Massive overfeeding and energy balance in men: the Guru Walla model

Pasquet, Patrick; Brigant, L; Froment, Anne; Koppert, G A; Bard, Denis; Garine, Igor de; Apfelbaum, M

doi:10.1093/ajcn/56.3.483

Cited by 85 publications

(63 citation statements)

References 35 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…Pasquet et al described the phenomenal positive energy balance occasionally achieved by members of the Massas population of Cameroon, when undergoing a seasonal 'fattening ceremony'. 68 By doubling habitual energy intake, Thrift: a guide to thrifty genes, thrifty phenotypes and thrifty norms JCK Wells men were able to increase body weight by 25% over 3 months, 70% of the weight gain comprising fat. Crosscultural studies have shown that Zulu men prefer fatter women in their native South Africa, but develop preferences for slimmer women if they move to the UK with greater energy availability.…”

Section: Culturally Transmitted Variability In Thriftmentioning

confidence: 99%

Thrift: a guide to thrifty genes, thrifty phenotypes and thrifty norms

Wells¹

2009

Int J Obes

View full text Add to dashboard Cite

There is a growing interest in evolutionary models of human adiposity. Frequent reference has been made to 'thrifty genes' or 'thrifty phenotypes', referring to a variety of metabolic or behavioural traits that in one or the other way imply frugality in the expenditure or storage of energy. However, there is confusion over how the strategy of thrift has been incorporated into human biology. At the broadest level, humans represent a thrifty species relative to other mammals, indicating that metabolic adaptations had a crucial role in the emergence of the Homo lineage, in particular in buffering reproduction from ecological stochasticity. In contemporary humans, some variability in adiposity may be attributable to genotypes systematically favoured in certain ecological settings. Genetic variability is also present within populations, and may be considered bet hedging (distributing risk across offspring to increase parental fitness). Bet hedging is an alternative to genetic drift for accounting for genetic variability in the absence of strong selective pressures. Contrasting with genetic variability emerging over the long-term, thrifty phenotypes represent a response to short-term ecological variability. Physiological plasticity allows the emergence of variability across the life course in response to ecological cues experienced directly or by very recent ancestors. Finally, cultural norms or individual preferences allow voluntary behavioural manipulation of thrift in individuals. Overall, there is a range of factors and processes both favouring and opposing thrifty genes, which may reflect moderate bet hedging rather than systematic adaptation. Plasticity protects the genome from selective pressures by tailoring the organism to ongoing ecological conditions. The fact that obesity can occur in different individuals through different genotypes, life histories and behaviours indicates that different treatments are also likely to be required.

show abstract

Section: Culturally Transmitted Variability In Thriftmentioning

confidence: 99%

Thrift: a guide to thrifty genes, thrifty phenotypes and thrifty norms

Wells¹

2009

Int J Obes

View full text Add to dashboard Cite

show abstract

“…This is assessed by using exogenous fatty acids labeled with C13 and integrated in the meal, and by measuring the C13 abundance in the expired air. [8][9][10] Since exogenous fat in the postprandial phase is mostly stored (in adipose tissue), the fraction oxidized is generally low, ranging from 10 to 20% of the exogenous fat intake, depending upon the conditions of measurements (duration) as well as the composition of the diet.…”

Section: àWhole Body Fat Oxidation ð1þmentioning

confidence: 99%

Concept of fat balance in human obesity revisited with particular reference to de novo lipogenesis

Schütz

2004

Int J Obes

View full text Add to dashboard Cite

The measurement of fat balance (fat input minus fat output) involves the accurate estimation of both metabolizable fat intake and total fat oxidation. This is possible mostly under laboratory conditions and not yet in free-living conditions. In the latter situation, net fat retention/mobilization can be estimated based on precise and accurate sequential body composition measurements. In case of positive balance, lipids stored in adipose tissue can originate from dietary (exogenous) lipids or from nonlipid precursors, mainly from carbohydrates (CHOs) but also from ethanol, through a process known as de novo lipogenesis (DNL). Basic equations are provided in this review to facilitate the interpretation of the different subcomponents of fat balance (endogenous vs exogenous) under different nutritional circumstances. One difficulty is methodological: total DNL is difficult to measure quantitatively in man; for example, indirect calorimetry only tracks net DNL, not total DNL. Although the numerous factors (mostly exogenous) influencing DNL have been studied, in particular the effect of CHO overfeeding, there is little information on the rate of DNL in habitual conditions of life, that is, large day-to-day fluctuations of CHO intakes, different types of CHO ingested with different glycemic indexes, alcohol combined with excess CHO intakes, etc. Three issues, which are still controversial today, will be addressed: (1) Is the increase of fat mass induced by CHO overfeeding explained by DNL only, or by decreased endogenous fat oxidation, or both? (2) Is DNL different in overweight and obese individuals as compared to their lean counterparts? (3) Does DNL occur both in the liver and in adipose tissue? Recent studies have demonstrated that acute CHO overfeeding influences adipose tissue lipogenic gene expression and that CHO may stimulate DNL in skeletal muscles, at least in vitro. The role of DNL and its importance in health and disease remain to be further clarified, in particular the putative effect of DNL on the control of energy intake and energy expenditure, as well as the occurrence of DNL in other tissues (such as in myocytes) in addition to hepatocytes and adipocytes.

show abstract

“…The only study in humans using this approach was the fascinating report of the`Guru Walla' overfeeding (Pasquet et al, 1992), a traditional fattening ritual in Cameroon wherein adolescent boys are deliberately overfed to an extraordinary degree. These young men ingest a high CHO diet (70%) containing 7000 kcalad; they gain 12 kg fat over 10 weeks while eating .…”

Section: Stoichiometry (Macronutrient Intake Vs Changes In Body Compomentioning

confidence: 99%

“…There have been no studies reported, to date, of even longer periods of CHO overfeeding at rates in excess of TEE (that is, comparable to the Guru Walla model, Pasquet et al, 1992) with direct measurement of liver or adipose tissue DNL.…”

Section: Dnl During Surplus Cho Dietsmentioning

confidence: 99%

De novo lipogenesis in humans: metabolic and regulatory aspects

1999

View full text Add to dashboard Cite

The enzymatic pathway for converting dietary carbohydrate (CHO) into fat, or de novo lipogenesis (DNL), is present in humans, whereas the capacity to convert fats into CHO does not exist. Here, the quantitative importance of DNL in humans is reviewed, focusing on the response to increased intake of dietary CHO. Eucaloric replacement of dietary fat by CHO does not induce hepatic DNL to any substantial degree. Similarly, addition of CHO to a mixed diet does not increase hepatic DNL to quantitatively important levels, as long as CHO energy intake remains less than total energy expenditure (TEE). Instead, dietary CHO replaces fat in the whole-body fuel mixture, even in the post-absorptive state. Body fat is thereby accrued, but the pathway of DNL is not traversed; instead, a coordinated set of metabolic adaptations, including resistance of hepatic glucose production to suppression by insulin, occurs that allows CHO oxidation to increase and match CHO intake. Only when CHO energy intake exceeds TEE does DNL in liver or adipose tissue contribute signi®cantly to the wholebody energy economy. It is concluded that DNL is not the pathway of ®rst resort for added dietary CHO, in humans. Under most dietary conditions, the two major macronutrient energy sources (CHO and fat) are therefore not interconvertible currencies; CHO and fat have independent, though interacting, economies and independent regulation. The metabolic mechanisms and physiologic implications of the functional block between CHO and fat in humans are discussed, but require further investigation. IntroductionIn this review, I will address the fate of surplus dietary carbohydrate (CHO) in humans. More speci®cally, the focus will be on conversion of CHO to fat, or de novo lipogenesis (DNL), with the question framed in quantitative terms: to what extent is surplus dietary CHO energy converted to fat? The various ways in which CHO content of the diet can be increased will be considered: increased CHO that replaces dietary fat (high-CHO low-fat, eucaloric diets); CHO added to a mixed diet, where CHO energy is less than total energy expenditure (TEE) but total energy intake exceeds TEE; and CHO consumption in excess of TEE. This review will therefore focus on the upper limits and consequences of increased CHO intake rather than on the lower limits and consequences of insuf®cient fat intake. Background and historical review

show abstract

Massive overfeeding and energy balance in men: the Guru Walla model

Cited by 85 publications

References 35 publications

Thrift: a guide to thrifty genes, thrifty phenotypes and thrifty norms

Thrift: a guide to thrifty genes, thrifty phenotypes and thrifty norms

Concept of fat balance in human obesity revisited with particular reference to de novo lipogenesis

De novo lipogenesis in humans: metabolic and regulatory aspects

Contact Info

Product

Resources

About