Program Loss Fat

One great mystery in this nutritional debate is how the Harvard School of Public Health and their epidemiologists keep finding such links between the omega 6 polyunsaturates and all manner of good health. My confusion comes in part because in all likelyhood the most omega 6 fats will be eaten by people eating a load of processed crap who by all accounts should not be the healithiest. If the epidemiologists take all those people out of the equation what are we even measuring? Just the leftover folks who eat salad and chicken and fish and walk their dogs every day. Hardly seems fair.

A Civil Twilight: River (right click to open in new window)

And yet, those crafty vegetable oils elude my ability to smack them down entirely. I've done some reading on the metabolism of the omega 6s and it doesn't make for very fun blog posts. Suffice it to say that *maybe* if you pour tons of O6 down the gullet there may be some compensatory reduction in the inflammatory pathways they ought to light up like a runway. It seems that the real key to staying healthy while eating commercial salad dressings, factory-farmed eggs, and chicken skin is to make sure you do NOT skimp on the omega 3s. Also, avoid trans fats like the plague (duh) because they can interfere with uptake of the omega 3s.

Earlier this week a paper from Nature tweeted by Stephan Guyenet and Mike Eades that adds more fuel to the anti-O6 argument.  Omega 6 in large amounts: fragile polyunsaturates, biologically active, evolutionarily novel, and not nearly as tasty as steak or olive oil. Is it a coincidence that the obesity epidemic began and peaked when enthusiasm for omega 6 was at it's highest? Come the late 90s and 00s, Mediterranean diets became more the rage. Veggie oil, king of low cholesterol, began to be edged out by the monounsaturates. Nevertheless, "during the 20th century, elevations in AA-PL have been estimated from the dramatic increase in dietary LA resulting from > 1000-fold increase in per capita consumption of soybean oil from 0.006 to 7.38% of energy." (Gah) (AA-PL = arachidonic acid phospholipids, or the amount of omega 6 derived compounds in cell membranes.  LA = linoleic acid, the primary dietary omega 6 found in soybean and corn oils, etc.)

We've heard the omega 6 obesity story before, and it has everything to do with the endocannabinoid system.  Here is one of several blog posts from 2011 where I broke it down into exrutiating detail.  In short, omega 6 fats are made into natural endocannabinoids, our own happy cannabis compounds. Smoking a ton of weed is associated with: hanging out listlessly on a couch in one's parents' basement watching Yo Gabba Gabba AND the munchies.

Central cannabis receptor activation is associated with increased eating and increased fat accumulation and fatty liver. So researchers thought they would take some happy mice and increase linoleic acid as a controlled dietary variable and see if it made the little guys fat via increased levels of endocannabinoids.

So the mice were fed pellets with and pastes with 20% protein, some carbs, and then mixtures of 7 different oils.  Lipids were extracted from the mice livers and brains and levels of endocannabinoids were measured.

Mice with 8% linoleic acid diets (comparable to modern human diets) had elevated levels of linoleic acid and arachdonic acid in the cell membranes (not surprising) compared to the historic 1% mice (ahem, human) diets.  Levels of the endocannabinoids were tripled in the 8% LA diets. Dietary LA increased body weight, food intake, and fat tissue in the mice.

Here's the key, however: Adding 1% EPA and DHA omega 3s to the mouse diets seemed to undo much of the problems caused by the gallons of omega 6. Omega 6 in the cell membranes dropped, as did the levels of endocannabinoids, as did the fatty tissue, weight, and overeating in the mice. These mice didn't look quite as nice metabolically or had as beautiful cell membranes as the 1% LA mice, but it was loads better than the 8% LA omega 3 deficient mice.

Dietary LA also increased leptin and decreased adiponectin.

In the human population, dietary consumption of soybean oil, poultry, shortening, and sugars (but not grains, beef, fish, eggs, dairy, or vegetables) were positively correlated with obesity in several epidemiology cohorts from 1909 to 1999.

Honestly, this paper is the strongest one yet I've seen maligning omega 6 fatty acid in vast quantities in the diet. One can't necessarily make the leap from the observational data in humans and the controlled data in the rats to an absolute causal relationship in humans, but hey, playing it safe with olive oil and avocados and rolling on the wild side with some saturated animal and tropical plant fats doesn't seem like it would be that unwise compared to toking it up on processed fried foods, no?