Powered in the knowledge that fats aren’t in and of them selves automatically ‘fattening’, our headlining culture committed reductionism suicide once more and we singled out certain fats for praise, and others for blame.
Some were labelled ‘heart-healthy’ while others ‘artery clogging’ in the pursuit of a template we all understand in our navigation of good and bad fats. I am a firm believer in education and understanding being key to our behaviour change; ten cents’ of human understanding equals ten dollars worth of medical sciences (Fischer 1879-1962).
Lets chew the fat, but first, some revision :)
BASIC FATS - REVISED
On a purely chemical level, fats or lipids comprise of a carbon backbone, which for simplicity sake are bound by varying amounts of Hydrogen. Each Carbon atom has an affinity for up to 4 Hydrogen atoms where it is bound by a single bond. In the situation where every Carbon atom has all four of its bonds connected to Hydrogen, it could be described as being ‘saturated’; hence we call these saturated fats (figure 1). The length of the Carbon chain dictates whether this chain is called a short (<5 carbons), medium(6-12 carbons) or long chain fatty acid (>12 carbons). (Wikipedia).
If however, the Carbon backbone does not have all its bonds connected to Hydrogen, it is no longer saturated and thus aptly named; Unsaturated. These fall into two main categories rather comically named MUFA and PUFA.
When there is only one (mono) Carbon missing a Hydrogen, this is called a Mono-unsaturated fatty acid (MUFA). If however, more than one (poly) bond is unbound to hydrogen, it is also named accordingly; Poly-unsaturated fatty acids (PUFA), please see figure two. The point where there is a missing Hydrogen can be seen and described as a ‘double bond’.
The point where this double bond is found in the Carbon chain is important for both definition and clinical purposes. In the bottom image of figure 3 there is more than one double bond (yellow C’s) illustrating that this is a polyunsaturated fatty acid with the first double-bond on the third Carbon from the left. There are a host of different types of these but as a category collectively we call them ‘Omega-3’ or n-3. If there is more than one double-bond (polyunsaturated) and the first one is on the sixth Carbon from the left we call it ‘Omega 6’ (n-6).
If there is only one double bond it is known as a Mono-unsaturated fatty acid on the ninth Carbon from the left and is otherwise known as the less commonly used term of ‘Omega-9’ (n-9).
Figure 3: The point where the first double bond in the Carbon is what distinguishes whether we are dealing with an omega 3, 6 or 9. Double bond on the third Carbon means omega 3 (lower chain), sixth Carbon means omega 6 (middle lower chain) and the less commonly used term omega 9 (middle upper chain).
GOOD FATS, BAD FATS
*Sidenote: the next section discusses some of the research in this area, although I have tried to keep it as simple as possible, you can skip to the 'closing thoughts' section if you want to jump some of the detail.
Oleic acid is the most common MUFA. These can be found in animal and vegetable foods – olive oil is the usual example – it makes up close to half of all the fat tissue in your body. Mono-unsaturated fatty acids are universally considered to be a healthy source of energy, provided you don't eat too much. Any dietary fat is easily converted to body fat.
Examples of high MUFA foods
- Nuts (almonds, brazil, cashews, hazelnuts, macademia, pecans, pistachios. walnut...)
- Nut butters (almond - my favourate, peanut, cashew, hazelnut...)
- Oils (olive, avocado, walnut, peanut, sunflower, safflower...)
Polyunsaturated fatty acids on the other hand are more interesting. There are two strands of this category that our body simply cannot create itself – it is in fact essential that we get them from our diet – again they were named so; essential fatty acids. The first is known as Linoleic acid (LA), an omega-6 PUFA; the second is alpha-linolenic acid (ALA) an omega-3 PUFA.
Linoleic acid is by far the most common PUFA in our diet and comes almost exclusively from three main sources; soybean, corn and cottonseed oils – none of which were a staple of the human diet a century ago. Interestingly, we get hardly any omega-3 fats through our diet.
Examples of high PUFA foods
- Fish oils (cod liver, salmon)
- Flaxseeds, whole
- Mayonnaise, light
- Vegetable oils (corn, flaxseed, grapeseed, sesame, soybean, cottonseed....)
There are two omega-3 fatty acids that have been linked to just about every important aspect of human health including cardiovascular and brain status; Eicosapentaenoic Acid (EPA) and Docosahexaenoic Acid (DHA). For a while fish oil was thought to prevent cardiovascular diseases however there is mounting evidence suggesting that the benefits are no longer quite so clear1.
There has also been debate over recent years of the importance of the omega 3:6 ratio. It is a foundation of the ‘paleo / caveman’ diet that our ancestors ate a near 1:1 ratio between the PUFAs. However over the past few thousand years with the rise of agriculture and processed foods the balance has shifted heavily in favour of omega-6 (more like 15-20+:1). Since omega-6 are associated with inflammation and omega-3s do the opposite it does lead to an important consideration, should we be trying to ‘re-calibrate’ our omega balance and reduce omega-6; the supposed ‘anti-inflammatory’ diet.
The literature here is well appraised in the March/April 2015 Alan Aragon Research Review (AARR)2. Chris Ramsden et al3 is one of the most significant outspoken critics of the American Heart Associations’ (2009) omega-6 recommendations of 5-10% total energy intake with this systematic review3. In 2013 the same author also used retrieved data from the Sydney-Diet-Heart-Study (SDHS), the longest ever controlled trial into the effects of omega-6 replacing saturated fat conducted between 1966-19734. This study was given significant weight in government guidelines as they found replacing saturated fat with safflower oil (75% omega-6) increased deaths from cardiovascular disease and coronary heart disease. A big deal.
The theory following Ramsdens findings certainly suggest reducing omega-6 PUFAs should translate to improved heart health. The best, most recent evidence we have however suggests you needn’t bother (see Johnson & Fritsche, 2012 direct quote below)
“This review clearly demonstrates that nearly no data are available from randomised, controlled intervention studies, among healthy non infant humans to show that the addition of LA (omega-6) to diets increases markers of inflammation. However the possibility that large intakes of LA increase markers of inflammation cannot be eliminated.
Nevertheless the outcome of this review should provide the dietetic community and other health professionals with a measure of reassurance regarding current dietary recommendations that emphasise optimal intake of both omega-6 and omega-3 PUFAs from sources such as soybean, canola, corn and safflower oils….” (Johnson & Fritsche, 2012)
As this systematic review of random controlled trials shows, our goal really ought to be to increase both PUFAs, 3 and 6 with no real concern about balancing them.
We can achieve more omega-3 through consuming fish, grass fed beef and free ranging eggs.
One of the best ways to achieve omega-6 is through nuts and seeds. In fact nuts are one of the strongest cases for not balancing your omegas – almonds have more than 2000 times as much omega-6 and are associated with a long list of health benefits. Those who eat nuts tend to be the leanest with the lowest risk of diabetes, respiratory problems and cardiovascular disease.6
So inflammatory omega-6 IS NOT a cause for concern regarding my cardiovascular health at all, including processed vegetable oils?!
The basis for cardiovascular disease is a process known as ‘atherosclerosis’ which was touched upon in chewing the fat part I, otherwise known as ‘clogged arteries’. This is essentially an inflammatory mechanism where the ‘bad’ cholesterol (LDL) gets trapped in the lining of our arteries and then a process called oxidation leads to a series of events and ultimately plaque formation that stiffens and blocks our blood flow system. The theory runs that each free carbon in the skeleton of PUFAs (revisit figure 2) is vulnerable to being ‘oxidised’ and leads to highly volatile compounds that damage our artery lining known as ‘free radicals’ and contributes to clogging arteries7. This has been demonstrated in animals at least8.
It is on this basis that saturated fats are also referred to as ‘more stable’ fats as they are less prone to oxidation, are therefore solid at room temperature and arguably more suitable to cook at higher temperatures before they are denatured.
USEFUL TIP: Cooking with fats as a rule of thumb:
- Ghee (clarified butter)
- Coconut oil
- Lard (pig fat)
- Tallow (beef fat)
- Duck fat
- Goose fat
These (saturated) fats are all solid at room temperature and arguably more stable against oxidation, therefore better tolerating higher temperatures.
Dressing with fats / oils:
- Olive oil, walnut oil, sesame oil, grapeseed oil, canola oil, avocado oil, macadamia nut oil, flaxseed oil or any other vegetable oils...
These oils have varying proportions of MUFA and PUFA in them and it seems generally good advice to not expose these to high temperatures and are best consumed as dressings.
RULES WERE MADE TO BE BROKEN
Provided we make otherwise heart healthy lifestyle choices (regular exercise, not smoking, stress regulation - discussed below) there is no reason marinading vegetables with an oil prior to cooking should be an issue. For example, olive oil drizzled over sweet potatoes, parsnips or a jacket potato. These are my personal favourites.
The best evidence we have however shows there is no causal link in the literature to suggest that a diet heavy in inflammatory omega-6 causes the ‘inflammatory’ diseases it has been associated with. In healthy people, who do not smoke, who regularly exercise and make otherwise positive lifestyle choices that do not lend themselves toward chronic stress and behaviours like excessive alcohol consumption, there is no damage in the arteries for any of the proposed processes of omega-6 PUFA or cholesterol mediated damage to take hold in the first place!2
The current literature warns that we cannot rule out a high PUFA intake in the presence of these co-morbid health conditions making things worse. However, to generalise this to healthy people would be like suggesting that carbohydrates are an issue for diabetics therefore everyone should avoid liberal carbohydrates, which would be equally illogical.
The very concept of industrially produced vegetable oils does not sit well with me if simply down to knowing how they are produced (discussed here). However, the research does suggest that in the presence of otherwise healthy lifestyle choices, the highest sources of omega-6 which are nuts and seeds and our vegetable oils (sunflower oil, safflower oil, canola oil, corn oil, rapeseed oil…..) should be of little concern, of course when exercising moderation. These foods are very easy to get a high density of calories in one sitting.
The advice to completely avoid vegetable oils is one I have conformed to in the past, falling into the very trap I strive to avoid – reductionism. When considering the bigger picture, the two major points from this literature review are as follows:
MUFA are good for you
PUFA are good for you.
There is no good reason to worry about the ratio of omega 3:6.
Surely, there are some fats that are bad for us??
Trans fats (margarine) have got to be bad for me??
The research can throw us some real curve balls where we least expect it. Find out why trans fats aren’t the villains you might think in the final part of this series. :)
Luke R. Davies :)
1. Hooper, L., Thompson, R. L., Harrison, R. A., Summerbell, C.D., Ness, A. R., Moore, H. J., Worthington, H. V., Durrington, P. N., Capps, N. E., Riemersma, R. A., Ebrahim, S. B. and Smith, G. (2006). Risks and Benefits of Omega-3 Fats for Mortality, Cardiovascular Disease, and Cancer: Systematic Review, British Medical Journal, 332(7544), P.752-60.
2. Aragon, A. (2015). Alan Aragon Research Review. Linoleum Acid - Does it deserve a Kick in the Nuts? March/April release.
3. Ramsden, C. E., Hibbeln, J. R., Majchrzak, S. F. and Davis, J. M. (2010). n-6 Fatty Acid-specific and Mixed Polyunsaturate Dietary Interventions have Different Effects on CHD Risk: a Meta-analysis of Randomised Controlled Trials, British Journal of Nutrition, 104(11), P.1586-600.
4. Ramsde, C. E., Zamora, D., Leelarthaepin, B., Majchrzak-Hong, S. F., Faurot, K. R., Suchindran, C. M., Ringel, A., Davis, J. M. and Hibbeln. J. R. (2013). Use of Dietary Linoleic Acid for Secondary Prevention of Coronory Heart Disease and Death: Evaluation of Recovered Data from the Sydney Diet Heart Study and Updated Meta-Analysis, British Medical Journal, 346
5. Johnson, G. H. and Fritsche, K. (2012). Effects of Dietary Linoleic Acid on Markers of Inflammation in Healthy Persons: a Systematic Review of Randomised Controlled Trials, Journal Acad Nutr Diet, 112(7), P.1029-41.
6. Guasch-Farrè, M., Bullò, M., Martinez-González, M. A., Ros, E., Corella, D., Estruch, R., Fitò, M., Aròs, F., Wärnberg, J., Fiol, M., Lapetra, J., Vinyoles, E., Lamuela-Raventrós, R. M., sERRA-mAJEM, l., Pintó, X., Ruiz-Gutiérrez, V., Basora, J. and Sala-Salvadó, J. (2013). Frequency of Nut Consumption and Mortality Risk in the PREDIMED Nutrition Intervention Trial, BMC Medicine, 11(164)
9. Aragon, A. and Schuler, L. (2014). The Lean Muscle Diet, Rodale inc, New York, USA, P.18.