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  #16   ^
Old Tue, Jun-05-18, 05:34
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teaser teaser is online now
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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.
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  #17   ^
Old Tue, Jun-05-18, 15:08
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teaser teaser is online now
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Plan: mostly milkfat
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https://www.sciencedaily.com/releas...80605130051.htm

Quote:
Another omega 6 is fattening theory....

Maternal fatty acid balance affects offspring obesity thorough gut microbial population

The balance between omega-6 and omega-3 fatty acids in the tissues of female mammals, which previous research has suggested can impact the incidence of obesity in their offspring, appears to do so through its effect on the microbial population of the infant's gastrointestinal tract. In the open-access journal Microbiome, a team of investigators from Massachusetts General Hospital (MGH) and University College Cork, Ireland, report finding that increasing levels of heart-healthy omega-3 fatty acids in female mice -- either during pregnancy or lactation -- reduced weight gain and metabolic disruptions in infant mice fed a high-fat diet.

"Our results suggest that a balanced ratio of omega 6/omega 3 fats in a mother's body during pregnancy and breastfeeding is critical for reducing the lifetime risk of obesity in children, and that the microbes in an infant's gut are key players in mediating this effect," says Jing X. Kang, MD, PhD, director of the Laboratory for Lipid Medicine and Technology in the MGH Department of Medicine, senior author of the report. "These findings can help us understand why so many people today are obese and develop ways to prevent the problem."

Both omega-6 and omega-3 fatty acids are essential to good health, but maintaining a relatively even balance between the two is important. The typical Western diet, heavy in meats and other animal products, can lead to excess omega-6 consumption, which can promote inflammation and may contribute to cardiovascular diseases and other health problems. It is well known that the microbial population -- or microbiota -- of the infant gut is largely influenced by that of the mother but also can be affected after birth by diet and other environmental factors.

Several studies have suggested that alterations in the dietary omega-6/omega-3 ratio can change the balance of gut microbial species, but there has been limited data on how or whether the maternal omega-6/omega-3 ratio affects the microbiota of their offspring and the associated risk of obesity. To investigate this question, the MGH team used a strain of transgenic mice they previously developed that -- in contrast to other mammals -- produce high levels of omega-3s in their tissues. These mice carry a gene called fat-1 -- usually found in C. elegans roundworms -- that converts the omega-6s normally abundant in mammalian tissues into omega-3s.

To separately investigate the impact of maternal fatty acid status during pregnancy and during lactation, the research team began with two groups of female mice -- one with the transgenic fat-1 gene and a nontransgenic or wild-type (WT) group -- that were mated to WT males. From the offspring of fat-1 females, the researchers selected only those that inherited WT genotypes for comparison with the offspring of WT females. Then equal numbers of both offspring groups were given to foster mothers from the other group for breastfeeding, resulting in four groups of infant mice:

offspring of fat-1 mothers fed by fat-1 mothers,
offspring of fat-1 mothers fed by WT mothers
offspring of WT mothers fed by fat-1 mothers
offspring of WT mothers fed by WT mothers.
This cross-fostering study design allows some offspring to be exposed to different fatty acids -- omega-6 or omega-3 -- during pregnancy and lactation without the need to feed different diets to the mothers, which can confound study results. All maternal mice were fed a high omega-6 diet during both pregnancy and lactation.

After the offspring were weaned at 4 weeks of age, the young mice were maintained on a high-fat diet for the subsequent three months. The researchers then found that, while maternal fatty acid profiles during gestation had some effect on offspring, the fatty acid balance in the mothers' milk -- which would be similar to that of their tissues -- had an even stronger effect. Among the WT offspring, those fed by fat-1 mothers had significantly lower omega 6/omega 3 ratios than those fed by WT mothers, and the ratios of fat-1 offspring fed by fat-1 mothers were lower than those fed by WT mothers. Similarly, the microbiota of all offspring reflected those of the foster mothers, patterns that persisted throughout the three months of high-fat feeding.

While the weights all the infant mice were similar when they were weaned, after three months of a high-fat diet, WT male offspring that had been fed by WT mothers gained significantly more weight than did WT males fed by fat-1 mothers. There were no significantly differences in weight gain among any of the female mice, suggesting that the influence of maternal fatty acid status on offspring weight gain was gender dependent. Markers of metabolic disruption at that time were lowest in fat-1 offspring fed by fat-1 mothers, implying that maternal omega-3s can mitigate the metabolic effects of a high-fat diet.

The results of this study, Kang suggests, imply that dietary omega-3 supplementation during pregnancy and especially during lactation could help reduce the future risk of obesity and related conditions in children. "Since we know that gut microbiota can have a profound effect on obesity-related disorders, research into interventions that target gut microbiota, including those that may improve omega 6/omega 3 ratios, should be a priority." Kang is an associate professor of Medicine at Harvard Medical School.


Of course they blame meat, because it contains omega 6 fatty acids. The animal fed to the mice in the study was corn.
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  #18   ^
Old Fri, Jun-08-18, 09:44
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BillyHW BillyHW is offline
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Not Being French. French people don't get fat. You are not French, therefore you get fat.
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  #19   ^
Old Fri, Jun-08-18, 11:33
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BillyHW BillyHW is offline
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Dehydration. You are not hungry, you are thirsty. But because you don't drink water you overeat, and get fat.
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  #20   ^
Old Fri, Jun-08-18, 14:24
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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.
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  #21   ^
Old Sun, Jun-10-18, 12:51
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BillyHW BillyHW is offline
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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.
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  #22   ^
Old Sun, Jun-10-18, 13:45
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Put your fork down in between bites.
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  #23   ^
Old Sun, Jun-10-18, 14:07
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Chemicals (e.g. RoundUp) and crap in our food.
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  #24   ^
Old Sun, Jun-10-18, 15:26
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Eating while watching TV.
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  #25   ^
Old Sun, Jun-10-18, 19:15
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BillyHW BillyHW is offline
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Blood Type. You don't eat right for your particular blood type, therefore you are fat.
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  #26   ^
Old Mon, Jun-11-18, 03:31
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Calianna Calianna is offline
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Quote:
Originally Posted by teaser
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.

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!)
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  #27   ^
Old Mon, Jun-11-18, 06:15
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teaser teaser is online now
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Posts: 12,702
 
Plan: mostly milkfat
Stats: 190/152.4/154 Male 67inches
BF:
Progress: 104%
Location: Ontario
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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?
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  #28   ^
Old Mon, Jun-11-18, 11:28
M Levac M Levac is offline
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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.

---

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.
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  #29   ^
Old Wed, Jun-13-18, 07:03
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Calianna Calianna is offline
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Plan: Atkins-ish (hypoglycemia)
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Quote:
Originally Posted by teaser
A mismatch between "perceived" hunger and homeostatic appetite.
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.
Quote:



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?



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.
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  #30   ^
Old Wed, Jun-13-18, 08:05
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teaser teaser is online now
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Plan: mostly milkfat
Stats: 190/152.4/154 Male 67inches
BF:
Progress: 104%
Location: Ontario
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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.

Quote:
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.


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.
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