Calorie restriction and susceptibility to intact pathogens

Kristan, Deborah M.

doi:10.1007/s11357-008-9056-1

Cited by 67 publications

(48 citation statements)

References 74 publications

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“…As previously noted, most people dying in modern famines die not because they run out of energy but because they have weakened immune systems that make them susceptible to disease (Speakman, 2006). Moreover, small mammals under caloric restriction show increased susceptibility to nematode infections and reduced ability to clear infections (Kristan, 2007(Kristan, , 2008.…”

Section: Dual-intervention Point Model and 'Drifty Gene' Hypothesismentioning

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: Dual-intervention Point Model and 'Drifty Gene' Hypothesismentioning

confidence: 99%

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

Speakman

2018

Journal of Experimental Biology

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“…Although weight loss and cachexia in the early stages of cancer progression are not as common as thought (Tisdale, 2002;Fearon et al, 2003;Fox et al, 2009), the B15% loss of body mass index caused by a moderate (20%) calorie restriction (Racette et al, 2006) would prevent its use in the great majority of cancer treatment scenarios. In addition, the effect of long-term restriction in delaying wound healing and impairing immune function Kristan, 2008;Reed et al, 1996) may impose a significant risk to cancer patients receiving chemotherapy, surgery or immunity-based treatments (Kim and Demetri, 1996).…”

Section: Dr and Cancer Treatmentmentioning

confidence: 99%

Fasting vs dietary restriction in cellular protection and cancer treatment: from model organisms to patients

2011

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“…Severe food restriction is very arduous and too difficult to practice and to sustain for most individuals. Importantly, long‐term exposure to a CR diet might also cause substantial side effects like amenorrhoea, osteoporosis, decreased fertility, and libido, impaired wound healing and increased susceptibility to infections 8, 9, 10, 11. Different variants of intermittent energy restriction (CR for intermittent periods of time) have been reported to have health‐promoting effects.…”

Section: Introductionmentioning

confidence: 99%

Intermittent calorie restriction largely counteracts the adverse health effects of a moderate‐fat diet in aging C57BL/6J mice

Lute

Boekschoten

Dijk

et al. 2017

Molecular Nutrition Food Res

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ScopeCalorie restriction (CR) has been shown to extend life‐ and health‐span in model species. For most humans, a life‐long CR diet is too arduous to adhere to. The aim of this study was to explore whether weekly intermittent CR can (1) provide long‐term beneficial effects and (2) counteract diet‐induced obesity in male aging mice.Methods and resultsIn this study, we have exposed C57Bl/6J mice for 24 months to an intermittent (INT) diet, alternating weekly between CR of a control diet and ad libitum moderate‐fat (MF) feeding. This weekly intermittent CR significantly counteracted the adverse effects of the MF diet on mortality, body weight, and liver health markers in 24‐month‐old male mice. Hepatic gene expression profiles of INT‐exposed animals appeared much more comparable to CR‐ than to MF‐exposed mice. At 12 months of age, a subgroup of MF‐exposed mice was transferred to the INT diet. Gene expression profiles in the liver of the 24‐month‐old diet switch mice were highly similar to the INT‐exposed mice. However, a small subset of genes was consistently changed by the MF diet during the first phase of life.ConclusionWeekly intermittent CR largely, but not completely, reversed adverse effects caused by a MF diet.

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Calorie restriction and susceptibility to intact pathogens

Cited by 67 publications

References 74 publications

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

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

Fasting vs dietary restriction in cellular protection and cancer treatment: from model organisms to patients

Intermittent calorie restriction largely counteracts the adverse health effects of a moderate‐fat diet in aging C57BL/6J mice

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