Table 1.
Impact of diverse diets on CRC risk and ISC biology
| Diet | CRC risk | Effects on ISCs |
|---|---|---|
| Calorie restriction | Decreased in humans and animal models (45–47, 52, 53) | Increased ISC number allows outcompeting of mutant ISCs (59) |
| Fasting | Fasting phase: decreased (54, 62) Refeeding: unknown, potentially increased (66) |
Fasting phase: lower cellular proliferation (61) Refeeding phase: increased proliferation (54, 56–58) |
| Vitamin D | Decreased in humans and animal models (67–72) | Enhances expression of stemness genes and reduces proliferation (74) |
| Vitamin C | Unknown (75–77) | Unknown |
| Fructose | Increased in animal models and some epidemiological associations (79, 81, 82) | Fuels aerobic glycolysis and increases de novo fatty acid synthesis (80) |
| HFD-induced obesity | Increased in animal models (32, 33, 92, 93) Obesity increases CRC risk in humans (44, 86) No effect was observed for HFD, without overeating, on CRC risk in humans (28) |
Increased proliferation and tumorigenicity (32, 33, 92, 93) Decreased MHC-II expression (34) |
| Carbohydrate-rich diet | Unknown | Unknown |
| Ketone bodies | Unknown in humans Decreased in animal models (103, 105) |
Enhanced NOTCH activity, ISC self-renewal, postinjury regeneration, and decreased secretory cell differentiation (104) Decreased proliferation (105) |
| Weight loss | Decreased (106–111) | Unknown |
Abbreviations: CRC, colorectal cancer; HFD, high-fat diet; ISC, intestinal stem cell; MHC-II, major histocompatibility complex class II.