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A SYSTEMATIC review published last month created a bit of a storm as to whether recommendations to reduce saturated fat in our diet were based on evidence.
The article, in Open Heart, claimed that no randomised controlled trial (RCT) had tested government recommendations to reduce saturated fat intake before they were introduced in 1977 in the US and in 1983 in the UK to help prevent coronary heart disease (CHD).
The paper stimulated an article in The Guardian with the alarming subtitle “Researchers claim dietary advice around fat consumption, followed by millions for the past 30 years, should never have been issued”.
Neither the Open Heart paper nor The Guardian article asks whether today’s diet/heart advice is in error.
RCTs are, of course, the ultimate test for pharmaceuticals. Patients are randomly given either the test drug or a placebo with no biological action. Compliance can be checked by measuring the drug in blood samples.
However, for nutrition research this is not usually possible. If a test food is added or removed, some other food must replace it to keep the calorie intake level, and compliance is hard to maintain and assess.
RCTs of dietary change are uncommon except for trials with pure micronutrients.
When reduced saturated fat has been researched in controlled human trials it has usually been replaced with foods containing polyunsaturated fat [PUF]. These diet trials tested the combined effect of removing saturated fat and adding PUF.
All these trials were completed between 1966 and 1989, before statins were available to lower plasma cholesterol.
Meta-analyses published in more recent times find that the combination of reduced saturated fat and increased PUF does lead to significantly fewer CHD events.
The low density lipoprotein (LDL)-cholesterol-raising effect of saturated fatty acids had been first reported in The Lancet in 1957.
Expert committees first recommended reducing saturated fat intake to prevent CHD in 1961 in the US and in 1976 in the UK, following a report of a joint working party of the Royal College of Physicians of London and the British Cardiac Society. These recommendations were then taken up by the governments of both countries and later in Australia.
When the committees which developed these recommendations in the US and the UK met they had other information available showing ecological CHD was common in communities with higher plasma cholesterols; prospective studies, including the Framingham study, showing people with high plasma cholesterols had more CHD events in the next 10 years; and RCT results consistent with benefits from reducing saturated fat and increasing PUF.
Lowering plasma LDL-cholesterol has been a major way to deal with the CHD epidemic. Age-standardised death rates from CHD started to come down rapidly 7 years after the dietary recommendations were first introduced in the US in 1961 and 7 years after the 1976 recommendation in the UK.
In 1995 statins were introduced and the mortality decline has continued.
There has been a vast amount of literature in the past 50-plus years that does not support the claims made in the Open Heart articles.
Advice to limit intake of saturated fat should continue.
Professor Stewart Truswell is emeritus professor of human nutrition at the University of Sydney.
COI: Professor Truswell was a member of the Royal College of Physicians committee in 1976 and wrote an editorial for The BMJ in 1984 about the UK Department of Health and Social Security’s report that followed the dietary advice of the Royal College of Physicians.
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“The interior surfaces of the heart and blood vessels are covered with endothelial cells, which reduce friction. When the blood becomes turbulent, endothelial cells divide much faster than normal. The division creates gaps in the coating of the vessel, allowing platelets and cholesterol to attach and form rough patches, and plaque begins to form.” [”Principles of Physics: A Calculus-Based Text, Volume 1” by Raymond A Serway, John W Jewett – Wadsworth Publishing Co Inc, 2011, p.499]
This degeneration is arteriosclerosis, with the rough patches causing blood clots. With increasing age, the liver produces more and more cholesterol in an effort to keep the cells lining the blood vessels in an elastic state* (culminating in excessive, and potentially dangerous, levels of cholesterol that could block arteries).
* A textbook employed worldwide [“Essentials of Human Anatomy and Physiology” (Tenth Edition) by Elaine N. Marieb – Pearson Education Limited 2014, p.80] says, “The cholesterol helps keep the cell membrane fluid.”
Lowering cholesterol reduces attachment of this lipid to the vessel. But it doesn’t affect other arteriosclerotic causative factors like platelets, endothelial cells and blood flow. Also – reduction of cholesterol, and fluidity, in cell membranes would increase friction between vessel walls and passing blood plasma/cells, eventually leading to rough patches and degeneration of vessels. Therefore; cholesterol-lowering drugs alter the pathway to, but do not cure or prevent, arteriosclerosis.
Both excess refined carbohydrates and excess saturated fat are implicated in chronic disease. There is no single “demon”. “Heart healthy carbohydrates” include plant-derived whole grains. Essentially every cultural diet includes plant-derived carbohydrate – either a grain or starchy root vegetable – as a staple. There is lots of robust evidence that a diet including whole-grains and plant-derived carbohydrates, within whole foods, enhances health in many ways – not just weight control and insulin resistance but also in bowel health and various cancers. It’s tempting to look for simplistic approaches, like declaring fructose to be “poison”, but physiology and chronic disease causation are much more complex than that. Finding a way to manage personal weight is great if done in a way consistent with overall health outcomes, but an understanding the overall health effects of diet is required when advising others or creating public policy.
Professor Truswell has documented that he was the most influential figure behind the introduction, in 1979, of Australia’s first dietary guidelines: http://apjcn.nhri.org.tw/server/apjcn/procnutsoc/1990-1999/1995/1995%20p…
He has explained that our 1979 guidelines were mainly a rebadged version of the (infamous) 1977 US dietary guidelines and that, importantly, our guidelines were introduced without a proper local review of the “science” on which the US guidelines were based. That science – insisting that saturated fat in meat and dairy foods causes heart disease and stroke – has now been shown to be faulty: http://ajcn.nutrition.org/content/91/3/535
If saturated fat were as harmful as Professor Truswell still insists, there would exist no reliable and repeatable randomised-controlled trials (RCTs) showing – as they do – that replacing supposedly heart-healthy carbohydrates with fat – including saturated fat – tends to fix obesity and type 2 diabetes while reducing the risk of cardiovascular disease: http://www.australianparadox.com/pdf/obesitysummit.pdf When one realises that obesity, type2diabetes and CVD are merely aspects of Metabolic Syndrome or insulin-resistance syndrome, the dietary evil shifts from being saturated fat in wholefoods to sugar and other refined cabohydrates.
Prof Truswell’s article is well-supported by high-quality review information. IN particular, Micha and Mozaffarian’s very thorough review, published in Lipids 2010, reaffirmed the evidence that reduction in saturated fat reduces the coronary risk, so long as the energy gap is not replaced by refined carbohydrates. The full paper can be accessed here: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2950931/
The reason for this pro-fat backlash is another discussion altogether. It appears to go with the assertion that “sugar is poison” and that fructose alone is to blame for all obesity or insulin resistance. Certainly excess sugar, beyond nutrient and energy balance, can contribute to chronic illness. That does not give saturated fat a free pass. I’d be interested in the opinions of others on the current pro-saturated-fat phenomenon.
In this comment I can’t offer details and references off the top of my head but maybe will inspire those who are aware of these things to chime in. Point one is that when you dig deeper you find or are reminded that not all saturated fats are the same and that there is a spectrum of effects on lipid profile that varies with chain length and the relative proportion of specific fatty acids. Second, LDL appears to be an imprecise marker for atherogenicity of the population of particles involved and that future studies would do well to include some of the recently elucidated markers, such as total particle number. The next iteration of research on this issue (of the impact of saturated fat on heart disease evolution) will hopefully take such nuances into account.