Calorie Restriction, Aging, and Cancer Prevention: Mechanisms of Action and Applicability to Humans

Hursting, Stephen D.; Lavigne, Jackie A.; Berrigan, David; Perkins, Susan N.; Barrett, J. Carl

doi:10.1146/annurev.med.54.101601.152156

Cited by 508 publications

(406 citation statements)

References 96 publications

Supporting

Mentioning

388

Contrasting

Unclassified

Order By: Relevance

“…While being difficult to practice, this approach has a lot of scientific merit for being able to extend average life spans of many species of animals including rats, mice, fish, and possibly primates (currently being tested). Along with this life span extension is a reduction in chronic diseases that are common to mankind, reviewed in Hursting et al [6]. A recent meta-analysis of 14 experimental studies found that energy restriction resulted in a 55% reduction in spontaneous tumors in laboratory mice [7].…”

Section: Reviewmentioning

confidence: 99%

Nutrition and cancer: A review of the evidence for an anti-cancer diet

Donaldson¹

2004

Nutr J

564

344

View full text Add to dashboard Cite

It has been estimated that 30–40 percent of all cancers can be prevented by lifestyle and dietary measures alone. Obesity, nutrient sparse foods such as concentrated sugars and refined flour products that contribute to impaired glucose metabolism (which leads to diabetes), low fiber intake, consumption of red meat, and imbalance of omega 3 and omega 6 fats all contribute to excess cancer risk. Intake of flax seed, especially its lignan fraction, and abundant portions of fruits and vegetables will lower cancer risk. Allium and cruciferous vegetables are especially beneficial, with broccoli sprouts being the densest source of sulforophane. Protective elements in a cancer prevention diet include selenium, folic acid, vitamin B-12, vitamin D, chlorophyll, and antioxidants such as the carotenoids (α-carotene, β-carotene, lycopene, lutein, cryptoxanthin). Ascorbic acid has limited benefits orally, but could be very beneficial intravenously. Supplementary use of oral digestive enzymes and probiotics also has merit as anticancer dietary measures. When a diet is compiled according to the guidelines here it is likely that there would be at least a 60–70 percent decrease in breast, colorectal, and prostate cancers, and even a 40–50 percent decrease in lung cancer, along with similar reductions in cancers at other sites. Such a diet would be conducive to preventing cancer and would favor recovery from cancer as well.

show abstract

Section: Reviewmentioning

confidence: 99%

Nutrition and cancer: A review of the evidence for an anti-cancer diet

Donaldson¹

2004

Nutr J

564

344

View full text Add to dashboard Cite

show abstract

“…leads to the production of reactive oxygen species (ROS). ROS are involved in a variety of biological phenomena, such as mutation, carcinogenesis and aging (1,2). In the multistage carcinogenesis model, ROS are associated not only with initiation, but also with promotion and progression.…”

Section: Introductionmentioning

confidence: 99%

Sequence-specific DNA damage by reactive oxygen species: Implications for carcinogenesis and aging

Oikawa

2005

Environ Health Prev Med

View full text Add to dashboard Cite

Reactive oxygen species (ROS) generated by environmental chemicals can cause sequence-specific DNA damage, which may lead to carcinogenesis and aging. We investigated the mechanism of DNA damage by environmental chemicals (catechol, propyl gallate and bisphenol-A), homocysteine and UVA radiation using human cultured cell lines and 32 P-labeled DNA fragments. Carcinogenic catechol induced piperidine-labile sites frequently at thymine residues in the presence of Cu(II) and NADH. Furthermore, catechol increased the formation of 8-oxo-7,8-dihydro-2'-deoxyguanosine (8-oxodG), a characteristic oxidative DNA lesion, in human leukemia cell line HL-60, but not in HP100, a hydrogen peroxide (H 2 O 2 )-resistant cell line derived from HL-60. Thus, it is concluded that oxidative DNA damage through generation of H 2 O 2 plays an important role in the carcinogenic process of catechol. In addition, an environmental factor, bisphenol-A, and a dietary factor, propyl gallate, also induced sequence-specific DNA damage via ROS generation.UVA, as well as UVB, contributes to photoaging. In humans, telomere shortening is believed to be associated with cell senescence. In this study, we investigated the shortening rate of telomeres in human WI-38 fibroblasts exposed to UVA irradiation. The telomere length (as measured by terminal restriction fragment length) in WI-38 fibroblasts irradiated with UVA decreased with increasing the irradiation dose. UVA irradiation with riboflavin caused damage specifically at the GGG sequence in the DNA fragments containing telomere sequence (TTAGGG) 4 . We concluded that the GGG-specific damage in telomere sequence induced by UVA irradiation participates in the increase of the telomere shortening rate.In this report, we show our experimental results and discuss the mechanisms of sequence-specific DNA damage in relation to carcinogenesis and aging.

show abstract

“…Moreover, tumor development and size is increased after subcutaneous injection of CRC cells in obese compared to non-obese mice (32). By contrast, animal studies have demonstrated that calorie restriction strongly inhibits cancer and slows tumor growth (33). In particular, calorie restriction inhibits spontaneous, transplanted, and carcinogen-induced colon cancer in mice and rats (34)(35)(36).…”

Section: Obesity and Colorectal Cancer Riskmentioning

confidence: 99%

Translational approaches to addressing complex genetic pathways in colorectal cancer

Early

Fontana

Davidson

2008

Translational Research

View full text Add to dashboard Cite

Colorectal cancer (CRC) is among the most prevalent cancers worldwide and represents a major public health challenge in the developed world. From the perspective of translational investigation, scientists have enormous opportunity to elucidate the molecular genetic mechanisms contributing to CRC pathogenesis since the majority of cancers arise from adenomatous precursor lesions. The process of adenoma growth and transformation is accompanied by cumulative mutations in dominant genetic pathways that confer a growth advantage. While this developmental process permits interrogation of informative pathways prior to the development of cancer, only a minority of adenomas progress to CRC. Accordingly, a major challenge for clinical translational investigators is to identify the molecular signatures that indicate increased likelihood for adenoma progression. By corollary, these molecular signatures include mutations in high penetrance alleles, including the Adenomatous Polyposis Coli (APC) gene as well as other alleles in the Wnt/β-catenin signaling pathway that specify increased genetic susceptibility to CRC. Interactions between these high penetrance alleles and other modifier genes as well as with environmental factors are of particular importance in understanding the complex network of events leading to CRC. This brief review will highlight three areas where important questions concerning genetic and environmental risk factors have fueled translational investigation into possible pathways leading to CRC.There have been substantial advances in the last two decades in our understanding of the molecular pathways that lead to colorectal cancer (CRC), the results of research that demonstrated the role of mutational activation of oncogenes coupled with loss of function of tumor suppressor genes in a model that advanced the concept of finite, but cumulative mutational events (summarized in (1)). These studies in preclinical, animal models as well as cell-based models, clinical observational and randomized studies in humans have led to a more complete understanding of the role of both environmental and genetic factors in CRC pathogenesis.One tangible result of this expanded scientific foundation is an emerging consensus that familial or inherited factors play an increasingly relevant role in our approach to patients with CRC(2). Examples of dominant genetic pathways include those governed by Adenomatous Polyposis Coli (APC) tumor suppressor gene, and also the microsatellite instability pathway 4 To whom communication should be directed

show abstract

Calorie Restriction, Aging, and Cancer Prevention: Mechanisms of Action and Applicability to Humans

Cited by 508 publications

References 96 publications

Nutrition and cancer: A review of the evidence for an anti-cancer diet

Nutrition and cancer: A review of the evidence for an anti-cancer diet

Sequence-specific DNA damage by reactive oxygen species: Implications for carcinogenesis and aging

Translational approaches to addressing complex genetic pathways in colorectal cancer

Contact Info

Product

Resources

About