Another thread reminded me of one of my favourites, the endocannabinoid excess theory. Setting aside type I which is basically the munchies.

Type II is suppposed to be caused by an excess of omega 6 fatty acids in the diet. They fed mice a high fat diet with either 1 percent omega 6 linoleic acid or 8 percent. The 8 percent mice got fat, the 1 percent mice did not.

They got curious about how this related to other macronutrient ratios. They tried medium fat and very low fat at 8 and 1 percent linoleic acid--both of these were fattening at 8 percent but not at 1 percent. So that's interesting, because a diet with 8 percent linoleic acid as pretty much the only fat source is still a very low fat diet. (I believe the 1 percent linoleic was still an 8 percent fat diet, since otherwise the two wouldn't be properly comparable, I'll check after).

Endocannabinoids are lipid molecules, various fatty acids are used to synthesize various endocannabinoids, linoleic acid is one of these fatty acids.

There's an endocannabinoid drug that was trialed on obesity, they backed off because one of its effects is depression. And depression certainly does result, sometimes, in a decrease in appetite. Maybe this belongs in the "self-medication through food" basket, as well. But maybe the mice were perfectly happy at 1 percent linoleic acid, there's a difference between endocannabinoid blockade and greater sensitivity that might occur if your normal production of endocannabinoid is just a little lower.

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3889814/

Full study. I checked, and they replaced the excess linoleic acid with olive and coconut oils. The diets did contain sucrose.


One thing that bothers me with these studies is that they did nothing to look for a threshold. Saturation of this effect could occur at way below 8 percent linoleic acid. What happens at 4 percent? 2?

The actual endocannabinoids involved require desaturation of the linoleic acid to arachidonic acid. 1 percent fish oil (or was it dha?) anyways a fairly small amount protected against the effect of linoleic acid, desaturase enzymes that produce dha from alpha linolenic acid also produce arachidonic acid from linoleic acid, preformed dha downregulates the enzymes involved. That throws up the question of the effect of preformed arachidonic acid, but since the prediction there is that an all meat diet should be fattening and it doesn't seem to be, I don't see much point in going too far down that path--although I wouldn't be that shocked if in a mixed diet with sugar and starch etc. arachidonic acid from meat did play a role.

https://www.sciencedaily.com/releas...80605130051.htm



Of course they blame meat, because it contains omega 6 fatty acids. The animal fed to the mice in the study was corn.

Not Being French. French people don't get fat. You are not French, therefore you get fat.

Dehydration. You are not hungry, you are thirsty. But because you don't drink water you overeat, and get fat.

That's always been a fun one. Maybe you're thirsty, not hungry. I think there's something to be said for not drinking your calories, maybe, there is an obvious risk of taking in excess sugar if you you ever drink is coke. Also if I sip cream in coffee all day, it doesn't seem to count as much as saving up that cream and just drinking it with my dinner, for satiety.

Fast Eating. You eat too fast, and don't give your stomach enough time to signal your brain that you're full, therefore you overeat, and therefore you are fat.

Put your fork down in between bites.

Chemicals (e.g. RoundUp) and crap in our food.

Eating while watching TV.

Blood Type. You don't eat right for your particular blood type, therefore you are fat.

Something along those lines showed up in a Dr Oz newspaper column not too long ago. I don't normally bother reading his quackery, but the headline sucked me in - it said something about easy or foolproof way to prevent obesity. I barely skimmed the article, reading just enough to see something about some kind of cabbanoids, comparing it to marijuana, and then all the usual stuff about avoiding fats, meat (especially red meat), making sure to eat plenty of hearthealthywholegrains, lots of fruit and veggies, and how 4 cups of raw spinach only has 25 calories. (So eat up on that spinach -at only 25 calories for a quart of it, you're going to need to eat bushels of it daily!)

A mismatch between "perceived" hunger and homeostatic appetite.

An interesting aside in this idea is a study on children with a gut problem of some type. They used glucose monitors to check the kid's blood glucose when they said they were hungry. The idea is that in healthy children, there's a dip in blood glucose when they experience hunger.

So if the kid's blood glucose was below a certain level, and they were hungry, they ate. Hunger without a dip in blood glucose, and they put it off for an hour. Supposedly eating this way helped them with their gut issue.

Another interesting thing--their reports of hunger started to coincide with that dip in blood glucose, more and more.

They also tried this in overweight adults. Same thing--they even reported that they learned to fairly reliably predict their own blood glucose measurement by how they felt. They don't seem to have taken over the weight loss world, but I always found the idea interesting. Can the body "learn" that it will only get fed if it lets blood glucose dip? Or learn to only associate feeding opportunities with that dip in blood glucose--discounting food cues etc. to some degree unless that condition is met?

Insulin resistance in the brain - insulin shuts down hunger when injected directly in the brain, when the brain becomes resistant to insulin, this effect does not occur, we eat more, grow fat.

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Teaser, blood glucose dips for some reason, likely cause is insulin spike. Cause of this insulin spike is likely pavlovian, i.e. a set of conditions are met, the usual response is triggered. The more carbs in previous meals, the greater this effect will be for next meal.

Or, ketosis rise. Insulin drops low enough to allow the liver to produce more ketones, which then activates insulin receptors in the liver, which then takes in more blood glucose for storage, blood glucose drops. This contradicts the idea that ketones suppress hunger, so we have to look elsewhere to explain why there's both more ketones and hunger simultaneously.

This can also be pavlovian. As a rule, fasting allows ketogenesis to ramp up. And fasting eventually leads to normal hunger. The two already occur simultaneously, effectively creating a set of conditions that only needs the meal and subsequent post-prandial effects of this meal for a pavlovian response to be established and reinforced at every subsequent fasting/meal cycle.

For this one, we could also argue it's all about insulin, but on this forum we're quite aware that ketosis is associated with a slew of distinct changes. So, in this pavlovian sense, the idea that there's a small insulin spike that causes a small blood glucose dip is obvious, but it's equally obvious that fasting/ketosis leads to a significant and systemic change which can provide this set of conditions to establish a pavlovian response.

Is this commonly known as "head hunger" as opposed to real hunger? Because this is something very common when your blood sugar spikes then crashes (from insulin along with the rest of the chemical/hormonal cascade). It feels like desperate hunger, even though your stomach may still be full of food - it can actually be distended because it's so full, and yet your brain is desperately screaming for you to eat again, because what it perceives is the blood sugar drop, the high insulin, and all the hormonal/chemical changes which indicate to your brain that you are extremely depleted, so eating as soon as possible is of the utmost importance.



I suppose you can be conditioned to experience an involuntary pavlovian reaction to almost anything, but I'd be almost willing to bet that the subjects of this study actually just learned to recognize how they felt when their blood sugar reached the level deemed acceptable for them to eat again.

I think the idea that "head" hunger is sort of less legitimate is false. Sometimes starving people lose their appetite after a number of days, but still report "head" hunger, an interest in food, this sort of makes sense to me as a safeguard. Removing the discomfort of starvation so an animal can function, but still having that safeguard of interest in food/high response to food cues means an animal has the capacity and interest to take advantage of what feeding opportunities do come up, prolonging survival.

Take rats, put them on a restricted feeding schedule. They'll binge, especially if it's oreo's. Are they little gluttons with no self-control? Are there conditions of uncertain food supply where this sort of strategy could increase survival? I think this stuff is there for a reason, besides making us feel bad about our lack of self-control.



This is really the thing I found most interesting, the idea that people could learn to sense their own glucose level.

Before people were talking much about IF, I remember a web page by a type II diabetic who took the simple tack of putting off eating during the day until his blood glucose reached a certain low, it worked pretty well for him.