Set point theory

from Wikipedia, the free encyclopedia

The set-point theory is a scientifically controversial thesis according to which the human body weight is genetically programmed and cannot be changed at will. It is represented, for example, by the controversial food chemist Udo Pollmer . According to this theory, most people have a relatively stable set point to which the weight automatically steers again in the event of deviations up or down. Just as a thermostat regulates the temperature in a room, there is an individual weight in adults that the body wants to maintain. This weight is called the set point weight .

theory

The term set point comes from the regulation theory of cybernetics and describes a set point . The theoretical model is based on the assumption that the body always tries to maintain a state of homeostasis . The setpoint for the weight is regulated by a "switching point" in the brain, called a ponderostat . It is suspected to be in the hypothalamus . The switching point constantly compares the actual value of the organism with the set target value and reacts to downward deviations with physical signals such as hunger . The so-called starvation metabolism, through which the body's basal metabolic rate is reduced in phases of under-caloric nutrition, is regarded as evidence for the set-point theory.

The set-point theory aims to explain why most obese people, despite repeated weight loss diets, do not lose weight in the long term and keep their excess weight . It assumes that an existing internal control mechanism for body weight, which determines the set point , is set too high for genetic reasons.

In a modified set point theory, e.g. B. represented by Keesey, the initially normal set point increases due to long-term overeating and then remains permanently at the new increased set point.

research

With the help of molecular biology , researchers are trying to prove such a control loop. However, the research is far from over. Most of the published research results relate to animal experiments.

In 1984, Leibel and Hirsch examined the energy requirements of weight-stable, fat and thin people. The energy requirement per square meter of body surface was comparable with 5989  kJ / m² / day (1432 kcal / m² / day) (thickness) and 5608 kJ / m² / day (1341 kcal / m² / day) (thin). After a diet, the energy requirements of the fat people fell to 4270 kJ / m² / day (1021 kcal / m² / day) below the value of the thin control group. The fat people took in 9079 kJ / day (2171 kcal / day), less than the thin with 9535 kJ / day (2280 kcal / day). And this, although they still weighed 60% more than the thin control group.

A 1968 study by Sims and colleagues attempted to increase weight by 15 to 25%. This required 25,000 to 42,000 kJ / day (6,000 to 10,000 kcal / day). Far more kJ were required than would actually be mathematically necessary to build up fat.

The Swede Fredrik Nyström examined the consequences of massive overeating in the case of sedentary lifestyle, similar to what was shown in the documentary Super Size Me , under laboratory conditions. In addition, 18 students doubled their calorie intake through fast food and avoided moving. According to the energy balance model, all students should have increased massively. This was not the case. The increase varied greatly from person to person.

See also

Web links

swell

  1. Petra Wiedmer, Gender-Specific Body Weight Regulation in Mice. Investigations on the set-point theory of body mass (diss.), P. 4 ff.
  2. a b Presentation of the set point theory
  3. B. Herd: Fat stays fat. In: The time of May 9, 2007
  4. S. Wolpert: Dieting Does Not Work, UCLA Researchers Report. ( Memento of January 30, 2012 in the Internet Archive ) April 3, 2007, accessed June 25, 2011
  5. Jeffrey S. Flier: Obesity Wars - Molecular Progress Confronts an Expanding Epidemic. In: Cell. 116, 2004, p. 337, doi : 10.1016 / S0092-8674 (03) 01081-X .
  6. DGE molecules regulate weight [1]
  7. ^ RL Leibel, J. Hirsch: Diminished energy requirements in reduced-obese patients. In: Metabolism: clinical and experimental Volume 33, Number 2, February 1984, pp. 164-170, PMID 6694559 .
  8. Sims EA, Horton ES: Endocrine and Metabolic Adaptation to Obesity and Starvation. Am J Clin Nutr 21 (1968) 12, pp. 1455-1470. PMID 4881681
  9. Kate Douglas: "Super size me" revisited - under lab conditions. New Scientist , Issue 2588, January 27, 2007
  10. ^ JA Levine, NL Eberhardt, MD Jensen: Role of nonexercise activity thermogenesis in resistance to fat gain in humans. In: Science Volume 283, Number 5399, January 1999, pp. 212-214, ISSN  0036-8075 . PMID 9880251 . ( Abstract )