Saturated fat is not the major issue
BMJ 2013; 347 doi: https://doi.org/10.1136/bmj.f6340 (Published 22 October 2013) Cite this as: BMJ 2013;347:f6340
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What happens if you eliminate all sources of saturated fat from the diet rather than just reduce their intake? The results obtained by two US researchers are impressive, showing the way to a safer and better standard of care in ischaemic heart disease.
A plant-rich Mediterranean diet is already recognised to be effective in the prevention of heart disease. Going a step further, evidence is mounting that a plant-based diet, consisting of unprocessed grains, legumes (beans, lentils and peas), vegetables and fruits, can prevent, arrest and even reverse coronary artery disease.
A leading advocate of this approach is Esselstyn, a US-based cardiac surgeon. In 1985 he recruited 24 patients with triple-vessel coronary artery disease for a research study, originally designed to last five years (1).
His goal was to achieve, through plant-based nutrition and cholesterol-lowering drugs, a serum cholesterol level less than 150 mg/dL (3.9 mmol/L), as is seen in cultures - for example Okinawa or rural areas of China - where coronary artery disease is rarely seen. Participants were asked to avoid oil, meat, fish, poultry and most dairy products; eat mostly unprocessed grains, legumes, vegetables and fruit; and consume alcohol and caffeine only in moderation. Patients were also given cholesterol-lowering drugs, as appropriate.
According to an article in The American Journal of Cardiology (2), 18 of the participants were followed for 12 years. Although as a group the participants had a history of 49 coronary events – increasing angina (chest pain), heart attack or bypass surgery – during the eight years prior to the study, all but one had no events after the study began. The exception was a patient who was off the study for two years and experienced angina. He has since resumed the study’s diet and medications, following a bypass operation.
The six patients who did not adhere to the diet were released from the study within the first 15 months and returned to standard care. All had further coronary events, 13 during the 12 years of follow-up. One patient who adhered to the program died shortly after the five-year mark from a cardiac arrhythmia. According to Esselstyn, this probably resulted from damage to the heart caused by the patient's original massive myocardial infarction prior to the start of the study. Angiograms taken just two months before this patient’s death had shown reversal of coronary lesions.
Prior to the study, Dr. Esselstyn’s group had average total cholesterol levels of 237 mg/dL (6.13 mmol/L). The group now averages 145 mg/dL (3.75 mmol/L). Low-density lipoprotein (LDL) cholesterol levels are around 82 mg/dL (2.12 mmol/L). About 70% of the participants have experienced regression of their disease, meaning that the plaques appeared smaller and smaller on successive angiograms.
Esselstyn feels that these results are particularly important because they show that this therapy arrests, rather than just slows, atherosclerosis. Patients become empowered and feel in control of the disease that previously dominated their lives.
Because adherence to the program was key, Esselstyn used methods to aid patients’ compliance. He conducted a 60-90 minute interview with each patient and the patient’s spouse at the start of the study. He monitored patient cholesterol and overall progress with office visits every two weeks for the first five years. Patients learned the results of their blood work by a personal phone call from Esselstyn the night of their office visit. And several times a year, participants and Esselstyn gathered at one of their homes to review treatment objectives, exchange menus and socialise.
This and other studies convincingly show that coronary artery disease can be reversed by aggressively lowering cholesterol through a very low fat vegetarian diet and, if needed to achieve the target cholesterol level, lipid-lowering drugs.
Esselstyn has expressed his view that it is “scientifically and ethically imperative to inform the public what constitutes an optimal diet. He follows the same diet as his patients. In 1985, his total cholesterol was around 185 mg/dL. It now hovers around 110. Esselstyn's website is at www.HeartAttackProof.com
Ornish has also shown that coronary artery disease is reversible using intensive lifestyle modifications (3).
Diet is of crucial importance not only in disease prevention but also because of the size of its associated environmental impact. The number of farm animals in the USA now equals the number of Americans multiplied by 32. On a global scale the environmental damage from livestock alone is truly gargantuan. Robert Goodland, who served as the World Bank's environmental advisor for over 20 years, has recalculated the contribution of livestock to global warming and found that it far exceeds previous estimates of around 18% (4). His most recent published estimate is 51%, a figure mentioned in a recent interview:
http://www.drmcdougall.com/health/education/videos/advanced-study-weeken...
Oppenlander has also examined food choices and their huge, multi-faceted impacts on the global environment in his book Comfortably Unaware (5). A lecture in which he effectively communicates the scale of the damage to our eco-systems is available online:
http://www.youtube.com/watch?v=Fws0f9s4Bas
Goodland strongly urges everyone who is concerned to improve our chances of preserving a liveable environment to get behind the twin goals of reforestation and widespread adoption of a sustainable plant-based diet.
References:
1. Esselstyn C. A strategy to arrest and reverse coronary artery disease: a 5-year longitudinal study of a single physician's practice. J Fam Pract.1995 Dec;41(6):560-8.
2. Esselstyn C. The Am J of Cardiology 1999 August 1; 84:339-341
3. Ornish. Intensive lifestyle changes for reversal of coronary artery disesase. JAMA 1998 Dec 16;280(23):2001-7.
4. Worldwatch Institute: Livestock emissions - still grossly underestimated? http://www.worldwatch.org/node/6297
5. Oppenlander, Comfortably Unaware – global depletion and food responsibility (published 2011).
Competing interests: No competing interests
It is disappointing to see so many letters in the BMJ clinging to the outdated notion that saturated fat is bad and vegetable fat is good. I would therefore like to draw attention to two little known points about animal fat.
Firstly, vegetable oil induces fatty liver disease and saturated fat reverses it. This has been demonstrated by comparing rats fed on corn oil and rats fed on beef fat [1].
Secondly, the mistaken advice to avoid saturated fat from animals has made most people short of the fat soluble vitamins A, D, E and K2. Vitamin K2 is distinct from vitamin K1 which is present in vegetables and is responsible for blood clotting. Vitamins A, D and K2 are needed together for normal calcium metabolism. Vitamins A and D are necessary for the production of the proteins osteocalcin and matrix gla protein (MGP). Osteocalcin attracts calcium into bones and teeth. MGP sweeps calcium out of soft tissues. To become active these proteins have to be switched on by vitamin K2 using gamma-carboxylation.
Vitamin K2 prevents osteoporosis and tooth decay through the action of osteocalcin. Fat soluble vitamins can be use to heal dental cavities. Vitamin K2 prevents coronary artery calcification and heart disease though the action of MGP. Lack of active MGP in the first trimester causes early calcification of the nasal septum and a hypoplastic maxilla which in turn causes crowded teeth and impacted wisdom teeth. Lack of vitamin K2 makes bones long and thin so increasing height through generations is due to poor nutrition not improving nutrition. Low levels of vitamin K2 result in calcification of elastin, the cause of double chins, piles and varicose veins. Another action of osteocalcin is to attach to Leydig cells and stimulate production of testosterone. This is why sperm counts are deteriorating.
Matters are made worse by the current fashion of treating people with high dose of vitamin D alone. This rapidly uses up meagre levels of vitamin K2. MGP remains inactive and coronary artery calcification results.
Francis Pottenger fed a vitamin K2 deficient diet to cats [2]. Due to an epigenetic effect successive generations became sicker and by the third generation they were so sick they could not reproduce. Humans will head the same way as Pottenger’s cats unless we realise that saturated fat and cholesterol are good for us [3].
References:
1. Beef fat prevents alcoholic liver disease in the rat, Alcohol Clin Exp Res. 1989 Feb;13(1):15-9
2. Pottenger’s Cats by Francis M Pottenger Jr MD
3. Fat and Cholesterol are Good for You by Uffe Ravnskov MD PhD
4. Vitamin K2 and the Calcium Paradox by Dr Kate Rheaume-Bleue
5. Nutrition and Physical Degeneration by Weston Price
Competing interests: No competing interests
If we can't see the wood for the trees, how can we expect to see the elephant in the room? Malhotra says that saturated fat has nothing to do with heart disease and may be protective. Nutrients are not eaten in isolation, and most of the saturated fat in our diet comes from animal foods. So is he saying that animal foods are safe for the heart? But this would be absurd given the solidity of the evidence in favour of plant-based nutrition: Ornish and Esselstyn have independently shown that ischaemic heart disease is reversible with a low-fat plant-based diet (1,2). This is on top of a mountain of observational evidence showing that plant-based diets prevent heart disease, something Malhotra appears to acknowledge by saying that a Mediterranean diet results in far better outcomes than can be obtained with statins. As a Mediterranean diet is low in saturated fat, this hardly fits with Malhotra's myth-busting ambitions.
Our attempts to understand how foods can promote health or cause disease by looking at one nutrient at a time have met with precious little success. Time after time this approach has failed us. We thought we could capture the benefits of vitamins by taking vitamin pills, but we found that this paradoxically increases mortality - we need to have these nutrients in their proper context, packaged up within the whole food, otherwise they don't work as we expect them to work.
Even protein, almost universally regarded as a uniquely beneficial nutrient, turns out to have unexpected problems. Fontana and Campbell have independently shown that a high protein intake accelerates ageing and promotes age-related degenerative diseases (3,4). Animal foods, characteristically rich in both protein and saturated fat, cause numerous adverse health effects via multiple mechanisms, including boosting IGF-1 and activating the NF-kB inflammation hub (5). Inflammation is now considered as a crucially important disease driver in heart disease, cancer, diabetes, obesity and other chronic diseases (6).
Finally, a diet based on animal foods is destructive not only to human health but also to the global climate. Oppenlander has drawn attention to the enormous environmental impact of the estimated 70 billion animals involved in food production (7). This cannot go on if we are to preserve a liveable environment.
When doctors ignore or deny the great problems associated with animal foods they use their position in society unwisely, undermine the health of the nation and, quite possibly, help shorten the lifespan of our entire civilisation.
1. Ornish. Intensive lifestyle changes for reversal of coronary artery disesase. JAMA 1998 Dec 16;280(23):2001-7.
2. Esselstyn C. A strategy to arrest and reverse coronary artery disease: a 5-year longitudinal study of a single physician's practice. J Fam Pract.1995 Dec;41(6):560-8.
3. Fontana, L. Long-term effects of calorie or protein restriction on serum IGF-1 and IGFBP-3 concentration in humans. Aging Cell 2008 October; 7(5): 681–687.
4. Campbell TC, The China Study (pub 2005); Whole - rethinking the science of nutrition (pub 2013)
5. Van Beek; Bc|10 links saturated fat overnutrition with hepatocellular NF-kB activation and insulin resistance; Cell Rep. 2012 May 31;1(5):444-52.
6. Weiss, Editorial: inflammation; Nature 454, 427 24 July 2008 doi:10.1038/454427a
7. Oppenlander, Comfortably Unaware - global depletion and food responsibility (pub 2011)
Competing interests: No competing interests
We should not partake of saturated fat?
Now olive oil we can consume by the vat.
We must all enjoy a diet ‘Mediterranish’
Including plenty of bread, olive oil and maybe oily fish.
Our hearts are struggling with difficulty to pump
Our arteries are clogging like an old tractor sump.
Our waistbands are expanding our bellies getting fatter
We can no longer find clothes which contour and flatter.
Diabetes looks likely - eat unlimited amounts of carbohydrate
Whilst your insulin supply exhaust and your kidneys dehydrate.
Where did it all go wrong, is it as bad as it would seem?
The kids eat up all their chips with some pop in between!
A pancake for breakfast, or make that a stack
They are labelled ‘fat free’ so it won’t matter jack.
Manufacturers pledge less saturated fat in biscuits, chocolate and cake
You can eat twice as many now, although they taste a bit fake.
Red meats they say are part of the heart unfriendly bunch
No more succulent roast beef and two veg for Sunday lunch?
Dairy foods are also deemed wrong, no milk in our tea – our way to revive
How will our Great British farmers ever survive?
Rats fed purely on ‘mono fats’ fail in their reproduction
Hardly the hot Latino lover way to seduction.
So the Med diet will bring us salvation,
But hang on we are hardly a sun drenched nation!
Is the Mediterranean diet the route to a healthy heart?
Surely lunch made by mama followed by a snooze play a major part.
May I also say if I can be so bold?
A Mediterranean diet will hardly keep out the cold.
Our culture and diet routine may seem very nationalistic
But shouldn’t our approach to diet and lifestyle be far more holistic?
Jane E Collis
Competing interests: No competing interests
It is well established that saturated fat increases LDL cholesterol. However in comparison to carbohydrates saturated fat also raises HDL cholesterol and reduces triglycerides with little effect on the total cholesterol :HDL ratio which is considered a better predictor of CHD events than total cholesterol alone. 1,2
The food source of saturated fat may have greater relevance. Most recently Otto et al revealed that a higher intake of dairy saturated fat was associated with a lower CVD risk but meat intake with an increased risk in the multi-ethnic study of atherosclerosis.3
Although there is evidence to support the replacement of saturated fat with polyunsaturated fat in reducing CHD events, this benefit may be more specific to omega 3, with higher omega 6 PUFA’s found commonly in industrialised vegetable oils implicated in pro-inflammatory, atherogenic oxidised LDL. This may explain why a re-analysis of unpublished data in the Sydney Heart study revealed that cardiac patients that replaced butter with omega 6 containing safflower oil and safflower oil containing margarine had increased all cause and cardiovascular mortality despite a 13% reduction in total cholesterol in this group.
Furthermore the exploitation of an unhelpful “low fat” mantra by the food industry has resulted in dietary prescriptions that have resulted in high refined carbohydrate diets, worsening obesity and fuelling atherogenic dyslipidaemia, a metabolic state defined by increased triglycerides, reduced HDL cholesterol and increased proportions of small dense LDL particles. A reduction in carbohydrate intake but not saturated fat appears to improve this dyslipidaemic profile.4
And two thirds of people admitted to hospital with acute myocardial infarction now qualify for a diagnosis of metabolic syndrome, with a 50% increased risk of mortality or rehospitalisation at one year.5
An over obsession with total calories consumed as opposed to the nutritional value of those calories has also proved be unhelpful and has been exploited by the food industry with the addition of cheap sugar to many processed foods. A 9 tea spoon sugared cola has less than 150 calories, but according to the EPIC study drinking just one can a day increased the risk of type 2 diabetes independent of BMI. Conversely the consumption of 4 table spoons of extra-virgin olive oil per day, approximating to 500 calories, as recommended in the PREDIMED study intervention arm significantly reduced heart attack and stroke risk. It’s perhaps instructive to note after a 2 year review of 16,000 studies Sweden has just become the first western nation to reject the “low fat” dietary dogma advocating a diet that is high fat and low in refined carbohydrates as the best for cholesterol profile and weight loss. Promoting a Mediterranean diet to reduce CVD risk and cognitive decline whilst simultaneously reducing population processed food and added sugar intake, which unlike fat and protein has no nutritional value, is the single dietary contributor to dental caries, and is driving the diseases of the metabolic syndrome may offer the best dietary solution to improving public health.
1. Mensink RP, Zock PL, Kester AD, 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 2003;77:1146–55.
2. Assmann G, Schulte H, von Eckardstein A, Huang Y. High-density lipoprotein cholesterol as a predictor of coronary heart disease risk. The PROCAM experience and pathophysiological implications for reverse cholesterol transport. Atherosclerosis 1996;124(suppl):S11–20.
3. de Oliveira Otto MC, Mozaffarian D, Kromhout D, Bertoni AG, Sibley CT, Jacobs DR Jr, Nettleton JA. Dietary intake of saturated fat by food source and incident cardiovascular disease: the Multi-Ethnic Study of Atherosclerosis.
Am J Clin Nutr. 2012 Aug;96(2):397-404. doi:10.3945/ajcn.112.037770.Epub 2012 Jul 3.
4. Krauss RM, Blanche PJ, Rawlings RS, Fernstrom HS, Williams PT Separate effects of reduced carbohydrate intake and weight loss on atherogenic dyslipidemia. Am J Clin Nutr 2006;83:1025–31,
5. Arnold SV, Lipska KJ, Li Y, Goyal A, Maddox TM, McGuire DK, et al.The accuracy and prognosis of in-hospital diagnosis of metabolic syndrome in patients with myocardial infarction. Prediabetes and the Metabolic Syndrome 2013 Congress, 20 April 2013.
Competing interests: No competing interests
Reading through the responses to Dr Malhotra’s paper, I was somewhat disheartened to see how many correspondents – both supporters and critics of the paper – argued their case solely from the position of statistical ‘risk factors’, as though we understand nothing of the underlying biochemical mechanism of atherosclerosis. Let us not confuse levels of cholesterol, triglycerides or particular lipoprotein subclasses with ‘mechanism’ – the majority of your correspondents used these as stand-alone risk factors, divorced from the underlying mechanisms that hold the only meaningful answers to the question of how diet is linked to cardiovascular disease.
Dr Malhotra is certainly on the right track. Whilst it is unclear precisely how atherosclerosis is initiated, it is evident that the ongoing process comprises a vicious cycle of inflammation and self-amplifying free-radical chain reactions, culminating in the modification of low density lipoprotein to an oxidised form (‘oxLDL’) which is avidly taken up via the scavenger-receptor pathway. The basic chemistry of LDL modification is ‘screaming out loud’ to us that polyunsaturated fatty acids, being far more susceptible to lipid peroxidation than their saturated relatives, should favour the process.
If we accept that a certain percentage of the LDL in the bloodstream is going to be converted to oxLDL, then of course lowering total LDL will lower the absolute level of the modified lipoprotein. It is an unfortunate coincidence, then, that the dietary measures commonly recommended to lower total LDL (‘the high in polyunsaturates/low in saturates’ mantra) can logically be assumed to promote oxLDL formation. Add to this the unfavourable increase in the ratio of ω-6/ω-3 fatty acid intake that has accompanied the increased consumption of vegetable oils by the populace and it is not too difficult to understand why cardiovascular disease is still prevalent.
Rather than intervening downstream to the LDL oxidation step, surely it would make more sense to consume diets which minimise LDL modification in the first place. Raised LDL per se is not the problem: prevent its oxidation and elevated levels should not be atherogenic.
Unfortunately such nuances will never be revealed by the adoption of a mechanism-blind statistical approach to the investigation of the links between diet and cardiovascular disease (however ‘objective’ this may seem). No matter how ‘significant’ your statistics, how perfectly ‘controlled’ your sample, number crunching should always be subservient to mechanism-based biological chemistry. Attempts to put numbers to risk factors in such isolation are as futile as those of the economists trying to tell us the cost/benefit ratio of the proposed HS2 rail link. I can work on a train as well as the next person, but it takes only one noisy child – or indeed an individual whose idea of ‘working’ on the train entails broadcasting their business loudly into a mobile phone – to put the best laid plans to waste. So it is with nutrition and cardiovascular disease: there are just too many variables in play to pin-point the role of particular dietary components using statistics.
Returning to the important question of how the maelstrom of events we refer to as atherosclerosis is initiated, most of the biochemical evidence suggests the process is a response-to-injury phenomenon. I favour a mechanism involving the glycation of proteins in the circulatory system (promoted by high glucose concentrations), leading to an immune response, of which inflammation and increased free-radical generation are integral features (the latter involving NADPH oxidase and NO synthase). No doubt other forms of injury can also initiate the process, including infection and mechanical damage to the vascular endothelium. However, I suspect that for the majority of the population the excessive consumption of glucose and fructose (as components of sucrose), both of which can ‘attach to’ proteins, is an important factor in the initiation of atherosclerosis. In this regard, I support the general gist of Dr Malhotra’s paper.
Competing interests: No competing interests
While the primary focus of Dr Malhotra’s observation was not on the evidence base for statins, one comment warrants clarification. He writes: “[t]he strongest evidence base for statins is in secondary prevention, where all patients after a myocardial infarction are prescribed maximum dose treatment irrespective of total cholesterol, because of statins’ anti-inflammatory or pleiotropic (coronary plaque stabilizing) effects. In this group the NNT is 83 for mortality over five years”. In fact, it was standard dose (i.e. pravastatin 40 mg, simvastatin 20-40 mg), not maximum dose statin therapy, that was shown to reduce total mortality in placebo-controlled, randomized controlled trials that enrolled participants with coronary heart disease.(1,2,3)
1. Scandinavian Simvastatin Survival Group. Randomised trial of cholesterol lowering in 4444 patients with coronary heart disease: The Scandinavian Simvastatin Survival Study (4S). Lancet 1994;344:1383-89.
2. The Long-Term Intervention with Pravastatin in Ischaemic Disease (LIPID) Study Group. Prevention of cardiovascular disease events and death with pravastatin in patients with coronary heart disease and a broad range of initial cholesterol levels. N Engl J Med 1998;339:1349-57.
3. Heart Protection Study Collaborative Group. MRC/BHF Heart Protection Study of cholesterol lowering with simvastatin in 20 536 high-risk individuals: a randomized placebo-controlled trial. Lancet 2002;360:7-22.
Competing interests: No competing interests
Dr Malhotra’s paper (1) provides some useful reminders regarding the causes of coronary heart disease (CHD) and the requirements for risk reduction but does include several instances where the existing literature has been misinterpreted.
The title is accurate. CHD has a complex aetiology and there is no single factor which can be regarded as “the major issue”. With that in mind it is not surprising that the relative importance of different risk factors can change over time. Many patients who now present with myocardial infarction are likely to be overweight and have features of the metabolic syndrome. Dyslipidaemia, dysglycaemia and raised blood pressure levels are now well-established risk factors for CHD. Given the pivotal role of central obesity in this constellation of cardiometabolic risk indicators, attempts to avoid and treat excess weight gain are central components of preventive cardiology.
In December 2012 and January 2013 the BMJ published systematic reviews and metaanalyses (commissioned by WHO) that demonstrated the potential for total fat and dietary free sugars to promote body fatness (2, 3). These findings are hardly surprising given the potential of both these macronutrients to increase the energy density of foods.
“Sugar” is increasingly regarded as the villain of the piece though many energy dense foods are rich in both sugar and fat. Sugar sweet beverages although not energy dense are also associated with excess weight gain. The BMJ sugars review provides convincing evidence that the effect of sugars in promoting body fatness is via their tendency to promote excessive calorie intakes rather than via some unique metabolic pathways, in those consuming self-selected diets (2). When calorie intakes are carefully controlled there is no effect on body weight when sugars are exchanged for other energy sources.
Whether free sugars and fructose in particular have an adverse effect on cardiometabolic risk independent of body weight is yet to be finally resolved. Individual studies suggest untoward effects on lipid and carbohydrate metabolism and distribution of body fatness but most of the studies involved higher intakes of sugars than usually consumed and were relatively short term. However a meta analysis of randomised controlled trials examining the effects of free sugars on blood pressure and lipids (presented at the 2013 Australia and New Zealand Obesity Society Conference, abstract available: http://www.anzos2013.org/2013-program/) suggests their potential to raise total cholesterol and triglyceride and blood pressure, especially diastolic pressure.
So, we would agree with Malhotra that replacement of fat with sugars in manufactured and other foods is totally inappropriate. However we would strongly dispute his conclusion that saturated fat is exonerated as a cause of coronary heart disease.
Contrary to Malhotra’s statement that “advice [to reduce saturated fat intake] has, paradoxically, increased our cardiovascular risks”(1) the past several decades have seen substantial declines in cardiovascular disease mortality (4), which have occurred in parallel with declines in both saturated fat intake and serum cholesterol levels in much of the western world (5). These ecological observations suggesting an association between total cholesterol and CHD, are supported by findings in cohort studies and clinical trials (6).
Metaanalysis of observational studies in nearly 900 000 adults in western countries showed a linear relationship between total cholesterol and CHD mortality, but not mortality from stroke, a more heterogeneous disease (6). A similar association has been repeatedly demonstrated between cholesterol and non-fatal CHD (7). Malhotra selectively cites two studies (both in low-risk Asian populations) which he claims show that “high cholesterol is not a risk factor” for CVD (8, 9). Both studies indeed reported associations between low cholesterol and mortality, however this association, which been repeatedly described, is likely due largely to confounding by pre-existing disease, including cancers, liver, respiratory and digestive diseases, malnutrition and smoking (10).
The direct evidence for an association between saturated fat intake and CHD is less clear, but this is hardly surprising. A recent meta-analysis of prospective cohort studies by Siri-Tarino et al (2010) suggested no association between saturated fat intake and CHD (11). However cohort studies may be confounded by not taking into account sources of replacement energy, misreporting of dietary saturated fat intakes or measurement error resulting in regression dilution effects, and by inappropriate adjustment for lifestyle factors (12). In pooled analyses of cohort studies inconsistent adjustment for potential intermediates in the diet-disease pathway, as well as for energy intake, may also result in residual confounding.
The findings are more clear when also considering what replaces saturated fat. In a data pooling study of 11 prospective cohort studies examining the effect on CHD risk of substituting carbohydrates or unsaturated fats for saturated fats, Jakobsen et al (2009) showed that replacing saturated fat with polyunsaturated fat resulted in a significant reduction in CHD risk whereas substitution with carbohydrate resulted in a modest increase in risk (13). Arguably the strongest confirmation of the diet-disease relationship comes from randomised controlled trials. In a metaanalysis of 8 relatively long-term trials Mozaffarian et al (2010) showed a significant reduction in CHD events in studies where saturated fat reduction was achieved by substitution primarily with polyunsaturated fat, thus confirming the findings of Jakobsen et al (14).
The influence of saturated fat intake on CHD is supported by many shorter term experimental studies examining the effects of saturated fats on metabolic biomarkers for CHD. Mensink et al. (2003) have aggregated data relating to the effects on blood lipids of substituting carbohydrates, mono or polyunsaturated fats for saturated fats in controlled experimental trials (15). In all comparisons replacement of saturated fat was associated with an improved total:HDL cholesterol ratio, with the greatest effect seen with polyunsaturated fat replacement.. Clinical trials involving cholesterol lowering by diet or drugs confirm CHD risk reduction in proportion to the extent of cholesterol lowering (16, 17).
Dietary advice is given in terms of foods or dietary patterns rather than nutrients. There is no evidence that any particular dietary pattern is superior when adhering to the core components of cardioprotection, including reduction of saturated fat and free sugars and an increase in the ratio of unsaturated to saturated fatty acids.
REFERENCES
1. Malhotra A. Saturated fat is not the major issue. BMJ 2013;347. doi: 10.1136/bmj.f6340.
2. Te Morenga L, Mallard S, Mann J. Dietary sugars and body weight: systematic review and meta-analyses of randomised controlled trials and cohort studies. BMJ 2013;346:e7492. doi: 10.1136/bmj.e7492.
3. Hooper L, Abdelhamid A, Moore HJ, Douthwaite W, Skeaff CM, Summerbell CD. Effect of reducing total fat intake on body weight: systematic review and meta-analysis of randomised controlled trials and cohort studies. BMJ 2012;345:e7666. doi: 10.1136/bmj.e7666.
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5. Farzadfar F, Finucane MM, Danaei G, Pelizzari PM, Cowan MJ, Paciorek CJ, Singh GM, Lin JK, Stevens GA, Riley LM. National, regional, and global trends in serum total cholesterol since 1980: systematic analysis of health examination surveys and epidemiological studies with 321 country-years and 3• 0 million participants. The Lancet 2011;377(9765):578-86.
6. Prospective Studies Collaboration. Blood cholesterol and vascular mortality by age, sex, and blood pressure: a meta-analysis of individual data from 61 prospective studies with 55 000 vascular deaths. The Lancet 2007;370(9602):1829-39. doi: http://dx.doi.org/10.1016/S0140-6736(07)61778-4.
7. Asia Pacific Cohort Studies Collaboration. Cholesterol, coronary heart disease, and stroke in the Asia Pacific region. International Journal of Epidemiology 2003;32(4):563-72. doi: 10.1093/ije/dyg106.
8. Nago N, Ishikawa S, Goto T, Kayaba K. Low cholesterol is associated with mortality from stroke, heart disease, and cancer: the Jichi Medical School Cohort Study. Journal of epidemiology / Japan Epidemiological Association 2011;21(1):67-74.
9. Bae J-M, Yang Y-J, Li Z-M, Ahn Y-O. Low Cholesterol is Associated with Mortality from Cardiovascular Diseases: A Dynamic Cohort Study in Korean Adults. J Korean Med Sci 2012;27(1):58-63.
10. Jacobs D, Blackburn H, Higgins M, Reed D, Iso H, McMillan G, Neaton J, Nelson J, Potter J, Rifkind B. Report of the Conference on Low Blood Cholesterol: mortality associations. Circulation 1992;86(3):1046-60.
11. Siri-Tarino PW, Sun Q, Hu FB, Krauss RM. Meta-analysis of prospective cohort studies evaluating the association of saturated fat with cardiovascular disease. The American journal of clinical nutrition 2010;91(3):535-46. doi: 10.3945/ajcn.2009.27725.
12. Mamdani M, Sykora K, Li P, Normand SL, Streiner DL, Austin PC, Rochon PA, Anderson GM. Reader's guide to critical appraisal of cohort studies: 2. Assessing potential for confounding. BMJ 2005;330(7497):960-2. doi: 10.1136/bmj.330.7497.960.
13. Jakobsen MU, O'Reilly EJ, Heitmann BL, Pereira MA, Balter K, Fraser GE, Goldbourt U, Hallmans G, Knekt P, Liu S, et al. Major types of dietary fat and risk of coronary heart disease: a pooled analysis of 11 cohort studies. The American journal of clinical nutrition 2009;89(5):1425-32. doi: 10.3945/ajcn.2008.27124.
14. Mozaffarian D, Micha R, Wallace S. Effects on coronary heart disease of increasing polyunsaturated fat in place of saturated fat: a systematic review and meta-analysis of randomized controlled trials. PLoS medicine 2010;7(3):e1000252. doi: 10.1371/journal.pmed.1000252.
15. Mensink RP, Zock PL, Kester AD, 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. The American journal of clinical nutrition 2003;77(5):1146-55.
16. Baigent C, Blackwell L, Emberson J, Holland LE, Reith C, Bhala N, Peto R, Barnes EH, Keech A, Simes J, et al. Efficacy and safety of more intensive lowering of LDL cholesterol: a meta-analysis of data from 170,000 participants in 26 randomised trials. Lancet 2010;376(9753):1670-81. doi: 10.1016/S0140-6736(10)61350-5.
17. Dayton S, Pearce ML, Goldman H, Harnish A, Plotkin D, Shickman M, Winfield M, Zager A, Dixon W. Controlled trial of a diet high in unsaturated fat for prevention of atherosclerotic complications. Lancet 1968;2(7577):1060-2.
Competing interests: No competing interests
It is important to highlight that this article provides a brief commentary on saturated fat and is based on limited evidence. Government advice to limit saturated fat intake to no more than 11% of total food energy in order to reduce the risk of cardiovascular disease is based on long standing evidence from the Committee on Medical Aspects of Food Policy (COMA) and is endorsed by the Scientific Advisory Committee on Nutrition, who now provides the UK with independent advice on nutrition. The advice is supported by a wealth of evidence and is also in line with more recent assessments made by the Institute of Medicine (2005), World Health Organization (2008) and the European Food Safety Authority (2010).
There is good evidence from randomised controlled trials (RCTs) to demonstrate that saturated fat consumption influences cholesterol levels and increases the risk of cardiovascular disease. For example, the RISCK study, a 6 month trial that analysed results from 548 men and women, found that total cholesterol and LDL cholesterol concentrations were significantly lower after consumption of diets lower in saturated fat compared to the control group (Jebb et al. 2010). Skeaff and Miller (2009) conducted a meta-analysis of 16 trials modifying the amount of saturated fat in the diet and found that, in studies which significantly lowered serum cholesterol by replacing saturated fat with polyunsaturated fat, both heart attacks and deaths from heart disease were significantly reduced. More recently a Cochrane Collaboration systematic review (Hooper et al. 2012) concluded that reducing saturated fat by reducing and/or modifying dietary fat intakes lowered the risk of cardiovascular events by 14%.
The combined results of 14 RCTs investigating statins also found that a reduction in LDL-cholesterol of 1mmol/L, sustained over a period of 5 years, reduced major vascular events by 23% (Cholesterol Treatment Trialists’ Collaborators, 2005). Chan et al (2011) conducted a meta-analysis of seven trials investigating the effect of intensive lipid lowering using statins. The intensive lipid lowering arm had reduced LDL levels and significantly lower risks for stroke, coronary events, and CVD and CHD deaths.
The UK National Diet and Nutrition Survey (NDNS) shows that people are still, on average, consuming saturated fat above recommendations (12.7% for food energy). Therefore based on the totality of the evidence, Public Health England will continue to advise people to consume a diet that is low in saturated fat and supports the Department of Health’s Responsibility Deal incentives to reduce saturated fat in foods.
In addition to focusing on reducing saturated fats, PHE supports broader changes to the diet including reductions in salt, sugar and calorie intake and increasing fruit and vegetable consumption.
Chan DK, O'Rourke F, Shen Q, Mak JC, Hung WT. (2011) Meta-analysis of the cardiovascular benefits of intensive lipid lowering with statins. Acta Neurol Scand. 124(3):188-95.
Cholesterol Treatment Trialists’ Collaborators. Efficacy and safety of cholesterol-lowering treatment: prospective meta-analysis of data from 90 056 participants in 14 randomised trials of statins. Lancet 2005;366:1267-78.
Department of Health. 46 Nutritional aspects of cardiovascular disease. Report on Health and Social Subjects. 1994. London: TSO.
EFSA Panel on Dietetic Products, Nutrition, and Allergies (NDA); Scientific Opinion on Dietary Reference Values for fats, including saturated fatty acids, polyunsaturated fatty acids, monounsaturated fatty acids, trans fatty acids, and cholesterol. EFSA Journal 2010; 8(3):1461.
IOM (Institute of Medicine). 2005. Dietary Reference Intakes for Energy, Carbohydrate,
Fiber, Fat, Fatty Acids, Cholesterol, Protein, and Amino Acids (Macronutrients). National Academies of Science, Washington DC.
Jebb SA, Lovegrove JA, Griffin BA, Frost GS, Moore CS, Chatfield MD, Bluck LJ, Williams CM, Sanders TA; RISCK Study Group. Effect of changing the amount and type of fat and carbohydrate on insulin sensitivity and cardiovascular risk: the RISCK (Reading, Imperial, Surrey, Cambridge, and Kings) trial. Am J Clin Nutr. 2010 Oct;92(4):748-58.
National Diet and Nutrition Survey: Headline Results from Years 1, 2 and 3 (combined) of the Rolling Programme 2008/09 – 2010/11
Skeaff CM & Miller J. Dietary fat and coronary heart disease: summary of evidence from prospective cohort and randomised controlled trials. Ann Nutr & Metab 2009;55:173-201.
WHO. 2008. Fats and fatty acids in human nutrition. Joint FAO/WHO Expert Consultation. Food and nutrition paper 91, WHO, Geneva.
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Re: Saturated fat is not the major issue
One thing which strikes me on reading of these responses is an overwhelming emphasis on the impact of specific components of foods (i.e. individual nutrients) rather than the actual whole foods themselves.
My understanding of traditional human diets is that numerous populations have until recently thrived on a wide range of differing diets (from very high to very low fat) and that the 'diseases of civilisation' only appear when they are introduced to industrially produced refined food products. It would therefore seem that searching for individual nutrients responsible for various conditions is an oversimplification of a complex issue. Michael Pollen summarised the ideas very well in his book 'In Defence of Food' with the advice that in order to maximise our chances of remaining healthy we should eat real food and not 'edible food like substances'
Competing interests: No competing interests