Anyway, I felt I needed to do a post on PUFAs (poly-unsaturated fatty acids). Previously, I did a post on how saturated fats are not bad for you. I don’t care what everyone else says. I don’t care what established authorities say. I’m an ISTJ. If you can’t provide a logically consistent argument. If you can’t adequately answer all the counter-arguments. If your conclusion isn’t in sync with other studies, or even with your own data. If your research techniques leave much to be desired. Then forget it, I’m not jumping on your bandwagon.
So, like, several years ago I was researching all this saturated fat nonsense and really trying to understand the process of lipid metabolism and atherosclerosis. I mean, LDL particles are getting damaged, and a bunch of cholesterol lipids are piling up in plaques in peoples’ arteries, and this does seem to be a pretty significant nationwide problem.
Forget that from my best scientific understanding, saturated fats would actually be protective. Forget that cholesterol isn’t even the main issue. Let’s get to the main issue as I identified it in my research: oxidation and inflammation.
Daniel Steinberg alludes to oxidation in his book The Cholesterol Wars when he starts talking about the scavenger receptor on macrophages and oxidatively modified LDL. He then talks about some study in which pobucol was able to arrest the progression of lesions in rabbits by blocking endothelial cell-induced LDL oxidation and that specifically the effect was not due to probucol’s LDL-lowering effect.
Anyway, where was I? Oh right, oxidation. So here’s the thing. Atherosclerosis is all about damage to your LDL particles. Steinberg may not have followed up on these insights, but I sure as hell did. The thing is macrophages are there for cleaning up. They don’t chomp up healthy LDL. There are some slides I’d like to share, but viewing them doesn’t make the whole thing much simpler.
As I studied all this, I started to come up with my own ideas what promotes atherosclerosis. My conclusions run fairly counter to Daniel Steinberg’s. Since PUFAs contain at least two double bonds, they are highly volatile*. This means prone to oxidation and free-radical damage. It is this sort of damage that macrophages are going to detect**. A diet rich in PUFAs would seem an undue risk for oxidative stress***.
Despite the very apparent risk in using PUFAs, which come mostly from seed and nut oils, we pretty much guarantee these oils will be rancid**** in the way we prescribe their use. I.e. using them as cooking oils and providing no warning about the solvents and heating processes that are used to extract these oils.
And it’s worse than that. As I’ve learned more, I’ve come to discover the high omega-6 ratio of most seed oils may itself be an issue, throwing the O6:O3 balance in our tissues out of whack and making them more pro-inflammatory.
Anyways, suffice it to say, I really haven’t seen any evidence exonerating seed oils, so I started to wonder, is there any context in which these oils would’ve been used in a traditional manner? I.e., would traditional cooking methods ever have had any use for canola, soybean, or corn oil? As far as I can tell, not on any massive scale, and certainly not for cooking. Thing is, seed oils are not like olive oil or palm oil. They’re not that easy to extract. What would extraction look like? Here’s Catherine Shanahan’s take on it in Deep Nutrition:
If we could somehow get canola oil out of the seed without exposing it to heat, it would be good for us, but nobody can.
Well, that’s not entirely true. In the old days, flax and rapeseed (a relative of canola) were gently extracted in the home using a small wedge press. Over the course of a day, the wedge would be tapped into the press a little further until, ever so slowly, the golden oil would start to drip, fresh and full of natural antioxidants and vitamins. These oils were not used to fry food, and therefore never exposed to damaging heat. If you aren’t up for installing a wedge press in your kitchen, a few small enterprises can provide flax, hemp, and other healthy omega-3 rich oils – none of which should ever be used for cooking.
So there’s the gist of it. Other than eating nuts straight up, this was about the extent to which seed oils were extracted and used in the diet. So what about expeller-pressed canola oil? Well, commercial extraction of seed oils involves hexane, followed by twenty or so additional stages of bleaching and deodorizing. Organic, expeller-pressed oil has only skipped the initial step of extraction using hexane.
So where does this lead me? It leads me to the point that I personally try to avoid all “vegetable” oils except olive oil, palm oil, or coconut oil. Note that seed oils are used in everything from “healthy” salad dressings to “unhealthy” mayo (so like, what’s the difference?). Eating out or eating processed foods or just stopping by the local deli, almost all the fats are from vegetable oils. It’s both sign and symptom of our major industrial agricultural system. There are actually very little saturated or animal fats in any of our restaurant or processed foods (unless you like French food). Show me a place that still cooks french fries in beef tallow, popcorn in coconut oil, or bakes pie crusts with lard. They exist, but they are few and far between. You can’t even buy decent lard, beef tallow, or coconut oil unless you know where to look.
No, I’m sorry, it’s not the saturated fats that are killing us. That’s just an easy scapegoat to a complex problem the heart***** of which lies with our industrial food system. But that system will not change easily. The real solution, on the individual level is to eat real foods. And I’m sorry to say it, but canola oil, soybean oil, safflower, sunflower, what have you… more often than not are part of the industrial food system.
*Compared to mono-unsaturated fats, having two places for oxygen to ineract doesn't make such interactions twice as likely for PUFAs. It makes them billions of times more likely.
**Again, macrophages are there to scavenge the junk. They will not soak up healthy LDL. Part of the whole process is that a macrophage sucks up a modified LDL, which then becomes a "foam" cell, and begins the whole atherosclerotic process.
***The body can protect PUFAs in serum for a short period, but it needs an adequate supply of anti-oxidants. If there is some disorder of your lipid metabolism and your LDL particles are spending more time in serum than they should (possibly indicated by high LDL particle count (LDL-P, not LDL-c)), then there is a much greater risk for oxidation.
****Rancidity refers to the chemical decomposition of fats, one pathway of which is oxidation.
*****No pun intended.
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