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  #1   ^
Old Sun, Jul-26-15, 19:00
teaser's Avatar
teaser teaser is offline
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Default Obesity research finds leptin hormone isn't the overeating culprit

I don't remember seeing this here, it's from back in May.

Quote:
For years, scientists have pointed to leptin resistance as a possible cause of obesity. Research, however, has found that leptin action isn't the culprit. Leptin is a hormone that plays a role in appetite and weight control. It is produced when we are well fed, and it signals to the brain that there is ample energy and therefore reduces eating.

For years, scientists have pointed to leptin resistance as a possible cause of obesity. Research led by investigators at the University of Cincinnati (UC) Metabolic Diseases Institute, however, found that leptin action isn't the culprit.

"Restoring leptin action will not be effective at reducing obesity because leptin action is normal as opposed to being impaired in obesity," says assistant professor Diego Perez-Tilve, PhD, who directed the study "Diet-Induced Obese Mice Retain Endogenous Leptin Action" which appeared in the science journal Cell Metabolism on May 14, 2015.

Leptin is a hormone that plays a role in appetite and weight control. It is produced, Perez-Tilve says, when we are well fed, and it signals to the brain that there is ample energy and therefore reduces eating.

Leptin has been a hormone of interest since 1994, he says, when scientists discovered that a particular strain of obese mouse couldn't produce leptin at all.

"That mouse was very obese because it was hungry all the time. When they treated the mouse with leptin, it stopped eating so much and started losing weight."

Perez-Tilve says scientists were initially puzzled because obese persons have leptin levels far higher than persons of average weight. They theorized that the body was making extra leptin to combat obesity and that the obese patients must therefore need more leptin than persons of average weight to signal the brain to stop eating. However, in human preclinical trials, "giving obese patients more leptin didn't work ... they ate the same and remained obese, so it was concluded that obesity was a state of leptin resistance," he says.

In the UC study, funded by the National Institutes of Health, the team headed by Perez-Tilve took a different approach. They blocked leptin action in both lean and obese mice. The results were that both sets of mice ate more and gained weight to the same extent, proving that "leptin action was not impaired in the obese mouse."

With obesity affecting more than one-third of Americans and taking a toll on the nation's health care system, Perez-Tilve says the results of this study show "we need to change our way of thinking about how to use leptin as a potential target for therapy to treat obesity."



http://www.sciencedaily.com/release...50518145437.htm
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  #2   ^
Old Mon, Jul-27-15, 09:09
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Nicekitty Nicekitty is offline
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I'm thinking that what drives hunger and satiety will turn out to be quite complex, not something that can be changed with a simple pill. There has to be several underlying mechanisms that give us cravings, and likewise turn us away, from the different elements of our diet, trying to get us to a balanced state with all our different nutrients needs satisfied. Of course this has gone horribly awry with our modern diet.
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  #3   ^
Old Mon, Jul-27-15, 09:32
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Kristine Kristine is offline
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Agreed. To me, the operative word here is THE. Leptin isn't THE overeating culprit. I thought that was already established. Even if you do have a screwed-up leptin system, it's probably not the only factor. Fixing that alone would probably be like slapping nicotine patches on people and expecting them to just magically cease smoking. The behavioural/emotional/cultural aspect is just as important to address.
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  #4   ^
Old Mon, Jul-27-15, 11:20
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Nancy LC Nancy LC is offline
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Yeah, they've discovered quite a few hormones that control appetite and energy expenditure.
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  #5   ^
Old Mon, Jul-27-15, 12:25
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khrussva khrussva is offline
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Over the past year and a half, I've been learning something new... what normal hunger and satiety really is. That is something that I really didn't have much experience with over the course of my life. I ate too much to ever be really 'hungry.' For most of my life I was not eating to hunger and certain foods (and we all know what they are) actually made me want to eat more. I was feeding a craving. I've found real hunger to be much more subtle in comparison. Satiety is a wonderful thing - I love it. Who'd have thought you could actually go for several hours and not be thinking about your next bite of food. Until recently, not me.

For me and what I think I've figured out for myself -- it all comes down to maintaining stable blood sugar. Crashing and low BG creates some sort of "need" for food that has nothing to do with real hunger. I don't think everybody experiences this and it is likely more prevalent in the obese. What ever is going on here, eating sugary junk starts a process that totally overrides what the naturally lean know of hunger and satiety. I've always felt that I was different than those people and they just didn't get it. Managing how much I eat each day is doable when normal hunger and satiety is the driving factor behind how much I eat. Eating high GI/processed carbs throws me into a completely different mode and I an numb to the feeling of feeling full. Feeling "stuffed" is what I used to think feeling "full" was. Feeling normal satiety is completely different. If I feel stuffed after I eat, then I overate -- past the feeling of satiety.

I think normal hunger and satiety was always there for me. It was just over-ridden by a different (and much more powerful) need. So the whole leptin discussion was for me, IMO, attempting to fix something that wasn't broken. They are barking up the wrong tree.

Last edited by khrussva : Mon, Jul-27-15 at 12:39.
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  #6   ^
Old Mon, Jul-27-15, 12:56
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deirdra deirdra is offline
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I am like you, and the LCHF LIFESTYLE is definitely key. Having a "normal" relationship with food makes you realize how many years were wasted starving on very low calorie HCLF diets, feeling flawed because it was so hard to resist foods while the "normal" people around us seemed to have such effortless self-restraint in the face of the same foods. Now I realize they were sated and not tempted or controlled by the food like we were.
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  #7   ^
Old Mon, Jul-27-15, 13:08
M Levac M Levac is offline
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Thanks, Teaser. It occurred to me that if we believe the problem is leptin resistance, we also have to conclude the default state is constant hunger. That makes no sense to me. I prefer to believe the default state is no hunger, then there's signals for both hunger and satiety, like for example ghrelin and leptin. If leptin isn't the problem, then the problem lies elsewhere, probably on the ghrelin side which is probably powerful enough to override leptin. That's just two hormones I know of, there's probably more things that regulate hunger and satiety, like enzymes, maybe ketones and fatty acids or even insulin. In the case of insulin however, it's probably not needed for satiety, i.e. when you eat a high-fat meal, you're still sated but there's barely any insulin produced from that meal.
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  #8   ^
Old Mon, Jul-27-15, 16:15
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teaser teaser is offline
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Lack of hunger as a default state makes sense. Anybody who isn't dangerously underweight has enough stores on their body to last a month or more without eating.

Insulin for satiety might make some sense, hunger is a classic symptom of insulin deficiency. That doesn't mean that it takes much though, insulin can be extremely low on a ketogenic diet or extended fast at the same time as hunger.
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  #9   ^
Old Mon, Jul-27-15, 17:05
M Levac M Levac is offline
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Yeah I meant in context, not in absolute terms. You're right, we still need normal insulin for things to work properly. Another thing I just thought of. It's the semi-starvation experiment findings and how they fit with this latest stuff about hunger. These subjects were constantly hungry yet they ate something. Compared to outright starvation where hunger disappears after a short time, it becomes obvious there's something going on with the stuff we eat. Besides the hunger/satiety signals independently of fat accumulation, I wonder if the fact that some stuff is obesogenic might also have an effect on hunger down the line or in parallel. You know, if the stuff we eat just makes us eat more but doesn't make us fatter, then I don't see much of a problem because then the surplus must obviously be spent somehow. But now it makes us both eat more and fatter. I think it's related to fasting insulin or in-between meals at least cuz that's when we grow fatter or leaner.
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  #10   ^
Old Wed, Jul-29-15, 01:03
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esw esw is offline
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Quote:
For me and what I think I've figured out for myself -- it all comes down to maintaining stable blood sugar. Crashing and low BG creates some sort of "need" for food that has nothing to do with real hunger. I don't think everybody experiences this and it is likely more prevalent in the obese. What ever is going on here, eating sugary junk starts a process that totally overrides what the naturally lean know of hunger and satiety. I've always felt that I was different than those people and they just didn't get it. Managing how much I eat each day is doable when normal hunger and satiety is the driving factor behind how much I eat. Eating high GI/processed carbs throws me into a completely different mode and I an numb to the feeling of feeling full. Feeling "stuffed" is what I used to think feeling "full" was. Feeling normal satiety is completely different. If I feel stuffed after I eat, then I overate -- past the feeling of satiety.


Khrussva-that is exactly how I have spent my life!! Eating HFLC keeps me stable of mind. Previous way of eating was all consuming, frightening and completely outwith my control. How could other people say no to those sugary comforting foods!!!!
Now, I know and accept this is what quick release carbs do to me, change my personality to a carb seeking missile . And yes, I don't think everyone is affected by carbs like this.
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  #11   ^
Old Wed, Jul-29-15, 02:55
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cotonpal cotonpal is online now
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Quote:
Originally Posted by esw
Khrussva-that is exactly how I have spent my life!! Eating HFLC keeps me stable of mind. Previous way of eating was all consuming, frightening and completely outwith my control. How could other people say no to those sugary comforting foods!!!!
Now, I know and accept this is what quick release carbs do to me, change my personality to a carb seeking missile . And yes, I don't think everyone is affected by carbs like this.


Me too. I was mostly ravenously hungry and occasionally completely overstuffed. I didn't understand "full". I was simply hungry almost all the time. Things are so much better now. When I first decided to go low carb I was sure my blood sugars were way out of wack, on a roller coaster of up and down, and that I was either diabetic or on my way there, like other members of my family. I didn't go to a doctor since I knew what to do to avoid diabetes, stop eating carbs. So I did, and the rest is history. I am lucky I grew up before the low fat era so that cutting carbs was the natural thing to do.

Jean
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  #12   ^
Old Wed, Jul-29-15, 06:24
teaser's Avatar
teaser teaser is offline
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Quote:
Originally Posted by M Levac
Yeah I meant in context, not in absolute terms. You're right, we still need normal insulin for things to work properly. Another thing I just thought of. It's the semi-starvation experiment findings and how they fit with this latest stuff about hunger. These subjects were constantly hungry yet they ate something. Compared to outright starvation where hunger disappears after a short time, it becomes obvious there's something going on with the stuff we eat. Besides the hunger/satiety signals independently of fat accumulation, I wonder if the fact that some stuff is obesogenic might also have an effect on hunger down the line or in parallel. You know, if the stuff we eat just makes us eat more but doesn't make us fatter, then I don't see much of a problem because then the surplus must obviously be spent somehow. But now it makes us both eat more and fatter. I think it's related to fasting insulin or in-between meals at least cuz that's when we grow fatter or leaner.


This reminds me of something I posted in another thread the other day;

Reposting from Fung thread... Dr. Fung often says that muscle is spared during fasting, as long as there's enough body fat...

http://www.ergo-log.com/leanmassfasting.html

This is a blog post on a rat study of severe calorie restriction vs. fasting that I found interesting. The blog itself is worth reading, there's also a link to the actual study here;


Quote:
The results from this study confirm that
the treatment used to induce weight loss can
influence the pattern of recovering of body
composition. Although the composition of weight loss was similar for food-restricted and
starved rats, the pattern and time course of
recovery of body fat was different for the two
groups of rats. The restricted rats regained a
large portion of their fat during the first 6 d
of refeeding, whereas body protein and
weight recovered steadily throughout the 17
d of refeeding. In the starved rats body protein
was almost totally replaced before there was a significant recovery of body fat. Although
there was a delay in replacement of
fat in starved-refed rats these animals were
more precise in returning body fat to control values than were the restricted-refed rats.


It took six days for the underfed rats to recover about the same amount of body protein that the starved rats recovered in two days.

Quote:
At the end of underfeeding the carcass weight of 40% -fed rats was 66 g less than that of 100%-ged controls. Of this weight loss, 28.2 g were fat and 11 g were protein. During the first 6 days of recovery, the 40%-fed rats regained 17 g (60%) of the fat and 7g (64%) of the protein.

The composition of weight loss in starved rats was the same as in restricted rats. Starvation had reduced carcass weight by 62 g. Fat accounted for 27.3 g, and protein accounted for 10.5 g of the weight loss. After 2 days of refeeding, 6 g (57%) of protein but only 3g (11%) of fat had been regained.


In the rats in this study at least, the fact that the two weight loss methods resulted in an equivalent ratio of lean mass to fat mass loss is irrelevant, once the effect of the refeed is taken into account.



In the Minnesota Starvation study, with refeeding, before lean mass returns to pre-diet levels, there was an overshoot of fat mass. There's an increase in appetite that remains until both fat mass and lean mass are recovered--and since fat mass recovers first, it's hypothesized that the appetite continues to be high until the lean mass is also recovered, and that this is what causes the increase in fat mass--not necessarily a drive to fatten with the body in "starvation" mode, but a continued increase in appetite needed for recovery of lean mass.

Quote:
Poststarvation hyperphagia and body fat overshooting in humans: a role for feedback signals from lean and fat tissues.


http://www.ncbi.nlm.nih.gov/pubmed/9062520
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