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Set point theory, as it pertains to human body weight, states that there is a biological control method in humans that actively regulates weight towards a predetermined set weight for each individual.[1] This may occur through regulation of energy intake (e.g. via increased or decreased appetite) or energy expenditure (e.g. via reduced metabolism or feelings of lethargy).[1][2] Set point theory explains why it is difficult for dieters to maintain weight loss over time, as calorie restriction may become less effective or more difficult to maintain as regulatory mechanisms in the body actively push the body back towards the set point weight.[3]
Set point theory differentiates between active compensation and passive compensation. Passive compensation describes processes where a decrease in body fat leads to less energy being expended, because one carries around less weight in daily activities. In addition to passive compensation, set point theory also posits active compensation. Here additional regulatory mechanism in the body affects energy expenditure or intake.[4]
Set point theory can be construed as implying weight regulation in a wide or tight range around the set point, in a symmetric or in an asymmetric manner (i.e. treating weight gain and loss either the same or differently), and may apply to regulation of body fat levels specifically (in a multi-compartment model) or to overall body weight.
Set point theory applies to both downward and upward adjustment of weight.[2][5] This return to the pre-change weight occurs faster than would be expected if individuals simply returned to their normal caloric intake and energy expenditure even after accounting for lower energy needs after weight loss, indicating an active response by the body encouraging weight gain.[4] While the set point applies to both deviations driven by weight loss and weight gain, the set point response driving a person to regain weight to regain the set point is stronger than the response to lose weight after gaining weight above the set point, implying that it may be easier to gain than to lose weight.
- ^ a b Cite error: The named reference
Role of set-point theorywas invoked but never defined (see the help page). - ^ a b Keesey, Richard E.; Hirvonen, Matt D. (1 September 1997). "Body Weight Set-Points: Determination and Adjustment". The Journal of Nutrition. 127 (9): 1875S–1883S. doi:10.1093/jn/127.9.1875S. PMID 9278574.
- ^ Ghanemi A, Yoshioka M, St-Amand J (2018). "Broken Energy Homeostasis and Obesity Pathogenesis: The Surrounding Concepts". J Clin Med. 7 (11): 453. doi:10.3390/jcm7110453. PMC 6262529. PMID 30463389.
{{cite journal}}: CS1 maint: multiple names: authors list (link) - ^ a b Cite error: The named reference
Alternative modelswas invoked but never defined (see the help page). - ^ Schwartz MW, Seeley RJ, Zeltser LM, Drewnowski A, Ravussin E, Redman LM; et al. (2017). "Obesity Pathogenesis: An Endocrine Society Scientific Statement". Endocr Rev. 38 (4): 267–296. doi:10.1210/er.2017-00111. PMC 5546881. PMID 28898979.
{{cite journal}}: CS1 maint: multiple names: authors list (link)