Why are trans fats worse than saturated fats?

Question

Saturated fat molecules have no double-bonded carbons, so they are long and straight, which means they stack easier and tend to form solids at room temperature, and solids are better at forming plaques in your arteries and interacting with cholesterol in the bloodstream.

Moving onward to hydrogenation, to my current understanding, if you hydrogenate vegetable oil all the way, you get saturated fats (no double bonds anywhere because you've shoved in so much hydrogen to occupy all the bonds). But for the purposes of making trans fats, it's usually partial hydrogenation.

I assume that most vegetable oils that get partially hydrogenated must be polyunsaturated fats to begin with (meaning more than one double-bond) because partial means you aren't replacing all the double bonds, so there must be at least two double-bonds present.

The result of partial hydrogenation means you remove these double bonds and start straightening out the chains, which makes them easier to stack (which is why trans fats tend to be solid or semisolid), like saturated fats.

My question:

Why are trans fats worse than saturated fats? It looks as though partial hydrogenation is simply taking a polyunsaturated fat and bringing it closer and closer to the status of a saturated fat, but not all the way. If the goal is to get a fat that is solid and lasts longer, why not just use a saturated fat?

And for whatever reason saturated fats aren't the answer: Isn't the end result of partial hydrogenation technically just another unsaturated fat? I thought unsaturated fats were considered healthy? So how are trans fats worse than fully-stackable saturated fats?

Or upon reflection maybe my question is, why are trans fats considered so much worse than other unsaturated fats? If all hydrogenation does is break up double bonds and insert hydrogen, straightening out any cis-kinks in the chain, doesn't this just generate the same acid with fewer double bonds and straighter chains? How is this any different than going out in nature and finding the same unsaturated fat, rather than going to the trouble of converting?

What's causing the difference, here? Where is my understanding breaking down?

Answer 1

Someone may very well give a more thorough answer but from what I understand, most naturally occurring unsaturated fats have their double bonds in the cis conformation which is generally higher in energy than the trans conformation.

Thus, the idea is that when you ingest trans fats (i.e. fats with a trans double bond) your body has to somehow hydrogenate this double bond before it can break it down further. This is more difficult for your body to do because it must either isomerize to a cis bond and then hydrogenate, or just hydrogenate the trans bond which is not easy for your body to do effectively. In some cases hydrogenation of trans fats can't actually happen because nature basically makes cis double bonds in fats (which sounds weird but is true) so your body has ways of breaking these fats down but not trans fats. So, the fat just gets stored or excreted without doing anything to it.

Answer 2

In my chemistry lab, one of the teaching experiments at my university involved nickel catalysed isomerisation of an alkene, as nickel is also the catalyst for hydrogenation.

This could explain why you end up with trans- fats from a cis- starting material.

Answer 3

First of all, the concept that saturated fats are the culprit in heart disease is hotly debated and the AMA has been removing, and pulling back on general guidelines about saturated fat. The opposing model would be the inflammatory model, and the primary pro-inflammatory fatty acid is linoleic acid (omega-6 PUFA). Furthermore PUFA's are much more capable of becoming oxidized species and carrying oxidizing groups to arterial linings resulting in oxidation damage. Most of the correlation of heart disease to fatty acid intake is independently explained by the trans fats that tended to be present in hydrogenated fats that also contained saturated fatty acids.

Mixed fats that contain PUFAs (polyunsaturated fatty acids) and MUFAs (monounsaturated fatty acids) can be hydrogenated to turn some of the UFAs into saturated fatty acids. This prevents rancidity and raises the smoke point of the fat because PUFAs are the easiest to go rancid, and to smoke under heat.

There are two general instances in which fats are hydrogenated. Liquid oils which are primarily MUFA and PUFA mixtures are hydrogenated to saturate those fatty acids, prevent onset of rancidity, and raise the smoke point. The main reason for the hydrogenation is not to make the fat solid, but to make it saturated so that those things happen. The second instance would be with a fatty acid mixture such as lard that contains saturated fatty acids, but also fractions of oleic acid and linoleic acid. Hydrogenation makes the lard more homogeneously solid and turns primarily the large 18 carbon oleic and linoleic fractions into 18 carbon saturated stearic acid. (There is actual evidence now that the primary reason that saturated fats were implicated in heart disease was because of the trans fat content in hydrogenated oils and lard. The evidence is the reduction in new cases of heart disease since the banning of trans fats).

The natural UFAs tend to have a cis structure, but the trans structure is more sterically stable because the large hydrocarbon tails on either side of the double bond will be further separated. Some of the broken double bonds are broken by the hyrdogenation process enough to allow a rotation before reforming and the majority of the products of the natural rotation will be trans once the double bond forms and locks down the rotation.

So why are trans fats made from primarily 18 carbon chains BAD? Most, if not all of the correlated risk to intake can be explained by an increase in LDL levels with no corresponding increase in HDL levels, so its not the trans fats forming the plaques but the fact that they tend to get repackaged as LDL and possibly only a small fraction of LDL molecules that account for most correlated heart disease risk. These LDL molecules also increase with higher dietary intake of fructose and linoleic acid and the findings are consistent with an inflammatory model (not a saturated fat model) of heart disease.

Answer 4

Saturated fat molecules have no double-bonded carbons, so they are long and straight, which means they stack easier and tend to form solids at room temperature, and solids are better at forming plaques in your arteries and interacting with cholesterol in the bloodstream.

This in invalid reasoning, because your arteries and the bloodstream are not at room temperature, they are at around 37 degrees Celsius where saturated fats are liquid.

Trans fats are unhealthy because the enzymes responsible for metabolizing them are "expecting" cis fats, and trans fats disrupt the whole metabolic chain. One of the side effects is raise of the low density lipoprotein cholesterol (LDL), which increases inflammation and risk of heart disease.