Nutrition Support To Patients Undergoing Gastrointestinal Surgery

Abstract

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.

No Effect of Energy Intake Overall on Risk of Endometrial Cancers: a Meta-analysis

“…Subsequently, numerous studies have consistently demonstrated that energy restriction could inhibit the development of a variety of spontaneous and induced tumors in rats and mice as well as non-human primates (Hursting et al, 2003;Zhu et al, 2003;Hursting et al, 2010;Klement et al, 2011). The essential biological rationale for anti-cancer effect of energy restriction would be endocrine regulation of cancer by insulin-like signals, which in turn may repress cell proliferation, disturb cell cycle, induce apoptosis and impair neovasculation of tumor tissue (Jiang et al, 2002;Zhu et al, 2003).…”

An Evolutionary and Mechanistic Perspective on Dietary Carbohydrate Restriction in Cancer Prevention

“…As a result, 'calorie restriction' remains popular among approaches to cancer control [129]. We therefore re-emphasize that the insulin/IGF-1 pathway is activated principally by dietary consumption of CHO, and glucose is most often the preferred energy substrate for cancer cells due to metabolic dysfunction, as described above [90,130,10]. Protein consumption also stimulates this pathway albeit to a lesser extent than glucose in humans [20].…”

“…Studies of CR in humans have generally addressed cancer treatment [6][7][8][9] but, most recently, carbohydrate-restricted diets, ketogenic diets, and so-called paleo diets which have de facto reduction of carbohydrate (CHO) as a common feature, have shown much promise for prevention [10]. It is understood, however that the discussion has outstripped both understanding of underlying mechanisms and the limited experimental support [11].…”

A Review of Cancer Immunotherapy and Nutritional Therapies

“…Cruciferous vegetables, such as broccoli, Brussels sprouts and cauliflower, are rich in powerful glucosinolates, which break down to form isothiocyanates that can cause cancer cells to commit suicide [14].…”