OVERVIEW
· Could one of our most prominent public health messages – to cut down on saturated fat – be fundamentally flawed?
· Worse still, could what we replace it with in our diets be doing even more damage?
· We challenge the orthodox view that simply eating more carbs, or more polyunsaturated fats, is the way to go.
· Forget saturated fats – the real answer to our heart health woes lie elsewhere.
If there’s one thing we know when it comes to heart disease prevention, it’s the need to reduce our intake of saturated fat. This is one of the pillars of international dietary health recommendations. And the message must have got through. A mighty 73% of Americans now know that saturated fat can cause heart disease1; 61% of the UK ‘correctly’ know we should be eating less saturated fat2. The UK’s Food Standards Agency states that a small drop in saturated fat intake (from 13.3% of calories to 11% or less) would save 3,500 lives a year, not to mention £1 billion for the economy3.
The evidence for saturated fat and heart disease sure looks conclusive. Because here’s the thing: saturated fat raises your ‘bad’ LDL cholesterol, which is a cast-iron cause of heart disease4.
The top five dietary sources of saturated fat in the UK are dairy (24%), meat (22%), fat spreads (11%), biscuits (cookies) and baked goods (8%), and chocolate confectionary (5%).
A sugar-coated fiasco
We can replace saturated fat with any nutrient – protein, carbohydrate, monounsaturated fats or polyunsaturated fats – and our LDL cholesterol levels reduce5,6. And with it goes our risk of heart disease… or so we’ve been told. The truth is, we’ve made a big fat mess out of it all. The way the unrelenting message is drummed into us, you’d think the evidence was watertight, wouldn’t you? Actually, it’s non-existent!
It may sound like heresy, but the research is there to back it. In 2010, a meta-analysis of 21 studies encompassing 347,747 subjects found no evidence to conclude that dietary saturated fat was associated with an increased risk of coronary heart disease, stroke or cardiovascular disease7. We know, that bit of information got our eyebrows raised, too.
Considering that negative studies are less likely to be published, and the low number of published studies on saturated fat that exist compared to the international attention it has received, we have to wonder how many other studies exonerating saturated fat have not made it into the public domain.
A large Japanese cohort study, also published in 2010, following 58,453 men and women for 14 years, found that those who consumed between 2.5g–11g of saturated fat per day (so, what would be deemed ‘ideal’) had a staggering 45% increased risk of stroke compared to those eating 18g or more per day, as well as a 22% increase in the risk of cardiovascular disease8. So where is all this compelling evidence that has tainted the reputation of saturated fats?
Irrespective of the lack of hard evidence over the last few decades, the ‘fat is bad’ mantra has hit home. Total fat and saturated fat intake has declined. And if something goes down in our diet, then something else will go up. As we’ve been banishing the fats, we’ve made up for them with a compensatory increase in carbohydrate intake. Data from the USA shows that about 50% of our calories now come from carbohydrates9. High-carb, low-fat diets rule, and when it comes to heart disease, this should be a good thing, right?
For every 1% increase in energy intake from saturated fat in place of carbohydrates, our ‘bad’ LDL cholesterol increases by about 0.03mmol/L10. All sounds good, in theory, but what about in reality? An analysis of US and European cohort studies found that if we replace just 5% of our energy intake from saturated fats with carbohydrates (such a drop would put us at recommended levels), we see a 7% increase in coronary events11. The thing is, when it comes to heart disease and cholesterol, it’s not just about our LDL levels. To look only at this factor, and ignore everything else, is far too simplistic. Carbohydrates can increase triglycerides12 (which are an established risk factor for heart disease) and decrease the ‘good’ HDL cholesterol12.
But it doesn’t stop there, and we need to go back to LDL. Sure, switch your saturated fats to carbs and your amount of LDL decreases, but what we’re rarely told is that not all LDL is the same; it can differ by its particle size. And anything that increases triglyceride levels, such as carbs, increases the amount of what’s known as ‘small low density LDL’13,14. It appears that these small LDL particles have a much greater atherogenicity – meaning they’ll clog up your artery walls in no time. Their smaller size allows greater penetration into the artery walls, reduces their ability to bind to the LDL receptor, which causes them to stay in our bloodstream longer, and makes them more susceptible to oxidation. It appears these negative effects of high carbohydrate intake are especially pronounced in the overweight population, which unfortunately is now the majority12.
When it comes to carbohydrates and risk of heart disease, it’s all about the quality of carbohydrate, which can be measured by its Glycemic Index (GI) – in other words, how high our blood sugar levels rise after consumption. In a cohort study of 53,644 men and women over 12 years, it was the high GI foods (the refined carbohydrates) which had a devastating effect on heart health15. Replacing 5% of calories from saturated fat with high-glycemic carbs was associated with a whopping 33% increase in heart attack occurrence. Switching saturated fat for medium GI carbs had no effect, whereas there was a suggestion that low GI carbs could possibly even lower the risk. It’s not hard to see how low GI carbohydrates wouldn’t increase risk, and may be beneficial. Here we’re talking about minimally processed grains, legumes, fruit and vegetables. So with these foods, we’re not just talking carbohydrates, but vitamins, minerals, phytonutrients and fibre, all of which are essential for overall and cardiovascular health. As well as this, it seems the deleterious effects of these ‘good’ carbohydrates on our lipid profile might be minimal12.
That’s all well and good, but this pattern of eating hardly defines the Western diet, does it? Our penchant is for high GI carbohydrates, which are all too often stripped of nutrients. We’re talking about the highly processed beige and white foods – bread and other baked goods, rice, pasta, breakfast cereals, potatoes and beverages – that characterize the Western diet. Not to mention the multitude of cleverly marketed goods lining our shelves that are laden with added sugar (they are supposedly ‘okay’ because they are ‘low fat’ – what a joke). What we’re left with is a continual sugar dump into our bloodstream, and the accompanying hormonal chaos that ensues, which leads to oxidative stress, inflammation, beta cell dysfunction and endothelial dysfunction16. Add to this raised triglycerides, reduced HDL and smaller LDL particle size, and it’s not difficult to see how high-GI junk dramatically increases our risk of heart disease.
To us, it’s become apparent that the hallowed public health message to reduce saturated fat, so loudly trumpeted, has backfired. It is a travesty and detrimental to our cardiovascular health. In the words of one researcher, ‘the obesity epidemic and growing intake of refined carbohydrates have created a “perfect storm” for the development of cardio-metabolic disorders’17.
Stolen credit
So, recommendations are now to replace saturated fat with polyunsaturated fats (or ‘PUFAs’ for short). Whereas saturated fats are mainly hard animal fats, polyunsaturated fats are mainly liquid vegetable oils. In a review of eight RCTs totalling 13,614 participants, it was found that if we switch 5% of our calorie intake from saturated fats to polyunsaturated fats, our coronary heart disease risk reduces by an impressive 10%18. A meta-analysis of 60 trials found replacing carbohydrates with polyunsaturated fats had the most favourable effect on improving our cholesterol profiles10.
There are two main types of polyunsaturated fats – omega-3 and omega-6. But with the omega-3s present in few food sources and only needed in relatively small amounts, they don’t offer an appropriate substitute for our saturated fat intake. Thus it is the omega-6s, with their much greater availability and consumption levels, that have received the accolades19. But that doesn’t mean that our heart disease woes are over. The fact is that government health agencies around the world have set a recommended limit on omega-6 consumption, which is typically an intake of about 4–8% of energy19,20. The US National Cholesterol Education Program states that ‘there are no large populations that have consumed large quantities of polyunsaturated fatty acids for long periods. Thus, high intakes have not been proven safe in large populations; this introduces a note of caution for recommending high intakes’21.
Omega-6 fats are found in vegetable oils – such as sunflower, corn, soybean, safflower and sesame – margarines, nuts, seeds, cereal grains and many processed foods (in the form of linoleic acid), and in meats, poultry, eggs and dairy products (in the form of arachidonic acid).
The big worry is that, on a biochemical level, eating too much omega-6 could contribute to inflammation in the body because the main type of omega-6 in the diet, linoleic acid, can be converted into arachidonic acid, which the body can then utilize to make pro-inflammatory chemicals19. While many people, including scientists, are concerned by this factor, it doesn’t actually appear to happen in humans because the conversion process is tightly regulated. So, even with higher intakes of linoleic acid, the increased conversion to arachidonic acid is minimal22. And contrary to what many think, it seems that a high omega-6 intake could even bring about a reduced inflammatory state19,23. But it is still all rather ambiguous and recommendations for upper intakes of omega-6 remain in place (with the exception of The American Heart Association, which recommends a minimum 5–10% of energy intake from omega-6 fats19).
So where does that leave us? Well, the omega-6 linoleic acid already makes up over 7% of energy intake in our diet24. This is predominantly through the greater than 1000-fold increase in soybean oil consumption that occurred in the twentieth century24. So what’s the point in recommending that we replace saturated fats with yet more omega-6 when we’re already consuming towards the upper end of recommended levels anyway? Considering that our alarming rates of heart disease have been accompanied by a dramatic rise in omega-6 consumption, are we really sure this is the table upon which we want to lay our bets?
One researcher who was unhappy to do so was Christopher Ramsden. When it comes to the trials that hail the polyunsaturated fats, we’re essentially talking about vegetable oils. While they are made up mostly of omega-6s, they also contain some omega-3s, which is worth mentioning. Ramsden and his colleagues, suspicious of the accolades accorded to the omega-6s, took the trials that were included in the meta-analyses for polyunsaturated fats and coronary heart disease risk and did something very interesting25. They split the trials into those that just increased omega-6 and those which used a mixed intervention increasing both omega-3s and omega-6s. The results were sobering indeed. RCTs that replaced saturated fat with just omega-6s produced no reduction in coronary heart disease. If anything, there were suggestions of an increased risk! So there we have it: another nutrient purported to save us from those ‘noxious’ saturated fats that just doesn’t hold up when put under scrutiny.
Unsung hero
With this revelation we see that it’s not the omega-6s that should be adorned with all the plaudits, but the omega-3s. More specifically, it’s the omega-3 fats EPA and DHA – the ones we find in oily fish – that are the true champions of our cardiovascular health. And are we so surprised? Just under 1g of EPA/DHA per day in a post-heart attack population is clinically proven to reduce death, non-fatal heart attack and non-fatal stroke by about 15%26. Omega-3s assist in stabilizing the electrical activity of the heart and in so doing, reduce the chances of developing arrhythmias, or an abnormal heart rhythmn27. Omega-3s are anti-thrombogenic (reducing the risk of blood clots), anti-inflammatory and therefore anti-atherogenic, and to top it off even have small effects on lowering blood pressure27.
Omega-3s lower triglyceride levels, with higher amounts used as an extremely effective treatment for hypertriglyceridemia, and thus decrease our small density LDL amounts, too. The omega-3 intake of the Japanese, with their fish-rich diet, hits near a gram per day, and they have extremely low levels of heart disease28. Here in the West, recommendations are to eat two servings of fish per week, of which one should be oily fish, and while even this may be a bit on the low side, only 19% of us achieve it29. As a result, our omega-3 EPA and DHA intake is a paltry 100–200mg per day30. Unsurprisingly, heart disease is rampant.
Amounts of fish supplying a gram of EPA/DHA are: herring 42–56g; salmon (farmed) 42–70g, (wild) 56– 98g; trout (85–98g); mackerel 56–238g; shrimp 308g; tuna (drained light tinned) 336g; cod (Atlantic) 350g, (Pacific) 644g; and haddock 420g31.
The beneficial health effects of omega-3 fish oils were first described in the Greenland Inuit. Consuming a diet rich in seafood appeared to proffer significant protection against coronary heart disease.
When we talk about omega-3, we’re essentially talking about fish, because no other dietary source comes close. In a 30-year trial of men (aged 40–55) in Chicago, eating an average of 35g of fish a day meant you had a 38% lower risk of death from coronary heart disease compared to those who didn’t eat fish32. A meta-analysis of 19 observational studies found that fish consumption was associated with a 14% lower risk of total coronary heart disease occurrence compared with little or no fish consumption33.
Omega-3 fats in the form of alpha-linolenic acid are found in some vegetable oils (e.g. rapeseed/canola and flax), some nuts and seeds (e.g. walnut and flax) and green leafy vegetables. However, the more potent forms of EPA and DHA omega-3 are found in cold-water fish and seafood.
Experts agree that we need a minimum of 500mg per day of EPA plus DHA combined to maintain cardiovascular health34. Consuming this level would be expected to significantly reduce the risk of death from coronary heart disease in healthy adults. For those with coronary heart disease, intakes of 1g per day are advised31.
Heart health is really only the beginning of the omega-3 story, and to stop there would do it an injustice. While the omega-6 fat arachidonic acid gets converted into pro-inflammatory factors in the body, the omega-3s fight aggressively for these same pathways to produce their less inflammatory factors. The upshot is that the omega-3-generated ones dampen down the overall inflammatory response. Getting sufficient omega-3 means that we can curb the activity of arachidonic acid in the body and with it reduce our levels of inflammation. Without sufficient omega-3 to keep arachidonic acid in check, we begin to see just why inflammation can become rampant in anyone following a typical Western diet. And that’s something to be wary of, as evidence is gathering to suggest that inflammation has a role to play in such diverse conditions as neurodegenerative diseases, obesity, type 2 diabetes, even cancer, to name but a few35,36. When it comes to the classic inflammatory disease, rheumatoid arthritis, data consistently shows an improvement in symptoms from using fish oils, although a minimum intake of 3g per day of EPA plus DHA combined is required for effective results37,38.
Fish stocks in the sea are under threat, so buy fish from sustainable sources wherever possible.
Now we must turn our attention to vegetarians and vegans. As we’ve seen in previous chapters, their predominant source of omega-3 is through plants providing alpha linolenic acid. And the conversion of this to the more potent EPA and DHA is poor. For these groups, their omega-6 to omega-3 ratio is of the utmost importance; ideally they should be striving for 4:1 or less. To achieve this they need to limit omega-6 oils. This can be done by switching from oils to wholefood sources such as sunflower seeds, pumpkin seeds, sesame seeds, walnuts, wheat germ and soy foods39. These provide smaller overall amounts of omega-6, while contributing other vital nutrients. Likewise, placing a greater emphasis on the omega-9 monounsaturated fats found in nuts, olives and olive oil, avocados and rapeseed/canola oil is a good strategy.
Little attention is given to monounsaturated fatty acids, but we could all probably benefit from increasing them. Monounsaturated-rich olive oil is a core component of the Mediterranean diet, which is strongly linked with lower cardiovascular and other inflammatory diseases40.
Incorporating good sources of the plant form of omega-3, alpha linolenic acid, is a must – good sources of this include flaxseed, hempseed, rapeseed/canola, walnuts and legumes (soy), as well as green leafy vegetables. A supplement of DHA-enriched microalgae (up to 300mg per day) is also encouraged39. DHA can also be converted back to EPA in small amounts in the body, helping to raise our EPA levels this way45.
Prime examples of omega-6-laden oils include safflower oil (75% omega-6), grapeseed oil (70% omega-6), sunflower oil (65% omega-6), corn oil (57% omega-6), cottonseed oil (52% omega-6), and soybean oil (51% omega-6)39.
THE SCIENCE BLAST: OMEGA OILS
So, there’s a bit of a competition going on here between omega-3 and omega-6, and it’s an idea that has fuelled the notion that we should aim to consume an ‘ideal’ ratio of these fats in our diet. If we look back to our hunter-gatherer ancestors, their natural diet would have provided a ratio of omega-6 to omega-3 fats of about 1–2:141. Just compare that to the ratio in our modern Western diet, which is more like 10:124 and could even be as high as 30:1!41 Because omega-6 can compete for the same enzymes and pathways in the body as omega-3, it’s proposed that scoffing large amounts of omega-6 (exactly as we see today) will overwhelm our omega-3, cancelling out their anti-inflammatory benefits.
However, most of our intake of omega-6 comes in the form of linoleic acid and, as we’ve seen, its conversion to arachidonic acid is tightly controlled, meaning that even the high amounts we consume are having a negligible impact. And while linoleic acid can compete with the omega-3s for incorporation into tissues, it seems it can also kick out arachidonic acid, so the net effect may actually be an anti-inflammatory one24. In the Los Angeles Veterans Study, a diet high in linoleic acid (15% of energy) actually reduced the amount of arachidonic acid in coronary atheroma phospholipids by 40%42. A US study found that, not only did linoleic acid intake not impede the anti-inflammatory actions of omega-3, but the greatest anti-inflammatory effect was seen from a combination of both omega-6 and omega-343. So you might hear a lot of talk about getting the correct ratio of omega-6 to omega-3, but you can forget it. It’s not the ratio that matters, it’s about bumping up our omega-3 intake to a meaningful level to reap the beneficial effects.
There is one caveat if you are a vegetarian or a vegan. Up to now when we’ve talked about omega-3, it’s been pretty much synonymous with fish. That’s because fish provides the potent omega-3 fats EPA and DHA. But plants also provide a type of omega-3 called alpha-linolenic acid, which is converted in the body to EPA/DHA. As we know, this conversion process is pretty poor, which means that alpha-linolenic acid accounts for quite a negligible supply of EPA/DHA. But what if you don’t eat any fish and rely solely on plant sources instead? This is where the omega-6 to omega-3 ratio (or more specifically the linoleic acid to alpha-linolenic acid ratio) is crucial.
Linoleic acid actually inhibits the conversion of alpha-linolenic acid to EPA and then to DHA19. The flipside is that if you reduce linoleic acid and increase alpha-linolenic acid it has the effect of reducing conversion to arachidonic acid and increasing conversion to EPA22,44. Therefore, vegetarians should not only increase their intake of omega-3 alpha-linolenic acid, but also reduce their omega-6 linoleic acid intake at the same time.
The enzymes that convert plant omega-3 fatty acids are highly dependent on our nutritional status, requiring adequate levels of pyridoxine, biotin, calcium, copper, magnesium and zinc39.
Alcohol inhibits conversion enzymes and depletes tissues of omega-3 fatty acids39.
THE PARTING SHOT
We’ve all been part of a big fat experiment, the results of which are out and they’re not good. Saturated fat was branded as public health enemy number one and we got so focused on it that we missed the true dietary disaster as our consumption of refined carbohydrates ran amok. So then we switched to the benefits of polyunsaturated fatty acids, and heralded the omega-6s as our saviour. Well, the results are coming back to roost there too, and it’s time to question the omega-6 ‘heart healthy’ certificate of authenticity. While not necessarily bad for us, it would be foolhardy to recommend any nutrient whose workings are not fully understood. There’s only one solution, and that’s to address the elephant in the room.
Saturated fat is simply not deserving of the bad rap it has received. That’s not a carte blanche to eat as much of it as you like – if we go to extremes there’s likely to be a price to pay. That’s the whole point here, getting back to the idea of balance. The reality is, the body is smart and all in all does a pretty good job in maintaining the status quo, as long as we do our bit too. The key is to give the body all the nutrients it needs to do this job, and right now that’s being prevented by the staggeringly low intake of omega-3 in our modern diet. If we are to tackle the burden of cardiovascular disease, promoting their intake is the road we have to take.
SUMMARY AND RECOMMENDATIONS
· Strong evidence implicating saturated fat in heart disease doesn’t exist.
· If you cut down on saturated fats and replace them with high GI carbohydrates, however, you will dramatically increase your risk of heart disease.
· Replacing saturated fats with omega-6 polyunsaturated fats is a dubious strategy too.
· It’s the omega-3 fats EPA and DHA that are truly deserving of our attention and our requirements can be satisfied by consuming two 170g servings of fish a week, with an emphasis on oily fish.