What you need to know about saturated fat and CVD
The effect of saturated fat on CVD outcomes. The debate put to bed
What’s the truth about dietary saturated fat intake and cardiovascular disease risk (CVD) risk? This is a topic we cover during my frequent diabetes education sessions. This is because diabetes significantly increases your risk of developing cardiovascular complications.
Usually I go through the spill of reducing saturated fat and increasing the ‘good unsaturated fatty acids to improve heart health. However, something has never sat right with me. This is because there has been conflicting messages in the media and amongst my fellow healthcare professionals about the role of diet and CVD risk.
Therefore, I found myself presenting on topics in good faith. Good faith the talks I have inherited from my healthcare services are up to date and reflect the best evidence. The problem is I hadn’t looked this up for myself. So when questions arise in my sessions challenging the information I felt somewhat uncomfortable. This is because I hadn’t looked at the research properly myself.
So I decided to try something novel to address this. I looked it up – properly. Not just a google search but instead conducted a pretty robust literature search. This will be my intention going forwards. Rather than more frequent less researched articles, I will try to capture the key research on the topic and mesh it with my experiences in practice. Hopefully this can provide a nice balanced approach to providing the most up to date clinical research on dietary and health topics.
If you know the history and have a good understanding of fats and just want a quick summary then the watch the video above or scroll down to the summary.
Low saturated fat – How it all started
If you’ll excuse the pun, fat has been at the heart of the cardiovascular debate since the 1940’s. Original research noticed a 70 fold increase in coronary deaths between 1920 and 1955. Researchers found people with CVD disease had a higher low density lipoprotein (LDL) cholesterol levels. This is now what we call ‘bad cholesterol.
Meanwhile, a key researcher in the development of the low fat recommendations known as Ancel Keys proposed the concentration of plasma cholesterol was proportional to the dietary saturated fat intake. Famous studies like the Framingham and 7 Countries studies appeared to confirm this. The 7 countries study looked at CVD incidence amongst different populations. He noticed countries with higher fat intakes had higher rates of CVD. It assessed 12,000 men between 40-59 years old and found positive correlations between coronary heart disease (CHD) mortality and total fat intake.
At a similar time research also looked at the relationship between sugar and CVD. Although some preliminary work demonstrated some relationship between the two, evidence was weaker than the link to fat.
As a result, the 1960’s guidelines reflected recommendations to reduce dietary fat intake with particular emphasis on reducing saturated fat.
Fast forward to present day and the association between saturated fat intake and CVD is not quite so clear. Many studies report conflicting evidence. The Cochrane data base of systematic reviews uses Skeaf’s (2009) review (https://www.karger.com/Article/Abstract/229002) as an example of a large scale study finding evidence to the contrary of the above studies.
The difference in evidence could be for many different reasons. Changing only 1 dietary nutrient can produce ripple effects that can’t always be accounted for. I could probably blog all day on the variations in research but let me highlight some key variables.
Variables which effect research outcomes
The study design will have a big impact on the outcome. Research studies tend to favour what we call randomised control studies. Such studies control as many external variables as possible and are therefore great at establishing cause and effect. It is this type of research which pharmaceutical companies use to test new medications.
Applying the study design to saturated fat intake there are many different problems that need to be addressed. How long is the study going to be? What participants will you include? Do they have existing CVD or not? If reducing total saturated fat in the diet what are you replacing it with, if at all? How many participants will you study? Will you include or exclude other risk factors such as smoking? Will the study be a randomised control study or will it be more of an observational study where researchers watch from the sidelines and see what happens?
I think you get the idea. Some studies called ‘Meta Analysis’ gather all the available studies in hope of identifying a conclusion. These are a great way to take stock of the evidence base as a whole and this is what I have primarily included in my own research.
These aren’t without their problems though. They too suffer from many of the above problems. The biggest problem comes from their inclusion criteria. To gain a fair and unbiased view of the literature you must compare similar studies. For example, including a study that looked at saturated fat intake and CVD outcomes over 1 year will unlikely demonstrate any significant findings. This is because it takes years before an effect will likely be seen in terms of disease. Think of smokers. You rarely see a smoker develop COPD within 5 years of smoking. The effect can take years. Therefore, including a study of only 1 year in duration will likely skew the results. Such a study would probably be excluded in a Meta Analysis of this kind.
So the system isn’t perfect. However, it’s the best we have. Often with enough participants, some clever maths and the recognition of the limitations of the study, a true conclusion can be formed.
What is Fat? – Caution – Science lesson coming up
There are many types of fat. So if we’re going to analyse it’s effect on CVD we need to know what we’re dealing with. So lets take a look at the different types of fat.
Fat is made up from several molecules. Glycerol forms a backbone of the structure allowing up to 3 carbon molecules to attach themselves to it. These carbon molecules can then bond with both additional carbon and/or hydrogen. Think of a chain linking together, where each kink can either be carbon or hydrogen.
The carbon atoms can also use single or double bonds when joining together. The number of carbon to carbon, carbon to hydrogen and type of bonds determines the type of fat we are dealing with.
Each carbon molecule will have a space to potentially bond with a hydrogen molecule. Therefore, the more carbon to carbon molecules joined together in a line will allow for potentially more hydrogen molecules to bond with them. The most common fats in the diet range between chains of 16 to 18 carbon molecules.
Carbon molecules with all their potential hydrogen slots taken are called saturated fats. The hydrogen spaces are fully saturated. Think a parking lot with every space taken.
When you have a double carbon bond, less hydrogen molecules join to the carbon molecules. In other words, you have spaces free in the car park. If one space is free we call this ‘mono’ (for one) and if more than one space is free, we call it ‘poly’ for many.
Types of fat
Therefore we have saturated (no double bonds), monounsaturated (1 double bond) and polyunsaturated fatty acids (more than one double bond). Each of these fats are triacylglycerols. We also have 2 other main categories of fats independent of triacyglycerols known as cholesterol and phospholipids, both of which support cell function. So we have 3 categories in total. Today we are focusing on the triacygylerols. These are saturated, monounsaturated and polyunsaturated fats. There is also an additional fat we will be discussing here today called ‘Trans fat’. This type of fat exists in very few natural foods and is typically the result of man made meddling. Also known as hydrogenated oils, these fats also effect human health.
Okay enough with the science. Lets get more practical. The functions of fat in the body are many. Fat is essential for human health. So even low fat guidelines should not be interpreted as no fat. Fat helps for energy storage, function of cell membranes, cell signalling, blood clotting, smooth muscle contraction and many more functions.
The different types of fat have different effects on the body and it is for this reason the debate exists about the optimal fat intake.
Saturated, monounsaturated, polyunsaturated and trans fatty acids
Hopefully if you’re still awake there is one more item to look at before we delve into the evidence. That is to look at the different triacylglycerols and show you the types of foods they exist in. No single food will have just one type of fat so when we discuss good sources of each we are talking about the foods with the highest composition.
Saturated fats are mainly found in animal products. Examples include cheese, pork, lamb, beef, milk, butter, lard, particularly fatty cuts of meat, cream, poultry with skin, etc. It seems a high intake of these foods increases your risk of developing CVD. This is because high intakes of saturated fat increases your LDL cholesterol or bad cholesterol.
Monounsaturated fats come mainly from oils such as olive oil, rapeseed oil, peanut oil, safflower oil, sesame oil and foods like avocado and nuts and seeds. Historically when I have presented on monounsaturated fats we explain these fats reduce your LDL cholesterol whilst having no effect on your ‘good’ high density lipoproteins (HDL) cholesterol. The question is whether this translates into improved CVD outcomes.
Polyunsaturated contain the essential fatty acids our body’s cannot make on their own. We have to eat these in the diet. You may know these as Omega 3 and Omega 6. These fats are also essential in maintaining optimal cell function.
There are 3 main types of omega 3 oils. Alpha linolenic acid (ALA), eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA).
Sources of ALA includes nuts and seeds and canola and soybean oils. Despite being a true essential fatty acid because our body’s can’t make it, ALA only acts as a precursor to the more metabolically active EPA and DHA versions. The problem with this is ALA has a low conversion rate to EPA and DHA meaning a lot of the benefit may be lost.
DHA & EPA
Therefore, current guidelines recommend cutting out the middle man and suggest eating rich sources of EPA and DHA which is oily fish. The current dietary recommendations support this advising 2 portions of fish per week with at least one of these being from an oily fish source.
Omega-6 fats are also essential, we must obtain some from food. They are important for regulating energy production (part of metabolism), bone, skin and hair health. Many foods contain omega-6 fats, particularly vegetable oils and nuts e.g. sunflower oil, soy and linseed oil.
Omega-6 fats include linoleic acid (LA), gamma-linolenic acid (GLA), dihomo-gamma-linolenic acid (DGLA) and arachidonic acid (ARA). Like ALA in the omega 3 category, each of these fats also act as a precursor to eicosanoids. Eicosanoids perform many functions in the body including cell signalling, inhibiting inflammation and immune response. There are multiple subfamilies of eicosanoids, including the most common prostaglandins, thromboxanes, leukotrienes and lipoxins. These help in the immune response and some research has indicated eating too many of these fats could be harmful to human health.
In fact a quick google search shows how in theory these foods could be harmful. The website Healthline suggests a recommended ratio of omega 6 to omega 3 ratio of 4:1. Healthline says, modern agricultural practices has shifted the ratio to more like 10-50:1. This means larger amounts of eicosanoids being produced. A presidential advisory from the American Heart Association (2017) does suggest certain animal feeds may increase the composition of omega 6 in food but does not go on to mention ideal ratios. It is beyond the scope of today to go into this in more detail and perhaps this may be an article for the future.
What we are concerned about ultimately, is whether any of these foods have any effect on CVD outcomes – regardless of theories or ideal ratios.
The Evidence for lowering saturated and total fat in the diet for improved CVD outcomes.
As mentioned I have attempted to use only credible studies looking at very large populations. My first port of call was a literature search using data bases such as Pubmed with an Open Athens account. I combined this with government guidelines both in the UK and the United states to try to get a balanced view.
The American Heart Association (2017) provide a rather robust review on the matter. They considered all the early evidence from the 50’s, 60’s and 70’s and balanced this against more recent studies. They concluded saturated fat increases LDL cholesterol, a major cause of atherosclerosis (hardening of the blood vessels) and CVD. Replacing saturated with polyunsaturated or monounsaturated fat decreases LDL cholesterol. Therefore, in theory reducing saturated fat indirectly reduces CVD. Furthermore, replacing fat with carbohydrates did not reduce the incidence of CVD. However, it was difficult to find out what type of carbohydrate was substituted for saturated fat amongst the studies.
After analysis they found the overall evidence supports replacing saturated fat with omega 6 fatty acids. They reported more favourable outcomes in reducing CVD incidence compared to replacement with other fats. The authors did not recommend reducing total fat intake as this wasn’t shown to demonstrate a clinical benefit. Instead, they recommend following a DASH (diet approaches to stop hypertension) or Mediterranean style diet.
The link between lowering total saturated fat intake and CVD outcomes was shown in a Cochrane review in 2015.
This review studied various different outcome measures. Primary outcomes looked at total mortality, cardiovascular events, heart attacks (fatal and non fatal), coronary heart disease mortality and blood lipids such as cholesterol.
The authors found you are at no less risk of CVD mortality when replacing saturated fat with other types of fat or carbohydrate. However, there was an overall 17% reduction in cardiovascular events when reducing saturated fat in the diet. When subgrouping the studies to look at individual effects, replacing saturated fat with polyunsaturated fat, the reduction was greater at 27%. Similar findings were not found when replacing saturated fat with monounsaturated fat, carbohydrate or protein.
Further analysis confirmed less cardiovascular events as cholesterol was reduced further. There was a modest suggestion that reducing saturated fat further and/or further increasing unsaturated fatty acids offered greater protection.
In other words, reducing your saturated fat intake may not have an effect on lifespan due to CVD but it will reduce the likelihood of suffering a CVD event e.g. heart attack, angina, hypertension etc. So you may be thinking no big deal if the mortality rate isn’t effected right? Well, what these studies do not measure is quality of life. From experience, patients in ill health have a reduced quality of life. So you may live as long with medical intervention but you may have serious complications.
Other Cochrane reviews have been published looking exclusively at omega 3 and omega 6 fatty acids. It seems omega 6 fatty acids produce the most benefit when it comes to reducing CVD events.
Take home messages
The researchers also raised an interesting point in their conclusion. Most individuals with active CVD will be on lipid lowering medication to prevent the likelihood of a CVD event. Therefore, the benefit of reducing saturated fat intake may be lost if patients are taking medication for their CVD. It is still likely beneficial to follow healthy eating guidance and I would always recommend this. However, in terms of active CVD, it seems reducing saturated fat intake alongside medical intervention will produce no further benefit.
What this does suggest though is prevention is the name of the game. The overall reduction in CVD when reducing saturated fat and replacing with mono or polyunsaturated fatty acids, carbohydrate or protein was 17%. This was increased to 27% if just looking at polyunsaturated fat. So if you don’t have active CVD and are taking no medication to lower your cholesterol, there appears to be a significant benefit.
What the evidence also seems to suggest is replacing saturated with hydrogenated oils (trans fats) increases the risk ratio of CVD. Moreover, when analysing the type of carbohydrate replacing saturated fat there is a risk increase if choosing more higher sugar and/or processed forms. The risk is reduced if you eat higher fibre carbohydrates such as vegetables, fruit and wholegrains.
A study in the British Medical Journal looked at this in 2013. They analysed 22 different studies looking at the total dietary fibre, types of fibre and events of CVD and CHD. Total fibre intake was inversely related with a risk of CVD. In other words, the more fibre you have the less chance of CVD you have.
Due to the restraints of writing a detailed blog around a full time job, unfortunately referencing as you would in a report is impossible. That is, if you ever want to publish the blog. Therefore, I endeavour to read around a subject, get the evidence, and feedback my findings. I try to get a well balanced view and look at the evidence from both sides. There is no agenda. I have listed all my sources below and if you want to look into this further and find contradictory evidence, please let me know.
Essentially, I’m trying to take the Doctor out of Google Doctor and get to the heart of the evidence.
Evidence has yet to prove saturated fat causes CVD. It does show it increases LDL a precursor to CVD but no direct link exists. The evidence also shows replacing saturated fat with polyunsaturated fat CVD events are improved.
If you google it, several articles make claims that the reduction of dietary saturated led to the obesengenic environment we find ourselves today. Perhaps this is true and the food industry to some extent sold the low fat recommendation at the expense of good nutrition.
BUT and it’s a big but, the dietary recommendations have never been to replace saturated fat with high sugar and processed foods. Instead wholegrains, vegetables, fruits and mono and polyunsaturated fats have been the staple of dietary advice for many years. If lowering one nutrient you need to be replace it with something else in order to not starve yourself. Carbohydrates are one of many used to compensate for this. Diets with modest amounts of carbohydrate, such as the Mediterranean diet, have been advised for many years. So low saturated fat doesn’t automatically result in an increase in processed carbohydrates.
According to the NICE guidelines advise people at high risk of or with CVD to reduce total fat intake to 30% or less of total energy intake. They should also reduce saturated fats to 7% or less of total energy intake and keep intake of dietary cholesterol below 300 mg/day. Where possible you should replace saturated fats with mono-unsaturated and polyunsaturated fats. Further information and advice can be found at NHS Choices. (NICE 2014).
CVD figures over the years
Mortality from CVD in the UK has fallen by roughly 60% since the 1980’s and 1990’s. This is attributed to reductions in major risk factors, mainly smoking. Drug treatment, including secondary prevention, accounts for the remaining 40%. Since 2000, immediate fatal CVD deaths have halved. However, morbidity appears to be rising. CVD costs the NHS billions. In 2003 the estimated cost to NHS in England was almost £6,940 million, rising to £7,880 million in 2010 (NICE, 2014).
Age is closely linked with CVD. It predominantly affects people older than 50 years. Risk factors for CVD include non-modifiable factors (such as age, sex, family history of CVD and ethnic background) and modifiable risk factors (such as smoking, raised blood pressure and lipids, obesity and alcohol intake). As you can see this blog only addresses one of these factors so there is a bigger picture.
The research shows replacing saturated fat with monounsaturated and omega 3 fatty acids does not reduce CVD. In reality most sources of good fats such as oily fish, olive oil, nuts etc have a combination of all fats with one type of fat being predominant. Therefore, eating a balanced diet consistent with current guidelines is good practice.
I would also like to highlight the evidence here only describes the relationship with CVD. It fails to show the other beneficial effects of monounsaturated fats and omega 3 foods. As mentioned these foods do provide essential functions in the body. Not meeting your requirement for these nutrients may manifest in other ways which are bad for your health.
I hope this article has cleared up some myths around saturated fat for you and hopefully you’ll comeback for more as I publish more articles.
Cochrane Database of Systematic Reviews Reduction in saturated fat intake for cardiovascular disease.
Cochrane Database of Systematic Reviews Omega-3 fatty acids for the primary and secondary prevention of cardiovascular disease (Review)
Cochrane Database of Systematic Reviews Omega-6 fats for the primary and secondary prevention of cardiovascular disease (Review)
Consumption of fruit and vegetable and risk of coronary heart disease: A meta-analysis of prospective cohort studies.
Dietary Fats and Cardiovascular Disease A Presidential Advisory From the American Heart Association
Dietary fibre intake and risk of cardiovascular disease: systematic review and meta analysis.
Dietary Linoleic Acid and Risk of Coronary Heart Disease: A Systematic Review and Meta-Analysis of Prospective Cohort Studies
Emerging Nutrition Science on Fatty Acids and Cardiovascular Disease: Nutritionists’ Perspectives
Fat, Sugar, Whole Grains and Heart Disease: 50 Years of Confusion. nutrients.
Monounsaturated Fatty Acids and Risk of Cardiovascular Disease: Synopsis of the Evidence Available from Systematic Reviews and Meta-Analyses
Monounsaturated Fatty Acid Intake and Stroke Risk: A Meta-analysis of Prospective Cohort Studies.
Monounsaturated fatty acids, olive oil and health status: a systematic review and meta-analysis of cohort studies