The core findings are that if you eat a diet with around 60% of calories from fat, then you end up lighter if that diet is based on safflower oil (omega 6 PUFA) and heavier if it's based on lard. Here's the table:
Well, there you go!
Safflower oil is more ketogenic than lard. It also allows greater fat loss during 72 hours of starvation, 10.3g of fat loss from safflower fed rats vs 3.9g from lard fed animals, here we are:
Mmmmmmmm, linoleic acid, the elixir of life and Weight Watchers' friend. And I thought it was obesogenic!
So what does the small print say? Lots!
First thing to make my ears prick up is that during the whole study the rats were only allowed to eat for 2 hours a day, in a single solid block. That means they were force fasted for 22 hours a day. We've noted from Table 3 that safflower oil allows greater weight loss under fasting conditions. So is it any surprise that the safflower rats ended up at 195g vs the 222g of the lard fed rats after eight weeks of this intermittent fasting? I'll come back to why in a moment.
In contrast most modern papers show that linoleic acid, the primary component of safflower oil, is grossly and transgenerationally obesogenic...
But that's because there is a difference between ad lib feeding and 22h per day forced fasting!
The difference is in the glucose levels. Look at these graphs from Fig 1, especially the glucose levels in the middle top graph:
Now, far be it for me to put words in to the mouth of a lab rat, but which group of rats is the hungriest? Which group becomes most hypoglycaemic perhaps? Even Dr You-are-confused-man-Guyenet seems to have, in an aberrant moment of lucidity, a glimmering of perception that hypoglycaemia makes you hungry. Or should I say drives eating behaviour? Did I ever even mention gluttony? If you are force fasted for 22h you can't overeat. You can't even eat to your metabolic needs without accessing significant amounts of stored fat.
Under full starvation a rat lives off of its fat. If linoleic acid is what is being released from the adipocytes under fasting conditions it provides significantly less FADH2 relative to NADH in to the electron transport chain of all fat burning cells than the mix of fatty acids from the adipocytes of lard fed rats. ie there is less physiological insulin resistance. This failure means you fail to keep glucose levels normal during starvation. Let's rub that in: Failure to develop physiological insulin resistance during starvation results in hypoglycaemia and hunger.
Exactly the same will happen in any soy oil fed USA citizen. The end result will still be the failure to develop the essential physiological insulin resistance which is needed to keep blood glucose normal during fasting.
When the average soy oil fattened American is asleep they HAVE to, finally, stop snacking on carbohydrate crap, which is the only way they can maintain a decent blood glucose level. At this time blood glucose falls, simply because their muscles stay insulin sensitive and glucose falls in to them. The brain will not accept hypoglycaemia. Some time, in the middle of the night, there has to be a Refrigerator Raid.
And, OMG, they eat calories! And calories count! Did I ever mention gluttony? Or, perhaps, is the Refrigerator Raid simple physiology?
The 22h daily fasted rats have a locked refrigerator. However hungry they feel due to hypoglycaemia, they are not getting any extra food. But why is there extra weight loss under starvation? Insulin was tricky to measure from a rat in the 1970s, but I know that the safflower loaded then starved rats had the lowest insulin as they are both insulin sensitive and hypoglycaemic. Low insulin = more lipolysis = more ketones and more weight loss. Logical.
Now let's go a step further. Blood glucose is low. It's low because the F:N ratio of linoleic acid is low and that's what is being released from adipocytes. This is metabolism. Individual cell by individual cell, it's a metabolic phenomenon. Picked up by the brain as hypoglycaemia.
Hypoglycaemia must drive food intake to avoid cerebral catastrophe. Glucose is not a neurotransmitter per se. The hypoglycaemia has to be converted to a neurotransmitter based message to affect behaviour. Oddly enough, a derivative of linoleic acid is a neurotransmitter. Linoleic acid is the parent molecule of the endocannabinoids. Even the cleanest nosed obesity researcher has heard of the munchies. Wouldn't it be funny if eating linoleic acid messed with your blood glucose level and this hypoglycaemia triggered the production of endocanabinoids from, you guessed, the parent molecule (of the hypoglycaemia!), linoleic acid within the brain? The same molecule which triggers the hypoglycaemia, making the hunger essential, in the first place.
You could view it as linoleic acid ingestion is a signal that hypoglycaemia is in the offing. If random evolution was looking for a substance to "choose" as a neurotransmitter to deal with hypoglycaemia, it might just be simplest to modify the basic lipid which is most prone to trigger low blood glucose throughout the body in the first place... You could then end up thinking that the endocannabinoids "just happen" to control appetite as a primary function. Of course, once the control system is in place you are all set to mess with it by demonising saturated fat and pushing corn and soy oils.
Well, I find the concept hysterical. But then I find most brain centred obesity research pretty amusing.
Peter
