. The result is spreadable straight out of the fridge, and tasty. This might just be the main benefit of the recipe. NZ refrigerators used to have a butter conditioner – a warm section of the fridge, just the right temperature to keep your butter spreadable. These went out with the anti-butter, saturated fat will kill you campaigning of the Heart Foundation and Rod Jackson in the 1990s. Such a loss…
Unlike the original Sunbutter, this mixture will have almost exactly the same fatty acid composition as your own fat stores (credit to Steve Phinney for this insight), and that’s exactly the kind of healthy fat you want to be running on.
And you don’t need to use anything to make it that you wouldn’t normally want in your food.
 Praagman J, de Jonge EA, Kiefte-de Jong JC, Beulens JW, Sluijs I, Schoufour JD, et al. Dietary Saturated Fatty Acids and Coronary Heart Disease Risk in a Dutch Middle-Aged and Elderly Population. Arterioscler Thromb Vasc Biol. 2016; 36(9): 2011-8.
 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 Nutr2016;103:356-65.
 Margarine intake and subsequent coronary heart disease in men. Gillman MW, Cupples LA, Gagnon D, Millen BE, Ellison RC, Castelli WP. Epidemiology. 1997 Mar;8(2):144-9.
 Liu Q, Rossouw JE, Roberts MB, Liu S, Johnson KC, Shikany JM, Manson JE, Tinker LF, Eaton CB. Theoretical Effects of Substituting Butter with Margarine on Risk of Cardiovascular Disease. Epidemiology. 2017 Jan;28(1):145-156.
 Hu FB, Stampfer MJ, Manson JE, et al. Dietary intake of α-linolenic acid and risk of fatal ischemic heart disease among women. Am J Clin Nutr. 1999; 69(5): 890-897.
 Use of dietary linoleic acid for secondary prevention of coronary heart disease and death: evaluation of recovered data from the Sydney Diet Heart Study and updated meta-analysis
 Seddon JM, Rosner B, Sperduto RD, et al. Dietary fat and risk for advanced age-related macular degeneration. Arch Ophthalmol 2001;119:1191–9.
 Seddon JM, Cote J, Rosner B. Progression of age-related macular degeneration: association with dietary fat, transunsaturated fat, nuts, and fish intake. Arch Ophthalmol 2003;121:1728–37.
 Heuberger RA, Mares-Perlman JA, Klein R, et al. Relationship of dietary fat to age-related maculopathy in the Third National Health and Nutrition Examination Survey. Arch Ophthalmol 2001;119:1833–8.
 Metayer C, Wang Z, Kleinerman RA, et al. Cooking oil fumes and risk of lung cancer in women in rural Gansu, China. Lung Cancer. 2002 Feb;35(2):111-7.
 Yu IT, Chiu YL, Au JS, Wong TW, Tang JL. Dose-response relationship between cooking fumes exposures and lung cancer among Chinese nonsmoking women. Cancer Res. 2006 May 1;66(9):4961-7.
 Wang DD, Li Y, Chuive SE, et al. Association of specific dietary fats with total and cause specific mortality. JAMA Intern Med. Published online July 5, 2016.
 Panel on Contaminants in the Food Chain. Risks for human health related to the presence of 3- and 2-monochloropropanediol (MCPD), and their fatty acid esters, and glycidyl fatty acid esters in food. EFSA Journal 2016;14(5):4426 [159 pp.].
Yesterday this headline appeared in Stuff.
Included in the article was a claim from Prof Rod Jackson that
“Butter consumption has increased and the underlying cause of heart disease is a diet high in saturated fat.”
Kiwis follow advice of advocates for high-fat, low-carb diets, who promote foods such as coconut oil and butter, to the detriment of their health, Jackson said.
“Everything was going in the right direction and now people are getting confused. Coconut fat should never go in your mouth, it’s saturated fat.”
We think this is a bit rich. A rise in heart disease was a predictable result of the huge increase in diabetes and obesity in recent years, the very epidemic we’ve been fighting with LCHF advice. The same reversal of mortality trends has happened in America, where LCHF is hardly being blamed. One place it’s not happening is Sweden, which has had mainstream LCHF diet advice and rising butter sales since 2008 – in Sweden heart attack death rates continue to drop steadily, with age-adjusted stats available as recently as 2015.
(In fact the Stuff article states that heart disease rates have already risen in Australia, a country which, as we shall see, is, according to Rod, eating far less butter than us, and where the dietary establishment has been suppressing LCHF advice viciously).
Another good reason why heart disease is rising is that we have an ageing population. The figures in Stuff were not age adjusted, there is a limit to how long life can be extended, and that limit is being reached all around the developed world. People have to die of something; we won’t really know if heart disease is rising until the statistics are age-adjusted – but we suspect it is, because this is an expected effect of a diabesity epidemic that Rod didn’t seem to think was very important with regard to heart disease when we spoke to him last.
How LCHF eating advice – a pattern of eating which reduces almost every cardiovascular risk factor – blood pressure, weight, triglycerides, HDL cholesterol, blood glucose and more – can be blamed for any increases in heart disease mortality is a wonder.
What about Rod’s claim that we’re eating more butter? He expanded on this in a recent edition of the Listener which re-opened the old debate, which is better, butter or margarine (non-dairy spreads)?
The case against butter was presented by Rod and Listener nutrition writer Jennifer Bowden, and the case for margarine was presented by oils and fats chemist Dr Laurence Eyres, so it was a balanced debate.
We don’t agree with their view that butter is bad for you, and causing untold health harms in New Zealand.
Before we go into it, we’re not telling people to eat butter. Olive oil is perfectly good and also has lots of uses. We just don’t see why the average person shouldn’t eat butter, especially in the context of a low carb diet. But we will point out that the category of margarine/non-dairy spread products suffers from multiple issues not addressed in the Listener article, which we’ll get to in a second part of this series.
So are we eating too much butter? First, we need to understand – just how much butter do we eat?
from Index Mundi – the 1986 spike is probably the result of an error that was corrected in 1996.
Professor Rod Jackson, interviewed by Nicky Pelligrino, told us the old historical narrative, that heart disease in NZ started falling as soon as butter intake started dropping from the 1960’s high of 20 Kg annually per capita (385g per week, on average, for every man, woman and child in the country), because saturated fat intakes fell, cholesterol fell, and so on.
The problem with this story is that saturated fat intakes fell slowly, there was a decline in monounsaturated fat too, and most of the replacement energy came from carbohydrates and products with trans fats (margarine became freely available in New Zealand in 1972). Any rise in polyunsaturated fat consumption was small and happened slowly, taking us from about 3% to 5% PUFA by the 1980’s.
There’s no version of the diet-heart hypothesis where a very gradual change of this type would cause a dramatic drop in heart attacks, effective immediately (or even at all, really). We were still eating diets high in saturated fat when heart disease started dropping, and we had been eating them for quite some time, and, per the classic version of the diet-heart hypothesis, coronary atherosclerosis is a slowly progressive disease and its reversal, if it happens at all, requires drastic dietary change.
In Rod Jackson’s version we started replacing butter with olive oil and canola in the late 60’s. No, we didn’t. Oils available in NZ in those days weren’t popular and usually tasted rancid, maybe because they got left in the cupboard for years. People didn’t really start using those products till the 1970’s, which was when the health food movement hit New Zealand. Canola oil wasn’t even invented till the mid-1990’s.
Be that as it may, the most remarkable claim in Rod Jackson’s story is that we are now eating as much butter as we did in the 1960’s. He’s on record from 2014 as saying that NZ per capita butter consumption was up to 11 Kg per annum in 2011, and now he’s saying it’s over 20 Kg and the highest in the world.
That’s right – every man woman and child in New Zealand eats, on average, 400g of butter every week (a block is 500g).
Judge Judy Scheindlin has a book titled “Don’t Pee on my Leg and Tell me it’s Raining”.
This is a case where a little observation on Rod’s part might help to correct a mistaken view. Is it really raining butter?
In the 1997 nutrition survey adult Kiwis (15+) were eating about 7.1% of the 35% of energy that came from dietary fat from butter (about 2.5% of total energy); children ate much less. In the 2008/9 survey, this was halved. Calculating from these figures, unlikely to be very reliable, only gives us around 2Kg a year. Yet even in this year Rod Jackson was quoted as saying “We average around 8kg a year – three times as much as Australians and 16 times more than the Japanese”. So according to Jackson, in 2008, before LCHF and Paleo became popular, the results of the Ministry of Health’s Food and Nutrition Study were completely and utterly wrong, and the average Kiwi was already eating more butter than a butter-friendly low-carber does today, and as much as the average inhabitant of France.
Rod’s data come from the Food and Agriculture Organization (FAO) of the UN, but there are other data available, which come from the dairy industry itself, and the International Dairy Federation has our per capita butter consumption for 2015 at 4.9 Kg, placing us in 7th equal place in world butter consumption.
They should know. But also look around you. My (GH) family of four eats and my (GS) family of five eat butter, and we don’t buy any non-dairy spreads. The two adults, but not the teenagers, eat LCHF (both GS and GH). We buy one 500g block most weeks (some weeks we don’t need to replace it). We use a little ghee too (GH). Together this adds up to about 550g butter fat; that’s 7.2 Kg per year per capita. But we’re exceptional families (maybe?), because someone is still buying the margarine and non-dairy spreads, someone is still cooking with soy and corn oil, and someone is still using vegetable shortening in their baking. Canola oil consumption in NZ is almost double that of butter, according to the industry data. These things haven’t gone away – and most of them didn’t exist in the 1960’s, when butter was the main fat in recipe books, and the only spread in the shops. We sometimes see butter in other people’s shopping trolleys, but more often see the cheaper oils and spreads. New Zealanders don’t eat more fat today than we did in the 60’s, so how do we fit all these oils and spreads in if we’re now eating the same amount of butter we ate back then?
Another factor is that Kiwis eat out more often and eat more processed and fast food than we did in the 1960’s. Takeaway food and processed food are hardly ever made with butter, and even restaurant food doesn’t supply much. The 1960’s equivalent of processed food was Edmonds’ Cookbook recipes made with equal quantities of butter, sugar and flour, or white bread with butter and jam, cheese, or luncheon meat (and if there were any adverse health effects of butter in the 1960’s NZ diet, you don’t need to look any further than those combinations, which accounted for most of the butter eaten).
So it looks to us that the IDF estimate of around 5 Kg per annum has to be much closer to the truth than the FAO estimate of 20 Kg, even if, as we expect, butter consumption per capita is increasing.
Why does this matter?
It’s important that public health advice be based on statistics that are as accurate as possible. Rod Jackson is fairly representative of the anti-saturated fat approach in New Zealand public health. In 2008 he called for a tax on butter (“professor calls for tax on poison butter“).
His colleagues present proposals modelling the effects of saturated fat taxes in New Zealand. If Jackson and his colleagues are basing their thinking on the FAO estimate, and it is badly wrong, as we think it may well be, then these models, such as they are, will be inaccurate. Further, if a scare story is published claiming we eat too much butter, and this is why we’re having heart attacks (sure, it has nothing to do with low-fat sugary treats and KFC cooked in canola oil), and the estimate of how much butter is being eaten in that story is out by a factor of 3 or 4, then the claim is based on an alternative fact.
Plainly, we need much more reliable data than we currently have to make any claims about butter consumption in NZ today.
As for the claim that coconut oil is somehow responsible – coconut oil is expensive. It’s not a big seller in supermarkets. It’s being bought by health conscious people and used as part of a diet that’s overall lowering their risk. It’s very unlikely to have come anywhere near the rise in heart attacks; we note that both the Stuff article and a recent Listener article focus on the stories of younger people who had heart attacks with no warning, because their cholesterol was low. So that hardly tells us that butter or coconut oil are dangerous – it tells us, rather, that Rod Jackson’s preferred risk marker is dangerously unreliable.
To make public health recommendations about a food like coconut oil is a step way past any criterion that should be used by public health practitioners. More specifically the criteria set out by Bradford Hill are simply not met. Its time to get sensible about public health recommendations around saturated fat and coconut oil.
For metabolic syndrome, maybe it’s time to look at other results, like the fasting TG/HDL ratio and HbA1c, and to start taking the epidemic of diabetes, obesity, and the metabolic syndrome more seriously, seriously enough to start applying effective measures like LCHF more widely.
Addendum: some more realistic data on the butter increase
Here’s some figures that seem to fit the facts. They come from the US Department of Agriculture’s yearly reports and are based on industry monitoring.
– From 2009 -2011, NZ butter consumption was at its lowest ever – 20 thousand metric tonnes. In 2012, about the time we (GS and GH) started to eat LCHF, Pete Evans went Paleo, and so on, it went up 5%, and went up another 4.7% in 2013. Consumption has stayed stable since then, on 22 thousand metric tonnes.
So a 10% increase over the lowest-ever consumption rate can possibly be attributed to LCHF, Paleo, and the Real Food movement, etc (and to New Zealand’s ever-growing population).
However, in 2013, rapeseed oil (canola) increased 5.71% and in the following year 2.70%
Palm oil consumption also increased by 36% in this period, and is now equal to butter consumption.
Soybean oil, the other main oil in spreads and other processed foods, fluctuated a fair bit but overall stayed stable during this period.
Canola and palm oil together – oils and spreads – accounted for a bigger increase in saturated fat intake in NZ than butter during the period in question, proving that Kiwis in general didn’t turn away from these foods at all.
In part 2 of this series we’ll look at What, if Anything, is Wrong with Margarine?
 Jody C. Miller, Claire Smith, Sheila M. Williams, Jim I. Mann, Rachel C. Brown, Winsome R. Parnell, C. Murray Skeaff. Trends in serum total cholesterol and dietary fat intakes in New Zealand between 1989 and 2009. Aust NZ J Public Health. 2016; Online; doi: 10.1111/1753-6405.12504.
By George Henderson and Grant Schofield
If you have a standard lipid test done in New Zealand and most other parts of the world, it will usually give a couple of ratios at the bottom. One of these is the fasting triglyceride-to-HDL cholesterol ratio.
It can also be calculated from the other measurements using this online calculator.*
Note that the reference range says that under 2 is ideal, 2-4 is “normal”, over 4 is high.
In our opinion TG/HDL ratios in the 2-4 range may be normal, but they are still likely to be unhealthy or predictive of future ill health. Why is this?
Fasting triglycerides (TG) are usually low (<1) in low carb, fat-adapted people. An exception can be during rapid weight loss.
If TG are high in the fasting state this indicates insulin resistance, and when triglycerides are too high their transfer to the HDL particles causes the HDL count to drop. Because the natural range of TG is fairly wide and context-dependent, the value of this single measurement is disputed, and HDL and the fasting TG/HDL ratio are taken as the more sensitive markers.
Another value is that these are cheap markers which are commonly tested. While there others that may be better, such as fasting insulin or 2-hour insulin, the TG/HDL ratio, especially considered in the context of other common measures including HbA1c and LDL cholesterol, often gives a valuable “look under the hood” at the state of metabolism and hormonal health.
We are constantly asked to comment on standard lipid panels. We think the TG/HDL ratio tells you a fair bit. So here’s our take.
First we will discuss evidence for HDL independently, then for the TG/HDL ratio.
This slide is from the SMART study group, and represents the risk for “all vascular events” in a lipid-lowering trial in 6,111 individuals with a previously diagnosed arterial disease. The controls were a group taking a low-dose statin that didn’t significantly lower their LDL. As you can see, only the control arm in the highest quartile for HDL at baseline had a significant risk reduction. The mean baseline TG/HDL ratios by HDL quartile were 6.2, 3.6, 2.9, and 1.6.
What’s intriguing about this is that these are people with pre-existing arterial disease, often from years earlier (historical). The high HDL quartile has the lowest rates of diabetes and metabolic syndrome and the lowest BMI (25.1 vs 28.1) and waist circumference (92 vs 99.3 cm), so does this group include more historical cases, and represent to a greater extent these men and women who, after their event or diagnosis, managed to improve their hormonal metabolism in various ways? We don’t know, because this kind of evidence isn’t supplied, but an earlier study from the SMART study group showed this interesting correlation between HDL , LDL and new events in a population at high risk (with high cholesterol or high blood sugar). Highest HDL (≥1.50 mmol/l) is protective in people with high LDL (≥2.5 mmol/l), whereas for those with low LDL, a lower HDL is sufficient (≥1.26). Again this is with a TG/HDL ratio of 1.6 in the combined upper HDL quintile, and 2.7 in the 4th quintile.
Some further evidence about TG and HDL comes from an older set of data, the Helsinki Heart Study. In this study a fibrate, Gemfibrozil, was used to lower cholesterol (fibrates lower triglycerides and small, dense LDL), and there was an untreated placebo arm (black bars). Here in this placebo arm we can clearly see the effect of triglycerides and HDL in reducing risk.
In the placebo group (n = 2,045), the low density lipoprotein cholesterol (LDL-C)/high density lipoprotein cholesterol (HDL-C) ratio was the best single predictor of cardiac events. This ratio in combination with the serum triglyceride level revealed a high-risk subgroup: subjects with LDL-C/HDL-C ratio greater than 5 and triglycerides greater than 2.3 mmol/l had a RR of 3.8 (95% CI, 2.2-6.6) compared with those with LDL-C/HDL-C ratio less than or equal to 5 and triglyceride concentration less than or equal to 2.3 mmol/l. In subjects with triglyceride concentration greater than 2.3 mmol/l and LDL-C/HDL-C ratio less than or equal to 5, RR was close to unity (1.1), whereas in those with triglyceride level less than or equal to 2.3 mmol/l and LDL-C/HDL-C ratio greater than 5, RR was 1.2. The high-risk group with LDL-C/HDL-C ratio greater than 5 and triglyceride level greater than 2.3 mmol/l profited most from treatment with gemfibrozil, with a 71% lower incidence of coronary heart disease events than the corresponding placebo subgroup. In all other subgroups, the reduction in CHD incidence was substantially smaller.
Summary so far: From both the SMART study and Helsinki we see that the TG/HDL ratio is especially important when LDL cholesterol is high. Why is this?
In this graph from a paper by Boizel et al you see that the TG/HDL ratio predicts LDL particle size. The proportion of small, dense atherogenic LDL particles rises sharply, and the proportion of intermediate and large particles falls, as the TG/HDL ratio increases in these patients (n=60 with type 2 diabetes and HDL ≥ 1 mmol/l).
The typical dyslipoproteinemia of type 2 diabetes is characterized by elevated VLDL, small (dense) LDL particles, and decreased HDL (4). The percentage of individuals having small LDL is increased by at least twofold in type 2 diabetes (5).
The prevalence of this qualitative abnormality of LDL has been reported to be surprisingly high, even in the absence of the characteristic diabetic dyslipidemia. Thus, up to 45% of patients with low triglyceride (TG) levels and an even higher percentage of patients with borderline hypertriglyceridemia have small LDL, in comparison with 30% in nondiabetic men and 10% in nondiabetic women (5–8).
Three prospective studies have established that small dense LDL is the best predictor
of future coronary artery disease (CAD) in nondiabetic subjects, even after adjustment for confounding by TG, LDL cholesterol, and HDL cholesterol levels (9).
These authors propose a TG/HDL ratio cut-off of 1.5 to diagnose atherogenic LDL particle size in people with type 2 diabetes.
The fasting TG/HDL ratio is highly correlated with 2-hour insulin (insulin levels 2 hours after consuming glucose) and, with a higher cut off, is also predictive of fasting hyperinsulinaemia. Insulin activates the same HMG-CoA reductase (HMGR) pathway that statins inhibit.[6, 7, 8] This explains why the protective effects of HDL and of statins are not at all additive, and why in SMART and Helsinki, as well as the JUPITER trial, lipid lowering treatments made little or no difference to high HDL and/or low TG groups, who were already at lower risk.
This evidence also predicts that drugs such as statins may be more effective than the large studies say they are when patients are carefully chosen on the basis of individual diagnostic markers, including the fasting TG/HDL ratio; bearing in mind, however, that this is an easy marker to change with a low carb healthy fat diet, which, if it changes the TG/HDL ratio, will also change LDL particle size and insulin levels for the better, amongst other things. There will be less chance of harmful side effects on the LCHF diet compared to drug interventions.
- LCHF will have an important and postive effect on the fasting TG/HDL ratio
- Fasting is critical. There has been a tendency in NZ, to go with non-fasted. We imagine this is just easier because of compliance issues. But it totally ruins the ratio as TG change rapidly when you eat. They are very prone to a rapid rise with carb intake because insulin fluxes carb-derived TG out of the liver.
- Fasted TG and HDL measures will mean your estimate of LDL (which is never directly measured) will be more accurate. So our advice is to do the blood lipid tests fasted for a more accurate and meaningful result.
Lowering of 2-hour post-prandial insulin response by a 20% carbohydrate diet vs 40% carbohydrate, from Gannon and Nuttall 2009.
*Note that the TG/HDL ratio in NZ is calculated using mg/dl values, as in the US, even though NZ lipid measurements themselves are given in mmol/L. mmol/L ratios, which give different numbers, are used in Europe, but all the literature we’re citing here is using the mg/dl ratios, which are in any case more convenient.
 van de Woestijne AP, van der Graaf Y, Liem A, Cramer MM, Westerink J, Visseren FJ. Low High-Density Lipoprotein Cholesterol Is Not a Risk Factor for Recurrent Vascular Events in Patients With Vascular Disease on Intensive Lipid-Lowering Medication. J Am Coll Cardiol.2013;62(20):1834-1841.
 Hajer GR, van der Graaf Y, Bots ML, Algra A, Visseren FL; SMART Study Group.
Low plasma HDL-c, a vascular risk factor in high risk patients independent of LDL-c.
Eur J Clin Invest. 2009 Aug;39(8):680-8. doi: 10.1111/j.1365-2362.2009.02155.x. Epub 2009 May 12.
 Manninen V, Tenkanen L, Koskinen P, et al.
Joint effects of serum triglyceride and LDL cholesterol and HDL cholesterol concentrations on coronary heart disease risk in the Helsinki Heart Study. Implications for treatment.
 Boizel R, Benhamou PY, Lardy B, Laporte F, Foulon T, Halimi S. Ratio of triglycerides to HDL cholesterol is an indicator of LDL particle size in patients with type 2 diabetes and normal HDL cholesterol levels. Diabetes Care. 2000 Nov;23(11):1679-85.
 Li C, Ford ES, Meng YX, Mokdad AH, Reaven GM.Does the association of the triglyceride to high-density lipoprotein cholesterol ratio with fasting serum insulin differ by race/ethnicity?
Cardiovasc Diabetol. 2008;28;7:4.
 Ness GC, Zhao Z, Wiggins L.
Insulin and glucagon modulate hepatic 3-hydroxy-3-methylglutaryl-coenzyme A reductase activity by affecting immunoreactive protein levels.
J Biol Chem. 1994 Nov 18;269(46):29168-72.
 Vincent TS, Wülfert E, Merler E.
Inhibition of growth factor signaling pathways by lovastatin. Biochem Biophys Res Commun. 1991 Nov 14;180(3):1284-9.
 Chen H, Ikeda U, Shimpo M, Shimada K.
Direct effects of statins on cells primarily involved in atherosclerosis.
Hypertens Res. 2000 Mar;23(2):187-92.
 Gannon MC, Nuttall FQ.
Control of blood glucose in type 2 diabetes without weight loss by modification of diet composition.
Nutrition & Metabolism2006;3:16
I’ve witten a lot about fuelling for training and racing for sport performance, especially endurance, and most especially Ironman triathlon. That’s what inspired What the Fat? Sport Performance, and several blogs about this guy: Bevan McKinnon and his sucess in using low carb healthy fat.
He’s now the current Ironman 70.3 and Ironman Hawaii World champion. That follows from his record time for an age grouper at Ironman NZ, Match 2016, and an group win in the ITU long course world champs in 2015.
Here’s the audio of my interview with Bevan following all this success and just exploring the in’s and out’s of nutrition in training and racing at the highest level.
Its a good listen with lots of gems from a very experienced athlete ad coach. Total time 34 minutes.
We recently had this letter on salt and hypertension published in the British journal, The Lancet. It’s unusual for the Lancet to publish favourable references to low carbohydrate diets. They tend to publish material supporting statins and fat-restricted dietary guidelines instead (thus setting up a series of controversies with the more reformist British Medical Journal. This probably helps the readership of both journals, and, by provoking open debate, generally advances the cause of science). So we’re very pleased that they thought the ideas in our letter sensible or informative enough to deserve publication.
Here we explain how we got drawn into this area, and why we think that the effects of LCHF on high blood pressure are relevant to people eating all kinds of diets.
Most people who start on a very low carbohydrate diet lose an extra pound or three or easily in the first week, and the conventional explanation is that this is nothing to get excited about as it’s water weight, water bound to glycogen that’s freed up when glycogen stores become depleted. We’ve never been happy with that explanation, because often the loss is much greater than the amount we’d expect from glycogen depletion.
In someone with hypertension, some of this water is actually part of the increased extracellular fluid volume that’s kept their blood pressure high. It’s good to be losing it.
In fact, if someone has high blood pressure, it’s very likely that they’ll be cutting down on medications quite soon after starting this diet – people with type 2 diabetes often reduce or come off blood pressure medication even before they cut down on blood sugar meds. We saw this in the very-low carb studies we reviewed for our New Zealand Medical Journal article on diabetes.
At the same time, you can start losing sodium easily, and you often need to supplement salt to keep your electrolytes in balance, when you cut carbs very low.
I’ve (GH) (and me (GS)) had this experience, getting cramps and feeling weak on a very low carbohydrate diet until I drank some water with extra salt, and I’ve also had the opposite experience of eating a salty high-carbohydrate meal in a Japanese restaurant and waking up visibly puffy from the retention of sodium and water. Such experiences are common.
The sodium (Na+) concentration in our body fluid needs to be kept within a quite narrow range, so if we’re retaining sodium we need to retain water and vice versa, and if losing, the opposite applies. And this system seems to be regulated by insulin – someone with type 1 diabetes who has no insulin will lose both electrolytes and fluid volume quickly.
So when we saw the study by Andrew Mente and colleagues in the Lancet, where most people tolerated high levels of salt long-term without increased systolic blood pressure or risk of CVD events or mortality, but in people with hypertension increases in blood pressure were associated with increasing sodium intakes, and increased CVD risk with high intakes, especially over 7 grams a day – which is a lot (in both groups low sodium intake, under 3 grams a day, was also associated with risk), we wondered whether the dietary context had an influence on this risk.
We looked to see what’s known about sodium reabsorption in the kidney, and found several experiments. The experiment we cited as our reference 5 has a particularly brilliant design – linking it to both the glucose and insulin concentrations in the blood. We also found that it’s well-accepted that essential hypertension is part of the metabolic syndrome, along with high insulin, elevated blood sugar, high triglycerides and low HDL.
(Essential hypertension is supposedly hypertension without known cause, it “just is”.
Actually, the distinction is to contrast it with hypertension secondary to some diagnosable physiological abnormality or disease – for example, portal hypertension, when cirrhosis of the liver inhibits the removal of blood by the liver from the portal vein, or hypertension due to kidney disease and so on.)
So it seems there may be a more coherent view of hypertension which explains why it appears in the context of metabolic syndrome.
We thought it is worthwhile for researchers to assess how much hypertension is associated with elevations in the insulin response to glucose. In other words, it’s worth looking for evidence as to whether this is (as we put it in our letter) due to to their not tolerating the amount of carbohydrate in their usual diet.
Because budgetary factors are important to the chances of any large study (the study in Mente et al was huge, n=133,118), we suggested the cheapest proxy for insulin, the fasting triglyceride/HDL ratio, which correlates quite well with the 2-hour insulin response to an OGTT in people without diabetes, and which are data that are in most people’s medical records already. The use of this proxy could be validated with the 2-hour insulin response to an OGTT in a subgroup if necessary. It can be seen in this study, chosen at random, that a doubling of the HDL/TG ratio (from ~2 to ~4 here) correlates with a doubling of the 2-hour insulin level (in table 2).
We already know that restricting carbohydrate in the diet is an effective tool for improving most cases of hypertension, but this sort of investigation would enable us to know with more certainty whether the consumption of modern high-carb diets lies somewhere on the causal pathway as well.
It’s not our position that dietary guidelines need to warn against high-carbohydrate diets – there’s no good evidence for that, they seem fine for plenty of people – but instead that they should supply clear information that restricted-carbohydrate diets are safe, and can be beneficial for weight management, blood sugar control, the management of blood pressure, and so on.
Researching this post brought up a very interesting animal study. In this experiment, a naturally hypertensive breed of rat was treated with high insulin doses. This greatly increased the animals’ blood pressure over baseline, and 4 of the 8 insulin treated rats suffered heart attacks – despite having no atherosclerosis, and not being fed cholesterol and high fat diets. Animals that are given atherosclerosis with high cholesterol diets don’t usually suffer heart attacks or other adverse effects. The placebo-treated hypertensive rats, and the insulin-treated normal rats, didn’t suffer heart attacks.
Demonstrating, perhaps, that high blood pressure plus high insulin is a dangerous combination, even when cholesterol is low. The discussion section of this paper is an interesting summary of the evidence for hyperinsulinaemia as causal in heart disease.
However, nothing in biology is ever quite as simple as we’d like it to be. Fuenmayor et al in 1998 found that insulin resistance in salt-sensitive, but not salt-resistant hypertension was worsened by high salt intakes. So these individuals may have an additional method to lower insulin, by avoiding high salt intakes. However high salt intake in this study was achieved by giving an extra 12 grams (3 teaspoons) of salt (4.6g sodium) a day on top of the low salt diet (this would take total intake to about 7g day), and this was not a cross-over study (7 days of low salt diet came first). Fasting and two-hour insulin in even the salt-resistant hypertensive cases was significantly higher than in non-hypertensive non-diabetics. The two-hour insulin is lower, as an artifact of the insulin suppression test used.
Fuenmayor et al concluded
Our observation is in line with the recent findings of increased insulin secretion in response to an oral glucose load in salt sensitive compared to salt resistant hypertensives. Therefore, carbohydrate administration (food intake) would induce silent hyperinsulinemia in salt sensitive patients. The elevated insulin levels may induce and worsen salt sensitivity and hypertension, and in the long term favor cardiovascular atherosclerotic complications.
Of course the quickest way to get too much salt and have your insulin raised too much by carbohydrate is to eat processed food. Avoid that, and it’s hard to overload on sodium just from occasional salty foods like feta, salted butter, and bacon. Use table salt (preferably iodised if you don’t eat a lot of seafood ) to taste. Have your blood pressure checked at the end of every doctor’s visit (seeing a doctor has been proven to raise your blood pressure, so only have it read once you’ve been seated for a while and have relaxed, if you can). If your blood pressure is too high, and you’re not eating heaps of salty or processed food, a LCHF diet may be a safer (and more effective) way to manage it than trying to cut salt as low as you can.
 Temelkova-Kurktschiev T, Henkel E , Schaper F, et al. Prevalence and atherosclerosis risk in different types of non-diabetic hyperglycemia. Is mild hyperglycemia an underestimated evil? Exp Clin Endocrinol Diabetes. 2000;108(2): 93-99.
 Zimlichman L, Zaidel S, Nofech-Mozes A et al. Hyperinsulinemia Induces Myocardial Infarctions and Arteriolar Medial Hypertrophy in Spontaneously Hypertensive Rats.
AJH 1997;10:646–653. zimlichman1997
 Fuenmayor N, Moreira E, Cubeddu LX. Salt sensitivity is associated with insulin resistance in essential hypertension. Am J Hypertens. 1998 Apr;11(4 Pt 1):397-402.
HDL cholesterol is one of the strongest predictors of both cardiovascular and cancer risk. It’s especially useful as this association seems to have no genetic basis, which implies it’s a modifiable risk factor. All non-drug interventions that improve health, for example by lowering weight, blood sugar, or inflammatory markers also raise HDL, including low carb diets, Mediterranean diets, and exercise. Raising HDL is usually considered a good thing. HDL is even called “good cholesterol” by the kind of ninnies who think that millennia of evolution have succeeded in producing something that deserves to be called “bad cholesterol”.
But there’s recent claims that high HDL is actually bad for cardiovascular disease at least,, after all.
CANHEART was a large (n= 631,762) pooled study in Canada, in which the association of HDL with mortality from CVD, cancer, and all other causes was determined over a follow-up period of 4.9 ± 0.4 years, during which there were 17,952 deaths.
Low HDL was associated with high death rates from all 3 causes, but surprisingly the CVD benefit plateaued at a fairly modest level, and very high HDL was associated with increased risk of non-CVD mortality. Especially levels over 90 mg/dl (2.33 mmol/l), but also over 70 mg.dl in men (1.81 mmol/l). CVD mortality overall was lowest in the range 51-90 mg/dl (1.32-2.23 mmol/l). These findings, as reported, supposedly debunk the idea that raising HDL is a good idea. Of course, raising HDL with drugs by sticking a spanner in the works at some point has never been an effective strategy and, as we shall see, there are genetic polymorphisms that give elevated HDL of little worth, but healthy diet and lifestyle changes that are reasonably expected to extend life always raise HDL a bit. Is this meaningless?
The levels associated with harm are very high HDL levels, and it’s relatively unusual to see levels this high in non-drinkers on LCHF diets, no matter how much coconut oil they eat. However, high alcohol intakes, as well as exposure to some drugs and toxins, can produce this effect, as can certain genetic variations. The conditions are collectively known as HALP, which is short for hyperalphalipoproteinaemia (we’ll stick with HALP).
One of the most common causes of HALP is alcoholism. Alcohol elevates HDL and at moderate intakes (around one standard drink a day) this is associated with benefit, but at high intakes there is no benefit and an increased risk of death from non-cardiovascular causes, including cancer. Ko at al in CANHEART claimed to have adjusted for excess alcohol intake, which was highest in those with highest HDL;
“Heavy alcohol consumption, as defined by the use of 5 or more drinks on 12 or more occasions per year was also included in the model for non-cardiovascular non-cancer death.”
I hate to break it to you, but getting drunk, even blind drunk, once a month will probably not raise your HDL much if at all. You really need to be a chronic alcoholic. In 2012, approximately 5 million Canadians (or 18 % of the population) aged 15 years and older met the criteria for alcohol abuse or dependence at some point in their lifetime, but how many at any one time qualify as chronically alcoholic is unknown. We know that Canadians have a per capita consumption of 10.2 litres of pure ethanol per year. That’s 27ml per day – a 200ml glass of wine – for every man, woman, and child over 15. If (for example) only 1 in 4 people drank regularly, that would be a bottle of wine a day each.
Even so, the data used in CANHEART to make the alcohol adjustment was far from complete.
“Since the use of smoking and alcohol was not available in entire CANHEART cohort, we imputed smoking status and heavy alcohol use for those with missing data based on the characteristics of the respondents to the Canadian Community Health Survey. Multiple imputation using complete observations and 10 imputation datasets was conducted. Smoking status was available for 5,093 individuals and alcohol use was available for 5,077 individuals who completed the survey.”
This was a tiny fraction of the 631,762 individuals in the study – less than 1% – and it involved voluntarily self-reported health data;
The Canadian Community Health Survey (CCHS), an ongoing Canada-wide population-based survey that collected information on self-reported health status, health determinants, and health care utilization
Alcohol intake is known to be misreported in dietary surveys by a factor of 2-3. Alcoholism is probably under-reported to health professionals to a much greater extent, especially in countries where health insurance is a major factor in access to care.
Another confounder is the effect of genetic polymorphisms. One genetic cause of very high HDL is a CETP defect.
“…the in vitro evidence showed large CE-rich HDL particles in CETP deficiency are defective in cholesterol efflux. Similarly, scavenger receptor BI (SR-BI) knockout mice show a marked increase in HDL-cholesterol but accelerated atherosclerosis in atherosclerosis-susceptible mice. Recent epidemiological studies in Japanese-Americans and in Omagari area where HALP subjects with the intron 14 splicing defect of CETP gene are markedly frequent, have demonstrated an increased incidence of coronary atherosclerosis in CETP-deficient patients. Thus, CETP deficiency is a state of impaired reverse cholesterol transport which may possibly lead to the development of atherosclerosis.”
The CANHEART authors, Ko et al, do not mention the likelihood of such conditions affecting their analysis. Even if we assume that both chronic alcoholism and genetic HALP are rare conditions, men with HDL over 90mg/l were less than 0.3% of the study population, and of these few men, only a few dozen died during the study. The exact number isn’t clear because the only mortality data given is for adjusted age-standardized rates per 1,000, but from total deaths and these rates we estimate it to be (at the very most) 70-80 deaths, of which 30-35 were non-cardiovascular and non-cancer deaths, out of about 2240 men. The majority of alcohol-related such deaths in Canada are due to alcoholic liver disease, motor vehicle accidents and alcohol-related suicides. Had Ko et al given a breakdown of non-cardiovascular causes of death for the highest HDL categories, it would have been relatively easy to tell how many of these were due to alcoholism.
Overall, people in the high HDL categories at baseline exercised more, had lower triglycerides, less diabetes, lower LDL, more ideal BMI, and ate more fruit and vege than people in the middle and lower ranges.
Did these things cause them to die at a higher rate?
Here’s an alternative explanation – the baseline characteristics represent only the vast majority of people in each category. The vast majority of people in each HDL category, even the highest, didn’t die. Even people with genetic HALP can be healthy. The people who died in the high HDL categories tended to be the people with alcoholism, drug induced HALP, and poorly-managed genetic HALP, and their baseline characteristics, had they been isolated, would have been quite different. These are the people for whom high HDL is not protective, and, as their numbers increased in categories of increasing HDL, the usual dose-response relationship between HDL and cardiovascular disease and cancer, seen in better-controlled populations, was lost.
(There would also have been metabolically healthy individuals who had low HDL for genetic reasons doing well in the low HDL category. For this reason the TG/HDL ratio and other available risk factors still need to be taken into consideration when evaluating HDL).
Healthy HALP seems to require low insulin and low triglycerides (TGs). This is exactly what we see in insulin-sensitive individuals, and in people whose HDL rises on the LCHF diet.
In hyperalphalipoproteinemia cases, we found a diminished TG/HDL-C plasma ratio that has been deemed as critically dependent on insulin activity. Although the plasma CETP activity measured by the exogenous method that reflects the plasma CETP concentration did not differ between the two groups the low TG/HDL-C likely is consequent to decreased endogenous CETP activity due to a diminished triglyceride availability from apoB-containing LP for exchange with HDL cholesteryl ester in hyperalphalipoprotaeinemia cases. In agreement with a primary role for insulin sensitivity in cholesterol metabolism and, to a considerable extent, in plasma HDL-C concentration variation, we found a diminished ALT level within the “reference” range in hyperalphalipoprotaeinemia cases, a result compatible with other reports relating ALT to insulin sensitivity.
A possible criticism is the way that Ko et al have interpreted the-lipid lowering trial data to support their thesis. This is only valid if their intention is to discourage the use of HDL as a drug target. (Incredibly, pharmaceutical companies have invested billions in developing drugs that inhibit CETP, and have continued to test these despite sometimes disastrous and always disappointing results, the latest trial ending as recently as 2016).
They say “Several contemporary studies have shown a lack of significant association of HDL-C levels and outcomes for patients on higher-intensity statins, with coronary artery disease, or who had undergone coronary artery bypass graft surgery (12,13,15).”
However, reference 12 states
“In 8901 (50%) patients given placebo (who had a median on-treatment LDL-cholesterol concentration of 2.80 mmol/L [IQR 2.43-3.24]), HDL-cholesterol concentrations were inversely related to vascular risk both at baseline (top quartile vs bottom quartile hazard ratio [HR] 0.54, 95% CI 0.35-0.83, p=0.0039) and on-treatment (0.55, 0.35-0.87, p=0.0047). By contrast, among the 8900 (50%) patients given rosuvastatin 20 mg (who had a median on-treatment LDL-cholesterol concentration of 1.42 mmol/L [IQR 1.14-1.86]), no significant relationships were noted between quartiles of HDL-cholesterol concentration and vascular risk either at baseline (1.12, 0.62-2.03, p=0.82) or on-treatment (1.03, 0.57-1.87, p=0.97). Our analyses for apolipoprotein A1 showed an equivalent strong relation to frequency of primary outcomes in the placebo group but little association in the rosuvastatin group.”
In other words, people in the top quartile for HDL and ApoA1 on placebo had the lowest vascular risk, and these people got little if any extra benefit from LDL lowering with a statin. And because we are looking at quartiles, not isolating a small number of people who have freakishly high HDL for some reason, there is a true dose-response effect of HDL between quartiles in the placebo arm.
This effect has been seen in multiple trials. Drug trials are likely to exclude alcoholics and binge drinkers.
The evidence tells us that the predictive value of HDL is excellent, but is lost when people are undergoing intensive treatment for coronary artery disease, a classic case of Goodhart’s law, “When a measure becomes a target, it ceases to be a good measure.” We see this again and again with intensive drug treatment to manipulate metabolic markers.
Thankfully, it doesn’t seem to apply to diet and lifestyle interventions.
What is HDL?
High-density lipoprotein or HDL is, like LDL, a large particle made up of various lipids and proteins (notably Apo A1 in the case of HDL, Apo B in the case of LDL) which is produced by the liver. Its role in cholesterol metabolism is to collect unwanted cholesterol, which is converted to cholesteryl esters (CE) by the addition of a fatty acid and transferred to LDL particles by CETP (cholesteryl ester transfer protein) for conveyance back to the liver. If CETP is deficient or inhibited CE accumulates in HDL, and LDL cannot complete its removal. Excess triglycerides (TG) from VLDL can also be transferred to HDL, and when the HDL particles become overloaded with TG they are unable to function as CE carriers and are removed from circulation, thus the association of high TG with low HDL and increased CVD risk.
 Ko DT, Alter DA, Guo H, et al. High-Density Lipoprotein Cholesterol and Cause-Specific Mortality in Individuals Without Previous Cardiovascular Conditions: The CANHEART Study. J Am Coll Cardiol. 2016;68(19):2073-2083. doi:10.1016/j.jacc.2016.08.038.
 Yamashita S, Maruyama T, Hirano K, Sakai N, Nakajima N, Matsuzawa Y.
Molecular mechanisms, lipoprotein abnormalities and atherogenicity of hyperalphalipoproteinemia.
Atherosclerosis. 2000 Oct;152(2):271-85.
 Leança CC, Nunes VS, Panzoldo NB et al. Metabolism of plasma cholesterol and lipoprotein parameters are related to a higher degree of insulin sensitivity in high HDL-C healthy normal weight subjects. Cardiovascular Diabetology 2013, 12:173.
 Ridker P.M., Genest J., Boekholdt S.M., et al; for the JUPITER Trial Study Group. HDL cholesterol and residual risk of first cardiovascular events after treatment with potent statin therapy: an analysis from the JUPITER trial. Lancet. 2010;376:333-339.
By George Henderson and Grant Schofield
Ancel Keys has become a kind of cartoon villain for dietary reformers for various reasons – allowing ecological epidemiological comparisons to dominate his thinking, attacking John Yudkin’s sugar hypothesis with made-up ecological claims, and basically (with a lot of help) bullying his rivals out of their labs and grants so that their science couldn’t undermine his and that of his mates.
Is there redemption? Did we get something wrong? Is he a good guy after all?
Ancel Keys had a first-class mind, and this was the main reason he won his battles. His work should not be ignored, any more than we should ignore the work of George Bernard Shaw or H.G. Wells because their ideas of social improvement led them eventually to support eugenics and dictators like Stalin. In this paper on the Roseto effect, Keys performs a valuable function – he debunks an early example of what would today be called ‘psychobollocks’. keys-roseto-2
The Italian immigrants of Roseto ate a diet high in red meat and animal fat (lard), and also high in starchy carbohydrate, the source of which no-one seems to have recorded. They avoided olive oil and had a seemingly low rate of heart attacks, supposedly due to relatively stress-free lives (the evidence for which was questionable). Keys shows that most of this supposed reduction in heart attacks is due to variation in coding the causes of death. And what is left over, he attributes to the Italians’ diets before immigration, and the fact that Italian immigrant diets had more monounsaturated fat and less saturated fat than the usual American diets. We also note (which Keys didn’t) that the inhabitants of Roseto drank wine instead of the soft drinks drunk by other Americans.
In this paper, Keys lays out the diet-heart hypothesis as it existed in 1965 –
But it is desirable to clarify the dietary problem.
STOUT et al.  discredit the hypothesis that dietary fat is important in atherogenesis
and its clinical complication in the form of coronary heart disease. Actually, the hypothesis that most proponents offer is not as simple as they indicate. One statement of the hypothesis is: “Atherogenesis in the coronary arteries is promoted by increasing concentration of cholesterol in the ß-lipoprotein in the blood plasma and this cholesterol concentration is raised by increasing the proportion of dietary calories supplied by saturated fatty acid, the poly-unsaturated fatty acids having a weaker opposing influence”.
A more modern and updated version of this, based on evidence from 60 controlled diet trials:  Just remember that Apo B is in LDL and similar particles, and tends to correlate with the small dense, and potentially harmful LDL sub-fraction. Keys knew about these, and they are resurfacing again today as an important marker of arterial health. Apo A1 is in the HDL sub-fraction which is associated with benefit.
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.
Apo B correlates to non-HDL cholesterol in people eating the normal diet, and less precisely to LDL cholesterol, whereas Apo A1 correlates with HDL cholesterol.
How did we get from this to a low fat diet?
Below we show you how. The low fat diet has potential to provide some benefit in improving particles. But the low carb diet is much better.
If we compare the 10% SFA, 30% fat dietary guidelines diet with a typical LCHF diet with unrestricted saturated fat, and fat from a variety of sources, we can see that the LCHF diet actually has the potential to lower Apo B much more than the low fat diet, despite having twice as much saturated fat. It also has more potential to increase Apo A1. The absolute levels of Apo B and Apo A1, and the ratios between them, are actually better predictors of heart disease risk than are LDL, HDL and their ratios.
The dietary guidelines diet:
Ignoring protein, only 20 % of this diet will lower Apo B, only 25% will increase Apo A1
50% UFA (5% PUFA)
50% of this diet will lower Apo B, 65% will raise Apo A1.
For some reason, when Ancel Keys came to test his hypothesis in 1968 in Minnesota, people were so opposed to increasing fat in the diet that he could only try to lower Apo B by replacing about 9% of the SFA in the diet with an equal amount of linoleic acid from corn oil (an intervention which wouldn’t have increased MUFA). This gave him a very small leverage in terms of Apo B compared to our example, offset by a negative effect on Apo A1.
He did this despite being on record as sceptical about the value of high linoleic acid (PUFA) intakes. Why? Maybe he had painted himself into a corner with his original ecological studies correlating fat with heart disease mortality. Maybe he had to compromise with the Harvard crew, Hegsted and Stare, who had already sold out to sugar interests. Even for someone as influential as Keys, setting up a big study was a co-operative effort that required the support of most of the major players in the field. In any case, the Minnesota study didn’t show that replacing SFA with linoleic acid reduced CHD mortality.
So, are there studies that support our hypothesis, that LCHF reduces CHD risk without SFA restriction? Just as in Keys day, few people can get funding for a long-term, large study that increases fat in the diet. The PREDIMED study is probably the only example; in this case, the diet arms with an increase in MUFA from olive oil (an extra 50g per day), or an increase in total unsaturated fats from nuts and olive oil (6 servings per week and 32g per day respectively), experienced lower risk of major CVD events compared to controls. (Those in the control group received small nonfood gifts, which was nice.) This is not a test of a high-SFA diet, as the subjects were complying with a supposed Mediterranean diet (i.e. not any real one but the version created recently by academics), but it does test the effect of increases in MUFA.
The median follow-up period was 4.8 years. A total of 288 primary-outcome events occurred: 96 in the group assigned to a Mediterranean diet with extra-virgin olive oil (3.8%), 83 in the group assigned to a Mediterranean diet with nuts (3.4%), and 109 in the control group (4.4%). Taking into account the small differences in the accrual of person-years among the three groups, the respective rates of the primary end point (major CVD events) were 8.1, 8.0, and 11.2 per 1000 person-years. The unadjusted hazard ratios were 0.70 (95% confidence interval [CI], 0.53 to 0.91) for a Mediterranean diet with extra-virgin olive oil and 0.70 (95% CI, 0.53 to 0.94) for a Mediterranean diet with nuts as compared with the control diet (P=0.015, by the likelihood ratio test, for the overall effect of the intervention). HRs for all but stroke were non-significant after multivariant adjustment.
There are a few recent epidemiological studies showing reduced CVD risk in higher-fat populations, with little or no adverse effect of SFA, including the high-quality Malmö Diet and Cancer Study. (n=28,098; 1250 deaths).
For men, a significant trend towards lower cardiovascular mortality in upper quartiles of total fat intake was observed (P = 0.028) with the RR for men in the fourth quartile being 0.65 (CI 0.45–0.94, P = 0.023) (Fig. 1). No difference was observed between quartiles of saturated fat intake for men. Having relatively high intakes of monounsaturated or polyunsaturated fats compared with saturated fats did not show benefit for either sex.
Although this association only exists for men in Malmö, this is important for 2 reasons – men have a much higher cardiovascular disease risk compared to women (3-4x in Sweden during these years), and cholesterol and LDL-cholesterol – the imprecise Apo B proxys – correlate with CVD risk in men in this age group, much more so than in women. Mean fat consumption by men in the upper quartile was 47.7% of energy – a respectable amount.
Similar findings came from the recent Harvard paper on fat and mortality in the combined Nurses’ Health Study and Health Professionals’ Follow-up Study (we wrote about this a while back).
After adjustment for known and suspected risk factors, dietary total fat compared with total carbohydrates was inversely associated with total mortality (hazard ratio [HR] comparing extreme quintiles, 0.84; 95% CI, 0.81-0.88; P < .001 for trend).
And, in memory of Keys, here’s a recent ecological (between-country) study: 
We found exceptionally strong relationships between some of the examined factors, the highest being a correlation between raised cholesterol in men and the combined consumption of animal fat and animal protein (r=0.92, p<0.001). The most significant dietary correlate of low CVD risk was high total fat and animal protein consumption. Additional statistical analyses further highlighted citrus fruits, high-fat dairy (cheese) and tree nuts. Among other non-dietary factors, health expenditure showed by far the highest correlation coefficients. The major correlate of high CVD risk was the proportion of energy from carbohydrates and alcohol, or from potato and cereal carbohydrates. Similar patterns were observed between food consumption and CVD statistics from the period 1980–2000, which shows that these relationships are stable over time. However, we found striking discrepancies in men’s CVD statistics from 1980 and 1990, which can probably explain the origin of the ‘saturated fat hypothesis’ that influenced public health policies in the following decades.
If the older epidemiological studies available to the original diet-heart enthusiasts didn’t show the same protective effects of total fat intake, this is perhaps because there was more trans fat in the food supply a few decades ago, or perhaps because modern studies are better controlled for carbohydrate quality and other factors.
The higher intakes in these studies of usual diets are usually around 40-50% fat, so they’re not actually low carb diets, but they are getting close, whereas our hypothetical LCHF example was 70% fat (which still allowed a generous hypothetical 75g of carbohydrate per day).
However – if Key’s hypothesis, and the prevailing appearance in his day of fat and SFA as associated with CVD mortality in epidemiology, was able to launch dozens of long-term studies of fat and saturated fat reduction for prevention of CVD, why is it that today, with a more up-to-date version of that hypothesis and at least as much epidemiological and experimental support for it, there are no trials, and instead we’re getting reheated leftovers of the old trials and their feeble and uncertain results, in the form of endless meta-analyses of the same data sets?
If you’ve read this far, you may appreciate this French documentary about the diet-heart hypothesis, which has some cool old footage of Ancel Keys and his crew.
There’s a particularly shocking bit in the middle where Jerry Stamler goes mad and starts telling us to throw away egg yolks. This marks the exact point at which the diet-heart hypothesis became an official licence to produce thousands of profitable low fat processed foods, with no regard for their actual nutritional value
* Nina Teicholz has pointed out that the only source of saturated fat associated with increased risk in this PREDIMED paper was “pastries and processed foods”. Meat, processed meats and dairy were safe sources of SFA.
 Keys A. Arteriosclerotic heart disease in a favored community. J chron Dis. 1966, Vol. 19, pp. 245-254.
 Mensink RP, Zock PL, Kester ADM, Katan MB. Effects of dietary fatty acids and carbohydrates on the ratio of serum total to HDL cholesterol and on serum lipids and apolipoproteins: a meta-analysis of 60 controlled trials. Am J Clin Nutr May 2003
vol. 77 no. 5 1146-1155. http://ajcn.nutrition.org/content/77/5/1146.full
 de Nijs T, Sniderman A, de Graaf J. ApoB versus non-HDL-cholesterol: diagnosis and cardiovascular risk management. Crit Rev Clin Lab Sci. 2013 Nov;50(6):163-71.
 Walldius G, Jungner I. The apo B/apo A-I ratio – a new predictor of fatal stroke, myocardial infarction and other ischaemic diseases – stronger than LDL and lipid ratios. Atherosclerosis. 2006;7(suppl):468. Abstract Th-W50.6.
 Ramsden CE, Zamora D, Majchrzak-Hong S et al. Re-evaluation of the traditional diet-heart hypothesis: analysis of recovered data from Minnesota Coronary Experiment (1968-73). BMJ 2016; 353
 Estruch R, Ros E, Salas-Salvadó J et al. Primary Prevention of Cardiovascular Disease with a Mediterranean Diet. N Engl J Med 2013; 368:1279-1290.
 Wang DD, Li Y, Chiuve SE et al. Specific Dietary Fats in Relation to Total and Cause-Specific Mortality.JAMA Intern Med. 2016 Aug 1;176(8):1134-45.
 Guasch-Ferré M, Babio N, Martínez-González MA, Corella D et al. Dietary fat intake and risk of cardiovascular disease and all-cause mortality in a population at high risk of cardiovascular disease. Am J Clin Nutr. 2015 Dec;102(6):1563-73. doi: 10.3945/ajcn.115.116046.
 Grasgruber P, Sebera M, Hrazdira E et al. Food consumption and the actual statistics of cardiovascular diseases: an epidemiological comparison of 42 European countries. Food & Nutrition Research [S.l.], v. 60, sep. 2016. http://www.foodandnutritionresearch.net/index.php/fnr/article/view/31694
A nice quote from reference :
The efficacy of replacing SFAs with carbohydrates depends on the effects on body weight in the long term, and that effect is uncertain.
Drs David Katz and Garth Davis are a good example of the type of crypto-vegan medical professional who believe in the power of the “plant based diet”. They have a knee jerk reaction to low carb diets, because they think these involve eating more meat.
Here’s a news flash – you can eat more meat on a low carb diet (because who knows if you ate any before), but you don’t need to, and you may well eat less, just because you’ll probably be eating less anyway, without much effort. …And LCHF well formulated is a high plant diet.
Newsflash 2: Cereals aren’t plants. They are highly processed foods made in factories.
Newsflash 3: You can eat a plant-based diet and be LCHF if you want.
But there’s more to it than just these revelations. There is a deeper unscientific criticism of LCHF, from scientists, which needs to be uncovered. Here it is.
They presented a blog on the Very Well website, a health and lifestyle platform which has also run more positive articles about LCHF, that’s critical of Drs Sarah Hallberg and Osama Hamdy’s recent opinion piece in the New York times saying that LCHF diets can be a viable alternative to bariatric surgery for diabetes.
Katz is from Yale (see his www site), and in our view is a “fence sitter” who criticises LCHF and other approaches which should be given as an option.
Katz introduces Davis, who then makes some numbered points. In our opinion these are all off the mark, and the condemnations of LCHF in particular include pseudoscientific scare stories; the sort of things that plant-based diet advocates fear will happen to them if they stop eating wholegrain cereals, but for which there is absolutely no evidence at all.
1. The authors imply that weight loss surgery is not effective.
Nowhere in the NYT article was it implied that bariatric surgery is ineffective.
In fact, though any surgery carries both a risk and a hefty price tag, there is good evidence that some forms of bariatric surgery are effective at reducing weight and reversing diabetes. Garth Davis, who is a bariatric surgeon, says “I see 80 percent to 85 percent of my gastric bypass patients off their diabetic medications five years later”, and this is a good result. Unless you are one of the other 15-20% (which is it?), some of whom may well have undergone a much bigger commitment than dieting for no improvement.
Dr Davis says “Long-term side effects of low-carb dieting may include high cholesterol, cardiovascular disease, kidney stones, bone loss, erectile dysfunction, malnutrition, and an increased risk of cancer.”
We have never heard of most of these; cholesterol usually goes down (if it’s high), it can sometimes go up, but there’s no evidence that rises in cholesterol related to carbohydrate restriction increase cardiovascular disease, and reason to think that they are at worst neutral. Why you would experience bone loss on any well-formulated diet, we can’t begin to think, but again there’s no record of this happening. A 24-month study of the Atkins diet found no new cases of kidney stones, and no change in bone density (in any case, these concerns belong to very high protein diets). As with erectile dysfunction; there’s no data on this either, but all these U.S. plant-based dudes seem to be very defensive about virility, maybe because of the scare stories about soy isoflavones. Malnutrition? That’s up to your dietitian, surely, but if you eat real food and mix up a good variety of animals and vegetables you can’t go wrong.
Cancer, of course, is the big scare story. We all know we’ll get cancer if we eat red meat or forget to eat our wholegrain fibres. Unfortunately there’s no good evidence for this. Diabetes (defined by high blood sugar) increases the risk of every cancer except prostate cancer, and a higher HDL level is associated with reduced risk, showing an obvious point at which diet influences risk. Ketogenic diets have actually shown promise for reducing cancer growth in early research.
As for meat, there is an interesting finding from the EPIC-Oxford study. It was a study of “health conscious” individuals (i.e. with less confounding from unhealthy behaviours), and in this population, which had a low mortality rate overall, vegetarians had a significantly higher rate of colorectal cancer than meat eaters.
“The incidence rate ratio for colorectal cancer in vegetarians compared with meat eaters was 1.39 (95% CI: 1.01, 1.91).“ 
Garth Davis fails to list the long-term side effects of bariatric surgery. Unlike the long-term low-carb diet side effects listed, these are not imaginary or conjectural but a matter of medical record. For example (these are just some listed)
Nutritional deficiencies are a common after-effect of surgery.
Between 13% and 36% of patients develop cholesterol gallstones after surgery, due to rapid weight loss, but only 10% develop symptoms requiring surgical intervention. (cholesterol gallstones are a common side-effect of rapid weight loss on low-fat diets, but not LCHF diets).
8% to 10% of patients developed incisional hernias after open bariatric surgery.
Less than 5% to 10% of patients have chronic problems with dumping syndrome, which can cause facial flushing, lightheadedness and diarrhoea after eating carbohydrate-rich meals. Most patients find that reducing their intake of carbohydrates and avoiding drinking liquids half an hour before and after eating improves their symptoms.
So some common side effects of bariatric surgery can be lessened or avoided by restricting carbs after surgery. Maybe this also helps to explain why 80-85% of Dr Davis’s patients can remain free of diabetes medications. These side effects are more common than the supposed serious side effects of LCHF, which have not been reported in RCTs, so we can’t even put a % figure on them.
2. They assume that patients who see bariatric surgeons have never tried dieting endlessly and over all types of diet before.
In fact, all of our practice’s patients have tried weight loss diets, multiple times. Many have dieted since “fat camps” as children. The number one diet our patients attempt is the Atkins diet (a popular low-carb approach), often numerous times, resulting in a fear of carbohydrates.
Nobody goes into surgery without having given a valiant effort at dieting. For many insurance companies, preoperative attempts at dieting are mandatory, and I know very few surgeons who would operate on a patient that has never tried to lose weight before.
If you go to a bariatric surgeon to reverse diabetes, clearly you have a serious medical problem. You want to be dieting in a way that’s supported and encouraged by your health providers. This is unlikely at present to be the Atkins diet (which can mean a number of different low carb approaches, including diets high in processed foods, or high in protein). Garth Davis plainly doesn’t support the LCHF approach, so his testimony about it can only be second-hand and anecdotal. Why might the “Atkins” diet fail these patients? There’s a clue in the recent Fat vs Carbs documentary on Welsh BBC TV. Presenter Jamie Owen goes on the LCHF diet to lose weight (it works, and his cholesterol goes down). Before he starts, his GP and the dietitian consulted say that he should follow it for “no longer than 3 weeks”. Really?
If you’re not supported in your efforts long-term, if you have “experts” sniping from the sidelines about cancer risk this and bone loss that, it takes a stubborn person to get good long-term results. Dr Sarah Hallberg, on the other hand, supports her type 2 diabetes patients to follow the LCHF diet, as does Dr David Unwin in the UK, and their patients don’t have a high failure rate at all. Plainly, if you do LCHF differently, you can get different results.
The bariatric surgeon is the ambulance at the bottom of the cliff. All other objections aside, it would be impossible to treat every case of diabetes by this method, no matter how effective.
3. The authors reveal a lack of knowledge as to the root mechanism that causes diabetes.
They seem to assume that diabetes is simply a result of high blood sugar, when in fact the high sugar is the symptom, not the cause, of diabetes. Lower carbohydrate intake will drop blood sugar, but it does not address the central issue—the body is no longer able to process the carbs.
In reality, diabetes is caused by uptake of fat into muscle and liver cells. This greatly impedes the body’s ability to make insulin receptors, and without insulin receptors, sugar cannot get into the cell. The low-carb diet will lower blood sugar, but it will not fix the underlying problem of insulin resistance.
Here, it is Davis and Katz who shows poor understanding of mechanisms. High carbohydrate intakes in people with type 2 diabetes push insulin high, and insulin is what governs the accumulation of fat in the body, including in muscle and liver (and pancreas) resulting in insulin resistance (insulin itself downregulates the insulin receptor if present in excess). On a very low carbohydrate diet, insulin drops and this fat is released and oxidised, restoring insulin sensitivity. Very low carb diets are highly effective for reducing liver fat (a bariatric surgeon should know this).
Sugar can get into cells without insulin receptors – glucose uptake is not the main problem in diabetes – instead, insulin resistance means that the liver doesn’t stop releasing glucose when you eat carbs. It’s the failure of insulin’s inhibitory effect that defines diabetes and results in high blood glucose.
The effects of this ‘black age’ are still with us because these incorrect hypotheses have, with the passage of time, been turned into dogma and become cast into ‘tablets of stone’ in undergraduate textbooks. They are also carried forward into postgraduate teaching. For example, even in well respected texts it is still common to find statements such as ‘The basic action of insulin is to facilitate glucose entry into cells, primarily skeletal muscle and hepatocytes.’ – Sonksen and Sonksen 
4. They suggest that the low-carb diet was the favored and only diet for diabetes until recently.
This is just false. In fact, at Duke University in the 1940s, Walter Kempner, MD, treated diabetes successfully with the Rice Diet.
Randomized clinical trials beginning in 1976 collectively highlight the efficacy of a plant-based diet in diabetes management. And recent studies funded by the National Institutes of Health (NIH) have shown us that plant-based diets are even more effective than the traditional American Diabetes Association (ADA) diet plan. As a result, the ADA includes plant-based eating patterns as a meal-planning option in their nutrition recommendations for people with diabetes.
In fact, Davis is distorting history here. The rice diet was never mainstream, and in any case was a highly restrictive inpatient diet, whereas pre-insulin LCHF diets like the Michigan Diet were designed to support patients with enough energy to stay active and keep working.
It doesn’t surprise us that plant-based diets are more effective than the ADA diet plan. As far as we know, every therapeutic diet that has ever been tested has been shown to be more effective than the ADA diet plan. Replacing refined carbs and denatured fats with their equivalents in real foods, even in plant form, is obviously going to slow the appearance of glucose in the blood and lower elevated insulin. That’s why the LCHF diet includes lots of non-starchy vegetables, low-sugar fruits, and fatty fruits and nuts. It’s often a plant-based diet too, if by that is meant a diet high in unprocessed plant food by volume.
Fifth: The authors insinuate that low-carb diets have somehow been erroneously abandoned and should be brought back.
The idea is that low-carb diets worked but the “low fat craze” prematurely, and inappropriately, ended the popularity of the low-carb diet. Low-carb diets have been around since the 1800s. There have been numerous best-selling books through the years touting low-carb dieting as the holy grail. Yet, the diet has repeatedly fallen out of favor, not because of some low fat conspiracy, but because side effects have kept it from being utilized long term.
One might ask, where is the rice diet now? Does anyone at all still use it?
In any case, this is not the reason the low-carb diet fell from favour. Its use declined in diabetes treatment because the mass-production of insulin made it seem unnecessary; its use for weight control declined after the 1960s for the reasons Dr David Ludwig gives in his recent JAMA article, and this – with very little testing, and no testing at all of the very low-carb diet – further.influenced diabetes recommendations.[7,8] After which time obesity and diabetes really did take off – if dietary treatment of these conditions had actually improved in the low-fat, low-animal fat era, this would probably not have happened.
Dr Sarah Hallberg and others are using the LCHF diet on an increasingly large scale and making it work for their patients. Instead of attacking them (and the real reason for this here seems to be opposition to the inclusion of animal foods and animal fats in the diet), why not study what they’re doing right? Hint: it involves including enough real foods – fatty animal foods and low carb vegetable foods – that people don’t feel deprived and persist in the diet long enough to adapt to it. It becomes a way of life – or, at least, a way of eating – that promotes health and enjoyment, and not a crash diet or another fad.
Telling a morbidly obese patient with diabetes to go on yet another low-carb diet is a form of fat shaming and is completely inappropriate management of this disease.
My suggestion to patients dealing with obesity and diabetes is to eat a predominantly whole foods, plant-based diet and to exercise.
Huh? Come again? The other guy’s diet advice is automatically fat-shaming, but your advice to eat virtuously and exercise (I bet they’ve never heard that before) isn’t?
 Friedman AN, Ogden LG, Foster GD et al. Comparative Effects of Low-Carbohydrate High-Protein Versus Low-Fat Diets on the Kidney. Clin J Am Soc Nephrol. 2012 Jul; 7(7): 1103–1111. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3386674/
 Key TJ, Appleby PN, Spencer EA et al. Cancer incidence in vegetarians: results from the European Prospective Investigation into Cancer and Nutrition (EPIC-Oxford). Am J Clin Nutr. 2009 May;89(5):1620S-1626S. doi: 10.3945/ajcn.2009.26736M. [link]
 Hamdan K, Somers S, Chand M. Management of late postoperative complications of bariatric surgery. Br J Surg. 2011 Oct;98(10):1345-55. doi: 10.1002/bjs.7568.
 Browning JD, Baker JA, Rogers T et al. Short-term weight loss and hepatic triglyceride reduction: evidence of a metabolic advantage with dietary carbohydrate restriction. Am J Clin Nutr. 2011 May;93(5):1048-52. doi: 10.3945/ajcn.110.007674. Epub 2011 Mar 2.
 P, Insulin: understanding its action in health and disease. Br. J. Anaesth. (2000) 85 (1): 69–79 doi:10.1093/bja/85.1.69
 Henderson G. Court of Last Appeal – The Early History of the High-fat Diet for Diabetes. J Diabetes Metab. 2016; 7:696. doi: 10.4172/2155-6156.100696
 Ludwig DS. Lowering the Bar on the Low-Fat Diet. JAMA. Published online September 28, 2016. doi:10.1001/jama.2016.15473
 Schofield GM, Henderson G, Thornley S. Very low-carbohydrate diets in the management of diabetes revisited. N Z Med J. 2016 Apr 1;129(1432):67-74.
Once again, the significance of a mouse study has been distorted by its authors and exaggerated by the media. It grabbed our attention because it was the lead front page story in our national newspaper the New Zealand Herald, no less. Also, because we’ve been big advocates for lower carb intakes, especially for the insulin resistant amongst us, it flies in the face on what we are on about.
So let’s have a look at what’s going on.
Common dietary advice has been turned on its head by new research finding that a low protein, high carbohydrate diet stimulates a hormone dubbed the “fountain of youth”.
The Sydney University group led by Dr Samantha Solon-Biet says a high-protein diet is good for reproductive health in younger adults, but recommends switching to a low-protein diet rich in vegetables and other natural carbohydrates from age 50 or 60 to live longer.
“A diet that optimises later-life health has a protein-to-carbohydrate ratio of 1:10,” Solon-Biet said.
The hormone this mouse study looks at is a protein called FGF-21. There is absolutely no evidence that this is a “fountain of youth” and really the myth of Ponce de León should be a warning to all these researchers – he never found the Fountain of Youth because it didn’t exist. Where this mouse research is interesting is because FGF-21, as well as having potentially useful effects in terms of insulin sensitivity, seems to be specifically important with regard to our appetite for sweet carbohydrates – when FGF-21 levels are high, carb cravings stop. So FGF-21 goes up when we eat carbs, so we know when to stop – but there’s such a thing as FGF-21 resistance, if levels are too high for too long we can become insensitive to it. FGF-21 levels also go up in other situations where we don’t need carbs – in prolonged fasting, or on a ketogenic diet. When you lose your sweet tooth after a few weeks on LCHF, that’s probably (in part) due to either a decrease in FGF-21 resistance or a rise in its level.
“FGF21 is increased in various conditions such as overfeeding, obesity, insulin resistance, starvation, protein/amino acid deprivation, low-protein ketogenic diets, and high carbohydrate feeding, yet the metabolic effects are very different in each nutritional context.”
But it’s very important to realise that thousands of proteins are involved in complex processes like the regulation of appetite. Maybe FGF-21 is to carbohydrate what leptin is to fat, but it’s very much early days still.
Auckland University Professor Wayne Cutfield said the Sydney study was based on mice, not humans, and looked at only one hormone called FGF21 out of a large number of hormones and other factors which interacted with each other.
“FGF21 is one of many factors involved in regulating our lifespan. To say that FGF21 is ‘the one’ is just not true,” he said.
Herald health and fitness commentator Lee-Anne Wann said people should not rush out and eat more carbohydrates to increase their FGF21.
“It’s great that they are looking at it. We’ve looked at other things like leptin which help manage our appetite, we are always finding new things,” she said. “But it’s too soon to be saying, ‘Oh my god, we should be increasing carbohydrates.”
In this instance the Herald reporter Simon Collins has done a good job (if we accept that these claims needed to be covered at all; but it will be big news in Australia for political reasons). The NZ experts he interviewed really don’t buy into the hype.
How was the study designed? In a somewhat confusing way. Mice were fed 25 different diets, and the paper isn’t clear what these were, except that they had various permutations of the 3 macronutrients. However, if they were the usual mouse diets, the carbohydrate would be mostly maltodextrin, the protein casein (just one of the proteins in milk, but the one which has a bit of a dodgy reputation when considered on its own). The fat could be anything – lard, cocoa butter, canola. Fortunately not much is being made of fat here.
But there’s a red flag – the mouse diet was not “rich in vegetables and other natural carbohydrates”. In fact, the odds are very high that it actually supplied none.
How were the results presented? Again in a somewhat confusing way. These scientists like using a novel kind of data visualisation, but fortunately they did provide this clearer summary.
Here’s your Fountain of Youth.
Eating a protein restricted, high carbohydrate diet maximises FGF21, but this results in an increased appetite for protein, for which FGF21 may be responsible.
If FGF21 was the Fountain of Youth, then, to exploit this, you would need to eat in such a way that you would always be craving protein, and then, if you did eat enough protein, you’d lose your FGF21 advantage.
This does not sound like much fun, even for a mouse. Protein foods are flavoursome, come in considerable variety, and are excellent sources of vitamins, minerals, essential fats, and energy. The LCHF diet isn’t, and the Paleo diet needn’t be, high protein at all, but for humans there is a real advantage to keeping muscle on our bodies (mice, for example, don’t need to open jars or lift the furniture often). This helps us to stay active, makes us more useful in our daily lives, and helps with physical and mental health. Losing muscle because of some fad diet idea (sic) that involves restricting protein for longevity (rather than for some measurable shorter term benefit, which you can actually check) is perhaps not the first thing that scientists should promote in the media. Surely every mouse experiment doesn’t have to generate a headline – there are enough human experiments to be going on with.
But I guess “high carbs key to long life” in a headline is just irresistible.
The discussion part of the paper is indeed interesting, and at least some of these 20 researchers really do know their stuff, but some of them seem to be extrapolating from it in the media as evidence that one type of traditional human diet out of thousands is healthier than all the others. The facts are, that
- all traditional, pre-industrial diets are more-or-less healthy except when resources are poor.
- populations eating diets high in meat and cheese (Sardinia) can be as long-lived as populations eating yams with low protein (Okinawa), and there are also shorter-lived populations eating both types of diet.
- if we are no longer eating these traditional diets, we are more likely to have have metabolic disease or other health conditions that are rare in traditional populations, and which usually respond to specific and perhaps novel dietary changes – even peasants emigrating from the Mediterranean 100 years ago were advised to stop eating carbohydrate foods if they became diabetic in their new homes. Such changes can reasonably be expected to improve longevity for the individual more often than not.
The article also mentioned the Mediterranean diet. This is not actually low in protein, nor high in carbohydrate, as far as we know. A new EPIC study shows that a high Mediterranean Diet Score (they tested 4 different Med Diet scoring systems) is associated with lower mortality in an English population (i.e. compared to the normal English diet, one shudders to think what that is today). One interesting finding is the cholesterol counts of those with low and high Med Diet Scores. Mean total cholesterol in both groups is 6.2 mmol/L, LDL is 4 and 3.9 respectively, HDL is 1.4 and 1.5, TGs are 1.9 and 1.7.
So even the high Mediterranean Diet Score consumers in the UK tend to have high cholesterol, and the diet doesn’t make a lot of difference to that, yet it reduces cardiovascular and total mortality. Interesting.
A few years ago researchers showed that cell phone radiation cures Alzheimer’s Disease in mice. I don’t remember those researchers going all over the media telling us to strap cell phones to our heads from age 50 or 60 to think better. What is it about diet researchers?
 Solon-Biet et al., Defining the Nutritional and Metabolic Context of FGF21 Using the Geometric Framework, Cell Metabolism (2016), http://dx.doi.org/10.1016/j.cmet.2016.09.001
 Tong TYN, Wareham NJ, Khaw K-T, Imamura F, Forouhi NG.
Prospective association of the Mediterranean diet with cardiovascular
disease incidence and mortality and its population impact in a non-Mediterranean
population: the EPIC-Norfolk study.
Tong et al. BMC Medicine (2016) 14:135
In the news recently is a review of statin benefits and side-effects in the Lancet which, using a controversial modelling method to predict population effects from the variable results of clinical trials, recommends that statins be prescribed more widely to healthy people to lower their risk of future heart attacks.
The claim is that side-effects are rare, but they seem to be more common, and more serious, in real life than Professor Rory Collins, lead author of the review, admitted when interviewed by the BBC. In our opinion, it’s not ethical to try to trivialise the side effects of any drug that can kill or cripple the people taking it, as Professor Collins did, whether or not the benefits outweigh the risks at a population level.
It’s also worth taking into account how these statin trials are typically designed and what that means for side effects, exclusion and interpretation. We’ve written about that before here.
A commenter on the What The Fat blog sent us this link to an Official Information Act request about the number of statin-related deaths and injuries in New Zealand.
Over the period 01 January 2001 through to 31 December 2014, this document details 1709 reports describing 3826 reaction terms – one report may have more than one reaction described. 21 cases resulted in an outcome of death however in 3 cases death was not related to the Statin medicine and 2 cases were unclassifiable.
So we have 1709 reports of statins causing injury, and 21 deaths of which 15 were considered to be caused by statins. No doubt there is considerable underreporting here, as many people prescribed a drug which produces adverse effects will stop taking it without telling the doctor, and many doctors will stop prescribing such a drug without reporting the incident, so these numbers will tend to represent serious cases that weren’t easily resolved.
Why do some people experience extreme toxic reactions from statins while others tolerate them? A simple explanation for some types of harm might be, that statins reduce the synthesis of cholesterol, which lowers LDL in the blood, but everyone with a raised LDL cholesterol who is prescribed statins may not have an excessive rate of cholesterol synthesis to begin with, as cholesterol synthesis is regulated by insulin. Someone with hyperinsulinaemia due to carbohydrate intolerance will tend to have an increased cholesterol synthesis, but this will often be accompanied by low or normal LDL levels. This may be why, in modern guidelines, LDL is no longer used as the sole guide to statin prescribing (the TG/HDL ratio is a better guide to insulin status).
Potentially, statins could cause enough of a cholesterol deficiency in cells to cause harm. This is how the NASA doctor Duane Graveline, who died recently, explained his own adverse reaction to statins, which caused him to suffer from amnesia. Professor Collins denies that amnesia is caused by statins; however all cases of amnesia in the New Zealand report (39) relate to the two statins, atorvastatin (Lipitor) and simvastatin (Zocor) which are fat-soluble and cross the blood brain barrier, just as Duane Graveline predicted. Of course it is likely that amnesia in elderly patients prescribed statins is often missed as a drug side-effect, with resulting under-reporting.
A more complex mechanism for harm is that statins can be metabolised to lactones in some people, and these statin lactones are three times more toxic than the statins themselves, especially to muscle cells. Statin lactones inhibit mitochondrial respiratory complex III, reducing its activity by 84% in this experimental paper, and smaller but significant reductions in CIII activity were found in muscle biopsies from patients suffering from statin myopathy.
In conclusion, we demonstrate that the Qo site of respiratory CIII is inhibited by several statin lactones and provide evidence for an association between this off-target effect and statin-induced myopathies. Consequently, polymorphisms of UGTs, the enzymes converting statin acids into lactones, and CIII could be predisposing factors in statin-induced myopathies. We showed that both G3PDH and b-oxidation stimulation can prevent statin-induced respiratory inhibition, providing a rationale for therapeutic intervention.
CIII is part of the mitochondrial electron transfer complex or ETC (also known as the respiratory complex) which is part of the machinery cells use to generate ready-use energy units (ATP) from food. Its inhibition has the effect of reducing the muscle cell’s ability to generate ATP, with apoptosis (self-destruction) of cells as an outcome. Fortunately the beta-oxidation step of fatty acid oxidation contributes to ATP through a separate mitochondrial transporter (not usually shown in diagrams, because “glucose is the most important energy source”), and this input is able to restore CIII activity – “Beta-oxidation also contributed to convergent electron flow into CIII (i.e. it stepped around the statin blockade) and reversed the effects, restoring CIII activity to 89% of normal”.
In this cell-culture experiment beta-oxidation was stimulated by adding palmitoyl-l-carnitine to the mixture; this is a molecule of saturated fat attached to a molecule of l-carnitine, which is the molecule that carries fatty acids into the mitochondria for beta-oxidation. Co-enzyme Q10 is the molecule that carries the electrons between complexes. It has been proposed that Co-enzyme Q10 and l-carnitine be used together to treat statin myopathy. However, increased beta-oxidation is also something that happens naturally in people eating the LCHF diet – it’s called fat-burning. (on the other hand G3PDH, interestingly, is activated by fructose, but also by glycerol, part of the fat molecule).
A further way in which statins can cause damage, this time to brain and nerve cells, is by inhibiting the synthesis of vitamin K2. Many plant foods contain vitamin K1, which the body converts to K2 (mostly in the liver, but also in the brain).
When this occurs in the brain the MK4 form of K2 produced is an essential co-enzyme for the synthesis of special sulfur-containing lipids called sulfatides. Low CNS sulfatide levels are associated with cognitive decline and seen in the early stages of Alzheimer’s disease.
The MK4 form of vitamin K2 is produced with the same enzyme (HMG-CoA reductase) that is targeted by statins.
From all these facts and hypotheses, we can arrive at a number of factors likely, at least in theory, to be protective to people using statins.
One is a fat-burning metabolism. Of course this is associated with low insulin levels and therefore unlikely to cause excessive cholesterol synthesis in the first place.
Another is l-carnitine. This is made in the body, but we get extra from animal foods, especially red meat. Another is co-enzyme Q10, we make this in the body but by using the same HMG-CoA reductase enzyme that makes cholesterol and vitamin K2. Co-Q10 is found in animal foods and also in vegetable oils.
Vitamin K2 is found in animal foods such as liver and eggs, in cheeses, and in other fermented foods such as natto and sauerkraut.
And cholesterol itself, of course, is only found in significant amounts in fatty animal foods, especially eggs, offal, and shellfish.
The irony is that the diet most likely to protect against statin side-effects (if that is in fact possible), is a high-fat diet with plenty of rich and tasty animal foods. Exactly the sort of diet you’ll be told to avoid by most of the doctors prescribing them.
We do have quite a few studies of carbohydrate-restricted diets in people taking statins showing that the combination is safe and results in added improvement.
In conclusion, these findings demonstrate that individuals undergoing statin therapy experience additional improvements in metabolic and vascular health from a 6 weeks CRD as evidenced by increased insulin sensitivity and resistance vessel endothelial function, and decreased blood pressure, triglycerides, and adhesion molecules.
And our favourite, the “high saturated fat and no-starch” diet.
An HSF-SA diet was prescribed for all patients; they were instructed to attempt to consume one half of all calories as saturated fat, primarily as red meat and cheese. Eggs and other low-fat forms of protein were allowed, regardless of cholesterol content. Fresh fruit and nonstarchy vegetables were prescribed in restricted amounts at each meal.
Starch was forbidden.
In patients with atherosclerotic cardiovascular disease, an HSF-SA diet results in weight loss after 6 weeks without adverse effects on serum lipid levels verified by nuclear magnetic resonance, and further weight loss with a lipid-neutral effect may persist for up to 52 weeks. All patients were obese (mean +/- SD body mass index [BMI], 39.0+/-7.3 kg/m2) and had been treated with statins before entry in the trial.
This diet contains every element that (in theory at least) should protect against statin side-effects. It’s high enough in fat and low enough in carbohydrate to stimulate beta-oxidation (and even supplies some fructose to activate G3PDH), it supplies vitamin K2, l-carnitine, Co-enzyme Q10 and cholesterol.
Take home points
- Statins inhibit the synthesis of cholesterol, excessive production of which is an effect of high insulin levels. Therefore, if statins do reduce heart attack risk, diets which lower insulin secretion by restricting carbohydrate should do so too. However, statins are only specific for one effect of excess insulin, whereas carbohydrate restriction reduces its effect on multiple pathways.
- Statins can damage muscles, with life-altering consequences, by inhibiting the mitochondrial CIII complex involved in the production of energy (ATP). Diets which activate fat-burning in muscles by restricting carbohydrate can restore energy production (in theory, based on experimental evidence).
- Statins can cause memory loss and neuropathy, probably by depleting vitamin K2 and cholesterol in the brain and nerves. High-fat, animal based diets are good sources of these nutrients, and also supply extra l-carnitine and Co-enzyme Q10 that may help to protect muscles.
As always, we are not cardiologists and are not qualified to prescribe statins or advise against using them. Those are decisions for your doctor and you (yes you!) to make when you weight up the likely benefits and harms and what weight to give to all of these combined.
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