UC (ulcerative colitis) patients have an increased risk of developing colorectal cancer compared with the normal population. The cause underlying this higher risk is not fully defined but includes nutritional and environmental factors concomitant with genetic alterations. We aimed to evaluate genetic stability in the colonic tissue of UC patients in clinical remission compared with the healthy population, and to establish a possible correlation between nutritional habits and these molecular assessments. UC patients (n 42) and healthy controls (n 37) participated in the study. All participants were histopathologically and medically diagnosed. Participants completed five separate 7 d dietary records, food-frequency questionnaires and validated 24 h recalls for nutritional assessment. The extent of chromosome 17 loss and the calculated chromosome index was determined in colon tissue biopsies by fluorescence in situ hybridisation. Correlations between the molecular and nutritional assessments were performed using Pearson's correlation coefficients. Significant differences in the nutritional intake of total fat (65 (SD 15) v. 89 (SD 25) g), cholesterol (330 (SD 168) v. 464 (SD 177) mg), dietary fibre (32 (SD 4.7) v. 9 (SD 4) g), vitamin A (1009 (SD 209) v. 506 (SD 204) μg), vitamin C (308 (SD 108) v. 72 (SD 53) mg) and folic acid (412 (SD 89 μg) v. 187 (SD 107)) were recorded for UC patients compared with controls. Significant correlations were found for the consumption of different food groups and the chromosome index for chromosome 17. The results of our study suggest that the nutritional habits adopted by UC patients during clinical remission may affect key cellular components of the colonic tissue, inducing a high degree of aneuploidy and genetic instability, and probably affecting the development of colon cancer.
- Fluorescence in situ hybridization
- Inflammatory bowel disease
- Nutritional habits
- Ulcerative colitis