Childhood Energy Intake and Cancer Mortality in Adulthood (original) (raw)
Related papers
European Journal of Cancer Prevention, 1999
Energy balance results from the exact equilibrium between caloric intake and caloric expenditure. A caloric intake larger than caloric expenditure results in overweight, even obesity, but other determinants, like hormonal dysfunction and/or genetic traits may play a part in obesity syndrome. Obesity, and even overweight, have been recognized as risk factors for the development of cancers. Human epidemiological studies, which have tended to establish the nature of the relationship between energy balance and cancer, are summarized first, with the influence of the various factors which act both on obesity and on cancer risk. Among these factors are the macronutrients responsible for the caloric intake, and some lifestyle factors (physical activity, drinking habits and tobacco use). Second, the animal studies help to distinguish between different relevant factors, and to understand some of the underlying mechanisms. However, the insulin-resistance syndrome, which appears to underlie the relationship between obesity and hormone-dependent cancers, and possibly colon cancer, is only relevant to human physiology because hormonal alterations are part of it. Prevention of hyperinsulinemia, insulin resistance and the accompanying visceral obesity appears to be a major public health task for the prevention of cancers.
Cancer and Energy Balance, Epidemiology and Overview
2010
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Effects of Energy Balance on Cancer in Genetically Altered Mice
The Journal of Nutrition, 2004
Evidence has accumulated from laboratory-based animal experiments and population-based human epidemiological studies that lifestyle factors that affect energy balance, such as caloric intake, nutritional status, and exercise, act in concert with genetic susceptibility to influence cancer development and progression. The use of animal models with specific genetic alterations, in combination with lifestyle modifications that alter overall energy balance, has contributed to a greater understanding of the mechanistic changes occurring during carcinogenesis and to the identification of points of intervention. Studies in our laboratory focusing on the role of energy balance and genetic susceptibility in mice deficient in one (ϩ/Ϫ) or both (Ϫ/Ϫ) alleles of the p53 tumor suppressor gene and mice with a mutant APC allele (APC Min) showed that calorie restriction decreases tumor burden, increases tumor latency, and decreases serum insulin-like growth factor (IGF)-1 and leptin levels. Data from our studies, combined with results from other animal and human studies, have established a role for IGF-1 in carcinogenesis. Studies using genetic models of cancer that have been interbred with mice with abnormal levels of IGF-1 will enable the examination of combined effects of energy balance and genetic alterations on the cancer process. Models that integrate lifestyle and genetic effects in a single system provide a physiologically intact system in which combination interventions and therapies for cancer prevention can be tested and validated, thus building a strong preclinical foundation that will inform the development of clinical trials and add perspective to epidemiological studies. J. Nutr. 134: 3394S-3398S, 2004. KEY WORDS: • energy balance • diet • nutrition • chemoprevention • transgenic • calorie restriction • insulin-like growth factor-1 • leptin Energy balance and lifestyle factors Energy balance, referring to a balance between caloric intake and expenditure, has received growing attention in the lay and scientific communities, given the role of overnutrition
Scientific Reports, 2016
Both chronic calorie restriction (CCR) and intermittent calorie restriction (ICR) have shown anticancer effects. However, the direct evidence comparing ICR to CCR with respect to cancer prevention is controversial and inconclusive. PubMed and Web of Science were searched on November 25, 2015. The relative risk (RR) [95% confidence interval (CI)] was calculated for tumor incidence, and the standardised mean difference (95% CI) was computed for levels of serum insulin-like growth factor-1 (IGF-1), leptin, and adiponectin using a random-effects meta-analysis. Sixteen studies were identified, including 11 using genetically engineered mouse models (908 animals with 38-76 weeks of follow-up) and 5 using chemically induced rat models (379 animals with 7-18 weeks of follow-up). Compared to CCR, ICR decreased tumor incidence in genetically engineered models (RR = 0.57; 95% CI: 0.37, 0.88) but increased the risk in chemically induced models (RR = 1.53, 95% CI: 1.13, 2.06). It appears that ICR decreases IGF-1 and leptin and increases adiponectin in genetically engineered models. Thus, the evidence suggests that ICR exerts greater anticancer effect in genetically engineered mouse models but weaker cancer prevention benefit in chemically induced rat models as compared to CCR. Further studies are warranted to confirm our findings and elucidate the mechanisms responsible for these effects. Cancer is, to some extent, a preventable disease that is presumably caused by a combination of genetic, environmental, and behavioural factors 1. Several reviews have discussed how diet and nutrition contribute to human cancer risk 2-6 by affecting the initiation, promotion and progression of cancers 7-9. Two main types of dietary restriction are chronic calorie restriction (CCR) and intermittent calorie restriction (ICR) (e.g., intermittent fasting, alternate-day fasting, or routine periodic fasting) 10-13. Two population-based studies have found a linear and inverse association between CCR and breast cancer risk 14,15. However, because CCR requires constant food restriction, the tolerance and compliance for fasting is unsatisfactory; therefore, the effect of CCR might not be as good as expected. Researchers have been looking for more feasible styles of calorie restriction (CR) with comparable or even superior results. Currently, ICR regimens have been found to be equivalent to, if not better than, CCR for weight loss, providing an alternative approach for weight loss that might be better suited to some individuals 16. Several population studies have shown that ICR can improve indicators of chronic diseases (e.g., insulin sensitivity, high density lipoprotein cholesterol and fat oxidation) 17-19. The question of whether ICR show better tumor inhibitory effects than CCR remains unanswered. Unfortunately, most research focuses on animal models. There is little evidence from human studies.
Transient caloric restriction and cancer risk (The Netherlands)
Cancer Causes & Control, 2007
Over the past century, many animal experiments have shown that caloric restriction can reduce the risk of cancer, a finding that proved to be highly reproducible. Many papers have been published on its potential for human health, but until know little evidence is available on its actual effects in humans. In Utrecht, The Netherlands, we have been investigating the effects of the 1944-1945 Dutch famine on breast cancer risk factors and breast cancer risk, and paradoxically the relatively short-term famine seemed to be related to increased breast cancer risk in later life. One of the differences between the famine situation and the large body of evidence from animal experiments is the duration of caloric restriction. Almost all animal experiments investigated sustained caloric restriction and information on the effects of short-term transient caloric restriction is very scarce. A search in the literature identified some animal experiments on shortterm transient caloric restriction and these seemed to be at least supportive to the famine findings. Because caloric restriction in humans for preventive health measures would be mostly short-term, it is important to extend animal research on short-term caloric restriction.
Lipids, 1986
The experiments reported are part of our effort to dissociate the tumor-enhancing effects of dietary fat and high caloric intake. Rats either were fed ad libitum diets containing 4% corn oil or their calories were restricted by 40% and their diets contained 13.1% corn oil. Incidence of 7,12-dimethylbenz(a)anthracene {DMBAHnduced mammary tumors was 80% in rats fed ad libitum and 20% in those fed the calorie-restricted diets. Incidence of 1,2-dimethylhydrazine (DMH)oinduced colon tumors was 100% in rats fed ad libitum and 53% in those whose caloric intake was restricted by 40%. The tumor yield {tumors per tumor-bearing rat) was significantly lower in rats on caloric restriction. In another series, rats were fed diets containing 5, 15 or 20% corn oil ad libitum or were fed calorie-restricted (by 25%} diets which provided 20 or 26.6% corn oil (therefore, the same absolute amount of fat was consumed in each of the pair-fed groups). Tumor incidence and tumor yield in the two calorie-restricted groups were similar to those seen in the rats fed 5% fat ad libitum; tumor burden {total g of tumor) was 45-65% lower in the calorie-restricted rats. The data suggest that caloric intake is a more stringent determinant of tumor growth than fat intake. 272-274 (1986).
European Journal of Clinical Nutrition, 2009
Objectives: To describe energy intake and its macronutrient and food sources among 27 regions in 10 countries participating in the European Prospective Investigation into Cancer and Nutrition (EPIC) study. Methods: Between 1995 and 2000, 36 034 subjects aged 35-74 years were administered a standardized 24-h dietary recall. Intakes of macronutrients (g/day) and energy (kcal/day) were estimated using standardized national nutrient databases. Mean Guarantor: MC Ocké. Contributors: MO carried out statistical analysis, prepared tables and figures and wrote the paper, taking into account comments from all co-authors. NS was the overall coordinator of this project and of the EPIC nutritional databases (ENDB) project. MO, NS, NL, SG, SB, PF, SS, VB, JL and EW were members of the writing group and gave input on statistical analysis, drafting of the paper and interpretation of results. The other co-authors were local EPIC collaborators involved in the collection of data, and in documenting, compiling and evaluating the subset of their national nutrient databases used in the ENDB. ER is the overall coordinator of the EPIC study. All co-authors provided comments and suggestions on the paper and approved the final version.
Energy and caloric restriction, and fasting and cancer: a narrative review
Supportive Care in Cancer, 2020
Dietary interventions have a significant impact on body metabolism. The sensitivity of cancer cells to nutrient and energy deficiency is an evolving characteristic of cancer biology. Preclinical studies provided robust evidence that energy and caloric restrictions could hinder both cancer growth and progression, besides enhancing the efficacy of chemotherapy and radiation therapy. Moreover, several, albeit low-powered, clinical trials have demonstrated clinical benefits in cancer patients. Future research will inform and firmly establish the potential efficacy and safety of these dietary interventions. Here, we review the current evidence and ongoing research investigating the relationship between various dietary restriction approaches and cancer outcomes.
Energy Balance and Carcinogenesis: Underlying Pathways and Targets for Intervention
Current Cancer Drug Targets, 2007
The prevalence of obesity, an established epidemiologic risk factor for many cancers, has risen steadily for the past several decades in the U.S. Particularly alarming are the increasing rates of obesity among children, portending continuing increases in the rates of obesity and obesity-related cancers for many years to come. Unfortunately, the mechanisms underlying the association between obesity and cancer are not well understood. In particular, the effects and mechanistic targets of interventions that modulate energy balance, such as reduced calorie diets and physical activity, on the carcinogenesis process have not been well characterized. The purpose of this review is to provide a strong foundation for future mechanistic-based research in this area by describing key animal and human studies of energy balance modulations involving diet, exercise, or pharmaceutical agents and by focusing on the interrelated pathways affected by alterations in energy balance. Particular attention in this review is placed on the components of the insulin/IGF-1/Akt pathway, which has emerged as a predominant target for disrupting the obesity-cancer link. Also discussed is the promise of global approaches, including genomics, proteomics, and metabolomics, for the elucidation of energy balance-responsive pathways. The ultimate goal of this work is to provide the missing mechanistic information necessary to identify targets for the prevention and control of cancers related to or caused by excess body weight.