Zitat Zitat von Vektor
@rantanplan
Eine einzelne Studie, ok. Allerdings steht etwas in der Praxis außer Frage: Personen mit Hyper- oder Hypothyreose haben einen erhöhten/erniedrigten Stoffwechsel. Schon mal Leute live gesehen, die über eine gewisse Zeitlang mit solchen SD-Hormonstörungen zu kämpfen haben? Da brauche ich keine Studie, die da irgendetwas widerlegt oder nicht, nur Augen.
...nicht falsch verstehen. Ich bezweifle nicht, dass Schilddrüsenhormone einen Einfluss haben. Die Praxis spricht hier wie so oft eine eigene Sprache. Ich wollte nur anfragen, wie sich so ein Ergebnis erklären läßt. Im übrigen ist dies nicht die einzige Studie, die zu diesem Ergebnis kommt.
Z.B. hat sich in der Vergangenheit gezeigt, dass ketogene Diäten den T3-Spiegel sehr stark absenken können, ohne, dass die metabolic rate in Mitleidenschaft gezogen wurde.

PS: Hat jemand vielleicht den gesamten Artikel des folgenden abstracts gelesen?

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

AG Dulloo, J Jacquet and L Girardier
Department of Physiology, Faculty of Medicine, University of Geneva, Switzerland. abdul.dulloo.unige.ch

An increase in the sensation of hunger and overeating after a period of chronic energy deprivation can be part of an autoregulatory phenomenon attempting to restore body weight. To gain insights into the role of fat and lean tissue depletion as determinants of such a hyperphagic response in humans, we reanalyzed the individual data on food intake and body composition available for the 12 starved and refed men in the classical Minnesota Experiment after a shift from a 12-wk period of restricted refeeding to an ad libitum refeeding period of 8 wk. For each individual, the following were determined: 1) the total hyperphagic response during the ad libitum refeeding period, calculated as the energy intake in excess of that during the prestarvation (control) period; 2) the degree of fat recovery and that of fat-free- mass (FFM) recovery before ad libitum refeeding, calculated as the deviation in fat and FFM from their respective prestarvation values (ie, the amount of fat or FFM before ad libitum refeeding as a percentage of fat or FFM during the control period); and 3) the deficit in energy intake before ad libitum refeeding, calculated as the difference between the energy intake during the period of restricted refeeding and that during the control period. The results indicate that 1) the total hyperphagic response is inversely correlated with the degree of fat recovery (r = -0.6) as well as with that of FFM recovery (r = -0.5), 2) the correlation between hyperphagia and FFM recovery persists after adjustment for fat recovery, and 3) the correlations between hyperphagia and fat recovery or FFM recovery persist after adjustment for the variance in the energy deficit during the preceding period of restricted refeeding. Taken together, these results in humans suggest that poststarvation hyperphagia is determined to a large extent by autoregulatory feedback mechanisms from both fat and lean tissues. These findings, which have implications for both the treatment of obesity and for nutritional rehabilitation after malnutrition and cachexia, have been integrated into a compartmental model of autoregulation of body composition, and can be used to explain the phenomenon of poststarvation overshoot in body fat.