Can't Stop Eating? Leptin Hormones

SideSteel

I think it's possible that you were simply spiking and lowering blood glucose somewhat rapidly and the lowering of it could trigger hunger signals.

Well, more than normal sugary stuff over the weekend. Then Monday back to normal diet, healthier choices, normal amount of food during the day up until dinner, the only sugar was the amount I normally take in coffee every day. Two plates of dinner, no dessert, but really really wanted to eat more. Stomach felt full but the desire to eat a 3rd plate of food. I wouldn't think that my blood glucose would be dropping at that point. I'm not on a VLCD, I am about 10 pounds from my goal weight so I'm not in a very big cut. Normally I get shaky and weak when I haven't eaten and glucose was dropping, totally different feeling here of being stuffed but wanting more food.

I see, if you were still hungry after returning to your normal diet then what I just said above was incorrect. Reading comprehension FTL on my part.

But that being said, I would doubt this has nothing to do with fructose induced leptin resistance from a few days of eating sweets.

Qskim

Leptin levels can fluctuate just like other hormones.
Severely obese individuals have higher levels of the hormone than those of normal weight.
Jeffrey Friedman who was head (?) of the team that discovered leptin in 1994 stated in a podcast that some severely overweight children were injected with the hormone once a week in trials and lost weight - hunger decreased.
It (leptin) influences every other hormone in the body but is not in itself reliant on other hormones.
It is the main transmitter from adipose tissue to the brain of our "full signal". How well this happens is what determines ab/normal weight levels.
Lol...that's all I can remember so far...currently reading "mastering leptin" by Byron Richards and please please let me finish the book before you bag it! I've always known about leptin and insulin resistance and ate accordingly before I came on MFP and lost as much weight doing so.

deksgrl

I just want to point out that, whatever the circumstance, you don't suddenly develop a hormone resistance in a month. It takes chronic overdoses (as far as I know) to cause that sort of thing.

Otherwise why aren't all kids diabetic for a week or two after Halloween? Hell, why am I not a diabetic yet? I steal all the good candies and keep them for myself and pass out all the crap I don't want to eat when kids come to my house trick or treating.

I'm not talking about diabetes, I'm talking about the fluctuation of Leptin.

ArroganceInStep

I'm not talking about diabetes, I'm talking about the fluctuation of Leptin.

I'm responding specifically to:

So, what is this Leptin hormone and what does the high fructose have to do with it, and why did that make me want to eat more even though I was full? Well, Leptin is the hormone that tells your brain that you are full, stop eating. When you have too much of this, it creates leptin resistance, where the leptin cannot cross the barrier to the brain, the brain does not get the message to stop eating. Basically, it makes you overeat, a lot. High Fructose Corn Syrup dramatically raises Leptin.

And saying that a month or so of bad eating for the holidays isn't suddenly going to make you Leptin resistant.

deksgrl

I'm not talking about diabetes, I'm talking about the fluctuation of Leptin.

I'm responding specifically to:

So, what is this Leptin hormone and what does the high fructose have to do with it, and why did that make me want to eat more even though I was full? Well, Leptin is the hormone that tells your brain that you are full, stop eating. When you have too much of this, it creates leptin resistance, where the leptin cannot cross the barrier to the brain, the brain does not get the message to stop eating. Basically, it makes you overeat, a lot. High Fructose Corn Syrup dramatically raises Leptin.

And saying that a month or so of bad eating for the holidays isn't suddenly going to make you Leptin resistant.

Mice become leptin resistant in 3 days of overfeeding. I don't know how long it takes for humans, but it doesn't seem out of the realm of possibilities that it would happen in a month.

ArroganceInStep

Mice become leptin resistant in 3 days of overfeeding. I don't know how long it takes for humans, but it doesn't seem out of the realm of possibilities that it would happen in a month.

A point I disagree with (though I don't know of any studies proving one way or the other so it's just speculation) but at least we're on the same page.

deksgrl

Some interesting studies though I haven't found one that addresses only leptin resistance and the amount of time it takes to develop.

http://www.ncbi.nlm.nih.gov/pubmed/22556394

Changes in insulin sensitivity precede changes in body composition during 14 days of step reduction combined with overfeeding in healthy young men.

Abstract

A lifestyle characterized by inactivity and a high-calorie diet is a known risk factor for impaired insulin sensitivity and development of Type 2 diabetes mellitus. To investigate possible links, nine young healthy men (24 ± 3 yr; body mass index of 21.6 ± 2.5 kg/m(2)) completed 14 days of step reduction (10,000 to 1,500 steps/day) and overfeeding (+50% kcal). Body composition (dual X-ray absorptiometry, MRI), aerobic fitness (maximal O(2) consumption), systemic inflammation and insulin sensitivity [oral glucose tolerance test (OGTT), hyperinsulinemic euglycemic clamp] were assessed before (day 0), during (days 3 and 7), and immediately after the intervention (day 14), with follow-up tests (day 30). Body weight had increased at days 7 and 14 (P < 0.05). The amount of visceral fat had increased at day 14 compared with day 0 (P < 0.05). The insulin response to the OGTT had increased at days 7 and 14 (P < 0.05). Insulin sensitivity, estimated using the Matsuda index, had decreased at days 3 and 7 (P < 0.01). At day 14, glucose infusion rates had decreased by ∼44% during the euglycemic clamps (P < 0.05). Also, plasma levels of leptin and adiponectin had increased (P < 0.05), whereas no changes were seen in inflammatory markers. At day 30, body weight and whole body adiposity were still elevated compared with day 0 (P < 0.05), whereas the insulin sensitivity as well as the insulin response to the OGTT did not differ from baseline. The glucose response to the OGTT was only affected at day 30, with a decrease compared with day 0. Our data show that insulin sensitivity was impaired after 3 days of inactivity and overfeeding. Impairments in insulin sensitivity occurred before changes in body composition, supporting the notion that the initial steps in impairment of insulin sensitivity may be linked directly to the effects of inactivity and a high calorie intake.

http://www.ncbi.nlm.nih.gov/pubmed/22412070

Sweetened beverage consumption, incident coronary heart disease, and biomarkers of risk in men.

Abstract
BACKGROUND:

Sugar-sweetened beverage consumption is associated with weight gain and risk of type 2 diabetes mellitus. Few studies have tested for a relationship with coronary heart disease (CHD) or intermediate biomarkers. The role of artificially sweetened beverages is also unclear.
METHODS AND RESULTS:

We performed an analysis of the Health Professionals Follow-Up Study, a prospective cohort study including 42 883 men. Associations of cumulatively averaged sugar-sweetened (eg, sodas) and artificially sweetened (eg, diet sodas) beverage intake with incident fatal and nonfatal CHD (myocardial infarction) were examined with proportional hazard models. There were 3683 CHD cases over 22 years of follow-up. Participants in the top quartile of sugar-sweetened beverage intake had a 20% higher relative risk of CHD than those in the bottom quartile (relative risk=1.20; 95% confidence interval, 1.09-1.33; P for trend <0.01) after adjustment for age, smoking, physical activity, alcohol, multivitamins, family history, diet quality, energy intake, body mass index, pre-enrollment weight change, and dieting. Artificially sweetened beverage consumption was not significantly associated with CHD (multivariate relative risk=1.02; 95% confidence interval, 0.93-1.12; P for trend=0.28). Adjustment for self-reported high cholesterol, high triglycerides, high blood pressure, and diagnosed type 2 diabetes mellitus slightly attenuated these associations. Intake of sugar-sweetened but not artificially sweetened beverages was significantly associated with increased plasma triglycerides, C-reactive protein, interleukin-6, and tumor necrosis factor receptors 1 and 2 and decreased high-density lipoprotein, lipoprotein(a), and leptin (P<0.02).
CONCLUSIONS:

Consumption of sugar-sweetened beverages was associated with increased risk of CHD and some adverse changes in lipids, inflammatory factors, and leptin. Artificially sweetened beverage intake was not associated with CHD risk or biomarkers.

Phrakman

should really stop blaming hormones for your inability to put the fork down. How bad do you want it?

Acg67

Some interesting studies though I haven't found one that addresses only leptin resistance and the amount of time it takes to develop.

http://www.ncbi.nlm.nih.gov/pubmed/22556394

Changes in insulin sensitivity precede changes in body composition during 14 days of step reduction combined with overfeeding in healthy young men.

Abstract

A lifestyle characterized by inactivity and a high-calorie diet is a known risk factor for impaired insulin sensitivity and development of Type 2 diabetes mellitus. To investigate possible links, nine young healthy men (24 ± 3 yr; body mass index of 21.6 ± 2.5 kg/m(2)) completed 14 days of step reduction (10,000 to 1,500 steps/day) and overfeeding (+50% kcal). Body composition (dual X-ray absorptiometry, MRI), aerobic fitness (maximal O(2) consumption), systemic inflammation and insulin sensitivity [oral glucose tolerance test (OGTT), hyperinsulinemic euglycemic clamp] were assessed before (day 0), during (days 3 and 7), and immediately after the intervention (day 14), with follow-up tests (day 30). Body weight had increased at days 7 and 14 (P < 0.05). The amount of visceral fat had increased at day 14 compared with day 0 (P < 0.05). The insulin response to the OGTT had increased at days 7 and 14 (P < 0.05). Insulin sensitivity, estimated using the Matsuda index, had decreased at days 3 and 7 (P < 0.01). At day 14, glucose infusion rates had decreased by ∼44% during the euglycemic clamps (P < 0.05). Also, plasma levels of leptin and adiponectin had increased (P < 0.05), whereas no changes were seen in inflammatory markers. At day 30, body weight and whole body adiposity were still elevated compared with day 0 (P < 0.05), whereas the insulin sensitivity as well as the insulin response to the OGTT did not differ from baseline. The glucose response to the OGTT was only affected at day 30, with a decrease compared with day 0. Our data show that insulin sensitivity was impaired after 3 days of inactivity and overfeeding. Impairments in insulin sensitivity occurred before changes in body composition, supporting the notion that the initial steps in impairment of insulin sensitivity may be linked directly to the effects of inactivity and a high calorie intake.

http://www.ncbi.nlm.nih.gov/pubmed/22412070

Sweetened beverage consumption, incident coronary heart disease, and biomarkers of risk in men.

Abstract
BACKGROUND:

Sugar-sweetened beverage consumption is associated with weight gain and risk of type 2 diabetes mellitus. Few studies have tested for a relationship with coronary heart disease (CHD) or intermediate biomarkers. The role of artificially sweetened beverages is also unclear.
METHODS AND RESULTS:

We performed an analysis of the Health Professionals Follow-Up Study, a prospective cohort study including 42 883 men. Associations of cumulatively averaged sugar-sweetened (eg, sodas) and artificially sweetened (eg, diet sodas) beverage intake with incident fatal and nonfatal CHD (myocardial infarction) were examined with proportional hazard models. There were 3683 CHD cases over 22 years of follow-up. Participants in the top quartile of sugar-sweetened beverage intake had a 20% higher relative risk of CHD than those in the bottom quartile (relative risk=1.20; 95% confidence interval, 1.09-1.33; P for trend <0.01) after adjustment for age, smoking, physical activity, alcohol, multivitamins, family history, diet quality, energy intake, body mass index, pre-enrollment weight change, and dieting. Artificially sweetened beverage consumption was not significantly associated with CHD (multivariate relative risk=1.02; 95% confidence interval, 0.93-1.12; P for trend=0.28). Adjustment for self-reported high cholesterol, high triglycerides, high blood pressure, and diagnosed type 2 diabetes mellitus slightly attenuated these associations. Intake of sugar-sweetened but not artificially sweetened beverages was significantly associated with increased plasma triglycerides, C-reactive protein, interleukin-6, and tumor necrosis factor receptors 1 and 2 and decreased high-density lipoprotein, lipoprotein(a), and leptin (P<0.02).
CONCLUSIONS:

Consumption of sugar-sweetened beverages was associated with increased risk of CHD and some adverse changes in lipids, inflammatory factors, and leptin. Artificially sweetened beverage intake was not associated with CHD risk or biomarkers.

ArroganceInStep

should really stop blaming hormones for your inability to put the fork down. How bad do you want it?

Reading comprehension ftw.

FredDoyle

should really stop blaming hormones for your inability to put the fork down. How bad do you want it?

And this precludes understanding the mechanism, why?

ArroganceInStep

Also the first study is far more interesting to me at least than the last. I'll have to read it some more, thanks.

Phrakman

should really stop blaming hormones for your inability to put the fork down. How bad do you want it?

And this precludes understanding the mechanism, why?

Dont really care about the science, all i see here is people looking for an out, dont want to blame themselves, want to blame some sort of hormone's.

ArroganceInStep

Dont really care about the science, all i see here is people looking for an out, dont want to blame themselves, want to blame some sort of hormone's.

Once again, reading comprehension ftw.

deksgrl

should really stop blaming hormones for your inability to put the fork down. How bad do you want it?

And this precludes understanding the mechanism, why?

Dont really care about the science, all i see here is people looking for an out, dont want to blame themselves, want to blame some sort of hormone's.

I am doing quite well, I'm not looking for an out. I was exploring the reason why after successful dieting and controlling appetite for over a year that there would be one day where there was that uncontrollable urge to eat. And there is a real scientific reason for that. If you are not interested, fine, don't comment.

FredDoyle

should really stop blaming hormones for your inability to put the fork down. How bad do you want it?

And this precludes understanding the mechanism, why?

Dont really care about the science, all i see here is people looking for an out, dont want to blame themselves, want to blame some sort of hormone's.

So your hasty generalization would be wrong then. Thanks for clearing that up.
...or you're a troll as your avatar would indicate.

SorchaEilis

Leptin resistance, IMO, is another excuse to justify obesity: "It's not MY fault, I'm leptin resistant!" The recommended 'cure' for leptin resistance? Healthy diet, portion control, and daily exercise. Hmm....

deksgrl

http://jcem.endojournals.org/content/82/4/1293.abstract?sid=c7a7d43e-1caa-4d7a-b8b6-f84ce587f213

"The data indicate that there are important gender-based differences in the regulation and action of leptin in humans. Serum leptin levels increase with progressive obesity in both men and women. However, for any given measure of obesity, leptin levels are higher in women than in men, consistent with a state of relative leptin resistance. These findings have important implications regarding differences in body composition in men and women. The observation that serum leptin is not related to energy expenditure rates suggests that leptin regulates body fat predominantly by altering eating behavior rather than calorigenesis."

http://jcem.endojournals.org/content/83/11/4140.abstract?sid=d43c27a2-4c9f-4720-bde6-f0249119ee1f

"The strongest distinction between the sexes in the level of organization of leptin concentration is not at the level of pulse organization or oscillation frequency, but, rather, in the mass or amount of leptin released (or removed) per unit time, indicating that women might be more resistant to the effects of leptin than men."

marsellient

Someone mentioned the production of dopamine as a response to eating sugar (in whatever form). Do any of you have thoughts or references about its relationship to appetite?

Thanks again for the previous references. I did say I know how my system responds to certain foods and therefore I stay away from them, and that I don't care why. That's not necessarily true. Like the OP I am interested in the science, but I've learned how my body responds without understanding why. I guess it would be smart to figure out why.