How Strongly Does Appetite Counter Weight Loss? Quantification of the Feedback Control of Human Energy Intake

Polidori, David; Sanghvi, Arjun; Seeley, Randy J.; Hall, Kevin D.

doi:10.1002/oby.21653

Cited by 164 publications

(207 citation statements)

References 44 publications

(69 reference statements)

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“…However, this theory does not accord with the general experience of individuals when dieting. Furthermore, under the settling point model, we would not expect to see any compensatory changes in energy expenditure or intake to resist changes in energy balance -yet such changes are routinely observed (Norgan and Durnin, 1980;Leibel et al, 1995;Horton et al, 1995;Dulloo et al, 1997;Dulloo and Jacquet, 1998;Goldberg et al, 1998;Weyer et al, 2001;Galgani and Santos, 2016;Hall et al, 2011Hall et al, , 2012Johannsen et al, 2012;Polidori et al, 2016). A review of 32 controlled feeding studies in humans concluded that the responses were most consistent with the set-point rather than the settling point model (Hall and Guo, 2017).…”

Section: Settling Point Theorymentioning

confidence: 99%

The evolution of body fatness: trading off disease and predation risk

Speakman

2018

Journal of Experimental Biology

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Human obesity has a large genetic component, yet has many serious negative consequences. How this state of affairs has evolved has generated wide debate. The thrifty gene hypothesis was the first attempt to explain obesity as a consequence of adaptive responses to an ancient environment that in modern society become disadvantageous. The idea is that genes (or more precisely, alleles) predisposing to obesity may have been selected for by repeated exposure to famines. However, this idea has many flaws: for instance, selection of the supposed magnitude over the duration of human evolution would fix any thrifty alleles (famines kill the old and young, not the obese) and there is no evidence that hunter-gatherer populations become obese between famines. An alternative idea (called thrifty late) is that selection in famines has only happened since the agricultural revolution. However, this is inconsistent with the absence of strong signatures of selection at single nucleotide polymorphisms linked to obesity. In parallel to discussions about the origin of obesity, there has been much debate regarding the regulation of body weight. There are three basic models: the setpoint, settling point and dual-intervention point models. Selection might act against low and high levels of adiposity because food unpredictability and the risk of starvation selects against low adiposity whereas the risk of predation selects against high adiposity. Although evidence for the latter is quite strong, evidence for the former is relatively weak. The release from predation ∼2-million years ago is suggested to have led to the upper intervention point drifting in evolutionary time, leading to the modern distribution of obesity: the drifty gene hypothesis. Recent critiques of the dual-intervention point/ drifty gene idea are flawed and inconsistent with known aspects of energy balance physiology. Here, I present a new formulation of the dual-intervention point model. This model includes the novel suggestion that food unpredictability and starvation are insignificant factors driving fat storage, and that the main force driving up fat storage is the risk of disease and the need to survive periods of pathogen-induced anorexia. This model shows why two independent intervention points are more likely to evolve than a single set point. The molecular basis of the lower intervention point is likely based around the leptin pathway signalling. Determining the molecular basis of the upper intervention point is a crucial key target for future obesity research. A potential definitive test to separate the different models is also described.

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Section: Settling Point Theorymentioning

confidence: 99%

The evolution of body fatness: trading off disease and predation risk

Speakman

2018

Journal of Experimental Biology

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“…These problems were recently addressed and the strength of the long-term energy intake feedback control circuit was quantified for the first time in humans. 88 …”

Section: Feedback Control Of Energy Intakementioning

confidence: 99%

“…88 The loss of glucose calories occurred without the subjects being directly aware of the calorie deficit and resulted in gradual weight loss. The subjects were found to progressively increase average energy intake by about 100 kcal/d per kilogram of lost weight – an effect more than 3-fold larger than the corresponding energy expenditure adaptations to weight loss.…”

Section: Feedback Control Of Energy Intakementioning

confidence: 99%

Obesity Energetics: Body Weight Regulation and the Effects of Diet Composition

2017

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Weight changes are accompanied by imbalances between calorie intake and expenditure. This fact is often misinterpreted to suggest that obesity is caused by gluttony and sloth and can be treated by simply advising people to eat less and move more. However, various components of energy balance are dynamically interrelated and weight loss is resisted by counterbalancing physiological processes. While low-carbohydrate diets have been suggested to partially subvert these processes by increasing energy expenditure and promoting fat loss, our meta-analysis of 32 controlled feeding studies with isocaloric substitution of carbohydrate for fat found that both energy expenditure (26 kcal/d; P <.0001) and fat loss (16 g/d; P <.0001) were greater with lower fat diets. We review the components of energy balance and the mechanisms acting to resist weight loss in the context of static, settling point, and set-point models of body weight regulation, with the set-point model being most commensurate with current data.

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“…At the same time there will be a small decrease in energy expenditure associated with the loss of body weight. Together, all else being equal, these effects will cause weight settle (plateau) at a new lower level (11,12,13,14) . How much lower will depend on the extent of the initial reduction in energy intake achieved by use of LCS.…”

Section: Energy Balancing and The Potential Usefulness Of Consuming Smentioning

confidence: 99%

The role of low-calorie sweeteners in the prevention and management of overweight and obesity: evidence v. conjecture

Rogers

2017

Proc. Nutr. Soc.

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By virtue of reducing dietary energy density, low-calorie sweeteners (LCS) can be expected to decrease overall energy intake and thereby decrease body weight. Such effects will be limited by the amount of sugar replaced by LCS, and the dynamics of appetite and weight control (e.g., acute compensatory eating, and an increase in appetite and decrease in energy expenditure accompanying weight loss). Consistent with these predictions, short-term intervention studies show incomplete compensation for the consumption of LCS v. sugar, and longer-term intervention studies (from 4 weeks to 40 months duration) show small decreases in energy intake and body weight with LCS v. sugar. Despite this evidence, there are claims that LCS undermine weight management. Three claims are that: (1) LCS disrupt the learned control of energy intake (sweet taste confusion hypothesis); (2) exposure to sweetness increases desire for sweetness (sweet tooth hypothesis); (3) consumers might consciously overcompensate for ‘calories saved’ when they know they are consuming LCS (conscious overcompensation hypothesis). None of these claims stands up to close examination. In any case, the results of the intervention studies comparing LCS v. sugar indicate that the effect of energy dilution outweighs any tendency LCS might conceivably have to increase energy intake.

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How Strongly Does Appetite Counter Weight Loss? Quantification of the Feedback Control of Human Energy Intake

Cited by 164 publications

References 44 publications

The evolution of body fatness: trading off disease and predation risk

The evolution of body fatness: trading off disease and predation risk

Obesity Energetics: Body Weight Regulation and the Effects of Diet Composition

The role of low-calorie sweeteners in the prevention and management of overweight and obesity: evidence v. conjecture

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