I was watching the lectures on essential fatty acids for my nutrition class last week, and learned something that for me was a major, Oprah-league, a ha!
High levels of insulin (which you might have if you eat a traditional Western diet and have insulin resistance) increases delta-5 desaturase. So what?
Well, it turns out that delta-5 desaturase helps convert DGLA — an omega 6 fatty acid derived from the linoleic acid in grain/vegetable oils — into arachidonic acid or AA (see below; click image for larger version).
Okay, so what you ask. Well here’s the thing. Lots of AA means increased inflammatory prostaglandins. This is not a good thing. It’s quite possibly the reason that obesity is associated with disease … as Gary Taubes says, “what makes you fat makes you sick.”
But wait, there’s more! High AA levels may mean higher levels of a substance called anandamide, which is a chemical that affects the same receptor in the brain that THC does … you know THC, it’s the active ingredient in pot. And when people smoke pot they often get … the munchies.
This presentation — New Directions in Understanding Obesity (PPT) — was my introduction to the endocannabinoid system (back in January), and I must say, I was giddy when I first skimmed it and I’ve been meaning to do a deeper dive for a while.
But the lecture on EFAs really connected the dots between our Western diet and its potential influence on the ECS. Eating processed foods high in insulin-raising sugar and omega 6 fats may contribute to a vicious cycle of overeating and increased appetite.
Western diet = inflammation + munchies?
Kurt Harris (and others) have lots of good stuff to say about the neolithic agents of disease, and I thought I pretty well understood the benefits of eliminating grains (especially wheat), sugar, and vegetable oils. But to borrow a phrase from across the pond, looking at the above implication of a diet high in sugar/refined grains and vegetable oils just gobsmacked me.
Like I said … A HA!
Smoke a blunt? Or eat fast food fries? Well, actually, there may be a difference (PDF, p. 59):
In comparison to the degree of overeating induced by THC, AEA [anandamide] displayed a reduced potency, but its effect was longer lasting
This is what makes me giddy about this area of research. It just makes for such a neat theory to explain one mechanism of overeating. Of course food is not addictive like cocaine or heroin. But what if it’s more insidious? I.e., the effect isn’t as strong (reduced potency) but it lasts and lasts and lasts? Hmmm.
[As an aside, I like what Dave Dixon had to say on Twitter in response to Dr. Eades’ report of a study showing brain activation in food addiction is the same as substance dependence: “Maybe more illuminating to say that substance addiction has same roots as food rewards.”]
Just say no
The link between AA and inflammation is well understood, so if for no other reason, eliminating (or at least minimizing) AA is essential to health. So whether or not you’re eating lots of carbs, you probably really want to minimize your grain/vegetable oil intake.
The link between the ECS and obesity, on the other hand, seems to have far less visibility. But researchers have have been looking at blocking ECS receptors via drugs to reduce appetite; too bad this has resulted in nasty side effects like increased pain and suicidal thoughts!
So we’re a long way off from conclusively knowing whether or not the ECS is involved in overeating and obesity. But in the meantime, I was struck by the end of Gary Taubes’ recent piece in the NY Times, “Is Sugar Toxic?“:
“I have eliminated refined sugar from my diet and eat as little as I possibly can,” [Craig Thompson, president of Memorial Sloan-Kettering Cancer Center] told me, “because I believe ultimately it’s something I can do to decrease my risk of cancer.” [Lewis Cantley, director of the Cancer Center at Beth Israel Deaconess Medical Center at Harvard Medical School] put it this way: “Sugar scares me.”
Sugar scares me too, obviously. I’d like to eat it in moderation. I’d certainly like my two sons to be able to eat it in moderation, to not overconsume it, but I don’t actually know what that means, and I’ve been reporting on this subject and studying it for more than a decade. If sugar just makes us fatter, that’s one thing. We start gaining weight, we eat less of it. But we are also talking about things we can’t see — fatty liver, insulin resistance and all that follows. Officially I’m not supposed to worry because the evidence isn’t conclusive, but I do.
As with sugar, the evidence regarding omega 6s, the endocannabinoid system and appetite isn’t conclusive, but eating a diet — like paleo — that reduces sugar and omega 6 sounds worth pursuing to me.
Update, 4/24/11: Emily Deans summarizes endocannabinoids and obesity. Money quote (emphasis mine):
SO – omega 6 fatty acids become endocannabinoids, which are associated with increased fat tissue, decreased insulin sensitivity, and leptin resistance. Oops! (But keep in mind we only have the “associated with” there, not the smoking gun. It’s just… such a pretty theory, I can’t help but squee a little.)
My sentiments exactly!!
Update, 9/27/12: Study in mice supports the connection: Dietary Linoleic Acid Elevates Endogenous 2-AG and Anandamide and Induces Obesity