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

Lee, C; Longo, Valter D.

doi:10.1038/onc.2011.91

Cited by 272 publications

(240 citation statements)

References 173 publications

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“…Different variants of intermittent energy restriction (CR for intermittent periods of time) have been reported to have health‐promoting effects. These beneficial health effects include improvements of body composition 12, 13, 14, skin wound healing 9, blood pressure and cardiovascular health markers 15, 16, neurological health and cognitive performance 17, 18, 19 and retarded tumor growth/formation 20, 21, 22, 23. By applying repetitive cycles of fasting/CR and regular eating, the negative side effects of CR are thought to be circumvented.…”

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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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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show abstract

“…4,5 Under conditions of caloric restriction, a state of reduced nutrient availability without causing malnutrition, TORC1 function is down-regulated causing decreased protein translation and increased autophagy. [6][7][8] At the cellular level, decreased availability of critical molecules, such as essential amino acids, 9,10 also leads to inhibition of TORC1 function, decreased rates of protein translation and increased autophagy. The inhibition of TORC1 function has been documented to significantly increase lifespan in a number of model organisms and non-human primates, as well as significantly reducing the development of age-related pathologies, such as cardiovascular disease, diabetes and cancer.…”

Section: Introductionmentioning

confidence: 99%

“…The inhibition of TORC1 function has been documented to significantly increase lifespan in a number of model organisms and non-human primates, as well as significantly reducing the development of age-related pathologies, such as cardiovascular disease, diabetes and cancer. 6,[11][12][13] Based on these observations, disruption of TOR signaling and function could be a viable strategy for increasing health and promoting healthier aging.…”

Section: Introductionmentioning

confidence: 99%

Rapamycin reduces fibroblast proliferation without causing quiescence and induces STAT5A/B-mediated cytokine production

Gillespie

MacKay

Sander

et al. 2015

Nucleus

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“…This highlights the link between the metabolic syndrome and cancer on the one hand and cancer and lifestyle factors like nutrition on the other. As indicated in Figure 2, restriction of dietary CHOs would counteract this signalling cascade by normalizing glucose and insulin levels in subjects with metabolic syndrome, in this way acting similar to calorie restriction/fasting [61,62]. Indeed, it has been shown in healthy subjects that CHO restriction induces hormonal and metabolic adaptions very similar to fasting [63][64][65][66].…”

Section: The Impact Of Insulin and Igf1mentioning

confidence: 99%

Nutrition Support To Patients Undergoing Gastrointestinal Surgery

Coles¹

2013

Clinical Nutrition

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Over the last years, evidence has accumulated suggesting that by systematically reducing the amount of dietary carbohydrates (CHOs) one could suppress, or at least delay, the emergence of cancer, and that proliferation of already existing tumor cells could be slowed down. This hypothesis is supported by the association between modern chronic diseases like the metabolic syndrome and the risk of developing or dying from cancer. CHOs or glucose, to which more complex carbohydrates are ultimately digested, can have direct and indirect effects on tumor cell proliferation: first, contrary to normal cells, most malignant cells depend on steady glucose availability in the blood for their energy and biomass generating demands and are not able to metabolize significant amounts of fatty acids or ketone bodies due to mitochondrial dysfunction. Second, high insulin and insulin-like growth factor (IGF)-1 levels resulting from chronic ingestion of CHO-rich Western diet meals, can directly promote tumor cell proliferation via the insulin/IGF1 signaling pathway. Third, ketone bodies that are elevated when insulin and blood glucose levels are low, have been found to negatively affect proliferation of different malignant cells in vitro or not to be usable by tumor cells for metabolic demands, and a multitude of mouse models have shown antitumorigenic properties of very low CHO ketogenic diets. In addition, many cancer patients exhibit an altered glucose metabolism characterized by insulin resistance and may profit from an increased protein and fat intake. In this review, we address the possible beneficial effects of low CHO diets on cancer prevention and treatment. Emphasis will be placed on the role of insulin and IGF1 signaling in tumorigenesis as well as altered dietary needs of cancer patients.

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

Cited by 272 publications

References 173 publications

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

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

Rapamycin reduces fibroblast proliferation without causing quiescence and induces STAT5A/B-mediated cytokine production

Nutrition Support To Patients Undergoing Gastrointestinal Surgery

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