Saturation be damned

Night time reading

I love interacting with this informed and educated community of ours who take responsibility for own health, read and interpret scientific articles, ask intelligent and incredibly tricky questions and look at the world through a prism of human evolution. It’s really really cool. I also don’t own a television or read newspapers. I know, I am missing out on the vital information on the recent exciting advances in the field of laundry detergents, easily foldable exercise equipment and female hygiene products. But I’ll take my chances.

So when I was approached recently by an Australian reporter to comment on why saturated fat might not be as bad as everyone thinks, I was temporarily stunned. Everyone still thinks that? An hour-long lunch outside in the company of co-workers brought me back to reality. Listening to the less-than-lithe lady lecturing a younger employee that “pasta is perfectly healthy as long as you avoid creamy sauces and stick with tomato-based ones and add psyllium husks to increase fibre” plunged me back to earth from the AHS12-induced heights.

Oh boy. On this planet, margarine is still a health food.

So I thought I’d write down some thoughts on fats, why we still need to talk about them, the strength of evidence and where we go from here. The article ended up being published at The Age and I was amused to see our hour-long phone conversation and the exchange of several emails with attached studies reduced to one sentence quoted from me, but I am not complaining since I think the article was quite well-balanced and hopefully gives people some food for thought. Here is the link.

If you are totally new to all this, I recommend that you read my post on fat basics and the slightly more complicated polyunsaturated fat primer.

Don’t all scientists and doctors agree that saturated fat is bad?

My main gripe with conventional advice to reduce saturated fat in the diet is that it makes it sound that everyone in science and medicine agrees that it is the right thing to do. They say “scientists” and you imagine a group of nerdy-looking men and women in lab coats and glasses with clipboards, all nodding in unison: “Saturated fat will kill you”.

Bad cow, bad!

Sorry, no. Far from it. In the year 2012 we still run trials on dietary fat and its effect on mortality, cardiovascular disease and weight. In fact, a Pubmed search on “dietary fat” yields close to 700 article from 2010 to present date.

If “saturated fat will kill you” is a done deal why do all these folks get research grants and waste years of their life on the pointless pursuit of the truth that has long been discovered and incorporated into every government-led nutrition advice?

And yet, the consensus is farther away than ever. Nutrition and Metabolism Society publishes critiques of the American Dietary Guidelines, as well as scores of papers on the subject. Then there is THINCS, The International Network of Cholesterol Skeptics, which really sounds like an evil mad scientist organisation from a Bond movie, but in fact has respected members like a biochemist Dr Mary Enig and a scientific researcher Dr Uffe Ravnskov.

Not to mention a fine gathering of clinicians, scientists, nutritionists, researchers, physiotherapists, bloggers at Harvard Law School this year for 2012 Ancestral Health Symposium, most of whom seemed to think that bacon is rad and margarine is bad.

Can you refute XYZ study and the rest of the body of evidence on saturated fat?

Yawn. I have no intention on memorising every study conducted in the last 50 years, no matter how bad or good they are. We have been eating fat, lard, meat, eggs, butter, ghee, coconut oil for thousands of years. I think the burden of proof lies on those who say that these traditional foods have been our silent killer all along. All I can do is to politely present the vast body of scientific evidence that does not support the lipid hypothesis (YES! IT IS STILL A HYPOTHESIS!)

Sarcasm alert. Lipid Hypothesis 2.0 = we have come to realise that total fat intake has no bearing on heart disease or weight (sorry! Our bad!) But it’s all about the type of fat. There are only 2 types of fat: saturated (=evil, comes from animals, eating animals is bad, you immoral cruel self-serving glutton) and unsaturated (=pure good, comes from vegetables, like cottonseed, soybean, canola and sunflower, botany be damned). Substituting unsaturated for saturated fat is the real reason why we are healthier, thinner and fitter than thousands of generations of traditional cultures because they couldn’t work out how to get 10% of their daily calories from PUFA, suckers.

 

He needs to be told how unhealthy he is from his 40% SAFA intake. Those coconuts will kill you, buddy! (Source: http://www.thatpaleoguy.com)

Several studies have shown improvement in CV markers and mortality when saturated fats were replaced with PUFA. Regardless of how good/bad sat fats are, shouldn’t we make the substitution just in case anyway?

This is a very common reasoning from many educated doctors and academics. They are now aware that sat fats are not much of a problem. Great. But what’s the harm in tinkering our diets if all we have is improvement, right?

Wrong.

I have a real problem with a blanket advice to increase PUFA in general as if they are all the same. PUFA are not all created equal, they have different physiological functions and effects on the body! (go back to basics). At the very least they should be differentiated into omega-3 and omega-6. However, even that’s too simplistic.

If you are planning on dividing fats on the basis of the biochemical structure and biological function, you have just only scratched the surface. Behold! All saturated fats are actually not the same either. Lauric fatty acid is metabolised differently and has different effects on serum lipid profiles than stearic. Even omega-3 are not a homogenous group (gasp!). The intake of the shorter-chained ALA (alpha-linolenic acid) does not come close to providing the same benefit as the long-chained DHA due to inefficient conversion.

Jacobsen’s analysis of 11 cohort studies, quoted in the article as the final proof of the miracle qualities of PUFA,  showed that substituting PUFA for SAFA seemed to reduce CV events and mortality. However, simplification, as usual, can only take you this far. The analysis lumped omega-3 and omega-6 PUFA together and did not take into account the deleterious effect of trans fatty acids separately from SAFA.

“Linoleic acid selective PUFA interventions produced no indication of benefit but rather a fairly consistent, but non-significant, signal toward increased risk of coronary heart disease and death. ” (Kuipers ER al, 2011, hyperlinked above)

That’s what happens when you simplify a complex concept. Why? Because the public are so dumb they won’t get it? Because 2 types of fat is quite enough to remember? And to make things even more visually and conceptually appealing let’s represent them as ying and yang, bad and good, dark and light?

So you have some studies, “they” have some studies. How do lay people know who to trust?

As much as I respect Evidence Based Medicine, I am well aware of its limitations. You can pull apart every study, point out the confounders, small sample size, confirmation bias, lack of double-blinding, the grant approved by a completely impartial third party with key investments in related area. Let’s not reduce the process to “Mine is bigger than yours.”

Nothing in biology makes sense except in the light of evolution“. Repeat this 5 times before going to bed every night.

How much omega-6 was available in our diet as Homo sapiens for 2 million years up to the advent of industrial processing? How much oil can you get out of a soybean without the benefit of extraction chemicals?

Aaaaaaah! Would you just tell me how much PUFA/SAFA/Carbs I should be eating?

Talking about macronutrients (fatty acids, carbs, etc) is useless unless it applies to food. If the advice to increase PUFA translates into “eat more fish” I will be the first one to shout it from the rooftops! But what if it translates into “eat more peanut butter”? Still PUFA! But are you going to get the same benefits? You don’t need to read an insightful review by Christopher Ramsden on omega-3 vs omega-6 to know that peanut butter ain’t gonna make you healthier than salmon. But sometimes we really really want to believe it. And deluding ourselves is oh so easy when somebody in a position of authority gives you the green light.

Yum

Focusing too much on macronutrients is what allowed abominations like “low fat banana bread” to become a healthy morning tea snack. The “reductionism” approach has successfully indicted natural foods such as eggs, coconut, avocado, butter. At the same time we have low fat sausage rolls, sugary cereal, margarine and other foods devoid of any nutrition, riding on the coat tails of the lipid hypothesis 2.0.

One of the benefits of using the evolutionary approach is that it allows you to make rational decisions about your life choices without having to double-check them with Pubmed. And it doesn’t involve re-enactment of Paleolithic times, although heaven knows, I find some modern social conventions really tedious (like people requesting to know how I am going on a Monday morning prior to my first cup of coffee). As the opponents of the Paleo approach correctly point out, we don’t really know what our ancestors ate. But I sure as hell know what they DIDN’T eat: excessive amounts of sugar, grains, seed oils and other industrially produced food-like substances. Not even almond flour cupcakes. Sorry.

Regulating your fat intake is easy: eat fish, seafood, meat (preferably grass-fed), eggs, some nuts, seasonal fruit and veggies.

Go back to eating food, not labels.

Lessons from history

Dairy products – foodstuffs made from mammalian milk.
Food Standards Agency UK

Cute child - check, sexist humour - check, false health claims - double check.

I hope you don’t eat margarine. Just like I hope you don’t smoke, drink alcohol excessively or do illicit drugs. Since margarine hasn’t been on my shopping radar for a while I just walk right past the brightly lit refrigerated shelves with hundreds of colourful tubs and packages straight to the “naughty corner” where a few lonely packs of butter have found refuge.

But recently a thought struck me as I was passing all that splendour: what is margarine doing in the dairy section of the supermarket? Or listed as “dairy” on the supermarket websites?

I will not bore you with the debunking of the so-called health claims of margarine. They all go along the lines of “we will save you from a certain death caused by the saturated fat in butter clogging your arteries”. Yawn. You can read  about the saturated fats here (Gary Taubes “What if It’s All Been a Big Fat Lie?”), here (Stephan Guyenet “Butter, Margarine and Heart Disease”) and here (Sylvan Lee Weinberg “The Diet-Heart Hypothesis: a Critique”).

Instead, I want to step away from the health conundrum to explore the history of margarine and its amazing rise from a lab-created inferior butter substitute to a major item in our shopping carts. I found myself more and more intrigued by the history (of food) as I get older which is scary because I find myself turning into my father: “Back in the days of the Empress Catherine the Great…” If you are under 30 and you are already bored come back in a few years.

History of margarine

Surprisingly enough, we can actually blame the French for the birth of margarine. The shortages of butter were crippling for the fat-loving nation in the middle of the 19th century. The war with Prussia was on the horizon and everyone knows you can’t feed cereal to soldiers. At the Paris World Exhibition in 1966 Louis Napoleon III announced a contest for the development of an acceptable butter substitute. In 1869 a French chemist by the name of Hippolyte Mège-Mouriés applied for a patent for a substance made from beef tallow emulsified with skim milk. He called it margarine, after a margaric fatty acid (considered a separate fatty acid at the time), and was subsequently awarded the government prize. The food industry began mass production but the product never took off. We can only imagine what the French public thought of spreading a colourless derivative of beef fat onto their morning croissants. My sympathies are entirely with them.

The Dutch firm Jurgen, one of the founding firms of Unilever (aha!),  bought the patent in 1870 and made a few improvements on the taste and the marketing. Other Northern European countries got in on the act, realising the potential of the new product.  It took awhile for the dairy industry to see the looming danger but by the end of the 19th century several countries had legislation in place to protect butter from the new kid on the block. The most bizarre of the margarine regulation laws was to have it coloured unappetising pink. Not surprisingly, it didn’t last.

As you can see at this point margarine is still largely an animal product. But with the growing shortages around the time of World War I and the development of food science new raw materials were required. The solution came in form of “vegetable” oils: soybean, cottonseed, canola, corn.

Quotation marks around “vegetable” are my little act of defiance against the food  industry which wants us to believe that these are vegetables because it makes it sound oh so wholesome. Until I see a potato oil on the shelf they are not vegetable oils (not even corn which is, of course, a grain)

The problem with oils is that they are, well, oily. But turns out that if you push hydrogen atoms through the oil under pressure in the presence of a metal catalyst such as nickel or palladium, you can solidify the oil. This basic biochemistry site gives a good description of what happens with unsaturated acids during hydrogenation.

Partial hydrogenation of unsaturated fatty acids leads to the formation of trans-fatty acids. Yep, we all know they are the real bad guys. Oops.

Over the next few decades margarine continued to develop as a combination of animal fats and seed oils. World War II brought the food rationing, relaxed legislation, (some might say more money behind the margarine manufacturers) which led to the margarine taking over the spread role from butter for the first time. The dairy industry was running out of ideas; their last resort was the colour advantage. Margarine companies were not allowed by law to mix yellow colouring into their product however they successfully circumvented that difficulty by selling a separate colouring which a housewife could mix with the margarine and serve to the unsuspecting dinner guests. The animal fat portion all but disappeared as the grain industries swelled up with government subsidies, especially in the US.

In the post war 1950 the diet-heart hypothesis started to make waves in the scientific and nutrition world and all of a sudden margarine went from a inferior and apologetic butter substitute for the poor to a heavily marketed health product. Housewives did not have to be ashamed of serving margarine in a butter dish any longer. Dr Ancel Keys said it was ok.

The rest, as they say, is history.  The word “margarine” is not even used very much anymore. Now we buy “spreads“, some of them are a combination of dairy and seed oils, some are pure seed oils promoted for their “heart healthy” polyunsaturated fat content. It is practically impossible to tease out which is which.

"When school is out each child needs their sandwich with Jurgen's Planta" 1916-1917. Run, kiddies, run!

Manufacturers still have to tread a thin marketing line between taste (the smooth softness and dairy aroma of butter) and the perceived unhealthfulness of saturated fats. Oh, how the tables have turned.  Now they apologise for butter. The fundamental difference between two products has been carefully ironed out and nowadays the terms “butter” and “margarine” are mostly interchangeable in the eyes of general public. So much so that if you ask for “butter” in a restaurant you are just as likely to get margarine.  If you attempt to raise the issue with an unsuspecting young waitress (poor thing,  she had no idea what she was in for when she was approaching my table), you’d be met with a blank look. Isn’t it the same thing? No, my dear, they are not. Just like when I order a piece of steak I don’t expect you to bring out a slab of tofu coloured red.

When can we restart calling these “foods” what they actually are? Imitation products,  lab-created and mass-produced to utilise agrarian commodities and chemically manipulated to suit the nutritional fad of the month.

And here is a little video on how to make butter.

How to make butter

Fat, glorious fat. Part II

If you have read the first post in this series and still came back for more I’m impressed. From the comments and messages that I have received (thank you all very very much) many of you appreciated going back to basic biochemistry. I don’t believe that science is an abstract concept, quite the opposite. Its applicability to everyday life is very underestimated by medical professionals and scientists alike. Either that or they believe that the public is really stupid and can’t possibly understand it. So instead they will just tell you what to do. No need to think. Baaaa.

So this particular discussion is going to be a little more in depth. I have really struggled to put together something which would be understandable but not simplistic. Please do not feel compelled to read it all at once if your eyes start glazing over. And yes, I had to skip over things and I’m hoping to get to those later.  I have about 5000 words sitting in my drafts.

To refresh your memory this is where we got to in the last post.

Let’s zoom in on PUFA. As I have mentioned before there are 3 families of PUFA: omega-3, omega-6 and some omega-9. I will leave that last group for now as these fatty acids are made in our body and seem to be less clinically relevant.

The other two families are often represented in the media and health circles as ying and yang. I don’t quite agree with that as you will see. Not a days goes by that you don’t hear of another miracle PUFA perform: from curing heart disease and diabetes to depression, weight loss and sexual performance. How biologically plausible are these claims? In other words, step 1 of the Framework of Common Sense requires us to ask a question: is it supported by what we know about human metabolism?

We know that PUFA are not the body’s preferred fuel. Instead they are an important component of cellular membranes, they initiate and control inflammation, they also participate in brain and retina formation in babies and are necessary for the synthesis of cellular messengers called endocannabinoids. Phew.

Sounds pretty important, right? However, PUFA are also involved in two of the most critical processes in our body: oxidation and inflammation. Both are essential to life, both are dangerous when they get out of control, both deserve a separate post so for now just keep them in the back of your mind

From general lets move to specifics. While the resident nutritionist on the Today show might believe that all omega fatty acids in their respective family are the same it is far from the truth.

I’m sure that all of you have heard of essential fatty acids. “Essentiality” in biochemical terms means that our body cannot synthesise these by itself and has to receive them via food. It also implies that without these essential fatty acids our health and maybe even life are seriously impaired. Two of the fatty acids in the PUFA family have been found to be “essential”: omega-3 alpha-linolenic acid (ALA from here) and omega-6 linoleic acid (LA). In the  beginning of the 20th century the studies by the Burr husband-wife team found that a lack of certain fats on a very restrictive diet makes some unfortunate rats very sick. Prior to this fats were considered important only as a source of energy and a delivery vehicle for vitamins A, D, E, K. It turned out that some fatty acids are much more than that.

Omega-3: parents, apple pies and essentiality

Let’s start with ALA. Its major function in the body is to be a parent, or the precursor, to the long chain omega-3 acids. When it is taken up from the diet it is converted to EPA and DHA, the two omega-3 siblings which cause much excitement in medical circles. EPA concentration in our body is very low as it seems to be converted immediately to its brother: DHA. However important EPA and DHA are, they are not “essential” in a biochemical sense, because we can synthesize them from ALA.

The problem is that this synthesis is not very efficient: the rate of conversion for ALA to EPA is around 8%. That is out of 1mg of ALA from flaxseed oil you will only make 0.08mg of EPA. DHA conversion rate is even poorer. It ranges from 0.5% in normal adults to 4% in young women (I’ll touch on that later).

Imagine you have decided to bake an apple pie on a Saturday afternoon. Maybe you are one of the millions of people who is still blissfully unaware that apple pie is not a health food. Maybe you will try to mitigate the damage by using margarine instead of butter. Maybe you had a rough week and you just don’t care. Back to the pie. There is no question that apples are “essential” to an apple pie. Most of us do not grow apples in our backyard or synthesise them in our bodies. You have to go and get apples from the outside source. But let’s say that the efficiency of apple:pie conversion is 8%. To get 800g of pure apple flesh after core removal, peeling, etc. you will need 10kg (Please note: demonstration purposes only. I did not actually measure apple:pie conversion so do not write saying you only needed 3 kg). To improve the efficiency of this process you can get an intermediate product like diced apples. You can even go and buy a whole apple pie, saving yourself all this headache.

In a similar way we don’t have to get our EPA/DHA from ALA (this is starting to sound like a children’s puzzle!). You can get your long chain omega-3 fatty acids directly from the diet. This way you will avoid the inefficient conversion and bypass the parent altogether. And as you know from the above, you don’t want to have to much of unnecessary oxidation-prone PUFA hanging around your body. Let’s focus on getting more bang for our nutritional buck.

And here are the long-awaited visuals.

Note: intermediate fatty acids have been omitted

This is something you need to know because the current nutritional recommendations push for more omega-3 in our diets. I will discuss the clinical evidence later but here we have the same problem as we had with every other advice: for the sake of “simplicity” all omega-3 are lumped together. Flaxseed oil, walnuts, canola oil – all contain high level of ALA, the parent molecule. They are also promoted as equally good sources of omega-3 as fish and other marine products, which are rich in EPA/DHA, the happy offspring. Meat, dairy and eggs, the way they are supposed to be (grassfed and pastured), never even get a mention.

Perfect example of opportunistic advertising

The implications are particularly important for vegetarians and vegans. And also everyone who heeds the Government advice (hello, Meatless Mondays!) and drastically reduces their meat consumption. This well-meaning study supplemented lactating women with flaxseed for 4 weeks in an attempt to increases DHA in their breast milk for the baby’s brain and retina development. The results saw a substantial rise in plasma ALA and every other intermediate fatty acid BUT the one they were actually aiming for: DHA. While it is possible that in vegetarians and vegans this process is amplified out of necessity to survive these results are still pretty poor.

Omega-6 is also “essential” but which one?

The biochemically “essential” parent FA in the omega-6 family is LA, linoleic acid. Just like in the case of omega-3 its essentiality is very relative. True, you can induce omega-6 deficiency in rats by feeding them nothing but purified sucrose, casein and some vitamins. Omega-6 deficiency was also found in very sick patients who received their nutrition via intravenous solution (TPN) with no omega-6 fats added. Needless to say that awkward oversight has seen been rectified and modern TPN solutions do not pose such issues. In reality you literally cannot take a step without tripping over LA nowadays. Ever since the happy days of Ancel Keys, McGovern committee, farming subsidies and industrialisation of food everything that is processed, packaged, patented and promoted (wow this was 4 p’s) contains this omega-6 FA.

In the body LA follows a series of reactions the result of which is a long chain omega-6 AA, Arachidonic Acid (I promise this is the last acronym). AA is a central player in the cascade of reactions which promote inflammation. Just like in my apple pie story you can also get AA directly from the diet, namely meat and poultry, eggs and organ meats. Inflammation is not all bad, it’s an essential part of our response to injury or infection and the first step of the healing process. But like all good things it has to come to an end. This is where the complexity and the innate wisdom of our bodies really hits you: AA itself promotes the synthesis of compounds which resolve the inflammation.

Note: intermediate fatty acids have been omitted

To help AA with this task we also have DHA and EPA from the omega-3 family. Therefore it is vital that we have a good balance between the key players of omega-3 and omega-6 family. I will cover inflammation and its main mediators, eicosanoids, in a later post.

One more thing to add to our little diagram is the enzymes which actually perform the conversion of short chain PUFA to long chain PUFA. Both families, omega-3 and omega-6, use the same enzymes and therefore they are in competition for them. Too much of the members of one family will interfere with the functioning of the other family. This is where the concept of a healthy 3:6 ratio comes from. High concentration of LA suppresses the conversion of ALA to EPA and DHA. On the other hand too much EPA can cause AA deficiency.

Let’s apply these new facts to a common diet and see where it leads us.

Warning: box food. Not for human consumption.

Most of the processed pre-packaged food come with a surprise addition of LA in form of soybean oil, sunflower oil, cottonseed oil, other unspecified vegetable oil. This is the source of LA which did not even exist a 100 years ago. Because you have heard about essential fatty acids and how important they are, you also go out of your way to buy health products which contain them like nuts and nut butters, seed trail mix, nut bars etc. You know all about the important omega-3 FAs so you buy flaxseed oil, walnuts and omega-3 fortified box food. The problem is that the overwhelming load of LA, inflammatory in its own right, is effectively shutting down the already-poor conversion of omega-3. And since you are getting most of your omega-3 from plant sources in the from of ALA you need that conversion!

So where does this all leave us? “Essentiality” is a biochemical concept which can be misleading if applied to the actual food. In reality the essential (=very important) fatty acids seem to be DHA and AA, possibly EPA. Even the most important PUFA are only needed in small quantities which is reflected in the composition of breast milk and animal tissues. The conventional wisdom tells us that just because they are essential more must be better. We can argue about the actual requirements (I bet you have noticed that I haven’t offered “the perfect ratio” or the required percentage of PUFA in the diet) however it is probably not very useful. Evolutionary clues should tell you that eating meat, some fish, eggs, pastured dairy and some plants will give you all the PUFA you need. Supplementing with artificial sources may just be akin to playing with fire.

Good sources of further basic information:

1. Weston A Price Foundation: Know your Fats by Mary Enig

2. IUPAC (International Union of Pure and Applied Chemistry) Lexicon of lipid nutrition  

3. DHA-EPA Omega 3 Institute (good for food sources)

4. SciTopics: Lipid Peroxidation

5. The medical biochemistry page: Omega-3, and -6 PUFAs

6. Julianne’s Paleo and Zone Nutrition: omega-3 and omega-6 post

And of course there are loads of posts from people much smarter than me like Peter from Hyperlipid, Stephan from WholeHealthSource, Dr Harris from Archevore and others addressing more intricate issues around PUFA.

Edit: a few typos and broken links, my bad.