Trans Fat Alternatives

[Trans-Fat Alternatives and Organics mp3]

Today’s episode is a discussion about the types of fat currently being used in food manufacturing and the restaurant industry to replace trans-fatty acids. We also discuss a recent meta-analysis published in the Annals of Internal Medicine about organic foods.

Carrie has written a great piece outlining the issue in Nutrition Nuts and Bolts, a blog run by another fellow UW Nutrition Science student.

I’d like to expound a bit on the chemical structure of fatty acids and why that is important.

The Basics

Fats are essentially chains of carbon. All carbon atoms must have four bonds; no more and no less. This means that when carbon is organized in a long chain two of the available bonds are attached to other carbons, and the remaining two bonds are attached to the most abundant atom in the universe: hydrogen. This type of fat, when all the available bonds are saturated with hydrogen, is known as a saturated fat.

The picture below is a representation of a saturated fat called palmitic acid. The black balls represent carbon, the white balls represent hydrogen, and the red balls at the end represent oxygen.

When fats are saturated they naturally take the shape of a kind of flat zig-zag structure because this is the most stable form.  This can allow for the fatty acids to neatly stack against each other, making them nearly always solid at room temperature.

By contrast, unsaturated fatty acids have one or more double bonds in the carbon chain. This produces kinks that prevent the fatty acids from forming a solid.


The main difference then, chemically speaking, between butter and oil is that the fatty acids in oil are chock-full of double bonds.

Where do trans-fats come in?

In the latter half of the 20th century saturated fats began to acquire a bad reputation. Various kinds of studies began to show that saturated fat was associated with heart diseases and cancers.1 Unsaturated fats, on the other hand, were largely considered to be healthier. Two problems though: when making biscuits or cookies or any number of other baked goods you really cannot substitute oil for butter.2 The second problem was that unsaturated fats are prone to oxidation and rancidity.

What do we do about this? Well, there was a process called hydrogenation that developed in the early 20th century to try and increase the shelf life of vegetable oils and fish oils. The resulting fats were actually more shelf-stable (because they were resistant to oxidation), cheaper to produce, were delicious, and could easily replace butter or lard in a recipe. This made them desirable to the food industry. Moreover, the fatty acids, although structurally similar to saturated fatty acids, were in fact unsaturated.

From Wikipedia:

In most naturally occurring unsaturated fatty acids, the hydrogen atoms are on the same side of the double bonds of the carbon chain (cis configuration — from the Latin, meaning “on the same side”). However, partial hydrogenation reconfigures most of the double bonds that do not become chemically saturated, twisting them so that the hydrogen atoms end up on different sides of the chain. This type of configuration is called trans, from the Latin, meaning “across.” The trans configuration is the lower energy form, and is favored when catalytically equilibrated as a side reaction in hydrogenation.

The fact that these fats were technically unsaturated led some health advocates to push for saturated fat to be replaced with trans-fat in common food products. Unfortunately, as we all know now trans fats are far worse than saturated fats in almost every way, at least in terms of human health.

Recently we’ve all been privy to the slow removal of trans fats from the food industry. Carrie and I discuss how it’s being done and what the implications might be.

Like I mentioned earlier, we also discussed organic foods and their latest controversy, but that portion will have its own forthcoming blog post.

  1. I’m not going to discuss the reasons for it in this blog post, but suffice it to say when saturated fats (as opposed to unsaturated fats) become incorporated into the lipid membranes of cells it starts to disrupt cell function. Membranes need to have a certain amount of fluidity and flexibility, but if they made up of mainly saturated fats then the cell membrane becomes rigid and it’s more difficult to do housekeeping chores like importing nutrients, exporting waste, cell signaling, etc. This is not the only reason for saturated fats negative health effects, but it’s a major one.
  2. Actually you can, but you won’t like the results.

Lipids, Inflammation, and Atherosclerosis

[Lipids, Inflammation, and Atherosclerosis mp3]

Today’s guest is the venerable Dr. Michael Rosenfeld, cardiovascular disease researcher and college professor extraordinaire. Most of his studies focus on atherosclerosis and the myriad factors that influence it.

Aside from being a pain-in-the-ass to pronounce, what exactly is atherosclerosis?

Before discussing the etiology of the disease it is important to have an understanding of how lipids are transported by the body. This is actually a more complex issue than one might suppose. Think about it: the human body is essentially an aquatic environment, and we all know that lipids are insoluble in water and will aggregate with other lipids in polar environments. So how would you be able to reliably and consistently transport dietary fat from your intestines to your liver and other organs and tissues as needed? You also need to consider that while some blood vessels are large in diameter others are quite small. Organisms like us have evolved a system to transport fats using what are called lipoproteins. They are basically tiny balls of triglycerides and cholesterol with a surface coat of various proteins and phospholipids that allow them to move about and interact in the polar environment of human plasma. There are essentially four kinds of lipoproteins: chylomicrons, very-low density lipoproteins (VLDL), low-density lipoproteins (LDL), and high-density lipoproteins (HDL). I won’t go into great detail about all of them right now, but each contains varying amounts of triglycerides and cholesterol and have slightly different proteins on their surfaces.

What do lipoproteins have to do with atherosclerosis? I’ll tell you. LDL particles are like the hot dog vendors at baseball games. They swim around the blood saying “Hiyoooo! Who needs cholesterol?? Get your cholesterol here! Use it for all kinds of things: bile salts, vitamin D, lipids rafts, testosterone… you name it! I got some fresh hot cholesterol just for you.” If a cell needs some cholesterol then it manufactures an LDL receptor, sticks it onto the cell membrane, and grabs any available circulating LDL. The LDL particle gets endocytosed and the cell can then use the delicious, gooey cholesterol for whatever it needs.

So what’s the problem? The problem is that LDL has a tendency to migrate through the endothelial cell layer of blood vessel walls and become trapped in the intima where it becomes oxidized or modified in some way. The oxidized/modified LDL particles trigger an immune response which ultimately leads to macrophages – informally known as scavengers or sometimes even garbage collectors – coming in and engulfing the oxidized/modified LDL. Now one of two things can happen here: 1) The cholesterol from macrophages can be handed off to HDL particles. The HDL can then take up this cholesterol and transport the it back to the liver to be recycled. The HDL could also give it to other lipoproteins in the blood. This process is known as reverse cholesterol transport. Or 2) The macrophage can hang out in the intima and continue to gobble-up incoming modified/oxidized LDL particles. This will lead to the formation of foam cells.1, 2


To make a long story short one or two or five foam cells within the vessel wall is no big deal, but over time, if the conditions are right, foam cells can accumulate within the vessel walls leading to a host of things you don’t want to happen with your arteries such as: narrowing of the blood vessel, chronic inflammation, recruitment of more macrophages, rupturing foam cells leading to all the oxidized LDL spilling out all over the place, migrating smooth muscle cells into the intima to wall-off the lesion, formation of a necrotic core filled with dead cells and cholesterol, and eventually rupture of the vessel wall (called a thrombosis) when all the contents spill out and can slow or stop the flow of blood. Platelets are then mobilized to repair the damage, but this probably only exacerbates the problem. If the thrombosis occurs in a coronary artery this can be deadly.


Inside an artery with advanced atherosclerosis

So what does this have to do with nutrition? There are several risk factors for atherosclerosis that can be manipulated via the diet. The following are risk factors that are considered to be “definitely modifiable” in the scientific and medical literature:

  • Cholesterol
  • HDL
  • Triglycerides
  • Blood Pressure
  • Cigarettes
  • Diabetes
  • Obesity
  • Sedentary Lifestyle
  • Alcohol

The following risk factors are classified as “potentially modifiable”

  • Lipoprotein(a)
  • Oxidized Lipids
  • Glucose Intolerance
  • Homocysteine

And there are some factors you just can’t do anything about

  • Age
  • Sex
  • Genetics

Now one might think that levels of cholesterol in the blood are directly related to the amount of cholesterol ingested in the diet. It appears to make logical sense, right? As it turns out dietary cholesterol doesn’t have a huge effect on circulating cholesterol. Most of us only absorb roughly 50% of dietary cholesterol. Even if you do ingest quite a bit of cholesterol from your diet your cells can compensate somewhat by down-regulating things like endogenous cholesterol synthesis. There is even a remarkable case study about a farmer that ate approximately 25 eggs a day (which adds up to an enormous amount of dietary cholesterol) and still had more or less normal serum cholesterol levels. The author claims that farmer was able to maintain cholesterol homeostasis by producing a ton of bile acids (made from cholesterol) and probably excreting most of it in the stool. Bear in mind, however, that this guy was probably an outlier as many case-studies are.

 

Okay, if dietary cholesterol doesn’t have a huge influence on serum cholesterol, then just what the hell does? Surprisingly saturated fat intake has a much larger effect on LDL than actual cholesterol intake. What do I mean by this? Well many studies have shown that if you subsist on a diet where your main source of fat is of the saturated kind, then it is likely that your LDL levels are high, but if you switched to fats consisting of mainly mono- and polyunsaturated fatty acids then your LDL levels are likely to drop significantly. Good news, right? Sure, olive oil all around! Oh, and with the caveat that your HDL levels could also decrease. Bummer. The good news is that LDL levels will decrease much more than the HDL. And just to further complicate matters the short and medium-chain saturated fatty acids commonly found in plant-based fats like coconut oil and palm oil don’t have the effect that other saturated fatty acids do when it comes to increasing serum cholesterol. This is because short-chain fatty acids (SCFA) and medium-chain fatty acids (MCFA) are processed differently by the body; they are not packaged into lipoproteins like other fats are but instead hitch a ride on serum albumin to get to their destinations. Think of the long-chain fatty acids (LCFA) as having to get on an enormous and crowded bus to get anywhere, whereas the SCFAs and the MCFAs are small and fit and can get on a bike to go where they need. That’s kinda where the metaphor stops, though.3

What else can you do to reduce your risk of atherosclerosis? They are all in the list.

  • If you’re obese you should lose weight, not just because of the reduced risk of atherosclerosis but also the substantial decreased risk in a legion of diseases, cancers, and what-have-you.
  • If you’re still smoking then I assume you are well aware of the above risks but choose to ignore them.
  • Get your blood pressure under control if you’re hypertensive.
  • Exercise regularly or at least semi-regularly.
  • Try not to get old. If you figure out how to do this let me know.
  • If you have Type 2 diabetes and you can’t shake it then at least learn to manage your glucose levels.
  • If you have hyperhomocysteinemia then you may have a B vitamin deficiency. Potentially an easy fix.
  • There are some gene therapies being studied right now if you have a genetic disorder that causes hypercholesterolemia.
  • There is also a large and growing body of evidence on phytochemicals and their antioxidant and protective effects.
  • There is also a substantial amount of evidence regarding omega-3 fatty acids and their role in modulating inflammation. Take this into account please.
  • If all else fails or you just want to keep eating steak and ice cream then talk to your doctor about statins.

This is all boilerplate stuff, of course. If you are reading this blog then I assume you are at least marginally interested in nutrition and already heed most of these recommendations. I didn’t get too much into inflammation in this post, but Dr. Rosenfeld and I talk about it more in the podcast. Inflammation truly deserves one or more posts on its own.

  1. Word on the street is that when the blokes that were first researching atherosclerosis were dissecting and examining diseased blood vessels they came upon a type of cell that looked like beer foam, and that’s how the foam cells got their name.
  2. It’s actually more complicated than that as you can probably imagine. It seems that if a macrophage ingests unmodified LDL then it can maintain normal cholesterol homeostasis, and get rid of the excess via reverse cholesterol transport. If the macrophage ingests a lot of oxidized LDL then it will become a foam cell.
  3. Wait… lemme try to extend it… So these buses sometimes get stuck on the highway and then the macrophage troll that hides underground comes and gobbles up the bus. If there are a bunch of buses then the troll will gobble those up as well and if he eats enough LDL buses then he morphs into the foam troll. Then foam troll can use his new powers of chemotaxis to silently call other trolls like a dog whistle and if enough buses and trolls show up then you have a traffic jam and everybody dies. Got it?

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