This entry is part 3 of 4 in the series Brad's Firm Pork Primer

The debate concluded with agreement by all that we need a randomized controlled trial to compare the effect of low and high intakes of LA. The trial should have typical US intakes of omega-3 PUFAs, with 7.5% energy from LA (the current US intake) in one group and 2.0% LA (historical intake) in the other. It would study cardiac endpoints and continue for about 5 years. — the report on the 2010 meeting of the International Society for the Study of Fatty Acids and Lipids (ISSFAL)

This is the third installment in my series about firm pork. For those of you who have been following the series it’s probably clear that the LA referenced in the above quote is linoleic acid, the main component of most vegetable oils. For the last 60 or so years the mainstream wisdom has been that vegetable oil is good because it lowers cholesterol levels but the truth is that the effect of linoleic acid on actual endpoints like diabetes, heart disease and cancer has rarely if ever been studied. This fact is shocking when you consider the explosive rise in consumption of RDB (refined, deodorized, bleached – it’s the industry’s term, not mine) vegetable oil over the last 100 years.

US Vegetable Oil Consumption Calories Per Day
1961 1971 1981 1991 2001 2011
276 379 484 549 638 701

In fact, vegetable oil is now the single largest caloric component in the american diet.

Dietary Component US Consumption – Calories Per Day
Vegetable Oil 701
Wheat 590
Added Sugars 569
Meat 432
Dairy 414

Let’s take a minute to talk about what it means to be a saturated fat or a polyunsaturated fat. A saturated fat is mostly composed of a chain of carbon atoms where each carbon is attached to two other carbons and two hydrogens in single bonds. The carbon chain is fairly straight and this means that saturated fats pack tightly together and are solid at room temperature. Monounsaturated fats, the main components in olive oil and most lards (depending on what the pigs are fed), have a single double bond, which creates a kink in the chain. These fats don’t pack as tightly together and are liquid at room temperature but solid in the refrigerator. Polyunsaturated fats have two or more double bonds, which means two or more kinks. They pack together even less densely and are therefore a liquid even in the refrigerator.

The differences between the fats don’t end with melting point. Saturated fats and monounsaturated fats can be synthesized by humans from carbohydrate or protein and are important structural elements in cell walls and other tissues. They are largely chemically inert. Polyunsaturated fats cannot be made by humans and therefore always come from diet. They are also necessary for some very important signalling pathways. This is why they are called “essential fatty acids” or EFAs – you must eat some of them to stay healthy, 1% of your diet or so. The pathways that they are involved in are highly complex, involving hard words like eicosanoids and prostoglandins, but ultimately are very important in inflammation. Generally speaking, the Omega-6 linoleic acid side of the pathway – the linoleic acid side – is thought to be pro-inflammatory and the Omega-3 side of the pathway is thought to be anti-inflammatory. It is, of course, not that simple but that’s enough background for now.

The last major difference between vegetable oils and more saturated fats is that saturated fats are highly stable and vegetable oils are highly prone to oxidation. The single bonds in saturated fat are highly stable. The carbons are fully bonded everywhere and thus happy. The double bonds in vegetable oil are reactive. Consider linseed oil. Linseed oil is used as a varnish or a paint binder or can polymerize into linoleum. Chemically, linseed oil is just oxidized flaxseed oil, a highly unsaturated vegetable oil that is all the rage as a health food supplement. Linseed oil is, in fact, so prone to oxidation that a pile of rags soaked in it can spontaneously combust. Linseed oil has been implicated in many a housefire.

So what does this have to do with your liver? First a little background. In the last several decades in America there has been a steep rise is rates of obesity, diabetes and non-alcoholic fatty liver disease. The last one you may never had heard of because it doesn’t get the publicity of the other two but something like a third of Americans have non-alcoholic fatty liver disease and there’s good reason to believe that metabolic syndrome (the pre-cursor to diabetes) begins in the liver.

Studies in rats have shown that the easiest way to give them liver disease and insulin resistance is to feed them a High-Fat High-Sugar diet (HFHS) but merely a High Fat Diet will ultimately do the same thing. Here’s the catch: these diets only work if the fats used are highly unsaturated. Saturated fat diets do not induce liver disease in rats. The diets that do induce liver damage seem to do it with “oxidative stress”. Remember how prone to oxidation vegetable oils are?

Here’s a beautiful experiment demonstrating just this point. Rats were given a steady diet containing ethanol (alcohol) for up to six months. One group was given beef fat, another lard and a third was given corn oil. “Rats fed tallow and ethanol developed none of the features of ALD, those fed lard and ethanol developed minimal to moderate disease, rats fed corn oil and ethanol developed the most severe pathology.” ALD is Alcoholic Liver Disease. Rats given highly saturated beef fat and a steady diet of alcohol don’t develop liver disease at all! To produce liver disease you need alcohol AND linoleic acid. You’ll notice that rats on lard based diets did a bit worse than rats on beef fat based diets, but still quite well. This is due to the higher linoleic acid content of this particular batch of lard compared to beef fat. Much more on this as the series goes on.

Here’s one more. Rats were given liver disease with dietary ethanol and fish oil (fish oil is HIGHLY prone to oxidation and induces full blown liver disease much faster than vegetable oil). One group of rats was flipped to a diet of ethanol and highly saturated palm oil and the liver disease was cured. The study cites decreased lipid peroxidation (fat oxidation) as the mechanism of action. Rats on a steady diet of alcohol can be cured of liver disease by removing the oxidation prone polyunsaturated fat – they’re cured by stable saturated fat!

Now look back at the table of top caloric sources in the american diet. Two of the three items are sugar and vegetable oil. We’ve already seen that one of the easiest ways to induce liver disease in rats is with a High Fat High Sugar diet. Is it any wonder that a third of us have liver disease?

I have one last anecdote. In the 2004 documentary “Super Size Me“, Morgan Spurlock sets out to eat every meal at McDonald’s for a month. All of the meals are washed down with soda (sugar). Most meals contain either french fries, hash browns, mayonnaise or salad dressing (vegetable oil). Before the diet Spurlock has a physical and gets a clean bill of health. After a month on sugar and vegetable oil? Liver disease.

Here’s the part where I bring this back around to pigs. I am a strong advocate of pork as a health food but that comes with one huge caveat. The composition of pork fat can vary wildly based on a variety of factors and in fact recent trends have conspired to send the linoleic acid content of most pork fat ever higher. I am trying to create pork fat with as little linoleic acid as possible. In my last article I talked about the vegetable oil content of various pig feeds. That is of the utmost importance but it’s not the only thing that counts towards determining pork fat composition. In the next article I’ll walk you through the factors that effect pork fat composition and why the trend has gone the wrong way in recent years.

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