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Old Fri, Feb-02-18, 08:35
teaser's Avatar
teaser teaser is offline
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Plan: mostly milkfat
Stats: 190/152.4/154 Male 67inches
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Location: Ontario
Default Hunger overrides sense of fullness after weight loss

https://www.sciencedaily.com/releas...80201123318.htm

Quote:
The levels of hormones that control hunger and fullness(satiety) both rise after weight loss, but individuals may only experience an increase in hunger, according to a new study. The study is published ahead of print in the American Journal of Physiology -- Endocrinology and Metabolism.

A team of researchers studied adult volunteers with severe obesity (body mass index greater than 40) who participated in a comprehensive weight loss program. The volunteers attended five sessions at a multidisciplinary rehabilitation program over the course of two years. During each three-week residential session, participants learned about interventions to aid weight loss, including eating a balanced, calorie-restricted diet, physical activity, talk therapy and nutrition education. Between program visits, participants were encouraged to continue with daily exercise and a healthy diet at home. The research team measured hunger and satiety hormone levels in the blood after the first four weeks of the trial and again after one and two years of continued weight loss. Investigators also recorded the participants' self-reported feelings of hunger and fullness at each of these intervals.

After one month of following the program, the volunteers' subjective sense of fullness after a meal was unchanged, but decreased at the one- and two-year marks, whereas self-reported hunger increased significantly after one and two years. The research team found increases in the levels of both the hunger and satiety hormones after one and two years of sustained weight loss. However, the boost in hunger hormones seemed to override the increase in satiety hormones, explained the researchers.

"This information is of importance for patients and health professionals working with this patient group, and strategies should be identified that can help patients deal with increased hunger in the long term," the researchers wrote.




The hormone I see referred to most often as a "hunger" hormone is ghrelin, I think you could also look at that as sort of a "switch from fed to fasted state" hormone, although that's a bit clunky.


https://www.ncbi.nlm.nih.gov/pubmed/11834429

Quote:
Ghrelin drives GH secretion during fasting in man.
Muller AF1, Lamberts SW, Janssen JA, Hofland LJ, Koetsveld PV, Bidlingmaier M, Strasburger CJ, Ghigo E, Van der Lely AJ.
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Abstract
OBJECTIVES:
In humans, fasting leads to elevated serum GH concentrations. Traditionally, changes in hypothalamic GH-releasing hormone and somatostatin release are considered as the main mechanisms that induce this elevated GH secretion during fasting. Ghrelin is an endogenous ligand of the GH secretagogue receptor and is synthesized in the stomach. As ghrelin administration in man stimulates GH release, while serum ghrelin concentrations are elevated during fasting in man, this increase in ghrelin levels might be another mechanism whereby fasting results in stimulation of GH release.

DESIGN AND SUBJECTS:
In ten healthy non-obese males we performed a double-blind placebo-controlled crossover study comparing fasting with and fasting without GH receptor blockade. GH, ghrelin, insulin, glucose and free fatty acids were assessed.

RESULTS:
While ghrelin levels do not vary considerably in the fed state, fasting rapidly induced a diurnal rhythm in ghrelin concentrations. These changes in serum ghrelin concentrations during fasting were followed by similar, profound changes in serum GH levels. The rapid development of a diurnal ghrelin rhythm could not be explained by changes in insulin, glucose, or free fatty acid levels. Compared with fasting without pegvisomant, fasting with pegvisomant did not change the ghrelin rhythm.

CONCLUSIONS:
These data indicate that ghrelin is the main driving force behind the enhanced GH secretion during fasting.



Ghrelin deficient mice become hypoglycemic when fasted, that enhanced growth hormone is needed to avoid this.

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4313585/



Quote:
Although the hunger-reducing effect of a ketogenic diet is well-documented, its main mechanisms of action are still elusive. The global picture is complicated by the contradictory role of ketosis on anorexigenic and orexigenic signals (summarized in Figure ​Figure4).4). Ketones (mainly BHB) can act both orexigenically or anorexigenically. In the orexigenic mechanism, it increases the circulating level of adiponectin, increasing brain GABA and AMPK phosphorylation and decreasing brain ROS production. The anorexigenic mechanism triggers a main normal glucose meal response, increasing circulating post-meal FFA (thus reducing cerebral NPY), maintaining CCK meal response and decreasing circulating ghrelin.


And since a ketogenic diet is closer to the fasted state, so a switch from fed to fasted is sort of less dramatic, and ketones themselves protect against hypoglycemia, a decrease in a circulating "fasted to fed" or "preventive of hypoglycemia" or even "hunger" hormone if you insist makes sense. Or maybe that's just cramming things into my personal bias.
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