Jesca Gm Brouwer1, Maureen Makama1, Geertruida J van Woudenbergh1,2, Hans Fa Vasen3, Fokko M Nagengast4, Jan H Kleibeuker5, Ellen Kampman1, Fränzel Jb van Duijnhoven6. 1. Division of Human Nutrition, Wageningen University & Research, Wageningen, Netherlands. 2. Christelijke Hogeschool, Ede, Netherlands. 3. Netherlands Foundation for the Detection of Hereditary Tumors, Leiden, Netherlands. 4. Department of Gastroenterology, Radboud University Medical Center, Nijmegen, Netherlands; and. 5. Department of Gastroenterology and Hepatology, University of Groningen, University Medical Center Groningen, Groningen, Netherlands. 6. Division of Human Nutrition, Wageningen University & Research, Wageningen, Netherlands; franzel.vanduijnhoven@wur.nl.
Abstract
Background: Persons with Lynch syndrome (LS) have high lifetime risk of developing colorectal tumors (CRTs) because of a germline mutation in one of their mismatch repair (MMR) genes. An important process in the development of CRTs is inflammation, which has been shown to be modulated by diet.Objective: We aimed to investigate the association between the inflammatory potential of the diet and the risk of CRTs in persons with LS.Design: We used the dietary intake of 457 persons with LS from a prospective cohort study to calculate the adapted dietary inflammatory index (ADII). The ADII was split into tertiles in which the highest tertile reflects the most proinflammatory potential of the diet. Cox proportional hazard models, with robust sandwich variance estimates to adjust for dependency within families, were used to calculate HRs and 95% CIs of CRTs by ADII tertile. HRs were adjusted for age, smoking status, and education level, and number of colonoscopies as a time-dependent variable. A potential effect measure modification was explored by stratifying the results by mutated MMR gene, sex, and a history of CRTs. We performed sensitivity analyses by repeating the analyses in non-nonsteroidal anti-inflammatory drug (NSAID) users (n = 315). Results: During a median follow-up time of 59 mo, 200 participants (43.8%) developed CRTs. No significant association was shown between highest compared with lowest ADII tertiles (HR for highest compared with lowest tertiles: 1.37; 95% CI: 0.80, 2.34). Stratification by mutated MMR gene, sex, and CRT history did not show significantly differential associations (P-interactions ≥ 0.64). In non-NSAID users, an HR of 1.60 (95% CI: 0.88, 2.93) for highest compared with lowest tertiles was shown. No significant effect modification was shown in this group either (P-interactions ≥ 0.24). Conclusion: A proinflammatory potential of the diet does not seem to be significantly associated with CRT risk in persons with LS.
Background: Persons with Lynch syndrome (LS) have high lifetime risk of developing colorectal tumors (CRTs) because of a germline mutation in one of their mismatch repair (MMR) genes. An important process in the development of CRTs is inflammation, which has been shown to be modulated by diet.Objective: We aimed to investigate the association between the inflammatory potential of the diet and the risk of CRTs in persons with LS.Design: We used the dietary intake of 457 persons with LS from a prospective cohort study to calculate the adapted dietary inflammatory index (ADII). The ADII was split into tertiles in which the highest tertile reflects the most proinflammatory potential of the diet. Cox proportional hazard models, with robust sandwich variance estimates to adjust for dependency within families, were used to calculate HRs and 95% CIs of CRTs by ADII tertile. HRs were adjusted for age, smoking status, and education level, and number of colonoscopies as a time-dependent variable. A potential effect measure modification was explored by stratifying the results by mutated MMR gene, sex, and a history of CRTs. We performed sensitivity analyses by repeating the analyses in non-nonsteroidal anti-inflammatory drug (NSAID) users (n = 315). Results: During a median follow-up time of 59 mo, 200 participants (43.8%) developed CRTs. No significant association was shown between highest compared with lowest ADII tertiles (HR for highest compared with lowest tertiles: 1.37; 95% CI: 0.80, 2.34). Stratification by mutated MMR gene, sex, and CRT history did not show significantly differential associations (P-interactions ≥ 0.64). In non-NSAID users, an HR of 1.60 (95% CI: 0.88, 2.93) for highest compared with lowest tertiles was shown. No significant effect modification was shown in this group either (P-interactions ≥ 0.24). Conclusion: A proinflammatory potential of the diet does not seem to be significantly associated with CRT risk in persons with LS.
Authors: Catherine M Phillips; Ling-Wei Chen; Barbara Heude; Jonathan Y Bernard; Nicholas C Harvey; Liesbeth Duijts; Sara M Mensink-Bout; Kinga Polanska; Giulia Mancano; Matthew Suderman; Nitin Shivappa; James R Hébert Journal: Nutrients Date: 2019-08-12 Impact factor: 5.717
Authors: Fränzel J B van Duijnhoven; Jesca G M Brouwer; Geertruida J van Woudenbergh; Ellen Kampman; Edith J M Feskens Journal: Adv Nutr Date: 2020-01-01 Impact factor: 8.701
Authors: Sara Moazzen; Francisco O Cortes-Ibañez; Bert van der Vegt; Behrooz Z Alizadeh; Geertruida H de Bock Journal: Eur J Nutr Date: 2021-08-02 Impact factor: 5.614